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Contents
Articles
Overview
Bipolar disorder 1 1 18 18 20 24 26 29 31 33 36 36 44 50 51 53 55 58 63 66 78 89 90 90 91 93 101 103 108 138 147
History
History of bipolar disorder Emil Kraepelin Karl Leonhard John Cade Mogens Schou Frederick K. Goodwin Kay Redfield Jamison
Symptoms
Hallucination Delusion Emotional dysregulation Anhedonia Dysphoria Suicidal ideation Sleep disorder Hypersomnia Insomnia Psychosis Racing thoughts
Bipolar spectrum
Bipolar spectrum Bipolar I Bipolar II Cyclothymia Dysthymia Major depressive disorder Schizoaffective disorder Mania
153 155 159 163 163 170 176 186 195 199 206 215 220 222 229 232 234 236 236 253 274 285 291 304 311 311 312 324 330 330 332
Treatment
Treatment of bipolar disorder Carbamazepine Gabapentin Lamotrigine Oxcarbazepine Topiramate Valproic acid Sodium valproate Valproate semisodium Lithium pharmacology Lithium carbonate Lithium citrate Lithium sulfate
Non-pharmaceutical treatment
Clinical psychology Electroconvulsive therapy Involuntary commitment Light therapy Psychotherapy Transcranial magnetic stimulation
Related subjects
Affective spectrum List of people with bipolar disorder Bipolar disorder in children
Organisations
International Society for Bipolar Disorders Icarus Project
References
Article Sources and Contributors Image Sources, Licenses and Contributors 335 343
Article Licenses
License 345
Overview
Bipolar disorder
Bipolar disorder
Classification and external resources ICD-10 ICD-9 OMIM DiseasesDB F31 [1] [2] , 296.1 [3] , 296.4 [10] [4] , 296.5 [5] , 296.6 [6] , 296.7 [7] , 296.8 [8]
296.0
125480 7812
[9]
309200
[11]
Bipolar disorder or bipolar affective disorder, historically known as manicdepressive disorder, is a psychiatric diagnosis that describes a category of mood disorders defined by the presence of one or more episodes of abnormally elevated energy levels, cognition, and mood with or without one or more depressive episodes. The elevated moods are clinically referred to as mania or, if milder, hypomania. Individuals who experience manic episodes also commonly experience depressive episodes, or symptoms, or a mixed state in which features of both mania and depression are present at the same time.[15] These events are usually separated by periods of "normal" mood; but, in some individuals, depression and mania may rapidly alternate, which is known as rapid cycling. Severe manic episodes can sometimes lead to such psychotic symptoms as delusions and hallucinations. The disorder has been subdivided into bipolarI, bipolarII, cyclothymia, and other types, based on the nature and severity of mood episodes experienced; the range is often described as the bipolar spectrum. Estimates of the lifetime prevalence of bipolar disorder vary, with studies typically giving values of the order of 1%, with higher figures given in studies with looser definitions of the condition.[16] The onset of full symptoms generally occurs in late adolescence or young adulthood. Diagnosis is based on the person's self-reported experiences, as well as observed behavior. Episodes of abnormality are associated with distress and disruption and an elevated risk of suicide, especially during depressive episodes. In some cases, it can be a devastating long-lasting disorder. In others, it has also been associated with creativity, goal striving, and positive achievements. There is significant evidence to suggest that many people with creative talents have also suffered from some form of bipolar disorder.[17] It is often suggested that creativity and bipolar disorder are linked. Genetic factors contribute substantially to the likelihood of developing bipolar disorder, and environmental factors are also implicated. Bipolar disorder is often treated with mood stabilizing medications and, sometimes, other psychiatric drugs. Psychotherapy also has a role, often when there has been some recovery of the subject's stability. In serious cases, in which there is a risk of harm to oneself or others, involuntary commitment may be used. These cases generally involve severe manic episodes with dangerous behavior or depressive episodes with suicidal ideation. There are widespread problems with social stigma, stereotypes, and prejudice against individuals with a diagnosis of bipolar disorder.[18] People with bipolar disorder exhibiting psychotic symptoms can sometimes be misdiagnosed as having schizophrenia, a serious mental illness.[19]
Bipolar disorder The current term bipolar disorder is of fairly recent origin and refers to the cycling between high and low episodes (poles). A relationship between mania and melancholia had long been observed, although the basis of the current conceptualisation can be traced back to French psychiatrists in the 1850s. The term "manic-depressive illness" or psychosis was coined by German psychiatrist Emil Kraepelin in the late nineteenth century, originally referring to all kinds of mood disorder. German psychiatrist Karl Leonhard split the classification again in 1957, employing the terms unipolar disorder (major depressive disorder) and bipolar disorder.
Depressive episode
Signs and symptoms of the depressive phase of bipolar disorder include persistent feelings of sadness, anxiety, guilt, anger, isolation, or hopelessness; disturbances in sleep and appetite; fatigue and loss of interest in usually enjoyable activities; problems concentrating; loneliness, self-loathing, apathy or indifference; depersonalization; loss of interest in sexual activity; shyness or social anxiety; irritability, chronic pain (with or without a known cause); lack of motivation; and morbid suicidal ideation.[21] In severe cases, the individual may become psychotic, a condition also known as severe bipolar depression with psychotic features. These symptoms include delusions or, less commonly, hallucinations, usually unpleasant.[22] A major depressive episode persists for at least two weeks, and may continue for over six months if left untreated.[23]
Manic episode
Mania is the signature characteristic of bipolar disorder and, depending on its severity, is how the disorder is classified. Mania is generally characterized by a distinct period of an elevated mood, which can take the form of euphoria. People commonly experience an increase in energy and a decreased need for sleep, with many often getting as little as 3 or 4 hours of sleep per night, while others can go days without sleeping.[24] A person may exhibit pressured speech, with thoughts experienced as racing.[25] Attention span is low, and a person in a manic state may be easily distracted. Judgment may become impaired, and sufferers may go on spending sprees or engage in behavior that is quite abnormal for them. They may indulge in substance abuse, particularly alcohol or other depressants, cocaine or other stimulants, or sleeping pills. Their behavior may become aggressive, intolerant, or intrusive. People may feel out of control or unstoppable, or as if they have been "chosen" and are "on a special mission" or have other grandiose or delusional ideas. Sexual drive may increase. At more extreme phases of bipolar I, a person in a manic state can begin to experience psychosis, or a break with reality, where thinking is affected along with mood.[26] Some people in a manic state experience severe anxiety and are very irritable (to the point of rage), while others are euphoric and grandiose. To be diagnosed with mania according to the Diagnostic and Statistical Manual of Mental Disorders (DSM), a person must experience this state of elevated or irritable mood, as well as other symptoms, for at least one week, less if hospitalization is required.[27]
Bipolar disorder Severity of manic symptoms can be measured by rating scales such as self-reported Altman Self-Rating Mania Scale[28] and clinician-based Young Mania Rating Scale.[29]
Hypomanic episode
Hypomania is generally a mild to moderate level of mania, characterized by optimism, pressure of speech and activity, and decreased need for sleep. Generally, hypomania does not inhibit functioning like mania.[30] Many people with hypomania are actually in fact more productive than usual, while manic individuals have difficulty completing tasks due to a shortened attention span. Some people have increased creativity while others demonstrate poor judgment and irritability. Many people experience signature hypersexuality. These persons generally have increased energy and tend to become more active than usual. They do not, however, have delusions or hallucinations. Hypomania can be difficult to diagnose because it may masquerade as mere happiness, though it carries the same risks as mania. Hypomania may feel good to the person who experiences it. Thus, even when family and friends learn to recognize the mood swings, the individual often will deny that anything is wrong.[31] Also, the individual may not be able to recall the events that took place while they were experiencing hypomania.[20] What might be called a "hypomanic event", if not accompanied by complementary depressive episodes ("downs", etc.), is not typically deemed as problematic: The "problem" arises when mood changes are uncontrollable and, more importantly, volatile or "mercurial". If unaccompanied by depressive counterpart episodes or otherwise general irritability, this behavior is typically called hyperthymia, or happiness, which is, of course, perfectly normal. Indeed, the most elementary definition of bipolar disorder is an often "violent" or "jarring" state of essentially uncontrollable oscillation between hyperthymia and dysthymia. If left untreated, an episode of hypomania can last anywhere from a few days to several years. Most commonly, symptoms continue for a few weeks to a few months.[32]
Associated features
Associated features are clinical phenomena that often accompany the disorder but are not part of the diagnostic criteria for the disorder. There are several childhood precursors in children who later receive a diagnosis of bipolar disorder. They may show subtle early traits such as mood abnormalities, full major depressive episodes, and ADHD.[35] BD is also accompanied by changes in cognitive processes and abilities. This include reduced attentional and executive capabilities and impaired memory. How the individual processes the world also depends on the phase of the disorder, with differential characteristics between the manic, hypomanic and depressive states.[36] Some studies have found a significant association between bipolar disorder and creativity.[37]
Causes
The causes of bipolar disorder likely vary between individuals. Twin studies have been limited by relatively small sample sizes but have indicated a substantial genetic contribution, as well as environmental influence. For bipolar I, the (probandwise) concordance rates in modern studies have been consistently put at around 40% in monozygotic twins (same genes), compared to 0 to 10% in dizygotic twins.[38] A combination of bipolar I, II and cyclothymia produced concordance rates of 42% vs 11%, with a relatively lower ratio for bipolar II that likely reflects
Bipolar disorder heterogeneity. The overall heritability of the bipolar spectrum has been put at 0.71.[39] There is overlap with unipolar depression and if this is also counted in the co-twin the concordance with bipolar disorder rises to 67% in monozigotic twins and 19% in dizigotic.[40] The relatively low concordance between dizygotic twins brought up together suggests that shared family environmental effects are limited, although the ability to detect them has been limited by small sample sizes.[39]
Genetic
Genetic studies have suggested many chromosomal regions and candidate genes appearing to relate to the development of bipolar disorder, but the results are not consistent and often not replicated.[41] Although the first genetic linkage finding for mania was in 1969,[42] the linkage studies have been inconsistent.[43] Meta-analyses of linkage studies detected either no significant genome-wide findings or, using a different methodology, only two genome-wide significant peaks, on chromosome 6q and on 8q21. Genome-wide association studies neither brought a consistent focus each has identified new loci.[43] Findings point strongly to heterogeneity, with different genes being implicated in different families.[44] A review seeking to identify the more consistent findings suggested several genes related to serotonin (SLC6A4 and TPH2), dopamine (DRD4 and SLC6A3), glutamate (DAOA and DTNBP1), and cell growth and/or maintenance pathways (NRG1, DISC1 and BDNF), although noting a high risk of false positives in the published literature. It was also suggested that individual genes are likely to have only a small effect and to be involved in some aspect related to the disorder (and a broad range of "normal" human behavior) rather than the disorder per se.[45] Advanced paternal age has been linked to a somewhat increased chance of bipolar disorder in offspring, consistent with a hypothesis of increased new genetic mutations.[46]
Physiological
Abnormalities in the structure and/or function of certain brain circuits could underlie bipolar. Two meta-analyses of MRI studies in bipolar disorder report an increase in the volume of the lateral ventricles, globus pallidus and increase in the rates of deep white matter hyperintensities.[47] [48] The "kindling" theory asserts that people who are genetically predisposed toward bipolar disorder can experience a series of stressful events,[49] each of which lowers the threshold at which mood changes occur. Eventually, a mood episode can start (and become recurrent) by itself. There is evidence of hypothalamic-pituitary-adrenal axis (HPA axis) abnormalities in bipolar disorder due to stress.[50] Other brain components which have been proposed to play a role are the mitochondria,[51] and a sodium ATPase pump,[52] causing cyclical periods of poor neuron firing (depression) and hypersensitive neuron firing (mania). This may only apply for type one, but type two apparently results from a large confluence of factors. Circadian rhythms and melatonin activity also seem to be altered.[53]
Environmental
Evidence suggests that environmental factors play a significant role in the development and course of bipolar disorder, and that individual psychosocial variables may interact with genetic dispositions.[45] There is fairly consistent evidence from prospective studies that recent life events and interpersonal relationships contribute to the likelihood of onsets and recurrences of bipolar mood episodes, as they do for onsets and recurrences of unipolar depression.[54] There have been repeated findings that between a third and a half of adults diagnosed with bipolar disorder report traumatic/abusive experiences in childhood, which is associated on average with earlier onset, a worse course, and more co-occurring disorders such as PTSD.[55] The total number of reported stressful events in childhood is higher in those with an adult diagnosis of bipolar spectrum disorder compared to those without, particularly events stemming from a harsh environment rather than from the child's own behavior.[56] Early
Bipolar disorder experiences of adversity and conflict are likely to make subsequent developmental challenges in adolescence more difficult, and are likely a potentiating factor in those at risk of developing bipolar disorder.[57]
Diagnosis
Diagnosis is based on the self-reported experiences of an individual as well as abnormalities in behavior reported by family members, friends or co-workers, followed by secondary signs observed by a psychiatrist, nurse, social worker, clinical psychologist or other clinician in a clinical assessment. There are lists of criteria for someone to be so diagnosed. These depend on both the presence and duration of certain signs and symptoms. Assessment is usually done on an outpatient basis; admission to an inpatient facility is considered if there is a risk to oneself or others. The most widely used criteria for diagnosing bipolar disorder are from the American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders, the current version being DSM-IV-TR, and the World Health Organization's International Statistical Classification of Diseases and Related Health Problems, currently the ICD-10. The latter criteria are typically used in Europe and other regions while the DSM criteria are used in the USA and other regions, as well as prevailing in research studies. An initial assessment may include a physical exam by a physician. Although there are no biological tests which confirm bipolar disorder, tests may be carried out to exclude medical illnesses such as hypo- or hyperthyroidism, metabolic disturbance, a systemic infection or chronic disease, and syphilis or HIV infection. An EEG may be used to exclude epilepsy, and a CT scan of the head to exclude brain lesions. Investigations are not generally repeated for relapse unless there is a specific medical indication. Several rating scales for the screening and evaluation of BD exist, such as the Bipolar spectrum diagnostic scale.[58] The use of evaluation scales can not substitute a full clinical interview but they serve to systematize the recollection of symptoms.[58] On the other hand instruments for the screening of BD have low sensitivity and limited diagnostic validity.[58]
Bipolar disorder This is a catchall category, diagnosed when the disorder does not fall within a specific subtype.[64] Bipolar NOS can still significantly impair and adversely affect the quality of life of the patient. The bipolar I and II categories have specifiers that indicate the presentation and course of the disorder. For example, the "with full interepisode recovery" specifier applies if there was full remission between the two most recent episodes.[65] Rapid cycling Most people who meet criteria for bipolar disorder experience a number of episodes, on average 0.4 to 0.7 per year, lasting three to six months.[66] Rapid cycling, however, is a course specifier that may be applied to any of the above subtypes. It is defined as having four or more episodes per year and is found in a significant fraction of individuals with bipolar disorder. The definition of rapid cycling most frequently cited in the literature (including the DSM) is that of Dunner and Fieve: at least four major depressive, manic, hypomanic or mixed episodes are required to have occurred during a 12-month period.[67] Ultra-rapid (days) and ultra-ultra rapid or ultradian (within a day) cycling have also been described.[68]
Differential diagnosis
There are several other mental disorders which may involve similar symptoms to bipolar disorder. These include schizophrenia,[69] schizoaffective disorder, drug intoxication, brief drug-induced psychosis, schizophreniform disorder and borderline personality disorder. Both borderline personality and bipolar disorder can involve what are referred to as "mood swings". In bipolar disorder, the term refers to the cyclic episodes of elevated and depressed mood which generally last weeks or months. The term in borderline personality refers to the marked lability and reactivity of mood, known as emotional dysregulation, due to response to external psychosocial and intrapsychic stressors; these may arise or subside suddenly and dramatically and last for seconds, minutes, hours or days. A bipolar depression is generally more pervasive with sleep, appetite disturbance and nonreactive mood, whereas the mood in dysthymia of borderline personality remains markedly reactive and sleep disturbance not acute.[70] Some hold that borderline personality disorder represents a subthreshold form of mood disorder while others maintain the distinctness, though noting they often coexist.[71]
Challenges
The experiences and behaviors involved in bipolar disorder are often not understood by individuals or recognized by mental health professionals, so diagnosis may sometimes be delayed for over 10 years.[72] The treatment lag is apparently not decreasing, even though there is increased public awareness of the condition. Individuals are commonly misdiagnosed.[73] An individual may appear simply depressed when they are seen by a health professional. This can result in misdiagnosis of Major Depressive Disorder. However, there is also a long-standing issue in the research literature as to whether a categorical classificatory divide between unipolar and bipolar depression is actually valid, or whether it is more accurate to talk of a continuum involving dimensions of depression and mania.[74] [75] It has been noted that the bipolar disorder diagnosis is officially characterised in historical terms such that, technically, anyone with a history of (hypo)mania and depression has bipolar disorder whatever their current or future functioning and vulnerability. This has been described as "an ethical and methodological issue", as it means no one can be considered as being recovered (only "in remission") from bipolar disorder according to the official criteria. This is considered especially problematic given that brief hypomanic episodes are widespread among people generally and not necessarily associated with dysfunction.[36] Flux is the fundamental nature of bipolar disorder.[76] Individuals with the illness have continual changes in energy, mood, thought, sleep, and activity. The diagnostic subtypes of bipolar disorder are thus static descriptionssnapshots, perhapsof an illness in continual flux, with a great diversity of symptoms and varying
Bipolar disorder degrees of severity. Individuals may stay in one subtype, or change into another, over the course of their illness.[77] The DSM-V, to be published in 2013, will likely include further and more accurate sub-typing (Akiskal and Ghaemi, 2006). The diagnosis of bipolar disorder can be complicated by coexisting psychiatric conditions such as obsessive-compulsive disorder, social phobia, panic disorder, or attention-deficit/hyperactivity disorder. Substance abuse may predate the appearance of bipolar symptoms, further complicating the diagnosis. A careful longitudinal analysis of symptoms and episodes, enriched if possible by discussions with friends and family members, is crucial to establishing a treatment plan where these comorbidities exist.[78]
Management
There are a number of pharmacological and psychotherapeutic techniques used to treat bipolar disorder. Individuals may use self-help and pursue recovery. Hospitalization may be required especially with the manic episodes present in bipolar I. This can be voluntary or (if mental health legislation allows and varying state-to-state regulations in the USA) involuntary (called civil or involuntary commitment). Long-term inpatient stays are now less common due to deinstitutionalization, although these can still occur.[79] Following (or in lieu of) a hospital admission, support services available can include drop-in centers, visits from members of a community mental health team or Assertive Community Treatment team, supported employment and patient-led support groups, intensive outpatient programs. These are sometimes referred to partial-inpatient programs.[80]
Psychosocial
Psychotherapy is aimed at alleviating core symptoms, recognizing episode triggers, reducing negative expressed emotion in relationships, recognizing prodromal symptoms before full-blown recurrence, and, practicing the factors that lead to maintenance of remission[81] Cognitive behavioural therapy, family-focused therapy, and psychoeducation have the most evidence for efficacy in regard to relapse prevention, while interpersonal and social rhythm therapy and cognitive-behavioural therapy appear the most effective in regard to residual depressive symptoms. Most studies have been based only on bipolar I, however, and treatment during the acute phase can be a particular challenge.[82] Some clinicians emphasize the need to talk with individuals experiencing mania, to develop a therapeutic alliance in support of recovery.[83]
Medication
The mainstay of treatment is a mood stabilizers such as lithium carbonate or lamotrigine.[84] [85] Lamotrigine has been found to be best for preventing depressions, while lithium is the only drug proven to reduce suicide in people with bipolar disorder.[86] These two drugs comprise several unrelated compounds which have been shown to be effective in preventing relapses of manic, or in the one case, depressive episodes. The first known and "gold standard" mood stabilizer is lithium,[87] while almost as widely used is sodium valproate,[88] also used as an anticonvulsant. Other anticonvulsants used in bipolar Sodium valproate is a common mood stabilizer disorder include carbamazepine, reportedly more effective in rapid cycling bipolar disorder, and lamotrigine, which is the first anticonvulsant shown to be of benefit in bipolar depression.[89] Depending on the severity of the case, anti-convulsants may be used in combination with lithium-based products or on their own.[90]
Bipolar disorder Atypical antipsychotics have been found to be effective in managing mania associated with bipolar disorder.[91] Antidepressants have not been found to be of any benefit over that found with mood stabilizers.[91] Omega 3 fatty acids, in addition to normal pharmacological treatment, may have beneficial effects on depressive symptoms, although studies have been scarce and of variable quality.[92] The effectiveness of topiramate is unknown.[93]
Prognosis
For many individuals with bipolar disorder a good prognosis results from good treatment, which, in turn, results from an accurate diagnosis. Because bipolar disorder can have a high rate of both under-diagnosis and misdiagnosis,[20] it is often difficult for individuals with the condition to receive timely and competent treatment. Bipolar disorder can be a severely disabling medical condition. However, many individuals with bipolar disorder can live full and satisfying lives. Quite often, medication is needed to enable this. Persons with bipolar disorder may have periods of normal or near normal functioning between episodes.[94] Prognosis depends on many factors such as the right medicines and dosage, comprehensive knowledge of the disease and its effects; a positive relationship with a competent medical doctor and therapist; and good physical health, which includes exercise, nutrition, and a regulated stress level. There are other factors that lead to a good prognosis, such as being very aware of small changes in a person's energy, mood, sleep and eating behaviors.[95]
Functioning
A recent 20-year prospective study on bipolar I and II found that functioning varied over time along a spectrum from good to fair to poor. During periods of major depression or mania (in BPI), functioning was on average poor, with depression being more persistently associated with disability than mania. Functioning between episodes was on average good more or less normal. Subthreshold symptoms were generally still substantially impairing, however, except for hypomania (below or above threshold) which was associated with improved functioning.[96] Another study confirmed the seriousness of the disorder as "the standardized all-cause mortality ratio among patients with BD is increased approximately two-fold." Bipolar disorder is currently regarded "as possibly the most costly category of mental disorders in the United States." Episodes of abnormality are associated with distress and disruption, and an elevated risk of suicide, especially during depressive episodes.[97]
Bipolar disorder
Mortality
Bipolar disorder can cause suicidal ideation that leads to suicidal attempts. One out of 3 people with bipolar disorder report past attempts of suicide or complete it,[101] and the annual average suicide rate is 0.4%, which is 10 to 20 times that of the general population.[102] The standardized mortality ratio from suicide in BD is between 18 and 25.[103]
Epidemiology
When broadly defined 4% of people experience bipolar at some point in their [104] life. The Disability-adjusted life year for bipolar disorder per 100,000inhabitants in 2002.no dataless than lifetime prevalence 180180186186190190195195200200205205210210215215220220225225230230235 of bipolar disorder type I, which includes at least a lifetime manic episode, has generally been estimated at 2%.[105] It is equally prevalent in men and women and is found across all cultures and ethnic groups.[106] A reanalysis of data from the National Epidemiological Catchment Area survey in the United States, however, suggested that 0.8 percent experience a manic episode at least once (the diagnostic threshold for bipolar I) and 0.5 a hypomanic episode (the diagnostic threshold for bipolar II or cyclothymia). Including sub-threshold diagnostic criteria, such as one or two symptoms over a short time-period, an additional 5.1 percent of the population, adding up to a total of 6.4 percent, were classed as having a bipolar spectrum disorder.[107] A more recent analysis of data from a second US National Comorbidity Survey found that 1% met lifetime prevalence criteria for bipolar 1, 1.1% for bipolar II, and 2.4% for subthreshold symptoms.[108] There are conceptual and methodological limitations and variations in the findings. Prevalence studies of bipolar disorder are typically carried out by lay interviewers who follow fully structured/fixed interview schemes; responses to single items from such interviews may suffer limited validity. In addition, diagnosis and prevalence rates are dependent on whether a categorical or spectrum approach is used. Concerns have arisen about the potential for both underdiagnosis and overdiagnosis.[109] Late adolescence and early adulthood are peak years for the onset of bipolar disorder.[110] [111] One study also found that in 10% of bi-polar cases, the onset of mania had happened after the patient had turned 50.[112]
History
Variations in moods and energy levels have been observed as part of the human experience since time immemorial. The words "melancholia" (an old word for depression) and "mania" have their etymologies in Ancient Greek. The word melancholia is derived from melas/, meaning "black", and chole/, meaning "bile" or "gall",[113] indicative of the term's origins in pre-Hippocratic humoral theories. Within the humoral theories, mania was viewed as arising from an excess of yellow bile, or a mixture of black and yellow bile. The linguistic origins of mania, however, are not so clear-cut. Several etymologies are proposed by the Roman physician Caelius Aurelianus, including the Greek word ania, meaning to produce great mental anguish, and manos, meaning relaxed or loose, which would contextually approximate to an excessive relaxing of the mind or soul (Angst and Marneros 2001). There are at least five other candidates, and part of the confusion surrounding the exact etymology of the word mania is its varied usage in the pre-Hippocratic poetry and mythologies (Angst and Marneros 2001). The basis of the current conceptualisation of manic-depressive illness can be traced back to the 1850s; on January 31, 1854, Jules Baillarger described to the French Imperial Academy of Medicine a biphasic mental illness causing recurrent oscillations between mania and depression, which he termed folie double forme (dual-form
Bipolar disorder insanity).[114] Two weeks later, on February 14, 1854, Jean-Pierre Falret presented a description to the Academy on what was essentially the same disorder, and designated folie circulaire (circular insanity) by him.(Sedler 1983) The two bitterly disputed as to who had been the first to conceptualise the condition. These concepts were developed by the German psychiatrist Emil Kraepelin (18561926), who, using Kahlbaum's concept of cyclothymia,[115] categorized and studied the natural course of untreated bipolar patients. He coined the term manic depressive psychosis, after noting that periods of acute illness, manic or depressive, were generally punctuated by relatively symptom-free intervals where the patient was able to function normally.[116] The term "manic-depressive reaction" appeared in the first American Psychiatric Association Diagnostic Manual in 1952, influenced by the legacy of Adolf Meyer who had introduced the paradigm illness as a reaction of biogenetic factors to psychological and social influences.[117] Subclassification of bipolar disorder was first proposed by German psychiatrist Karl Leonhard in 1957; he was also the first to introduce the terms bipolar (for those with mania) and unipolar (for those with depressive episodes only).[118]
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Cultural references
Kay Redfield Jamison, a clinical psychologist and Professor of Psychiatry at the Johns Hopkins University School of Medicine, profiled her own bipolar disorder in her memoir An Unquiet Mind (1995).[119] In her book, Touched with Fire (1993), she argued for a connection between bipolar disorder and artistic creativity.[120] Several films have portrayed characters with traits suggestive of the diagnosis that has been the subject of discussion by psychiatrists and film experts alike. A notable example is Mr. Jones (1993), in which Mr. Jones (Richard Gere) swings from a manic episode into a depressive phase and back again, spending time in a psychiatric hospital and displaying many of the features of the syndrome.[121] In The Mosquito Coast (1986), Allie Fox (Harrison Ford) displays some features including recklessness, grandiosity, increased goal-directed activity and mood lability, as well as some paranoia.[122] In the Australian TV drama Stingers, Detective Luke Harris (Gary Sweet) is portrayed as having bipolar disorder and shows how his paranoia interfered with his work. As research for the role, Sweet visited a psychiatrist to learn about manic-depressive illness. He said that he left the sessions convinced he had the condition. TV specials, for example the BBC's The Secret Life of the Manic Depressive,[123] MTV's True Life: I'm Bipolar, talk shows, and public radio shows, and the greater willingness of public figures to discuss their own bipolar disorder, have focused on psychiatric conditions, thereby, raising public awareness. On April 7, 2009, the nighttime drama 90210 on the CW network, aired a special episode where the character Silver was diagnosed with bipolar disorder. A public service announcement (PSA) aired after the episode, directing teens and young adults to the Child and Adolescent Bipolar Foundation website for information and to chat with other teens.[124] Stacey Slater, a character from the popular BBC soap EastEnders, has been diagnosed with the disorder. After losing her friend Danielle Jones, Stacey began acting strangely; and the character had to come to terms with the prospect that, like her mother, Jean Slater, she suffers from bipolar disorder. The high-profile storyline was developed as part of the BBC's Headroom campaign.[125] The Channel 4 soap Brookside had earlier featured a story about bipolar disorder when the character Jimmy Corkhill was diagnosed with the condition.[126] Dean Sullivan, the actor who played Jimmy, was presented with a Special Achievement Award at the 2003 British Soap Awards for the role.[126]
Bipolar disorder
11
Specific populations
In children
Emil Kraepelin in the 1920s noted that mania episodes were rare before puberty.[127] In general BD in children was not recognized in the first half of the twentieth century. This issue diminished with an increased following of the DSM criteria in the last part of the twentieth century.[127] [128] While in adults the course of BD is characterized by discrete episodes of depression and mania with no clear symptomatology between them, in chidren and adolescents very fast mood changes or even chronic symptoms are the norm.[129] On the other hand pediactric BD instead of euphoric mania commonly develops with outbursts of anger, irritability and psychosis, less common in adults.[127] [129]
Lithium carbonate is the only drug approved for children by the FDA
The diagnosis of childhood BD is controversial,[129] although it is not under discussion that BD typical symptoms have negative consequences for minors suffering them.[127] Main discussion is centered on whether what is called BD in children refers to the same disorder than when diagnosing adults,[127] and the related question on whether adults criteria for diagnosis are useful and accurate when applied to children.[129] Regarding diagnosis of children some experts recommend to follow the DSM criteria.[129] Others believe that these criteria do not separate correctly children with BD from other problems such as ADHD, and emphasize fast mood cycles.[129] Still others argue that what accurately differentiates children with BD is irritability.[129] The practice parameters of the AACAP encourage the first strategy.[127] [129] American children and adolescents diagnosed of BD in community hospitals increased 4-fold reaching rates of up to 40% in 10 years around the beginning of the current century, while in outpatient clinics it doubled reaching the 6%.[129] The data suggest that doctors had been more aggressively applying the diagnosis to children. The reasons for this increase are unclear. Consensus regarding the diagnosis in the pediatric age seems to apply only to the USA. Studies using DSM criteria show that up to 1% of youth may have BD.[127] Treatment involves medication and psychotherapy.[129] Drug prescription usually consists in mood stabilizers and atypical antipsychotics.[129] Among the formers lithium is the only compound approved by the FDA for children.[127] Psychological treatment combines normally education on the disease, group therapy and cognitive behavioral therapy.[129] Chronic medication is often needed.[129] Current research directions for BD in children include optimizing treatments, increasing the knowledge of the genetic and neurobiological basis of the pediatric disorder and improving diagnostic criteria.[129] The DSM-V has proposed a new diagnosis which is considered to cover some presentations currently thought of as childhood-onset bipolar.[130] [131]
In the elderly
There is a relative lack of knowledge about bipolar disorder in late life. There is evidence that it becomes less prevalent with age but nevertheless accounts for a similar percentage of psychiatric admissions; that older bipolar patients had first experienced symptoms at a later age; that later onset of mania is associated with more neurologic impairment; that substance abuse is considerably less common in older groups; and that there is probably a greater degree of variation in presentation and course, for instance individuals may develop new-onset mania associated with vascular changes, or become manic only after recurrent depressive episodes, or may have been diagnosed with bipolar disorder at an early age and still meet criteria. There is also some weak evidence that mania is less intense and there is a higher prevalence of mixed episodes, although there may be a reduced response to treatment. Overall there are likely more similarities than differences from younger adults.[132] In the elderly, recognition and treatment
Bipolar disorder of bipolar disorder may be complicated by the presence of dementia or the side effects of medications being taken for other conditions.[133]
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References
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Bipolar disorder
[123] "The Secret Life of the Manic Depressive" (http:/ / www. bbc. co. uk/ health/ tv_and_radio/ secretlife_index. shtml). BBC. 2006. . Retrieved February 20, 2007. [124] "Child and Adolescent Bipolar Foundation special 90210 website" (http:/ / www. bpkids. org/ 90210). CABF. 2009. . Retrieved April 7, 2009. [125] "EastEnders' Stacey faces bipolar disorder" (http:/ / www. bbc. co. uk/ pressoffice/ pressreleases/ stories/ 2009/ 05_may/ 14/ stacey. shtml). BBC Press Office. May 14, 2009. . Retrieved May 28, 2009. [126] Tinniswood, Rachael (May 14, 2003). "The Brookie boys who shone at soap awards show". Liverpool Echo (Mirror Group Newspapers). [127] McClellan J, Kowatch R, Findling RL (January 2007). "Practice parameter for the assessment and treatment of children and adolescents with bipolar disorder". J Am Acad Child Adolesc Psychiatry 46 (1): 10725. doi:10.1097/01.chi.0000242240.69678.c4. PMID17195735. [128] Anthony, James; Scott, Peter (1960). "Manic-depressive psychosis in childhood". J Child Psychol Psychiatry 1: 5372. doi:10.1111/j.1469-7610.1960.tb01979.x. [129] Leibenluft E, Rich BA (2008). "Pediatric bipolar disorder". Annu Rev Clin Psychol 4: 16387. doi:10.1146/annurev.clinpsy.4.022007.141216. PMID17716034. [130] http:/ / www. dsm5. org/ Proposed%20Revision%20Attachments/ Justification%20for%20Temper%20Dysregulation%20Disorder%20with%20Dysphoria. pdf [131] http:/ / www. dsm5. org/ Newsroom/ Documents/ Diag%20%20Criteria%20General%20FINAL%202. 05. pdf [132] Depp CA, Jeste DV (October 2004). "Bipolar disorder in older adults: a critical review". Bipolar Disord 6 (5): 34367. doi:10.1111/j.1399-5618.2004.00139.x. PMID15383127. [133] Trinh NH, Forester B (2007). "Bipolar Disorder in the Elderly: Differential Diagnosis and Treatment" (http:/ / www. psychiatrictimes. com/ bipolar-disorder/ article/ 10168/ 54481). Psychiatric Times 24 (14). .
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Cited texts
Goodwin FK, Jamison KR (1990). Manic-Depressive Illness. New York: Oxford University Press. ISBN0-19-503934-3. Goodwin FK, Jamison KR (2007). Manic-Depressive Illness: Bipolar Disorders and Recurrent Depression, 2nd Edition. New York: Oxford University Press. ISBN0-19-513579-2.
Further reading
Contemporary first-person accounts Simon, Lizzie. 2002. Detour: My Bipolar Road Trip in 4-D. New York: Simon and Schuster. ISBN 0-7434-4659-3. Behrman, Andy. 2002. Electroboy: A Memoir of Mania. New York: Random House. ISBN 0-375-50358-7. Hornbacher, Marya. 2008. Madness: A Bipolar Life. ISBN 978-0618754458. Lovelace, David. 2008. Scattershot: My Bipolar Family. New York: Dutton Adult. ISBN 0-525-95078-8. Managing bipolar disorder Berk, Lesley (March 5, 2009). Living with Bipolar. Vermilion. ISBN9780091924256. Bipolar disorder in children Greenberg, Rosalie. 2008. Bipolar Kids: Helping Your Child Find Calm in the Mood Storm. ISBN 978-0-7382-1113-8 Papolos, Demetri, and Papolos, Janice. 2007. The Bipolar Child: The Definitive and Reassuring Guide to Childhood's Most Misunderstood Disorder -- Third Edition. ISBN 978-0-7679-2860-1 Raeburn, Paul. 2004. Acquainted with the Night: A Parent's Quest to Understand Depression and Bipolar Disorder in His Children. Earley, Pete. Crazy. 2006. New York: G. P. Putnam's Sons. ISBN 0-399-15313-6. A father's account of his son's bipolar disorder. Classic works on bipolar disorder Kraepelin, Emil. 1921. Manic-depressive Insanity and Paranoia ISBN 0-405-07441-7 (English translation of the original German from the earlier eighth edition of Kraepelin's textbook now outdated, but a work of major historical importance).
Bipolar disorder Mind Over Mood: Cognitive Treatment Therapy Manual for Clients by Christine Padesky, Dennis Greenberger. ISBN 0-89862-128-3
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External links
Bipolar Disorder overview (http://www.nimh.nih.gov/health/publications/bipolar-disorder/complete-index. shtml) from the U.S. National Institute of Mental Health website NICE Bipolar Disorder clinical guidelines (http://www.nice.org.uk/Guidance/CG38) from the U.K. National Institute for Health and Clinical Excellence website Bipolar Disorder (http://www.dmoz.org/Health/Mental_Health/Disorders/Mood/Bipolar_Disorder/) at the Open Directory Project
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History
History of bipolar disorder
Varying moods and energy levels have been a part of the human experience since time immemorial. The words "melancholia" (an old word for depression) and "mania" have their etymologies in Ancient Greek. The word melancholia is derived from melas/, meaning "black", and chole/, meaning "bile" or "gall",[1] indicative of the terms origins in pre-Hippocratic humoral theories. Within the humoral theories, mania was viewed as arising from an excess of yellow bile, or a mixture of black and yellow bile. The linguistic origins of mania, however, are not so clear-cut. Several etymologies are proposed by the Roman physician Caelius Aurelianus, including the Greek word ania, meaning to produce great mental anguish, and manos, meaning relaxed or loose, which would contextually approximate to an excessive relaxing of the mind or soul (Angst and Marneros 2001). There are at least five other candidates, and part of the confusion surrounding the exact etymology of the word mania is its varied usage in the pre-Hippocratic poetry and mythologies (Angst and Marneros 2001). The idea of a relationship between mania and melancholia can be traced back to at least the 2nd century AD. Soranus of Ephesus (98177 AD) described mania and melancholia as distinct diseases with separate etiologies;[2] however, he acknowledged that many others consider melancholia a form of the disease of mania (Cited in Mondimore 2005 p.49). A clear understanding of bipolar disorder as a mental illness was recognized by early Chinese authors. The encyclopedist Gao Lian (c. 1583) describes the malady in his Eight Treatises on the Nurturing of Life (Ts'un-sheng pa-chien).[3] The earliest written descriptions of a relationship between mania and melancholia are attributed to Aretaeus of Cappadocia. Aretaeus was an eclectic medical philosopher who lived in Alexandria somewhere between 30 and 150 AD (Roccatagliata 1986; Akiskal 1996). Aretaeus is recognized as having authored most of the surviving texts referring to a unified concept of manic-depressive illness, viewing both melancholia and mania as having a common origin in black bile (Akiskal 1996; Marneros 2001). Avicenna, a Persian physician and psychological thinker who wrote The Canon of Medicine in 1025, identified bipolar disorder as a manic depressive psychosis, which he clearly distinguished from other forms of madness (Junun) such as mania, rabies, and schizophrenia (Junun Mufrit or severe madness).[4] The basis of the current conceptualisation of manic-depressive illness can be traced back to the 1850s; on January 31, 1854, Jules Baillarger described to the French Imperial Academy of Medicine a biphasic mental illness causing recurrent oscillations between mania and depression, which he termed folie double forme (dual-form insanity).[5] Two weeks later, on February 14, 1854, Jean-Pierre Falret presented a description to the Academy on what was essentially the same disorder, and designated folie circulaire (circular insanity) by him.(Sedler 1983) The two bitterly disputed as to who had been the first to conceptualise the condition. These concepts were developed by the German psychiatrist Emil Kraepelin (18561926), who, using Kahlbaum's concept of cyclothymia,[6] categorized and studied the natural course of untreated bipolar patients. He coined the term manic depressive psychosis, after noting that periods of acute illness, manic or depressive, were generally punctuated by relatively symptom-free intervals where the patient was able to function normally.[7] After World War II, Dr. John Cade, an Australian psychiatrist, was investigating the effects of various compounds on veteran patients with manic depressive psychosis. In 1949, Cade discovered that lithium carbonate could be used as a successful treatment of manic depressive psychosis.[8] Because there was a fear that table salt substitutes could lead to toxicity or death, Cade's findings did not immediately lead to treatments. In the 1950s, U.S. hospitals began
History of bipolar disorder experimenting with lithium on their patients. By the mid-'60s, reports started appearing in the medical literature regarding lithium's effectiveness. The U.S. Food and Drug Administration did not approve of lithium's use until 1970.[9] The term "manic-depressive reaction" appeared in the first American Psychiatric Association Diagnostic Manual in 1952, influenced by the legacy of Adolf Meyer who had introduced the paradigm illness as a reaction of biogenetic factors to psychological and social influences.[10] Subclassification of bipolar disorder was first proposed by German psychiatrist Karl Leonhard in 1957; he was also the first to introduce the terms bipolar (for those with mania) and unipolar (for those with depressive episodes only).[11] In 1968, both the newly revised classification systems ICD-8 and DSM-II termed the condition "manic-depressive illness" as biological thinking came to the fore.[12] The current nosology, bipolar disorder, became popular only recently, and some individuals prefer the older term because it provides a better description of a continually changing multi-dimensional illness. Empirical and theoretical work on bipolar disorder has throughout history "seesawed" between psychological and biological ways of understanding. Despite the work of Kraepelin (1921) emphasizing the psychosocial context, conceptions of bipolar disorder as a genetically based illness dominated the 20th century. Since the 1990s, however, there has been a resurgence of interest and research in to the role of psychosocial processes.[13]
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References
[1] Liddell, Henry George and Robert Scott (1980). A Greek-English Lexicon (Abridged Edition). United Kingdom: Oxford University Press. ISBN0-19-910207-4. [2] "Bipolar_disorders_beyond_major_depression_and_euphoric_mania" (http:/ / assets. cambridge. org/ 97805218/ 35176/ excerpt/ 9780521835176_excerpt. pdf) (PDF). cambridge.org. . Retrieved 2008-02-16. [3] http:/ / www. nmh. gov. tw/ nmh_web/ english_version/ exhibition/ exhibition_s0703. cfm [4] Youssef, Hanafy A.; Youssef, Fatma A.; Dening, T. R. (1996). "Evidence for the existence of schizophrenia in medieval Islamic society". History of Psychiatry 7 (25): 5562 [57]. doi:10.1177/0957154X9600702503. PMID11609215. [5] Circular insanity, 150 years on. PMID15506718. [6] Millon, Theordore (1996). Disorders of Personality: DSM-IV-TM and Beyond. New York: John Wiley and Sons. pp.290. ISBN0-471-01186-X. [7] Kraepelin, Emil (1921) Manic-depressive Insanity and Paranoia ISBN 0-405-07441-7 [8] Cade JF (September 1949). "Lithium salts in the treatment of psychotic excitement" (http:/ / www. who. int/ docstore/ bulletin/ pdf/ 2000/ issue4/ classics. pdf) (PDF). Med. J. Aust. 2 (10): 34952. PMID18142718. . [9] Mitchell PB, Hadzi-Pavlovic D (2000). "Lithium treatment for bipolar disorder" (http:/ / www. who. int/ docstore/ bulletin/ pdf/ 2000/ issue4/ classics. pdf) (PDF). Bull. World Health Organ. 78 (4): 5157. PMC2560742. PMID10885179. . [10] Goodwin & Jamison. pp. 6061. [11] Goodwin & Jamison. p62 [12] Goodwin & Jamison. p88 [13] Alloy, LB; Abramson, LY; Urosevic, S; Walshaw, PD; Nusslock, R; Neeren, AM (2005). "The psychosocial context of bipolar disorder: environmental, cognitive, and developmental risk factors.". Clinical psychology review 25 (8): 104375. doi:10.1016/j.cpr.2005.06.006. PMID16140445.
Emil Kraepelin
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Emil Kraepelin
Emil Kraepelin (15 February 1856, Neustrelitz 7 October 1926, Munich) was a German psychiatrist. H.J. Eysenck's Encyclopedia of Psychology identifies him as the founder of modern scientific psychiatry, as well as of psychopharmacology and psychiatric genetics. Kraepelin believed the chief origin of psychiatric disease to be biological and genetic malfunction. However, Kraepelin was criticized for considering schizophrenia as a biological illness in the absence of any detectable histologic or anatomic abnormalities.[1] :221 While Kraepelin tried to find organic causes of mental illness, he adopted many theses of positivist medicine, but the basis for understanding is not etiology, as the causes of madness cannot be established with any precision.[2] His theories dominated psychiatry at the start of the twentieth century and, despite later psychodynamic incursions by Sigmund Freud and his disciples, appeared to enjoy a revival at century's end.
Emil Kraepelin
Kraepelin, the son of a civil servant, was born in 1856 in Neustrelitz, in the Mecklenburg district of Germany. He was first introduced to biology by his brother Karl, 10 years older and, later, the director of the Zoological Museum of Hamburg.
Early career
Kraepelin began his medical studies at 18, in Leipzig and Wurzburg, Germany. At Leipzig, where he studied neuropathology under Paul Flechsig and experimental psychology with Wilhelm Wundt, he wrote a prize-winning essay, "The Influence of Acute Illness in the Causation of Mental Disorders." He received his M.D. in 1878. In 1879, Kraepelin went to work with Bernhard von Gudden at the University of Munich, where he completed his thesis, "The Place of Psychology in Psychiatry". Returning to the University of Leipzig in 1882, he worked in Wilhelm Heinrich Erb's neurology clinic and in Wundt's psychopharmacology laboratory. His major work, "Compendium der Psychiatrie", was first published in 1883. In it, he argued that psychiatry was a branch of medical science and should be investigated by observation and experimentation like the other natural sciences. He called for research into the physical causes of mental illness and established the foundations of the modern classification system for mental disorders. Kraepelin proposed that by studying case histories and identifying specific disorders, the progression of mental illness could be predicted, after taking into account individual differences in personality and patient age at the onset of disease.[3]
Grave in Heidelberg
Emil Kraepelin In 1884 he became senior physician in Leubus and the following year he was appointed director of the Treatment and Nursing Institute in Dresden. In 1886, at the age of 30, Kraepelin was named professor of psychiatry at the University of Dorpat (later the University of Tartu) in what is today Estonia (see Burgmair Vol IV). Four years later, he became department head at the University of Heidelberg, where he remained until 1904. Whilst at Dorpat he became the director of the eighty-bed University Clinic. There he began to study and record many clinical histories in detail and "was led to consider the importance of the course of the illness with regard to the classification of mental disorders." Ten years later he announced that he had found a new way of looking at mental illness. He referred to the traditional view as "symptomatic" and to his view as "clinical". This turned out to be his paradigm-setting synthesis of the hundreds of mental disorders classified by the 19th century, grouping diseases together based on classification of syndromes common patterns of symptoms rather than by simple similarity of major symptoms in the manner of his predecessors. In fact, it was precisely because of the demonstrated inadequacy of such methods that Kraepelin developed his new diagnostic system.
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Emil Kraepelin
22
Alzheimer
Kraepelin postulated that there is a specific brain or other biological pathology underlying each of the major psychiatric disorders. As a colleague of Alois Alzheimer, and co-discoverer of Alzheimer's disease, it was his laboratory which discovered its pathologic basis. Kraepelin was confident that it would someday be possible to identify the pathologic basis of each of the major psychiatric disorders.
Influence
Kraepelin's great contribution in classifying schizophrenia and manic-depression remains relatively unknown to the general public, and his work, which had neither the literary quality nor paradigmatic power of Freud's, is little read outside scholarly circles.[4] Kraepelin's contributions were to a large extent marginalized throughout a good part of the twentieth century, during the success of Freudian etiological theories. However, his views now dominate psychiatric research and academic psychiatry, and today the published literature in the field of psychiatry is overwhelmingly biological in its orientation. His fundamental theories on the etiology and diagnosis of psychiatric disorders form the basis of all major diagnostic systems in use today, especially the American Psychiatric Association's DSM-IV and the World Health Organization's ICD system. In that sense, not only is Kraepelin's significance historical, but contemporary psychiatric research is also heavily influenced by his work.
Psychology
Kraepelin, being a disciple of Wilhem Wundt, had a life long interest in experimental psychology. In the Heidelberg and early Munich years he edited Psychologische Arbeiten, a journal on experimental psychology. One of his own famous contributions to this journal also appeared in the form of a monograph (105 p.) entitled ber Sprachstrungen im Traume (on language disturbances in dreams).[5] Kraepelin, on the basis on the dream-psychosis analogy, studied for more than 20 years language disorder in dreams in order to study indirectly schizophasia. The dreams Kraepelin collected are mainly his own. They lack extensive comment by the dreamer. In order to study them the full range of biographical knowledge available today on Kraepelin is necessary (see e.g. Burgmair et al., I-VII).
Honors
He was elected a member of the Royal Swedish Academy of Sciences in 1908.
References
[1] Cohen, Bruce (2003). Theory and practice of psychiatry (http:/ / books. google. com/ books?id=H8ZrAAAAMAAJ). Oxford University Press. pp.221. ISBN0195149378. . [2] Thiher, Allen (2005). Revels in Madness: Insanity in Medicine and Literature (http:/ / books. google. com/ books?id=G_Ww-9iiKe0C& pg=PT137& dq). University of Michigan Press. ISBN0472089994. . [3] http:/ / findarticles. com/ p/ articles/ mi_g2699/ is_0005/ ai_2699000523/ [4] On the reception of Kraepelin's work in the 20th century, see Eric J. Engstrom and Matthias Weber. Making Kraepelin History: A Great Instauration? In: History of Psychiatry 18.3 (2007): 267-273. [5] http:/ / books. google. com/ books?id=8RxWAAAAMAAJ& printsec=titlepage& source=gbs_summary_r& cad=0
Burgmair, Wolfgang & Eric J. Engstrom & Matthias Weber, et al., eds. Emil Kraepelin. 7 vols. Munich: belleville, 2000-2008. Vol. VII: Kraepelin in Munich, Teil II: 1914-1920 (2009), ISBN 978-3-933510-96-9 Vol. VI: Kraepelin in Munich, Teil I: 1903-1914 (2006), ISBN 3-933510-95-3 Vol. V: Kraepelin in Heidelberg, 1891-1903 (2005), ISBN 3-933510-94-5 Vol. IV: Kraepelin in Dorpat, 1886-1891 (2003), ISBN 3-933510-93-7 Vol. III: Briefe I, 1868-1886 (2002), ISBN 3-933510-92-9
Emil Kraepelin Vol. II: Kriminologische und forensische Schriften: Werke und Briefe (2001), ISBN 3-933510-91-0 Vol. I: Persnliches, Selbstzeugnisse (2000), ISBN 3-933510-90-2 Kraepelin, E. (1906). ber Sprachstrungen im Traume. Leizpig: Engelmann. (http:/ / books. google. com/ books?id=8RxWAAAAMAAJ&printsec=titlepage&source=gbs_summary_r&cad=0)
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External links
Extensive bibliography of English translations of Kraepelin's works (http://www.kraepelin.org/_wsn/page3. html) Extensive bibliography of works by and about Kraepelin's including those in the original German (http://www. mpipsykl.mpg.de/) International Kraepelin Society contact (http://www.kraepelin.org/) Kraepelin's monograph ber Sprachstrungen im Traume (http://www.archive.org/details/ bersprachstrung00kraegoog) Pulse-Project Audio Lecture: Dr. Octavian Buda on From Psychiatry in Dorpat to Eugenics in Munich: The late works of Emil Kraepelin. (http://www.pulse-project.org/node/150) For biographies of Kraepelin see: engstrom.de/KRAEPELINBIOGRAPHY.pdf (http://www.engstrom.de/KRAEPELINBIOGRAPHY.pdf) uni-leipzig.de/~psy/eng/kraep-e.html (http://www.uni-leipzig.de/~psy/eng/kraep-e.html) and ebsrv.ucsu.edu/facstaff/tbrown/times/obits/kraepelin.htm (http://websrv.ucsu.edu/facstaff/tbrown/times/obits/ kraepelin.htm) For English translations of Kraepelin's work see: On Uprootedness (1921) (http://hpy.sagepub.com/content/21/3/340.full.pdf+html) Emil Kraepelin's Clinical Self-Assessment (1920) (http://hpy.sagepub.com/content/13/49/98.full.pdf+html) Psychiatric Observations on Contemporary Issues (1919) (http://hpy.sagepub.com/content/3/10/256.full. pdf+html) On the Question of Degeneration (1908) (http://hpy.sagepub.com/content/18/3/399.full.pdf+html) The Directions of Psychiatric Research (1887) (http://hpy.sagepub.com/content/16/3/350.full.pdf+html)
Karl Leonhard
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Karl Leonhard
Karl Leonhard (March 21, 1904 in Edelsfeld, Bavaria, Germany April 23, 1988 in East Berlin, GDR) was a German psychiatrist, who stood in the tradition of Carl Wernicke and Karl Kleist. He created a complex classification of psychotic illnesses called nosological. His work covered Psychology, Psychotherapy, Biological psychiatry and Biological psychology. Moreover he created a classification of Nonverbal communication. He was born as the sixth of eleven children, his father being a Protestant minister. His medical education (at Erlangen, Berlin and Munich) was completed in 1928 and he worked as a physician at psychiatric hospitals in Erlangen, then a year later Gabersee and from 1936 Frankfurt am Main, to which last he was called by Karl Kleist. During the period of the Third Reich in order to save his patients from being killed by means of the T-4 Euthanasia Program, he stopped making diagnoses that would endanger a patient. In particular he stopped making any diagnoses of schizophrenia. He became a professor at Frankfurt in 1944 and a professor at Erfurt in the Soviet zone of Germany in 1954. In 1957 he became director of the psychiatric department at the Charit Hospital linked to the Humboldt University in East Berlin. He wanted to move back to West Germany in the sixties, but was refused the permission by the East German authorities. As compensation he got increased support for his scientific work. During his lifetime he interviewed more than 2000 psychotic patients, latterly with Dr Sieglinde von Trostorff. According to Helmut Beckmann (see "Books" below), editors of Western journals rejected his papers because "they were not in conformity with the standard practice of Anglo-American psychiatry and also because he pursued without compromise his own path derived from his findings." Most of his work was not translated into English. However summaries of Leonhard's views were included by Frank Fish in his "Schizophrenia" of 1962 (2nd edition 1976 ISBN 0-7236-0334-0) and "Clinical Psychopathology" of 1967 (2nd edition 1985 ISBN 0-7236-0605-6) which were widely read, if not understood, in their day. Today diagnosis for psychotic patients and mentally or otherwise ill persons are most commonly placed by ICD or DSM criteria. Psychosis will in general appear as an affective disorder (e.g. psychotic depression), a form of schizophrenia (e.g. catatonic type of schizophrenia) or a schizophrenia-like disorder, like the schizoaffective disorder for example.
Karl Leonhard Exalted Euphoria Confabulatory Euphoria Indifferent Euphoria The Cycloid Psychosis Anxiety-Happiness Psychosis Exited-Inhibited Confusion Psychosis Hyperkinetic-Akinetic Motility Psychosis The Unsystematic Schizophrenias Affective Paraphrenia Cataphasia (Schizophasia) Periodic Catatonia The Systematic Schizophrenias Simple Systematic Schizophrenias Catatonic Forms Parakinetic Catatonia Manneristic Catatonia Proskinetic Catatonia Negativistic Catatonia Speech-Prompt Catatonia Sluggish Catatonia Hebephrenic Forms Foolish Hebephrenia Eccentric Hebephrenia Shallow Hebephrenia Autistic Hebephrenia Paranoid Forms Hypochondrical Paraphrenia Phonemic Paraphrenia Incoherrent Paraphrenia Fantastic Paraphrenia Confabulatory Paraphrenia Expansive Paraphrenia Combined Systematic Schizophrenias Combined Systematic Catatonias Combined Systematic Hebephrenias Combined Systematic Paraphrenias Early Childhood Schizophrenias
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Karl Leonhard
26
Books
Die defektschizophrenen Krankheitsbilder, Leipzig: Thieme 1936 Classification of Endogenous Psychoses and their Differentiated Etiology [1], 2nd edition edited by Helmut Beckmann. New York/Wien: Springer-Verlag 1999 ISBN 3-211-83259-9 Der menschliche Ausdruck in Mimik, Gestik und Phonik, Leipzig: Barth 1969 - 3 Aufl. Wuerzburg 1997.
References
Internationale Wernicke-Kleist-Leonhard Gesellschaft [2] Menschenkunde.de [3] PsychiatrieOnline.org [4]
References
[1] [2] [3] [4] http:/ / books. google. com/ books?id=DVlvcsfFWeAC& lpg=PR1& pg=PR1#v=onepage& q& f=false http:/ / www. wkl-society. de/ http:/ / www. menschenkunde. net/ artikel/ kl-werk. htm http:/ / ajp. psychiatryonline. org/ cgi/ content/ full/ 155/ 10/ 1309
John Cade
This article is about the Australian psychiatrist. For the leader of the Kent Rebellion, see Jack Cade. For the former Maryland State Senator, see John A. Cade For the Louisiana Republican state chairman, see John H. Cade, Jr.
John Cade AO
Born 18 January 1912 Murtoa, Victoria, Australia 16 November 1980 (aged68) Fitzroy, Victoria, Australia
Died
Occupation psychiatrist; army medical officer; medical scientist; mental health practitioner; prisoner of war (Australian); public servant Spouse Children Parents Estana Evelyn Jean Charles John (1938), David (1940), Mary (1947), Peter (1948), Richard (1950) Dr David & Ellen Cade
Dr John Frederick Joseph Cade AO (18 January 1912 16 November 1980) was an Australian psychiatrist credited with discovering (in 1948) the effects of lithium carbonate as a mood stabilizer in the treatment of bipolar disorder (then known as manic depression). In an age where the standard treatments for psychosis were electroconvulsive therapy and lobotomy, lithium had the distinction of being the first effective medication available to treat a mental illness.
John Cade
27
Early life
John Cade was born in Murtoa,[1] in the Wimmera region of Victoria, Australia. John's father David was Murtoa's general practitioner. Ellen, John's mother, and younger brothers David and Frank completed the family. When John was a small boy, his father left for World War I and served in Gallipoli and France. On return from the war, his father suffered from 'war weariness' and had difficulty in continuing in general practice. Therefore, his father sold the practice and accepted a position with the Mental Hygiene Department. Over the next 25 years, Dr Cade Sr became medical superintendent at several Victorian mental hospitals, namely Sunbury, Beechworth and Mont Park. John and his brothers spent many of their younger years living within the grounds of these institutions, which had a great bearing on John's later deep understanding of the needs of the mentally ill.[2] John was educated at Scotch College, Melbourne, matriculating in 1928. He then studied medicine at the University of Melbourne, graduating at the age of 21 years with honours in all subjects. He became a House Officer at St Vincent's Hospital and then Royal Children's Hospital before becoming severely ill with bilateral pneumococcal pneumonia. While he was convalescing, John fell in love with one of his nurses, Jean. They married in 1937.[2]
World War II
Like his father before him, Cade left his young family to fight for Australia in the Armed Forces in World War II. Cade was appointed captain, Australian Army Medical Corps, A.I.F., on 1 July 1940 and posted to the 2nd/9th Field Ambulance.[3] Although trained as a psychiatrist, Dr. Cade served as a surgeon and departed for Singapore in 1941 on RMS Queen Mary. He was promoted to major in September 1941. After the Fall of Singapore to Japan, he became a prisoner of war at Changi Prison from February 1942 to September 1945.[2] During his imprisonment, he reportedly would observe some fellow inmates having strange, vacillating behaviour. He thought perhaps a toxin was affecting their brains and when it was eliminated through their urine, they lost their symptoms.
John Cade
28
Troubled Minds
In 2004, Film Australia and SBS screened the documentary 'Troubled Minds The Lithium Revolution',[7] a 60 minute documentary portraying John Cade's discovery of the use of Lithium in mental illness. The documentary received international recognition winning the main prize at the International Vega Awards for Excellence in Scientific Broadcasting. Troubled Minds was also recognised locally with writer/director Dennis K. Smith winning the AWGIE Award for Best Documentary.[8]
Notes
[1] Some authors state Cade was born in Horsham, one of the larger towns in the Wimmera area. However other authors, notably Cade's son Jack Cade, state John Cade was born in Murtoa, a town 32 kilometres (20mi) NE of Horsham. [2] Cade, Jack F. (1999). "John Frederick Joseph Cade: family memories on the occasion of the 50th anniversary of his discovery of the use of lithium in mania". The Australian and New Zealand journal of psychiatry 33 (5): 615618. doi:10.1080/j.1440-1614.1999.00624.x. PMID10544983. [3] Ironside, Wallace (1993). "Cade, John Frederick Joseph (19121980)" (http:/ / www. adb. online. anu. edu. au/ biogs/ A130374b. htm). Australian Dictionary of Biography. Canberra: Australian National University. . Retrieved 22 September 2008. [4] Cade, John FJ (3 September 1949). "Lithium salts in the treatment of psychotic excitement". Medical Journal of Australia 2 (36): 349352. [5] "It's an Honour Officer of the Order of Australia" (http:/ / www. itsanhonour. gov. au/ honours/ honour_roll/ search. cfm?aus_award_id=883814& search_type=quick& showInd=true). . Retrieved 22 November 2008. [6] "100 Years of Australian Innovation lithium for manic depression" (http:/ / www. biotechnology-innovation. com. au/ innovations/ pharmaceuticals/ manic_depression. html). . Retrieved 11 October 2008. [7] Troubled Minds: The Lithium Revolution (http:/ / www. imdb. com/ title/ tt1201166/ ) at the Internet Movie Database [8] "2005 AWGIE Award Winners" (http:/ / www. awg. com. au/ artman/ uploads/ awgie_2004_winners. pdf) (pdf). Australian Writers' Guild. . Retrieved 22 September 2008.
John Cade
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References
Mitchell PB, Hadzi-Pavlovic D. John Cade and the discovery of lithium treatment for manic depressive illness. Medical Journal of Australia, 1999, 171: 262264. and Ref. No. 00-0612 Bulletin of the World Health Organization, 2000, 78 (4) Mitchell PB. On the 50th anniversary
Mogens Schou
Mogens Schou (24 November 1918 29 September 2005) was a Danish psychiatrist whose groundbreaking research into Lithium led to its utilization as a treatment for bipolar illness. His work ultimately benefited thousands of patients worldwide.
Early years
Schou was born in Copenhagen, Denmark, on 24 November 1918. His father was a psychiatrist and medical director of a large mental hospital. Schou chose to study medicine with a specific view to doing research on manic-depressive illness (now more commonly referred to as bipolar disorder). He graduated with a degree in medicine from the University of Copenhagen in 1944. After his training in clinical psychiatry he also studied experimental biology.
Research
Schou had a long and distinguished career dedicated to research on therapeutic uses of lithium rooted in his deep concern for all patients with mood disorders, initially inspired by the depression and manic-depressive illness that afflicted many of his relatives. The psychopharmacological era began in earnest in 1949, with the article published by John Cade about the observed antimanic action of Lithium in Australia. Intrigued by these findings Schou, who in the meantime joined the Psychiatric Research Institute of the Aarhus University in Denmark, confirmed these findings in a double-blind placebo-controlled study with his co-workers. This marked the beginning of Schou's illustrious association with lithium. Since then, there have been a number of interlinked research themes that run through Schou's work. In the 1960s, Schou and Poul Baastrup discovered that long-term lithium treatment prevents the recurrences of illness in bipolar and some unipolar patients and they were understandably exhilarated. During the early 1960s, G. P. Hartigan, Poul Chr. Baastrup and Schou independently made sporadic observations that were suggestive of lithium also having prophylactic properties in manic-depressive illness. Subsequently, Baastrup and Schou joined together and in a non-blind lithium trial saw their preliminary observations confirmed. They even deemed the results so significant that they concluded that lithium is the first drug demonstrated as a clear-cut prophylactic agent against one of the major psychoses. However, the Schou-Baastrup prophylaxis hypothesis was met with great resistance by British psychiatry. To Aubrey Lewis and Michael Shepherd, lithium was dangerous nonsense. Shepherd, seconded by Harry Blackwell, simply characterized it as a therapeutic myth, which, in their opinion, was based on serious methodological shortcomings and spurious claims. Even terms such as unethical and unscientific were used. After painful consideration of the ethical aspects invoked, Schou and Baastrup undertook a unique double-blind trial of prospective-discontinuation design and with random allocation of manic-depressive patients (already on lithium) to lithium or placebo, unparalleled in psychiatry. It fully confirmed their hypothesis, published in The Lancet in 1970. Thus, lithium prophylaxis had also become established as evidence based. Lithium became the first-choice mood stabilizer in bipolar affective disorder.
Mogens Schou He was aware of some of the limitations of lithium treatment. He welcomed the introduction of other prophylactic agents into the market. From the available observations he concluded, however, that anti-epileptics and atypical anti-psychotics act on different kinds of bipolar patients to lithium. After he discovered lithium's prophylactic action in mood disorders, he tirelessly researched all its aspects and did not spare any effort to make the treatment available to all those in need. Millions of patients with recurrent mood disorders benefited because of his research. In 1990, authorities on manic-depressive illness such as Fred Goodwin and Kay Redfield Jamison characterized the ground-breaking discovery of lithium prophylaxis as one of the most important advances in modern psychiatry. He was an author of more than 500 publications, including texts, research papers, articles and book chapters. He was Emeritus Professor of the Psychiatric Hospital in Risskov, Denmark.
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References
Grof, Paul (2006). "Mogens Schou (19182005)" [1]. Neuropsychopharmacology 31 (4): 891892. doi:10.1038/sj.npp.1301018. Retrieved 2008-08-02. Schioldann, Johan (23 March 2006). "Obituary Mogens Schou 19182005" [2]. Australasian Psychiatry 14 (1): 116117. doi:10.1111/j.1440-1665.2006.02239.x. Retrieved 2008-08-02. Obituary Mogens Schou [3]
References
[1] http:/ / www. nature. com/ npp/ journal/ v31/ n4/ full/ 1301018a. html [2] http:/ / www3. interscience. wiley. com/ journal/ 118565544/ abstract?CRETRY=1& SRETRY=0 [3] http:/ / www. mooddisorderscanada. ca/ Mogens_Schou. pdf
Frederick K. Goodwin
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Frederick K. Goodwin
Frederick K. Goodwin
Born April 21, 1936 Cincinnati, Ohio
Occupation Psychiatrist, Research professor Spouse Rosemary Goodwin, MSW Website http:/ / drgoodwin. com [1]
Frederick K. Goodwin is a psychiatrist and Clinical Professor of Psychiatry at George Washington University [2] [3] where he is also director of the Center on Neuroscience, Medical Progress, and Society. He is a specialist in bipolar disorder (also known as manic-depressive illness) and recurrent depression.[4] Goodwin received his M.D. from St. Louis University, and was a psychiatric resident at the University of North Carolina in Chapel Hill. Goodwin joined the National Institute of Mental Health (NIMH) in 1965, and was its director from 1992 to 1994. Prior to that he held a Presidential appointment as head of the Alcohol, Drug Abuse, and Mental Health Administration,[5] served as NIMH Scientific Director and Chief of Intramural Research from 1981 to 1988. He was the first to report a controlled study on the antidepressant effects of lithium.[6] [7] He is a member of the Institute of Medicine of the National Academy of Sciences[8] and a fellow of the ACNP. He is a founder of the journal Psychiatry Research, and on the editorial boards of a number of other journals. He was president of the Psychiatric Research Society, elected in 1998.[9] Dr. Goodwin is a recipient of the major research awards in his field including the Hofheimer Prize from the American Psychiatric Association, the International Anna-Monika Prize for Research in Depression, the Edward A. Strecker Award,[10] the Nola Maddox Falcone Prize from NARSAD,[11] the McAlpin Research Award from the National Mental Health Association, the Distinguished Service Award from the National Alliance on Mental Illness, and the Research Award from the American Foundation for Suicide Prevention. He was the first recipient of the Psychiatrist of the Year from Psychiatric Times, and the Fawcett Humanitarian Award of the NDMDA (now the Depression and Bipolar Support Alliance. Dr. Goodwin was one of only five psychiatrists on the Current Contents list of the most frequently cited scientists in the world and one of 12 listed in The Best Doctors in the U.S.[12]
Frederick K. Goodwin independently supported Dr. Goodwin's claim.[14] In 2008, Sen. Charles Grassley (IA-R) conducted investigations regarding possible conflicts of interest between various academic psychiatrists and pharmaceutical companies. Sen. Grassley found no impropriety regarding Dr. Goodwin. The Times article, however, implied that Sen. Grassley uncovered some wrongdoing.[13] Dr. Goodwin issued a statement that The New York Times article and the follow-up editorial were filled with misstatements of fact and false implications.[15] The Infinite Mind program, which was independently produced and distributed, was slated to end its production at the end of 2008 due to a lack of funding. Nevertheless, following the controversy, NPR cancelled the broadcast of reruns of the show on its Sirius Satellite Radio channel.[12]
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Awards
Hofheimer Prize from the American Psychiatric Association International Anna-Monika Prize for Research in Depression Edward A. Strecker Award Falcone Prize from NARSAD McAlpin Research Award from the National Mental Health Association Distinguished Service Award from NAMI Research Award from the American Foundation for Suicide Prevention "Psychiatrist of the Year" from Psychiatric Times (first recipient) Fawcett Humanitarian Award from the National Depressive and Manic Depressive Association (first recipient) A.E. Bennett Award from the Society of Biological Psychiatry Psychopharmacology Research Award from the American Psychological Association Lifetime Achievement Award from the International Review of Bipolar Disorders Public Service Award from the Federation of American Societies for Experimental Biology (FASEB) Hope Award from the Depression and Bipolar Support Alliance
Publications
With Kay Redfield Jamison, Goodwin wrote Manic-Depressive Illness, the first psychiatric text to win the "Best Medical Book" award from the Association of American Publishers and Manic-Depressive Illness: Bipolar Disorders and Recurrent Depression. In addition, Dr. Goodwin has authored over 470 academic papers.
References
[1] [2] [3] [4] [5] http:/ / drgoodwin. com http:/ / www. gwupsychiatry. org/ faculty. html http:/ / john. gwumc. edu/ FacultyList/ searchmachine http:/ / drgoodwin. com/ index. php?page=bio Accessed on March 2, 2011 "New Director Named for Drug, Alcohol Research" (http:/ / pqasb. pqarchiver. com/ washingtonpost/ access/ 73617785. html?FMT=ABS& FMTS=ABS:FT& date=Jul+ 12,+ 1988& author=& pub=The+ Washington+ Post+ (pre-1997+ Fulltext)& edition=& startpage=z. 18& desc=New+ Director+ Named+ for+ Drug,+ Alcohol+ Research). July 12, 1988. . [6] . PMID4896983. [7] . PMID4556087. [8] http:/ / www. iom. edu/ Global/ DIrector/ Detail. aspx?id=0000045478 [9] http:/ / www. elsevier. com/ wps/ find/ journaleditorialboard. cws_home/ 522773/ editorialboard [10] http:/ / www. med. upenn. edu/ psych/ Strecker_recipients. html [11] http:/ / www. narsad. org/ ?q=node/ 128/ prizes [12] http:/ / drgoodwin. com/ index. php?page=bio [13] Harris, Gardiner (November 22, 2008). "Radio Host Has Drug Company Ties" (http:/ / www. nytimes. com/ 2008/ 11/ 22/ health/ 22radio. html?hp). The New York Times. . [14] http:/ / www. onthemedia. org/ transcripts/ 2008/ 11/ 28/ 01
Frederick K. Goodwin
[15] http:/ / drgoodwin. com/ index. php?page=nyt
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Academic contributions
Her book Manic-Depressive Illness (co-authored with Frederick K. Goodwin) is the classic textbook on bipolar disorder. Her seminal works among laypeople are her memoir An Unquiet Mind, which details her experience with severe mania and depression, and Night Falls Fast: Understanding Suicide, providing historical, religious, and cultural responses to suicide, as well as the relationship between mental illness and suicide. In Night Falls Fast, Jamison dedicates a chapter to American public policy and public opinion as it relates to suicide. Her second memoir, Nothing Was the Same, examines her relationship with her second husband, the psychiatrist Richard Jed Wyatt, who was Chief of the Neuropsychiatry Branch of the National Institute of Mental Health until his death in 2002.
Kay Redfield Jamison In her study Exuberance: The Passion for Life, she cites research which suggests that 15 percent of people who could be diagnosed as manic depressive may never actually become depressed; in effect, they are permanently 'high' on life. She mentions President Theodore Roosevelt as an example. Touched with Fire: Manic-Depressive Illness and the Artistic Temperament is Jamison's exploration of how bipolar disorder can run in artistic or high-achieving families. As an example, she cites Lord Byron and his relatives.
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Personal life
Jamison, in an interview [4], said she was an "exuberant" person, yet she longed for peace and tranquility; but in the end, she preferred "tumultuousness coupled to iron discipline" over leading a "stunningly boring life." In her memoir An Unquiet Mind, she concluded: I long ago abandoned the notion of a life without storms, or a world without dry and killing seasons. Life is too complicated, too constantly changing, to be anything but what it is. And I am, by nature, too mercurial to be anything but deeply wary of the grave unnaturalness involved in any attempt to exert too much control over essentially uncontrollable forces. There will always be propelling, disturbing elements, and they will be there until, as Lowell put it, the watch is taken from the wrist. It is, at the end of the day, the individual moments of restlessness, of bleakness, of strong persuasions and maddened enthusiasms, that inform one's life, change the nature and direction of one's work, and give final meaning and color to one's loves and friendships. Jamison is an Episcopalian[5] and was married to Richard Wyatt until his death in 2002.[6] Wyatt was a psychiatrist who studied schizophrenia at the National Institutes of Health. Their romance is detailed in the memoir Nothing Was the Same.
Bibliography
Manic-Depressive Illness (1990) (with Frederick K. Goodwin), ISBN 0-19-503934-3 Manic-Depressive Illness (2007) (with Frederick K. Goodwin), second edition Touched with Fire: Manic-Depressive Illness and the Artistic Temperament (1993) (includes a study of Lord Byron's illness), ISBN 0-684-83183-X An Unquiet Mind (1995) (autobiography), ISBN 0-679-76330-9 Night Falls Fast: Understanding Suicide (1999), ISBN 0-375-70147-8 Exuberance: The Passion for Life (2004), ISBN 0-375-40144-X Nothing Was the Same: A Memoir (2009), ISBN 0-307-26537-4
References
[1] Downer, Joanna (October 1, 1997). "Physician, Heal Thyself" (http:/ / www. time. com/ time/ printout/ 0,8816,987104,00. html). Time. . Retrieved July 27, 2011. [2] http:/ / www. st-andrews. ac. uk/ graduation/ laureationaddresses/ [3] "General Seminary's 189th Commencement on May 18" (http:/ / gts. edu/ index. php?option=com_content& view=article& id=1159:general-seminarys-189th-commencement-on-may-18-& catid=68:frontpage-news). The General Theological Seminary. May 5, 2011. . Retrieved July 27, 2011. [4] http:/ / www. mcmanweb. com/ article-247. htm [5] Night Falls Fast, p. 310 [6] O'Connor, Anahad (June 12, 2002). "Richard J. Wyatt, 63, Is Dead; Led Studies of Schizophrenia" (http:/ / www. nytimes. com/ 2002/ 06/ 12/ us/ richard-j-wyatt-63-is-dead-led-studies-of-schizophrenia. html). The New York Times. . Retrieved July 27, 2011.
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External links
An Interview with Kay Jamison on Charlie Rose Show - 17 mins video (http://www.charlierose.com/shows/ 1999/10/26/1/an-interview-with-kay-redfield-jamison) Faculty Profile at JHU (http://www.hopkinsmedicine.org/psychiatry/expert_team/faculty/J/Jamison.html)
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Symptoms
Hallucination
Hallucination
Classification and external resources
My eyes at the moment of the apparitions by August Natterer. ICD-10 ICD-9 DiseasesDB MeSH R44 [1] [2] [3] [4]
780.1 19769
D006212
A hallucination, in the broadest sense of the word, is a perception in the absence of a stimulus. In a stricter sense, hallucinations are defined as perceptions in a conscious and awake state in the absence of external stimuli which have qualities of real perception, in that they are vivid, substantial, and located in external objective space. The latter definition distinguishes hallucinations from the related phenomena of dreaming, which does not involve wakefulness; illusion, which involves distorted or misinterpreted real perception; imagery, which does not mimic real perception and is under voluntary control; and pseudohallucination, which does not mimic real perception, but is not under voluntary control.[5] Hallucinations also differ from "delusional perceptions", in which a correctly sensed and interpreted stimulus (i.e. a real perception) is given some additional (and typically bizarre) significance. Hallucinations can occur in any sensory modality visual, auditory, olfactory, gustatory, tactile, proprioceptive, equilibrioceptive, nociceptive, thermoceptive and chronoceptive. A mild form of hallucination is known as a disturbance, and can occur in any of the senses above. These may be things like seeing movement in peripheral vision, or hearing faint noises and/or voices. Auditory hallucinations are very common in paranoid schizophrenia. They may be benevolent (telling the patient good things about themselves) or malicious, cursing the patient etc. Auditory hallucinations of the malicious type are frequently heard like people talking about the patient behind their back. Like auditory hallucinations, the source of their visual counterpart can also be behind the patient's back. Their visual counterpart is the feeling of being looked-stared at, usually with malicious intent. Frequently, auditory hallucinations and their visual counterpart are experienced by the patient together.
Hallucination Hypnagogic hallucinations and hypnopompic hallucinations are considered normal phenomena. Hypnagogic hallucinations can occur as one is falling asleep and hypnopompic hallucinations occur when one is waking up. Hallucinations can be associated with drug use (particularly deliriants), sleep deprivation, psychosis, neurological disorders, and delirium tremens.
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Classification
Hallucinations may be manifested in a variety of forms.[6] Various forms of hallucinations affect different senses, sometimes occurring simultaneously, creating multiple sensory hallucinations for those experiencing them.
Visual
The most common modality referred to when people speak of hallucinations. These include the phenomena of seeing things which are not present or visual perception which does not reconcile with the consensus reality. There are many different causes, which have been classed as psychophysiologic (a disturbance of brain structure), psychobiochemical (a disturbance of neurotransmitters), and psychological (e.g. meaningful experiences consciousness). Numerous disorders can involve visual hallucinations, ranging from psychotic disorders to dementia to migraine, but experiencing visual hallucinations does not in itself mean there is necessarily a disorder.[7] Visual hallucinations are associated with organic disorders of the brain and with drug and alcohol related illness.[8] Sometimes internal imagery can overwhelm the sensory input from external stimuli when sharing neural pathways, or if indistinct stimuli is perceived and manipulated to match one's expectations or beliefs, especially about the environment. This can result in a hallucination.[9]
Auditory
Auditory hallucinations (also known as paracusia),[10] are the perception of sound without outside stimulus. Auditory hallucinations can be divided into two categories: elementary and complex. Elementary hallucinations are the perception of sounds such as hissing, whistling, an extended tone, and more. In many cases, tinnitus is an elementary auditory hallucination. However, some people who experience certain types of tinnitus, especially pulsatile tinnitus, are actually hearing the blood rushing through vessels near the ear. Because the auditory stimulus is present in this situation, it does not qualify as a hallucination. Complex hallucinations are those of voices, music, or other sounds which may or may not be clear, may be familiar or completely unfamiliar, and friendly or aggressive, among other possibilities. Hallucinations of one or more talking voices, are particularly associated with psychotic disorders such as schizophrenia, and hold special significance in diagnosing these conditions. However, many people not suffering from diagnosable mental illness may sometimes hear voices as well.[11] One important example to consider when forming a differential diagnosis for a patient with paracusia is lateral temporal lobe epilepsy. Despite the tendency to associate hearing voices, or otherwise hallucinating, and psychosis with schizophrenia or other psychiatric illnesses, it is crucial to take into consideration that even if a person does exhibit psychotic features, they do not necessarily suffer from a psychiatric disorder on its own. Disorders such as Wilson's disease, various endocrinological disorders, numerous metabolic disturbances, multiple sclerosis, systemic lupus erythematosis, porphyria, sarcoidosis, and many others can present with psychosis. Musical hallucinations are also relatively common in terms of complex auditory hallucinations and may be the result of a wide range of causes ranging from hearing-loss (such as in musical ear syndrome, the auditory version of Charles Bonnet syndrome), lateral temporal lobe epilepsy,[12] arteriovenous malformation,[13] stroke, lesion, abscess, or tumor.[14] The Hearing Voices Movement is a support and advocacy group for people who hallucinate voices, but do not otherwise show signs of mental illness or impairment.
Hallucination
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Command hallucinations
Command hallucinations are hallucinations in the form of commands.[15] The contents of the hallucinations can range from the innocuous to commands to cause harm to the self or others.[15] Command hallucinations are often associated with schizophrenia. People experiencing command hallucinations may or may not comply with the hallucinated commands, depending on circumstances. Compliance is more common for non-violent commands.[16]
Olfactory
Phantosmia is the phenomenon of smelling odors that aren't really present. The most common odors are unpleasant smells such as rotting flesh, vomit, urine, feces, smoke, or others. Phantosmia often results from damage to the nervous tissue in the olfactory system. The damage can be caused by viral infection, brain tumor, trauma, surgery, and possibly exposure to toxins or drugs.[17] Phantosmia can also be induced by epilepsy affecting the olfactory cortex and is also thought to possibly have psychiatric origins. Phantosmia is different from parosmia, in which a smell is actually present, but perceived differently from its usual smell. Olfactory hallucinations can also appear in some cases of associative imagination, for example, while watching a romance movie, where the man gifts roses to the woman, the viewer senses the roses' odor (which in fact does not exist). Olfactory hallucinations have also been reported in migraine, although the frequency of such hallucinations is unclear.[18] [19]
Tactile hallucinations
Tactile hallucinations are the illusion of tactile sensory input, simulating various types of pressure to the skin or other organs. One subtype of tactile hallucination, formication, is the sensation of insects crawling underneath the skin and is frequently associated with prolonged cocaine or amphetamine use[20] or with withdrawal from alcohol or benzodiazepines. However, formication may also be the result of normal hormonal changes such as menopause, or disorders such as peripheral neuropathy, high fevers, Lyme disease, skin cancer, and more.[20]
Gustatory
This type of hallucination is the perception of taste without a stimulus. These hallucinations, which are typically strange or unpleasant, are relatively common among individuals who have certain types of focal epilepsy, especially temporal lobe epilepsy. The regions of the brain responsible for gustatory hallucination in this case are the insula and the superior bank of the sylvian fissure.[21] [22]
Hallucination
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Stages of a hallucination
1. 2. 3. 4. 5. Emergence of surprising or warded-off memory or fantasy images[24] Frequent reality checks[24] Last vestige of insight as hallucinations become "real"[24] Fantasy and distortion elaborated upon and confused with actual perception[24] Internal-external boundaries destroyed and possible pantheistic experience[24]
Cause
Hallucinations can be caused by a number of factors.
Hypnagogic hallucination
These hallucinations occur just before falling asleep, and affect a surprisingly high proportion of the population. The hallucinations can last from seconds to minutes, all the while the subject usually remains aware of the true nature of the images. These may be associated with narcolepsy. Hypnagogic hallucinations are sometimes associated with brainstem abnormalities, but this is rare.[25]
Peduncular hallucinosis
Peduncular means pertaining to the peduncle, which is a neural tract running to and from the pons on the brain stem. These hallucinations usually occur in the evenings, but not during drowsiness, as in the case of hypnagogic hallucination. The subject is usually fully conscious and then can interact with the hallucinatory characters for extended periods of time. As in the case of hypnagogic hallucinations, insight into the nature of the images remains intact. The false images can occur in any part of the visual field, and are rarely polymodal.[25]
Delirium tremens
One of the more enigmatic forms of visual hallucination is the highly variable, possibly polymodal delirium tremens. Individuals suffering from delirium tremens may be agitated and confused, especially in the later stages of this disease. Insight is gradually reduced with the progression of this disorder. Sleep is disturbed and occurs for a shorter period of time, with rapid eye movement sleep.
Hallucination
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Migraine coma
This type of hallucination is usually experienced during the recovery from a comatose state. The migraine coma can last for up to two days, and a state of depression is sometimes comorbid. The hallucinations occur during states of full consciousness, and insight into the hallucinatory nature of the images is preserved. It has been noted that ataxic lesions accompany the migraine coma.[25]
Focal epilepsy
Visual hallucinations due to focal seizures differ depending on the region of the brain where the seizure occurs. For example, visual hallucinations during occipital lobe seizures are typically visions of brightly colored, geometric shapes that may move across the visual field, multiply, or form concentric rings and generally persist from a few seconds to a few minutes. They are usually unilateral and localized to one part of the visual field on the ipsilateral side of the seizure focus, typically the temporal field. However, unilateral visions moving horizontally across the visual field begin on the contralateral side and move towards the ipsilateral side.[21] Temporal lobe seizures, on the other hand, can produce complex visual hallucinations of people, scenes, animals, and more as well as distortions of visual perception. Complex hallucinations may appear real or unreal, may or may not be distorted with respect to size, and may seem disturbing or affable, among other variables. One rare but notable type of hallucination is heautoscopy, a hallucination of a mirror image of one's self. These "other selves" may be perfectly still or performing complex tasks, may be an image of a younger self or the present self, and tend to be only briefly present. Complex hallucinations are a relatively uncommon finding in temporal lobe epilepsy patients. Rarely, they may occur during occipital focal seizures or in parietal lobe seizures.[21] Distortions in visual perception during a temporal lobe seizure may include size distortion (micropsia or macropsia), distorted perception of movement (where moving objects may appear to be moving very slowly or to be perfectly still), a sense that surfaces such as ceilings and even entire horizons are moving farther away in a fashion similar to the dolly zoom effect, and other illusions.[28] Even when consciousness is impaired, insight into the hallucination or illusion is typically preserved.
Schizophrenic hallucination
Hallucinations caused by schizophrenia.
Drug-induced hallucination
Hallucinations caused by the consumption of psychoactive substances such as LSD or DMT.
Pathophysiology
Hallucination Various theories have been put forward to explain the occurrence of hallucinations. When psychodynamic (Freudian) theories were popular in psychology, hallucinations were seen as a projection of unconscious wishes, thoughts and wants. As biological theories have become orthodox, hallucinations are more often thought of (by psychologists at least) as being caused by functional deficits in the brain. With reference to mental illness, the function (or dysfunction) of the neurotransmitters glutamate and dopamine are thought to be particularly important.[29] The Freudian interpretation may have an aspect of truth, as the biological hypothesis explains the physical interactions in the brain, while the Freudian deals with the origin of the theme of the hallucination. Psychological research has argued that hallucinations may result from biases in what are known as metacognitive abilities.[30] These are abilities that allow us to monitor or draw inferences from our own internal psychological states (such as intentions, memories, beliefs and thoughts). The ability to discriminate between internal (self-generated) and external (stimuli) sources of information is considered to be an important metacognitive skill, but one which may break down to cause hallucinatory experiences. Projection of an internal state (or a person's own reaction to another's) may arise in the form of hallucinations, especially auditory hallucinations. A recent hypothesis that is gaining acceptance concerns the role of overactive top-down processing, or strong perceptual expectations, that can generate spontaneous perceptual output (that is, hallucination).[31]
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Treatments
There are few treatments for many types of hallucinations. However, for those hallucinations caused by mental disease, a psychologist or psychiatrist should be alerted, and treatment will be based on the observations of those doctors. Antipsychotic and atypical antipsychotic medication may also be utilized to treat the illness if the symptoms are severe and cause significant distress. For other causes of hallucinations there is no factual evidence to support any one treatment is scientifically tested and proven. However, abstaining from hallucinogenic drugs, managing stress levels, living healthily, and getting plenty of sleep can help reduce the prevalence of hallucinations. In all cases of hallucinations, medical attention should be sought out and informed of one's specific symptoms.
Epidemiology
One study from as early as 1895[32] reported that approximately 10% of the population experienced hallucinations. A 1996-1999 survey of over 13,000 people[33] reported a much higher figure, with almost 39% of people reporting hallucinatory experiences, 27% of which were daytime hallucinations, mostly outside the context of illness or drug use. From this survey, olfactory (smell) and gustatory (taste) hallucinations seem the most common in the general population.
Further reading
Johnson FH (1978). The anatomy of hallucinations. Chicago: Nelson-Hall Co. ISBN 0-88229-155-6. Bentall RP, Slade PD (1988). Sensory deception: a scientific analysis of hallucination. London: Croom Helm. ISBN 0-7099-3961-2. Aleman A, Lari F (2008). Hallucinations: The Science of Idiosyncratic Perception. American Psychological Association (APA). ISBN 1-4338-0311-9.
Hallucination
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References
[1] [2] [3] [4] [5] http:/ / apps. who. int/ classifications/ icd10/ browse/ 2010/ en#/ R44 http:/ / www. icd9data. com/ getICD9Code. ashx?icd9=780. 1 http:/ / www. diseasesdatabase. com/ ddb19769. htm http:/ / www. nlm. nih. gov/ cgi/ mesh/ 2011/ MB_cgi?field=uid& term=D006212 Leo P. W. Chiu (1989). "Differential diagnosis and management of hallucinations" (http:/ / sunzi1. lib. hku. hk/ hkjo/ view/ 21/ 2100448. pdf) (PDF). Journal of the Hong Kong Medical Association 41 (3): 2927. . [6] Chen E. and Berrios G.E. (1996) Recognition of hallucinations: a multidimensional model and methodology. Psychopathology 29: 54-63. [7] Visual Hallucinations: Differential Diagnosis and Treatment (2009) (http:/ / www. ncbi. nlm. nih. gov/ pmc/ articles/ PMC2660156/ ) [8] semple,David."oxford hand book of psychiatry" oxford press.2005. [9] Horwitz, M. (1975). Hallucinations: An information-processing approach. New York: Wiley. pp.163194. [10] "Medical dictionary" (http:/ / medical-dictionary. thefreedictionary. com/ paracusia). . [11] Thompson, Andrea (September 15, 2006). "Hearing Voices: Some People Like It" (http:/ / www. livescience. com/ humanbiology/ 060915_hearing_voices. html). LiveScience.com. . Retrieved 2006-11-25. [12] Engmann, Birk; Reuter, Mike: Spontaneous perception of melodies hallucination or epilepsy? Nervenheilkunde 2009 Apr 28: 217-221. ISSN 0722-1541 [13] Murat Ozsarac, Ersin Aksay, Selahattin Kiyan, Orkun Unek, F. Feray Gulec, De Novo Cerebral Arteriovenous Malformation: Pink Floyd's Song 'Brick in the Wall' as a Warning Sign, The Journal of Emergency Medicine, In Press, Corrected Proof, Available online 13 August 2009, ISSN 0736-4679, DOI: 10.1016/j.jemermed.2009.05.035. [14] "Rare Hallucinations Make Music In The Mind" (http:/ / www. sciencedaily. com/ releases/ 2000/ 08/ 000809065249. htm). ScienceDaily.com. August 9, 2000. . Retrieved 2006-12-31. [15] Beck-Sander, A.; Birchwood, M.; Chadwick, P. (1997). "Acting on command hallucinations: A cognitive approach". The British journal of clinical psychology / the British Psychological Society 36 ( Pt 1): 139148. PMID9051285. [16] Lee, T. M.; Chong, S. A.; Chan, Y. H.; Sathyadevan, G. (2004). "Command hallucinations among Asian patients with schizophrenia". Canadian journal of psychiatry. Revue canadienne de psychiatrie 49 (12): 838842. PMID15679207. [17] Phantom smells (http:/ / www. doctorhoffman. com/ wwphant. htm) [18] Wolberg FL, Zeigler DK (1982). "Olfactory Hallucination in Migraine". Archives of Neurology 39 (6): 382. PMID7092619. [19] Sacks, Oliver (1986). Migraine. Berkeley: University of California Press. pp.7576. ISBN9780520058897. [20] Berrios G E (1982) Tactile Hallucinations. Journal of Neurology, Neurosurgery and Psychiatry 45: 285-293 [21] Panayiotopoulos, Chrysostomos P. A clinical guide to epileptic syndromes and their treatment: based on the ILAE classification and practice parameter guidelines. 2. ed. London: Springer, 2007. [22] Barker, P. 1997. Assessment in Psychiatric and Mental Health Nursing In Search of the Whole Person. UK: Nelson Thornes Ltd. p245. [23] Barker, P. 1997. Assessment in Psychiatric and Mental Health Nursing in Search of the Whole Person. UK: Nelson Thornes Ltd. P245. [24] Horowitz MJ (1975). "Hallucinations: An Information Processing Approach". In West LJ, Siegel RK. Hallucinations; behavior, experience, and theory. New York: Wiley. ISBN0-471-79096-6. [25] Manford M, Andermann F (Oct 1998). "Complex visual hallucinations. Clinical and neurobiological insights" (http:/ / brain. oxfordjournals. org/ cgi/ content/ abstract/ 121/ 10/ 1819). Brain 121 ((Pt 10)): 181940. doi:10.1093/brain/121.10.1819. PMID9798740. . [26] Mark Derr (2006) (http:/ / www. nytimes. com/ 2006/ 02/ 14/ health/ 14case. html?ex=1151121600& en=04560d31e7926bee& ei=5070) Marilyn and Me, "The New York Times" February 14, 2006 [27] Engmann, Birk (2008). "Phosphenes and photopsias - ischaemic origin or sensorial deprivation? - Case history" (http:/ / www. psycontent. com/ content/ m507n73711u73652/ ?p=400b10f998844a6abe524fcf44626323& pi=1) (in German). Z Neuropsychol. 19 (1): 713. doi:10.1024/1016-264X.19.1.7. . [28] Bien CG, Benninger FO, Urbach H, Schramm J, Kurthen M, Elger CE (2000) Localizing value of epileptic visual auras. Brain 123:244253 PubMed (http:/ / www. ncbi. nlm. nih. gov/ pubmed/ 10648433?dopt=Abstract/ ) [29] Kapur S (Jan 2003). "Psychosis as a state of aberrant salience: a framework linking biology, phenomenology, and pharmacology in schizophrenia" (http:/ / ajp. psychiatryonline. org/ cgi/ pmidlookup?view=long& pmid=12505794). Am J Psychiatry 160 (1): 1323. doi:10.1176/appi.ajp.160.1.13. PMID12505794. . [30] Bentall RP (Jan 1990). "The illusion of reality: a review and integration of psychological research on hallucinations" (http:/ / content. apa. org/ journals/ bul/ 107/ 1/ 82). Psychol Bull 107 (1): 8295. doi:10.1037/0033-2909.107.1.82. PMID2404293. . [31] Grossberg S (Jul 2000). "How hallucinations may arise from brain mechanisms of learning, attention, and volition". J Int Neuropsychol Soc 6 (5): 58392. doi:10.1017/S135561770065508X. PMID10932478. [32] Francis Nagaraya, Myers FWH et al. (1894). "Report on the census of hallucinations". Proceedings of the Society for Psychical Research 34: 25394. [33] Ohayon MM (Dec 2000). "Prevalence of hallucinations and their pathological associations in the general population" (http:/ / linkinghub. elsevier. com/ retrieve/ pii/ S0165178100002274). Psychiatry Res 97 (23): 15364. doi:10.1016/S0165-1781(00)00227-4. PMID11166087. .
Hallucination
43
External links
Hearing Voices Network (http://www.hearing-voices.org/) "Anthropology and Hallucinations" (http://www.psychanalyse-paris.com/843-Anthropology-and.html), chapter from The Making of Religion "The voice inside: A practical guide to coping with hearing voices" (http://www.mind.org.uk/help/ medical_and_alternative_care/the_voice_inside_coping_with_hearing_voices) Psychology Terms (http://dictionary-psychology.com)
Delusion
44
Delusion
Delusion
Classification and external resources ICD-10 ICD-9 MeSH F22 297 [1] [2] [3]
D003702
A delusion is a false belief held with absolute conviction despite superior evidence.[4] Unlike hallucinations, delusions are always pathological (the result of an illness or illness process).[4] As a pathology, it is distinct from a belief based on false or incomplete information, dogma, poor memory, illusion, or other effects of perception. Delusions typically occur in the context of neurological or mental illness, although they are not tied to any particular disease and have been found to occur in the context of many pathological states (both physical and mental). However, they are of particular diagnostic importance in psychotic disorders including schizophrenia, paraphrenia, manic episodes of bipolar disorder, and psychotic depression.
Definition
Although non-specific concepts of madness have been around for several thousand years, the psychiatrist and philosopher Karl Jaspers was the first to define the three main criteria for a belief to be considered delusional in his 1913 book General Psychopathology.[5] These criteria are: certainty (held with absolute conviction) incorrigibility (not changeable by compelling counterargument or proof to the contrary) impossibility or falsity of content (implausible, bizarre or patently untrue)[6] Furthermore, when a false belief involves a value judgment, it is only considered as a delusion if it is so extreme that it cannot be or ever can be proven true (example: a man claims that he flew into the sun and flew back home. This would be considered a delusion). [7]
Types
Delusions are categorized into four different groups: Bizarre delusion: A delusion that is very strange and completely implausible; an example of a bizarre delusion would be that aliens have removed the affected person's brain. Non-bizarre delusion: A delusion that, though false, is at least possible, e.g., the affected person mistakenly believes that he is under constant police surveillance. Mood-congruent delusion: Any delusion with content consistent with either a depressive or manic state, e.g., a depressed person believes that news anchors on television highly disapprove of him, or a person in a manic state might believe he is a powerful deity. Mood-neutral delusion: A delusion that does not relate to the sufferer's emotional state; for example, a belief that an extra limb is growing out of the back of one's head is neutral to either depression or mania.[8]
Delusion
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Themes
In addition to these categories, delusions often manifest according to a consistent theme. Although delusions can have any theme, certain themes are more common. Some of the more common delusion themes are:[8] Delusion of control: This is a false belief that another person, group of people, or external force controls one's general thoughts, feelings, impulses, or behavior. Nihilistic delusion: This is a false belief that one does not exist or has become deceased.[9] Delusional jealousy (or delusion of infidelity): A person with this delusion falsely believes that a person is lying to them or that a spouse or lover is having an affair, with no proof to back up their claim. Delusion of guilt or sin (or delusion of self-accusation): This is a false feeling of remorse or guilt of delusional intensity. Delusion of mind being read: The false belief that other people can know one's thoughts. Delusion of reference: The person falsely believes that insignificant remarks, events, or objects in one's environment have personal meaning or significance. Erotomania A delusion where someone believes another person is in love with them. Religious delusion: Any delusion with a religious or spiritual content. These may be combined with other delusions, such as grandiose delusions (the belief that the affected person is a god, or chosen to act as a god, for example).[10] [11] Somatic delusion: A delusion whose content pertains to bodily functioning, bodily sensations, or physical appearance. Usually the false belief is that the body is somehow diseased, abnormal, or changedfor example, infested with parasites. Delusions of parasitosis (DOP) or delusional parasitosis: a delusion in which one feels infested with an insect, bacteria, mite, spiders, lice, fleas, worms, or other organisms. Affected individuals may also report being repeatedly bitten. In some cases, entomologists are asked to investigate cases of mysterious bites. Sometimes physical manifestations may occur including skin lesions.[12] Delusion of poverty: The person strongly believes that he is financially incapacitated. Although this type of delusion is less common now, it was particularly widespread in the days before state support.[13]
Grandiose delusions
Grandiose delusions are distinct from grandiosity, in that the sufferer does not have insight into his loss of touch with reality. An individual is convinced he has special powers, talents, or abilities. Sometimes, the individual may actually believe they are a famous person or character (for example, Napoleon). Grandiose delusions or delusions of grandeur are principally a subtype of delusional disorder but could possibly feature as a symptom of schizophrenia and manic episodes of bipolar disorder.[14] Grandiose delusions are characterized by fantastical beliefs that one is famous, omnipotent, or otherwise very powerful. The delusions are generally fantastic, often with a supernatural, science-fictional, or religious bent. In colloquial usage, one who overestimates one's own abilities, talents, stature or situation is sometimes said to have 'delusions of grandeur'. This is generally due to excessive pride, rather than any actual delusions.
Delusion
46
Persecutory delusions
Persecutory delusions are the most common type of delusions and involve the theme of being followed, harassed, cheated, poisoned or drugged, conspired against, spied on, attacked, or obstructed in the pursuit of goals. Persecutory delusions are a condition in which the affected person believes - wrongly they are being persecuted. Specifically, they have been defined as containing two central elements:[15] 1. The individual thinks that harm is occurring, or is going to occur. 2. The individual thinks that the persecutor has the intention to cause harm. According to the DSM-IV-TR, persecutory delusions are the most common form of delusions in schizophrenia, where the person believes they are "being tormented, followed, tricked, spied on, or ridiculed."[16] In the DSM-IV-TR, persecutory delusions are the main feature of the persecutory type of delusional disorder. When the focus is to remedy some injustice by legal action, they are sometimes called "querulous paranoia".[17]
Diagnosis
The modern definition and Jaspers' original criteria have been criticised, as counter-examples can be shown for every defining feature. Studies on psychiatric patients show that delusions vary in intensity and conviction over time, which suggests that certainty and incorrigibility are not necessary components of a delusional belief.[18] Delusions do not necessarily have to be false or 'incorrect inferences about external reality'.[19] Some religious or spiritual beliefs by their nature may not be falsifiable, and hence cannot be described as false or incorrect, no matter whether the person holding these beliefs was diagnosed as delusional or not.[20]
In other situations the delusion may turn out to be true belief.[21] For example, delusional jealousy, where a person believes that their partner is being unfaithful (and may even follow them into the bathroom believing them to be seeing their lover even during the briefest of partings) may result in the faithful partner being driven to infidelity by the constant and unreasonable strain put on them by their delusional spouse. In this case the delusion does not cease to be a delusion because the content later turns out to be true. In other cases, the delusion may be assumed to be false by a doctor or psychiatrist assessing the belief, because it seems to be unlikely, bizarre or held with excessive conviction. Psychiatrists rarely have the time or resources to check the validity of a persons claims leading to some true beliefs to be erroneously classified as delusional.[22] This is known as the Martha Mitchell effect, after the wife of the attorney general who alleged that illegal activity was taking place in the White House. At the time her claims were thought to be signs of mental illness, and only after the Watergate scandal broke was she proved right (and hence sane). Similar factors have led to criticisms of Jaspers' definition of true delusions as being ultimately 'un-understandable'. Critics (such as R. D. Laing) have argued that this leads to the diagnosis of delusions being based on the subjective understanding of a particular psychiatrist, who may not have access to all the information that might make a belief otherwise interpretable. R.D. Laing's hypothesis has been applied to some forms of projective therapy to "fix" a delusional system so that it cannot be altered by the patient. Psychiatric researchers at Yale University, Ohio State University and the Community Mental Health Center of Middle Georgia have used novels and motion picture films as the focus. Texts, plots and cinematography are discussed and the delusions approached tangentially.[23] This use of fiction to decrease the malleability of a delusion was employed in a joint project by science-fiction author Philip
John Haslam illustrated this picture of a machine described by James Tilly Matthews called an "air loom," which Matthews believed was being used to torture him and others for political purposes.
Delusion Jose Farmer and Yale psychiatrist A. James Giannini. They wrote the novel Red Orc's Rage, which, recursively, deals with delusional adolescents who are treated with a form of projective therapy. In this novel's fictional setting other novels written by Farmer are discussed and the characters are symbolically integrated into the delusions of fictional patients.This particular novel was then applied to real-life clinical settings.[24] Another difficulty with the diagnosis of delusions is that almost all of these features can be found in "normal" beliefs. Many religious beliefs hold exactly the same features, yet are not universally considered delusional. These factors have led the psychiatrist Anthony David to note that "there is no acceptable (rather than accepted) definition of a delusion."[25] In practice psychiatrists tend to diagnose a belief as delusional if it is either patently bizarre, causing significant distress, or excessively pre-occupies the patient, especially if the person is subsequently unswayed in belief by counter-evidence or reasonable arguments. It is important to distinguish true delusions from other symptoms such as anxiety, fear, or paranoia. To diagnose delusions a mental state examination may be used. This test includes appearance, mood, affect, behavior, rate and continuity of speech,evidence of hallucinations or abnormal beliefs, thought content, orientation to time, place and person, attention and concentration, insight and judgment, as well as short-term memory.[26] Johnson-Laird suggests that delusions may be viewed as the natural consequence of failure to distinguish conceptual relevance. That is, the person takes irrelevant information and puts it in the form of disconnected experiences, then it is taken to be relevant in a manner that suggests false causal connections. Furthermore, the person takes the relevant information, in the form of counterexamples, and ignores it.[27]
47
Causes
To define delusional thinking in a specific patient, it is important to consult a local psychiatrist who can make a thorough examination before diagnosing the problem.[37] Explaining the causes of delusions has been challenging and several theories have been developed. One is the genetic or biological theory, which states that close relatives of people with delusional disorder are at increased risk of delusional traits. Another theory is the dysfunctional cognitive processing, which states that delusions may arise from distorted ways people have of explaining life to themselves. A third theory is called motivated or defensive delusions. This one states that some of those persons who
Delusion are predisposed might suffer the onset of delusional disorder in those moments when coping with life and maintaining high self-esteem becomes a significant challenge. In this case, the person views others as the cause of their personal difficulties in order to preserve a positive self-view.[38] This condition is more common among people who have poor hearing or sight. Also, ongoing stressors have been associated with a higher possibility of developing delusions. Examples of such stressors are immigration or low socio-economic status.[39] Researcher, Orrin Devinsky, MD, from the NYU Langone Medical Center, performed a study that revealed a consistent pattern of injury to the frontal lobe and right hemisphere of the human brain in patients with certain delusions and brain disorders. Devinsky explains that the cognitive deficits caused by those injuries to the right hemisphere, results in the over compensation by the left hemisphere of the brain for the injury, which causes delusions.[40] A study carried out by a team from The Warwick Medical School at the University of Warwick, Coventry, England, led by Andrea Schreier, Ph. D., indicated that children who suffered bullying are more likely to develop psychotic symptoms in early adolescence. The background facts demonstrated that hallucinations and delusions are common in childhood as well as in adulthood and that children who experience such symptoms are more prone to develop psychosis later in life. Furthermore, the study demonstrated that the risk of psychotic symptoms, including delusions, was multiplied by two for children who suffered bullying at age eight or ten. The authors remark that bullying can cause chronic stress that may have an effect on a genetic predisposition to schizophrenia and result in setting off the symptoms.[41]
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References
[1] [2] [3] [4] [5] [6] [7] [8] [9] http:/ / apps. who. int/ classifications/ icd10/ browse/ 2010/ en#/ F22 http:/ / www. icd9data. com/ getICD9Code. ashx?icd9=297 http:/ / www. nlm. nih. gov/ cgi/ mesh/ 2011/ MB_cgi?field=uid& term=D003702 "Delusion" (http:/ / wordnetweb. princeton. edu/ perl/ webwn?s=delusion). Princeton - Wordnet. . Retrieved 8 April 2011. Jaspers, Karl (1913). Allgemeine Psychopathologie. Ein Leitfaden fr Studierende, rzte und Psychologen.. Berlin: J. Springer. Jaspers 1997, p.106 "Terms in the Field of Psychiatry and Neurology" (http:/ / www. abess. com/ glossary. html#D). . Retrieved 2010-08-06. Source: http:/ / www. minddisorders. com/ Br-Del/ Delusions. html Berrios G.E., Luque R. (1995). "Cotard Syndrome: clinical analysis of 100 cases". Acta Psychiatrica Scandinavica 91 (3): 185188. doi:10.1111/j.1600-0447.1995.tb09764.x. PMID7625193. [10] "Religious delusions are common symptoms of schizophrenia." (http:/ / www. sciforums. com/ showthread. php?t=51361). . Retrieved 17 April 2011. [11] M, Raja. "Religious delusion" (http:/ / www. sanp. ch/ pdf/ 2000/ 2000-01/ 2000-01-058. PDF). . Retrieved 17 April 2011. [12] "Difference between delusion and phobia" (http:/ / www. livingwithbugs. com/ del_pho. html). . Retrieved 2010-08-06. [13] Barker, P. 1997. Assessment in Psychiatric and Mental Health Nursing In Search of the Whole Person. UK: Nelson Thornes Ltd. P243. [14] Diagnostic and Statistical Manual of Mental Disorders Fourth edition Text Revision (DSM-IV-TR) American Psychiatric Association (2000) [15] Freeman, D. & Garety, P.A. (2004) Paranoia: The Psychology of Persecutory Delusions. Hove: PsychoIogy Press. ISBN 1-84169-522-X [16] Diagnostic and statistical manual of mental disorders: DSM-IV. Washington, DC: American Psychiatric Association. 2000. p.299. ISBN0-89042-025-4. [17] Diagnostic and statistical manual of mental disorders: DSM-IV. Washington, DC: American Psychiatric Association. 2000. p.325. ISBN0-89042-025-4. [18] Myin-Germeys I, Nicolson NA, Delespaul PA (April 2001). "The context of delusional experiences in the daily life of patients with schizophrenia". Psychol Med 31 (3): 48998. PMID11305857. [19] Spitzer M (1990). "On defining delusions" (http:/ / linkinghub. elsevier. com/ retrieve/ pii/ 0010-440X(90)90023-L). Compr Psychiatry 31 (5): 37797. doi:10.1016/0010-440X(90)90023-L. PMID2225797. . [20] Young, A.W. (2000). "Wondrous strange: The neuropsychology of abnormal beliefs". In Coltheart M., Davis M.. Pathologies of belief. Oxford: Blackwell. pp.4774. ISBN0-631-22136-0. [21] Jones E (1999). "The phenomenology of abnormal belief" (http:/ / muse. jhu. edu/ journals/ philosophy_psychiatry_and_psychology/ toc/ ppp6. 1. html). Philosophy, Psychiatry and Psychology 6: 116. . [22] Maher B.A. (1988). "Anomalous experience and delusional thinking: The logic of explanations". In Oltmanns T., Maher B.. Delusional Beliefs. New York: Wiley Interscience. ISBN0-471-83635-4.
Delusion
[23] Giannini AJ (2001). "Use of fiction in therapy". Psychiatric Times 18 (7): 56. [24] AJ Giannini. Afterword. (in) PJ Farmer. Red Orc's Rage.NY, Tor Books, 1991, pp.279-282. [25] David AS (1999). "On the impossibility of defining delusions". Philosophy, Psychiatry and Psychology 6 (1): 1720. [26] "Diagnostic Test List for Delusions" (http:/ / www. wrongdiagnosis. com/ symptoms/ delusions/ tests. htm). . Retrieved 2010-08-06. [27] "A New Definition of Delusional Ideation in Terms of Model Restriction" (http:/ / neuro. psychiatryonline. org/ cgi/ content/ full/ 13/ 3/ 403-a). . Retrieved 2010-08-06. [28] Sims, Andrew (2002). Symptoms in the mind: an introduction to descriptive psychopathology. Philadelphia: W. B. Saunders. pp.127. ISBN0-7020-2627-1. [29] Morimoto K, Miyatake R, Nakamura M, Watanabe T, Hirao T, Suwaki H (June 2002). "Delusional disorder: molecular genetic evidence for dopamine psychosis" (http:/ / www. nature. com/ npp/ journal/ v26/ n6/ full/ 1395864a. html). Neuropsychopharmacology 26 (6): 794801. doi:10.1016/S0893-133X(01)00421-3. PMID12007750. . [30] Mazure CM, Bowers MB (1 February 1998). "Pretreatment plasma HVA predicts neuroleptic response in manic psychosis". Journal of Affective Disorders 48 (1): 836. doi:10.1016/S0165-0327(97)00159-6. PMID9495606. [31] Yamada N, Nakajima S, Noguchi T (February 1998). "Age at onset of delusional disorder is dependent on the delusional theme". Acta Psychiatrica Scandinavica 97 (2): 1224. doi:10.1111/j.1600-0447.1998.tb09973.x. PMID9517905. [32] Tamplin A, Goodyer IM, Herbert J (1 February 1998). "Family functioning and parent general health in families of adolescents with major depressive disorder". Journal of Affective Disorders 48 (1): 113. doi:10.1016/S0165-0327(97)00105-5. PMID9495597. [33] Sims, Andrew (2002). Symptoms in the mind: an introduction to descriptive psychopathology. Philadelphia: W. B. Saunders. pp.128. ISBN0-7020-2627-1. [34] Draguns JG, Tanaka-Matsumi J (July 2003). "Assessment of psychopathology across and within cultures: issues and findings" (http:/ / linkinghub. elsevier. com/ retrieve/ pii/ S0005796702001900). Behav Res Ther 41 (7): 75576. doi:10.1016/S0005-7967(02)00190-0. PMID12781244. . [35] Stompe T, Friedman A, Ortwein G, et al (1999). "Comparison of delusions among schizophrenics in Austria and in Pakistan" (http:/ / content. karger. com/ produktedb/ produkte. asp?typ=fulltext& file=psp32225). Psychopathology 32 (5): 22534. doi:10.1159/000029094. PMID10494061. . [36] Birkmayer W, Danielczyk W, Neumayer E, Riederer P (1972). "The balance of biogenic amines as condition for normal behaviour" (http:/ / www. springerlink. com/ index/ N11474QQ25R5U236. pdf) (PDF). J. Neural Transm. 33 (2): 16378. doi:10.1007/BF01260902. PMID4643007. . [37] "Delusional Disorder Definition" (http:/ / www. delusional. com/ ). . Retrieved 2010-08-06. [38] "Delusional Disorder" (http:/ / www. minddisorders. com/ Br-Del/ Delusional-disorder. html). . Retrieved 2010-08-06. [39] "Causes of Delusional Disorder" (http:/ / www. depression-treatment-help. com/ mental-disorders/ delusional-disorder. htm). . Retrieved 2010-08-06. [40] "What causes delusions?" (http:/ / machineslikeus. com/ news/ what-causes-delusions). . Retrieved 2010-08-06. [41] "Children Who Suffered Bullying Are More Likely To Develop Psychotic Symptoms In Early Adolescence" (http:/ / www. medicalnewstoday. com/ articles/ 149130. php). . Retrieved 2010-08-06.
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Cited text Jaspers, Karl (1997). General Psychopathology. 1. Baltimore: Johns Hopkins University Press. ISBN0-8018-5775-9.
Further reading
Bell V, Halligan PW, Ellis H (2003). "Beliefs about delusions" (http://mindfull.spc.org/vaughan/ Bell_et_al_2003_BeliefsAboutDelusions.pdf) (PDF). The Psychologist 16 (8): 418423. Blackwood, Nigel J.; Howard, Robert J.; Bentall, Richard P.; Murray, Robin M. (April 2001). "Cognitive Neuropsychiatric Models of Persecutory Delusions" (http://ajp.psychiatryonline.org/cgi/content/abstract/158/ 4/527). American Journal of Psychiatry 158 (4): 527539. doi:10.1176/appi.ajp.158.4.527. PMID11282685. Coltheart M., Davies M., ed (2000). Pathologies of belief. Oxford: Blackwell. ISBN0-631-22136-0. Persaud, R. (2003). From the Edge of the Couch: Bizarre Psychiatric Cases and What They Teach Us About Ourselves. Bantam. ISBN0-553-81346-3.
Emotional dysregulation
50
Emotional dysregulation
Emotional dysregulation (ED) is a term used in the mental health community to refer to an emotional response that is poorly modulated, and does not fall within the conventionally accepted range of emotive response. ED may be referred to as labile mood[1] or mood swings. Possible manifestations of emotional dysregulation include angry outbursts or behavior outbursts such as destroying or throwing objects, aggression towards self or others, and threats to kill oneself. These variations usually occur in seconds to minutes or hours. Emotional dysregulation can lead to behavioral problems and can interfere with a person's social interactions and relationships at home, in school, or at place of employment. Emotional dysregulation can be associated with an experience of early psychological trauma, brain injury, or chronic maltreatment (such as child abuse, child neglect, or institutional neglect/abuse), and associated disorders such as reactive attachment disorder.[2] Emotional dysregulation may present in people with psychiatric disorders such as bipolar disorder, borderline personality disorder, and Complex post-traumatic stress disorder.[3] [4] ED is also found among those with autism spectrum disorders, including Asperger syndrome.[3]
Etymology
The word dysregulation is a neologism created by combining the prefix "dys" to "regulation" According to Webster's, dys has various roots. With Latin and Greek roots, it is akin to Old English t-, te- apart and in Sanskrit dus- bad, difficult.
References
[1] Beauchaine, T., Gatzke-Kopp, L., Mead, H., (2007). Polyvagal Theory and developmental psychopathology: Emotion dysregulation and conduct problems from preschool to adolescence. Biological Psychology, 74, 174-184. [2] Daniel Schechter, Erica Willheim (2009). Disturbances of attachment and parental psychopathology in early childhood. Infant and Early Childhood Mental Health Issue. Child and Adolescent Psychiatry Clinics of North America, 18(3), 665-687. [3] Pynoos, R., Steinberg, A., & Piacentini, J. (1999), Bipolar Disorder, and Asperger Syndrome. A developmental psychopathology model of childhood traumatic stress and intersection with anxiety disorders. Biological Psychiatry, 46, 1542-1554. [4] Schore, A., (2003). Affect dysregulation and disorders of the self. New York: Norton.
Anhedonia
51
Anhedonia
In psychology and psychiatry, anhedonia ( /nhidoni/ an-hee-doh-nee-; Greek: - an-, "without" + hdon, "pleasure") is defined as the inability to experience pleasure from activities usually found enjoyable, e.g. hobbies, exercise, social interaction or sexual activity. Anhedonia can be a characteristic of mental disorders including mood disorders, schizoaffective disorder, schizoid personality disorder and schizophrenia. Affected schizophrenic patients describe themselves as feeling emotionally empty.[1] Mood disturbances are commonly observed in many psychiatric disorders. Disturbing mood changes may occur resultant to stressful life events and they are not uncommon during times of physical illness.[2] While anhedonia can be a feature of such mood changes, they are not mutually inclusive.
Causes
Researchers theorize that anhedonia may result from the breakdown in the brain's reward system, involving the neurotransmitter dopamine. Studies by Paul Keedwell, MD, then of King's College, found that the brains of clinically depressed subjects had to work harder to process rewarding experiences.[3] [4]
Significance in depression
As a clinical symptom in depression, anhedonia rates highly in making a diagnosis of this disorder. The Diagnostic and Statistical Manual of Mental Disorders (DSM) describes a "lack of interest or pleasure" but these can be hard to tell apart given that people become less interested in things which do not give them pleasure. The DSM criterion of weight loss is probably related to it and many depressed people with this symptom describe a lack of enjoyment of food. People suffering from anhedonia in association with depression generally feel good in the morning and unhappy in the evenings and can portray any of the non-psychotic symptoms and signs of depression.[5]
Sexual anhedonia
Sexual anhedonia in males is also known as 'ejaculatory anhedonia'. This condition means that the person will ejaculate with no accompanying sense of pleasure. The condition is most frequently found in males, but women can suffer from lack of pleasure when the body goes through the orgasm process as well. Sexual anhedonia may be caused by: Hyperprolactinaemia Hypoactive sexual desire disorder (HSDD), also called inhibited sexual desire Low levels of the hormone testosterone Spinal cord injury Multiple Sclerosis Use (or previous use) of SSRI antidepressants[6] Use (or previous use) of antidopaminergic neuroleptics[7] [8] Fatigue Physical illness
It is very uncommon that a neurological examination and blood tests can determine the cause of a specific case of sexual anhedonia. Patients may be prescribed sustained-release bupropion to aid in treatment, which has been shown to relieve sexual dysfunction even in patients without depression.[9]
Anhedonia
52
References
[1] Hales R., Yudofsky S., Talbott J. 1999. Textbook of Psychiatry 3rd ed. Washington DC: The American Psychiatric Press. [2] Gelder, Michael G.; Mayou, Richard; Geddes, John; Geddes, John (2005). Psychiatry (3rd ed.). Oxford University Press. pp.2, 99. ISBN978-0-19-852863-0. [3] "No Pleasure, No Reward -- Plenty of Depression" (http:/ / www. mcmanweb. com/ no_pleasure. html) by John McManamy; URL accessed 2009-02-17 [4] Surguladze, S. (2003). "Neural systems underlying affective disorders". Advances in Psychiatric Treatment 9 (6): 44655. doi:10.1192/apt.9.6.446. [5] Tomb, David A. (1 August 2007). Psychiatry (http:/ / books. google. com/ books?id=lt0-i8xLINoC). Lippincott Williams & Wilkins. p.44. ISBN978-0-7817-7452-9. . Retrieved 18 December 2010. [6] Csoka, Antonei; Bahrick, Audrey; Mehtonen, Olli-Pekka (2007). "Persistent Sexual Dysfunction after Discontinuation of Selective Serotonin Reuptake Inhibitors". Journal of Sexual Medicine 5 (1): 227233. doi:10.1111/j.1743-6109.2007.00630.x. PMID18173768. [7] Tupala, E; Haapalinna, A; Viitamaa, T; Mnnist, PT; Saano, V (1999). "Effects of repeated low dose administration and withdrawal of haloperidol on sexual behaviour of male rats". Pharmacology & toxicology 84 (6): 2925. PMID10401732. [8] Martin-Du Pan, R (1978). "Neuroleptics and sexual dysfunction in man. Neuroendocrine aspects". Schweizer Archiv fur Neurologie, Neurochirurgie und Psychiatrie = Archives suisses de neurologie, neurochirurgie et de psychiatrie 122 (2): 285313. PMID29337. [9] Crenshaw, Theresa L.; Goldberg, James P.; Stern, Warren C. (1987). "Pharmacologic modification of psychosexual dysfunction". Journal of Sex & Marital Therapy 13 (4): 23952. doi:10.1080/00926238708403896. PMID3121861.
External links
Anhedonia - Bipolar Disorder Symptoms (http://www.bipolardisordersymptoms.info/bipolar-symptoms/ anhedonia.htm) No Pleasure, No Reward (http://www.mcmanweb.com/no_pleasure.html) Forum: "Ejaculation without orgasm" forum (hisandherhealth.com) (http://www.hisandherhealth.com/ sexual-health-bulletin-boards/7-mens-sexual-health/39385-ejaculation-without-orgasm-ejaculatory-anhedonia) Forum: "Ejaculatoryanhedonia.com" (http://www.ejaculatoryanhedonia.com/)
Dysphoria
53
Dysphoria
Dysphoria (from Greek (dysphoros), from -, difficult, and , to bear) (semantically opposite of euphoria) is medically recognized as a mental and emotional condition in which a person experiences intense feelings of depression, discontent and indifference to the world around them.[1] Mood disorders can induce dysphoria, often with a heightened risk of suicide, especially in persons with bipolar disorder who are in a depressive phase.[1] As the term refers only to a condition of mood, dysphoria may be experienced in response to ordinary life events, such as great illness or grief. Dysphoria can also be chemically induced by some commonly used psychoactive drugs, such as typical and atypical antipsychotics.[2]
Related conditions
The following conditions may include dysphoria as a symptom: Clinical depression (unipolar) and dysthymia Bipolar disorder[1] and cyclothymia Premenstrual Syndrome Premenstrual dysphoric disorder Stress Adjustment disorder with depressed mood Anxiety disorders such as PTSD. Gender identity disorder, sometimes called gender dysphoria Personality disorders such as borderline personality disorder and antisocial personality disorder Substance withdrawal Body dysmorphic disorder Hypoglycemia Schizophrenia Sexual Dysfunction Species dysphoria, a feeling of having been "born in the wrong body." Insomnia[3] Chronic pain[4]
Dysphoria
54
Notes
[1] Abbess, John F. "Glossary of terms in the field of psychiatry and neurology" (http:/ / www. abess. com/ glossary. html). . Retrieved 2006-11-18. [2] Neuroleptic (antipsychotic) dysphoria | biopsychiatry.com (http:/ / biopsychiatry. com/ neuroleptics. htm) [3] Rosa RR, Bonnet MH (2000). "Reported chronic insomnia is independent of poor sleep as measured by electroencephalography". Psychosom Med 62 (4): 47482. PMID10949091. [4] Chapman CR, Gavrin J (June 1999). "Suffering: the contributions of persistent pain". Lancet 353 (9171): 22337. doi:10.1016/S0140-6736(99)01308-2. PMID10393002.
References
Abbess, John F. "Glossary of terms in the field of psychiatry and neurology" (http://www.abess.com/glossary. html). Retrieved 2006-11-18. "Dysphoria." Alleydog.com Psychology Glossary. Metcalf, Matthew; and Coop, Andrew (2005). "Kappa Opioid Antagonists: Past Successes and Future Prospects" (http://www.aapsj.org/view.asp?art=aapsj070371). The AAPS Journal (American Association of Pharmaceutical Scientists) 7 (3): E704E722. doi:10.1208/aapsj070371. ISSN1522-1059. PMC2751273. PMID16353947. Retrieved 2006-11-19. Read, Kimberly (2006). "What is dysphoria?" (http://bipolar.about.com/cs/faqs/f/faq_dysphoria.htm). Your Guide to Bipolar Disorder. About.com. Retrieved 2006-11-19.
Suicidal ideation
55
Suicidal ideation
Suicidal ideation
Classification and external resources ICD-10 ICD-9 R45.8 [1] [2]
V62.84
Suicidal ideation is a common medical term for thoughts about suicide, which may be as detailed as a formulated plan, without the suicidal act itself. Although most people who undergo suicidal ideation do not commit suicide, some go on to make suicide attempts.[3] The range of suicidal ideation varies greatly from fleeting to detailed planning, role playing and unsuccessful attempts, which may be deliberately constructed to fail or be discovered, or may be fully intended to succeed. In a study conducted in Finland, 22% of the suicides examined had discussed suicidal intent with a health care professional in their last office visit.[4]
Risk factors
Psychiatric disorders
Major depressive disorder Anorexia nervosa Post-traumatic stress disorder (PTSD) Adjustment disorder Schizophrenia Borderline personality disorder Panic disorder Body dysmorphic disorder Dissociative identity disorder Social anxiety disorder Substance abuse Bipolar disorder Gender identity disorder Autism
Life events
Grief Sexual abuse Relationship breakup Unemployment Rejection Remorse Financial problems
Suicidal ideation
56
Past history
History of previous suicide attempt Family history of parasuicide
References
[1] http:/ / apps. who. int/ classifications/ icd10/ browse/ 2010/ en#/ R45. 8 [2] http:/ / www. icd9data. com/ getICD9Code. ashx?icd9=V62. 84 [3] Gliatto, Michael F.; Rai, Anil K. (March 1999). "Evaluation and Treatment of Patients with Suicidal Ideation" (http:/ / www. aafp. org/ afp/ 990315ap/ 1500. html). American Family Physician 59 (6). PMID10193592. . Retrieved 2007-01-08. [4] Halgin, Richard P.; Susan Whitbourne (2006). Abnormal psychology : clinical perspectives on psychological disorders. Boston : McGraw-Hill. pp.267272. ISBN0-07-322872-9.
Further reading
Beck, AT; Steer, RA; Kovacs, M; Garrison, B (1985). "Hopelessness and eventual suicide: a 10-year prospective study of patients hospitalized with suicidal ideation". Am J Psychiatry 142 (5): 559563. PMID3985195. Uncapher, H (20002001). "Cognitive biases and suicidal ideation in elderly psychiatric inpatients". Omega 42 (1): 2136. Uncapher, H; Gallagher-Thompson, D; Osgood, NJ (1998). "Hopelessness and suicidal ideation in older adults". The Gerontologist 38 (1): 6270. PMID9499654.
Suicidal ideation
57
External links
Evaluation and Treatment of Patients with Suicidal Ideation (http://www.aafp.org/afp/990315ap/1500.html) Suicidal Thoughts (http://www.aamft.org/imis15/content/Consumer_Updates/Suicidal_Thoughts.aspx) National Suicide Prevention Lifeline--warning signs (http://www.suicidepreventionlifeline.org/GetHelp/ SuicideWarningSigns.aspx)
Sleep disorder
58
Sleep disorder
Sleep disorder
Classification and external resources ICD-10 ICD-9 F51 [1] , G47 [2] [4] , 780.5 [5]
307.4
[3]
, 327
A sleep disorder, or somnipathy, is a medical disorder of the sleep patterns of a person or animal. Some sleep disorders are serious enough to interfere with normal physical, mental and emotional functioning. A test commonly ordered for some sleep disorders is the polysomnography. Disruptions in sleep can be caused by a variety of issues, from teeth grinding (bruxism) to night terrors. When a person suffers from difficulty in sleeping with no obvious cause, it is referred to as insomnia.[9] In addition, sleep disorders may also cause sufferers to sleep excessively, a condition known as hypersomnia. Management of sleep disturbances that are secondary to mental, medical, or substance abuse disorders should focus on the underlying conditions. Some proposed Sleep Disorders include Sleep-Related NeurogenicTachypnea, Sleep-Related Laryngospasm and Sleep Choking Syndrome [10]
Common disorders
The most common sleep disorders include: Primary insomnia: Chronic difficulty in falling asleep and/or maintaining sleep when no other cause is found for these symptoms. Bruxism: Involuntarily grinding or clenching of the teeth while sleeping. Delayed sleep phase syndrome (DSPS): inability to awaken and fall asleep at socially acceptable times but no problem with sleep maintenance, a disorder of circadian rhythms. (Other such disorders are advanced sleep phase syndrome (ASPS), non-24-hour sleep-wake syndrome (Non-24), and irregular sleep wake rhythm, all much less common than DSPS, as well as the transient jet lag and shift work sleep disorder.) Hypopnea syndrome: Abnormally shallow breathing or slow respiratory rate while sleeping. Narcolepsy: Excessive daytime sleepiness (EDS) often culminating in falling asleep spontaneously but unwillingly at inappropriate times. Cataplexy: a sudden weakness in the motor muscles that can result in collapse to the floor. Night terror: Pavor nocturnus, sleep terror disorder: abrupt awakening from sleep with behavior consistent with terror. Parasomnias: Disruptive sleep-related events involving inappropriate actions during sleep; sleep walking and night-terrors are examples. Periodic limb movement disorder (PLMD): Sudden involuntary movement of arms and/or legs during sleep, for example kicking the legs. Also known as nocturnal myoclonus. See also Hypnic jerk, which is not a disorder. Rapid eye movement behavior disorder (RBD): Acting out violent or dramatic dreams while in REM sleep (REM sleep disorder or RSD) Restless legs syndrome (RLS): An irresistible urge to move legs. RLS sufferers often also have PLMD. Situational circadian rhythm sleep disorders: shift work sleep disorder (SWSD) and jet lag.
Sleep disorder Sleep apnea, and mostly obstructive sleep apnea: Obstruction of the airway during sleep, causing lack of sufficient deep sleep; often accompanied by snoring. Other forms of sleep apnea are less common. The air is blocked from entering into the lungs, causing the individual to unconsciously gasp for air. The individual will pause for an average of ten seconds in order to breathe. This is commonly found in overweight, middle-aged men but is also found in people who have suffered from stroke. Sleep paralysis: is characterized by temporary paralysis of the body shortly before or after sleep. Sleep paralysis may be accompanied by visual, auditory or tactile hallucinations. Not a disorder unless severe. Often seen as part of narcolepsy. Sleepwalking or somnambulism: Engaging in activities that are normally associated with wakefulness (such as eating or dressing), which may include walking, without the conscious knowledge of the subject. Nocturia: A frequent need to get up and go to the bathroom to urinate at night. It differs from Enuresis, or bed-wetting, in which the person does not arouse from sleep, but the bladder nevertheless empties.[11] Somniphobia: a dread of sleep.
59
Types
Dyssomnias - A broad category of sleep disorders characterized by either hypersomnolence or insomnia. The three major subcategories include intrinsic (i.e., arising from within the body), extrinsic (secondary to environmental conditions or various pathologic conditions), and disturbances of circadian rhythm. MeSH [12] Insomnia: An inability to get the amount of sleep needed to restore our physical and mental condition. Insomnia is often a symptom of a mood disorder (i.e., emotional stress, anxiety, depression) or underlying health condition (i.e., asthma, diabetes, heart disease, pregnancy or neurological conditions). [13] Narcolepsy: A chronic neurological disorder (or dyssomnia), which is caused by the brain's inability to control sleep and wakefulness.[14] Sleep Disordered Breathing (SDB), including (non exhaustive): Several types of Sleep apnea Snoring Upper airway resistance syndrome Restless leg syndrome Periodic limb movement disorder Hypersomnia Recurrent hypersomnia - including Kleine-Levin syndrome Posttraumatic hypersomnia "Healthy" hypersomnia Circadian rhythm sleep disorders Delayed sleep phase syndrome Advanced sleep phase syndrome Non-24-hour sleep-wake syndrome Parasomnias - A category of sleep disorders that involve abnormal and unnatural movements, behaviors, emotions, perceptions, and dreams in connection with sleep. REM sleep behaviour disorder Sleep terror (or Pavor nocturnus)- Characterized by a sudden arousal from deep sleep with a scream or cry, accompanied by some behavioral manifestations of intense fear.[15] Sleepwalking (or somnambulism)
Sleep disorder Sleep sex (or sexsomnia) Exploding head syndrome - Waking up in the night hearing loud noises. Medical or Psychiatric Conditions that may produce sleep disorders Psychosis (such as Schizophrenia) Mood disorders Depression Anxiety Panic Alcoholism Sleeping sickness - a parasitic disease which can be transmitted by the Tsetse fly.
60
Medications and somatic treatments may provide the most rapid symptomatic relief from some sleep disturbances. Some disorders, such as narcolepsy, are best treated pharmacologically. Others, such as chronic and primary insomnia, may be more amenable to behavioral interventions, with more durable results. Chronic sleep disorders in childhood, which affect some 70% of children with developmental or psychological disorders, are under-reported and under-treated. Sleep-phase disruption is also common among adolescents, whose school schedules are often incompatible with their natural circadian rhythm. Effective treatment begins with careful diagnosis using sleep diaries and perhaps sleep studies. Modifications in sleep hygiene may resolve the problem, but medical treatment is often warranted.[16] Special equipment may be required for treatment of several disorders such as obstructive apnea, the circadian rhythm disorders and bruxism. In these cases, when severe, an acceptance of living with the disorder, however well managed, is often necessary. Some sleep disorders have been found to compromise glucose metabolism.[17]
Sleep disorder
61
Sleep medicine
Due to rapidly increasing knowledge about sleep in the 20th century, including the discovery of REM sleep and sleep apnea, the medical importance of sleep was recognized. The medical community began paying more attention than previously to primary sleep disorders, such as sleep apnea, as well as the role and quality of sleep in other conditions. By the 1970s in the USA, clinics and laboratories devoted to the study of sleep and sleep disorders had been founded, and a need for standards arose.
Sleep Medicine is now a recognized subspecialty within internal medicine, family medicine, pediatrics, otolaryngology, psychiatry and neurology in the United States. Certification in Sleep Medicine shows that the specialist: "has demonstrated expertise in the diagnosis and management of clinical conditions that occur during sleep, that disturb sleep, or that are affected by disturbances in the wake-sleep cycle. This specialist is skilled in the analysis and interpretation of comprehensive polysomnography, and well-versed in emerging research and management of a sleep laboratory."[19] Competence in sleep medicine requires an understanding of a myriad of very diverse disorders, many of which present with similar symptoms such as excessive daytime sleepiness, which, in the absence of volitional sleep deprivation, "is almost inevitably caused by an identifiable and treatable sleep disorder", such as sleep apnea, narcolepsy, idiopathic central nervous system (CNS) hypersomnia, Kleine-Levin syndrome, menstrual-related hypersomnia, idiopathic recurrent stupor, or circadian rhythm disturbances.[20] Another common complaint is insomnia, a set of symptoms which can have a great many different causes, physical and mental. Management in the varying situations differs greatly and cannot be undertaken without a correct diagnosis. Sleep dentistry (bruxism, snoring and sleep apnea), while not recognized as one of the nine dental specialties, qualifies for board-certification by the American Board of Dental Sleep Medicine (ABDSM). The resulting Diplomate status is recognized by the American Academy of Sleep Medicine (AASM), and these dentists are organized in the Academy of Dental Sleep Medicine (USA).[21] The qualified dentists collaborate with sleep physicians at accredited sleep centers and can provide oral appliance therapy and upper airway surgery to treat or manage sleep-related breathing disorders.[22] In the UK, knowledge of sleep medicine and possibilities for diagnosis and treatment seem to lag. Guardian.co.uk quotes the director of the Imperial College Healthcare Sleep Centre: "One problem is that there has been relatively little training in sleep medicine in this country certainly there is no structured training for sleep physicians."[23] The Imperial College Healthcare site[24] shows attention to obstructive sleep apnea syndrome (OSA) and very few other sleep disorders.
Normison (temazepam) is a benzodiazepine commonly prescribed for insomnia [18] and other sleep disorders.
Sleep disorder
62
References
[1] [2] [3] [4] [5] [6] [7] [8] [9] http:/ / apps. who. int/ classifications/ icd10/ browse/ 2010/ en#/ F51 http:/ / apps. who. int/ classifications/ icd10/ browse/ 2010/ en#/ G47 http:/ / www. icd9data. com/ getICD9Code. ashx?icd9=307. 4 http:/ / www. icd9data. com/ getICD9Code. ashx?icd9=327 http:/ / www. icd9data. com/ getICD9Code. ashx?icd9=780. 5 http:/ / www. diseasesdatabase. com/ ddb26877. htm http:/ / www. emedicine. com/ med/ topic609. htm http:/ / www. nlm. nih. gov/ cgi/ mesh/ 2011/ MB_cgi?field=uid& term=D012893 Hirshkowitz, Max (2004). "Chapter 10, Neuropsychiatric Aspects of Sleep and Sleep Disorders (pp 315-340)" (http:/ / books. google. no/ books?id=XKhu7yb3QtsC& pg=PA315& lpg=PA315& dq="Max+ Hirshkowitz"#v=onepage& q="Max Hirshkowitz"& f=false). In Stuart C. Yudofsky and Robert E. Hales, editors (Google Books preview includes entire chapter 10). Essentials of neuropsychiatry and clinical neurosciences (4 ed.). Arlington, Virginia, USA: American Psychiatric Publishing. ISBN9781585620050. . Retrieved 2009-12-06. "...insomnia is a symptom. It is neither a disease nor a specific condition. (from p. 322)" [10] Thorpy, Michael J. "PROPOSED SLEEP DISORDERS." The International Classification of Sleep Disorders: Diagnostic and Coding Manual. Rochester: American Sleep Disorders Association, 1990. Print. [11] www.sleepfoundation.org (http:/ / www. sleepfoundation. org/ article/ sleep-related-problems/ nocturia-and-sleep) [12] http:/ / www. ncbi. nlm. nih. gov/ entrez/ query. fcgi?cmd=Retrieve& db=mesh& list_uids=68020920& dopt=Full [13] Melinda Smith, M.A., Lawrence Robinson, Robert Segal, M.A. (September 2011). Sleep Disorders and Sleeping Problems (http:/ / helpguide. org/ life/ sleep_disorders. htm). . [14] National Institute of Neurological Disorders and Stroke (June 27, 2011). NINDS Narcolepsy (http:/ / www. ninds. nih. gov/ disorders/ narcolepsy/ narcolepsy. htm). . [15] Thorpy, Michael J. "PARASOMNIACS." The International Classification of Sleep Disorders: Diagnostic and Coding Manual. Rochester: American Sleep Disorders Association, 1990. Print. [16] Ivanenko A and Massey C (October 1, 2006). "Assessment and Management of Sleep Disorders in Children" (http:/ / www. psychiatrictimes. com/ sleep-disorders/ article/ 10168/ 52051). Psychiatric Times 23 (11). . [17] Keckeis M, Lattova Z, Maurovich-Horvat E, Beitinger PA, Birkmann S, Lauer CJ, Wetter TC, Wilde-Frenz J, Pollmcher T. (2010). Finkelstein, David. ed. "Impaired Glucose Tolerance in Sleep Disorders". PloS 1 3 (5): 9444. doi:10.1371/journal.pone.0009444. PMC2830474. PMID20209158. [18] Dictionary | Definition of Temazepam (http:/ / www. websters-online-dictionary. org/ definitions/ Temazepam) [19] "American Board of Medical Specialties : Recognized Physician Specialty and Subspecialty Certificates" (http:/ / www. abms. org/ Who_We_Help/ Physicians/ specialties. aspx). . Retrieved 2008-07-21. [20] Mahowald, M.W. (March 2000). "What is causing excessive daytime sleepiness?: evaluation to distinguish sleep deprivation from sleep disorders" (http:/ / web. archive. org/ web/ 20080530012343/ http:/ / www. postgradmed. com/ issues/ 2000/ 03_00/ mahowald. shtml). Postgraduate Medicine 107 (3): 10823. doi:10.3810/pgm.2000.03.932. PMID10728139. Archived from the original (http:/ / www. postgradmed. com/ issues/ 2000/ 03_00/ mahowald. shtml) on 2008-05-30. . Retrieved 2008-07-27. [21] "About AADSM" (http:/ / aadsm. org/ ). Academy of Dental Sleep Medicine. 2008. . Retrieved 2008-07-22. [22] "About the ADBSM" (http:/ / www. abdsm. org/ ). American Board of Dental Sleep Medicine. . Retrieved 2008-07-22. [23] Wollenberg, Anne (July 28, 2008). "Time to wake up to sleep disorders" (http:/ / www. guardian. co. uk/ commentisfree/ 2008/ jul/ 28/ health). Guardian News and Media Limited. . Retrieved 2008-08-03. [24] "Sleep services" (http:/ / www. imperial. nhs. uk/ services/ sleepservices/ index. htm). Imperial College Healthcare NHS Trust. 2008. . Retrieved 2008-08-02.
External links
Sleep Problems (http://www.rcpsych.ac.uk/mentalhealthinfoforall/problems/sleepproblems/sleepingwell. aspx) - information leaflet from mental health charity The Royal College of Psychiatrists List of sleeping disorders (http://insomniahelp.info/insomnia-therapy/list-of-sleeping-disorders) Sleep Disorders ePatient website (http://www.sleepdisorders.com/)
Hypersomnia
63
Hypersomnia
Hypersomnia
Classification and external resources ICD-10 ICD-9 F51.1 [1] , G47.1 [2] [4] , 307.43 [5] -307.44 [6] , 327.1 [7] , 780.53 [8] -780.54 [9]
291.82
[3]
, 292.85
Hypersomnia is a disorder characterized by excessive amounts of sleepiness. There are two main categories of hypersomnia: primary hypersomnia (also called idiopathic hypersomnia) and recurrent hypersomnia (also called primary recurrent hypersomnia). Both have the same symptoms but differ in how often they occur.[12]
Symptoms
Those who suffer from hypersomnia have recurring episodes of excessive daytime sleepiness (EDS) which is different from feeling tired due to lack of or interrupted sleep at night. They are compelled to nap repeatedly during the day, often at inappropriate times such as at work, during a meal, or in conversation. These daytime naps usually provide no relief from symptoms. Patients with hypersomnia often experience prolonged night sleep and have difficulty waking from long sleep, feeling disoriented upon doing so. Other symptoms may include anxiety, increased irritation, decreased energy, restlessness, slow thinking, slow speech, loss of appetite, hallucinations, and memory difficulty. Some patients lose the ability to function in family, social, occupational or other settings. Typically, hypersomnia is first recognized in adolescence or young adulthood.[13] These symptoms are present in both types of hypersomnia. A sufferer from primary hypersomnia displays these symptoms continually for months or even years. Recurrent hypersomnia is characterized by recurring periods of symptoms many times throughout the year mixed with periods of normal sleep-wake cycles. Kleine-Levin syndrome is the most well-known form of recurrent hypersomnia, though it is very rare; sufferers often sleep up to eighteen hours a day and yet do not feel refreshed upon waking.
Causes
Hypersomnia can be caused by brain damage and disorders such as clinical depression, uremia and fibromyalgia. Hypersomnia can also be a symptom of other sleep disorders such as narcolepsy, sleep apnea, restless leg syndrome and periodic limb movement disorder. It may also occur as an adverse effect of taking certain medications (e.g. some psychotropics for depression, anxiety, or bipolar disorder), of withdrawal from some medications, or of drug or alcohol abuse. A genetic predisposition may be a factor.[13] People who are overweight may be more likely to suffer from hypersomnia. Although studies have shown a correlation between a lack of sleep and weight gain, sleeping at the level of a hypersomniac can also lead to considerable weight gain. This is because excessive sleeping decreases metabolic energy consumption, making weight loss more difficult. Sleep disorders of this nature provoke or initiate weight gain due to a tendency to attempt to manage low energy levels by eating non-complex carbohydrates. Another possible cause is an infection of mononucleosis, as several instances of hypersomnia have been found to arise immediately after such an infection. It can also be caused in children by influenza.
Hypersomnia Two people with excessive daytime sleepiness and prolonged nocturnal sleep were treated for their subclinical hypothyroidism, effecting significantly decreased sleep time and daytime sleepiness.[14] When the cause of the hypersomnia cannot be determined, it is considered to be idiopathic hypersomnia.
64
Epidemiology
Hypersomnia is an uncommon disorder, less than 5% of adults complain of EDS. The disorder usually occurs between ages 1530 and develops slowly over a period of years.
Diagnosis
To be diagnosed with hypersomnia, one must display symptoms for at least a month and the disorder must have a significant impact on the patient's life. The diagnosis is not given if the hypersomnia is a result of medication or of another disorder.
Treatment
From the website of the US National Institute of Neurological Disorders and Stroke: Treatment is symptomatic in nature. Stimulants, such as amphetamine, methylphenidate, and modafinil, may be prescribed. Other drugs used to treat hypersomnia include clonidine, levodopa, bromocriptine, antidepressants, and monoamine oxidase inhibitors. Changes in behavior (for example avoiding night work and social activities that delay bed time) and diet may offer some relief. Patients should avoid alcohol and caffeine.[13] These drug therapies may or may not work; hypersomnia is a lifelong disorder and recent research theorizes to treat the hypothalamus as a probable solution.
References
[1] http:/ / apps. who. int/ classifications/ icd10/ browse/ 2010/ en#/ F51. 1 [2] http:/ / apps. who. int/ classifications/ icd10/ browse/ 2010/ en#/ G47. 1 [3] http:/ / www. icd9data. com/ getICD9Code. ashx?icd9=291. 82 [4] http:/ / www. icd9data. com/ getICD9Code. ashx?icd9=292. 85 [5] http:/ / www. icd9data. com/ getICD9Code. ashx?icd9=307. 43 [6] http:/ / www. icd9data. com/ getICD9Code. ashx?icd9=307. 44 [7] http:/ / www. icd9data. com/ getICD9Code. ashx?icd9=327. 1 [8] http:/ / www. icd9data. com/ getICD9Code. ashx?icd9=780. 53 [9] http:/ / www. icd9data. com/ getICD9Code. ashx?icd9=780. 54 [10] http:/ / www. emedicine. com/ med/ topic3129. htm [11] http:/ / www. nlm. nih. gov/ cgi/ mesh/ 2011/ MB_cgi?field=uid& term=D006970 [12] "Hypersomnia causes, adults, drug, person, people, used, effect, Definition, Description, Causes and symptoms, Demographics, Diagnosis, Treatments, Prognosis" (http:/ / www. minddisorders. com/ Flu-Inv/ Hypersomnia. html). Minddisorders.com. 1999-02-15. . Retrieved 2010-08-05. [13] National Institutes of Health (June 2008). "NINDS Hypersomnia Information Page" (http:/ / www. ninds. nih. gov/ disorders/ hypersomnia/ hypersomnia. htm). . Retrieved 2009-01-23. [14] "Elsevier" (http:/ / www. ghpjournal. com/ article/ S0163-8343(08)00130-8/ abstract). Ghpjournal.com. . Retrieved 2010-08-05.
Hypersomnia
65
External links
06-081c. (http://www.merck.com/mmhe/sec06/ch081/ch081c.html) at Merck Manual of Diagnosis and Therapy Home Edition 14-173c. (http://www.merck.com/mmpe/sec14/ch173/ch173c.html) at Merck Manual of Diagnosis and Therapy Professional Edition -483065848 (http://www.gpnotebook.co.uk/simplepage.cfm?ID=-483065848) at GPnotebook med/3129 (http://www.emedicine.com/med/topic3129.htm#) at eMedicine - "Primary Hypersomnia" National Sleep Foundation (http://www.sleepfoundation.org/) Sleep Education.com: Idiopathic Hypersomnia (http://www.sleepeducation.com/Disorder.aspx?id=48)
Insomnia
66
Insomnia
Insomnia
Classification and external resources ICD-10 ICD-9 F51.0 [1] , G47.0 [2] [4] , 327.0 [5] , 780.51 [6] , 780.52 [7]
307.42
[3]
, 307.41
[9]
Insomnia (or sleeplessness) is most often defined by an individual's report of sleeping difficulties.[10] While the term is sometimes used in sleep literature to describe a disorder demonstrated by polysomnographic evidence of disturbed sleep, insomnia is often defined as a positive response to either of two questions: "Do you experience difficulty sleeping?" or "Do you have difficulty falling or staying asleep?"[10] Thus, insomnia is most often thought of as both a sign and a symptom[10] [11] that can accompany several sleep, medical, and psychiatric disorders, characterized by persistent difficulty falling asleep and/or staying asleep or sleep of poor quality. Insomnia is typically followed by functional impairment while awake. One definition of insomnia is difficulties initiating and/or maintaining sleep, or nonrestorative sleep, associated with impairments of daytime functioning or marked distress for more than 1 month."[12] Insomnia can be grouped into primary and secondary, or comorbid, insomnia.[13] [14] [15] Primary insomnia is a sleep disorder not attributable to a medical, psychiatric, or environmental cause.[16] A complete diagnosis will differentiate between: insomnia as secondary to another condition, primary insomnia co-morbid with one or more conditions, or free-standing primary insomnia.
Classification
Types of insomnia
Insomnia can be classified as transient, acute, or chronic. 1. Transient insomnia lasts for less than a week. It can be caused by another disorder, by changes in the sleep environment, by the timing of sleep, severe depression, or by stress. Its consequences sleepiness and impaired psychomotor performance are similar to those of sleep deprivation.[17] 2. Acute insomnia is the inability to consistently sleep well for a period of less than a month. Insomnia is present when there is difficulty initiating or maintaining sleep or when the sleep that is obtained is non-refreshing or of poor quality. These problems occur despite adequate opportunity and circumstances for sleep and they must result in problems with daytime function. [18] [19] 3. Chronic insomnia lasts for longer than a month. It can be caused by another disorder, or it can be a primary disorder. People with high levels of stress hormones or shifts in the levels of cytokines are more likely to have Chronic insomnia.[20] Its effects can vary according to its causes. They might include muscular fatigue, hallucinations, and/or mental fatigue. Some people that live with this disorder see things as if they are happening in slow motion, wherein moving objects seem to blend together. Chronic insomnia can cause double vision.[17]
Insomnia
67
Subjective insomnia
Some cases of insomnia are not really insomnia in the traditional sense. People experiencing sleep state misperception often sleep for normal durations, yet severely overestimate the time taken to fall asleep. They may believe they slept for only four hours while they, in fact, slept a full eight hours.
Insomnia Certain neurological disorders, brain lesions, or a history of traumatic brain injury Medical conditions such as hyperthyroidism and rheumatoid arthritis[26] Abuse of over-the counter or prescription sleep aids (sedative or depressant drugs) can produce rebound insomnia Poor sleep hygiene, e.g., noise Parasomnias, which include such disruptive sleep events as nightmares, sleepwalking, night terrors, violent behavior while sleeping, and REM behavior disorder, in which the physical body moves in response to events within dreams A rare genetic condition can cause a prion-based, permanent and eventually fatal form of insomnia called fatal familial insomnia.[27] Physical exercise. Exercise-induced insomnia is common in athletes, causing prolonged sleep onset latency.[28] Sleep studies using polysomnography have suggested that people who have sleep disruption have elevated nighttime levels of circulating cortisol and adrenocorticotropic hormone They also have an elevated metabolic rate, which does not occur in people who do not have insomnia but whose sleep is intentionally disrupted during a sleep study. Studies of brain metabolism using positron emission tomography (PET) scans indicate that people with insomnia have higher metabolic rates by night and by day. The question remains whether these changes are the causes or consequences of long-term insomnia.[26] A common misperception is that the amount of sleep required decreases as a person ages. The ability to sleep for long periods, rather than the need for sleep, appears to be lost as people get older. Some elderly insomniacs toss and turn in bed and occasionally fall off the bed at night, diminishing the amount of sleep they receive.[29] Eluned Summers-Bremner further discusses various modes of insomnia in his book 'Insomnia: A Cultural History.'
68
Diagnosis
Specialists in sleep medicine are qualified to diagnose the many different sleep disorders. Patients with various disorders including delayed sleep phase syndrome are often mis-diagnosed with primary insomnia. When a person has trouble getting to sleep, but has a normal sleep pattern once asleep, a circadian rhythm disorder is a likely cause. In many cases, insomnia is co-morbid with [30] another disease, side-effects from medications, or Potential complications of insomnia. a psychological problem. Approximately half of all diagnosed insomnia is related to psychiatric disorders.[31] In depression in many cases "insomnia should be regarded as a co-morbid condition, rather than as a secondary one;" insomnia typically predates psychiatric symptoms.[31] "In fact, it is possible that insomnia represents a significant risk for the development of a subsequent psychiatric disorder."[10] Knowledge of causation is not necessary for a diagnosis.[31]
Insomnia
69
Treatment
It is important to identify or rule out medical and psychological causes before deciding on the treatment for insomnia.[32] Attention to sleep hygiene is an important first line treatment strategy and should be tried before any pharmacological approach is considered.[33] Pharmacological treatments have been used mainly to reduce symptoms in acute insomnia; their role in the management of chronic insomnia remains unclear.[13]
Non-pharmacological
Non-pharmacological strategies are superior to hypnotic medication for insomnia because tolerance develops to the hypnotic effects. In addition, dependence can develop with rebound withdrawal effects developing upon discontinuation. Hypnotic medication is therefore only recommended for short-term use, especially in acute or chronic insomnia.[34] Non pharmacological strategies however, have long lasting improvements to insomnia and are recommended as a first line and long term strategy of managing insomnia. The strategies include attention to sleep hygiene, stimulus control, behavioral interventions, sleep-restriction therapy, paradoxical intention, patient education and relaxation therapy.[35] Reducing the temperature of blood flowing to the brain slows the brain's metabolic rate thereby reducing insomnia. [36] EEG biofeedback has demonstrated effectiveness in the treatment of insomnia with improvements in duration as well as quality of sleep.[37] Stimulus control therapy is a treatment for patients who have conditioned themselves to associate the bed, or sleep in general, with a negative response. As stimulus control therapy involves taking steps to control the sleep environment, it is sometimes referred interchangeably with the concept of sleep hygiene. Examples of such environmental modifications include using the bed for sleep or sex only, not for activities such as reading or watching television; waking up at the same time every morning, including on weekends; going to bed only when sleepy and when there is a high likelihood that sleep will occur; leaving the bed and beginning an activity in another location if sleep does not result in a reasonably brief period of time after getting into bed (commonly ~20 min); reducing the subjective effort and energy expended trying to fall asleep; avoiding exposure to bright light during nighttime hours, and eliminating daytime naps. A component of stimulus control therapy is sleep restriction, a technique that aims to match the time spent in bed with actual time spent asleep. This technique involves maintaining a strict sleep-wake schedule, sleeping only at certain times of the day and for specific amounts of time to induce mild sleep deprivation. Complete treatment usually lasts up to 3 weeks and involves making oneself sleep for only a minimum amount of time that they are actually capable of on average, and then, if capable (i.e. when sleep efficiency improves), slowly increasing this amount (~15 min) by going to bed earlier as the body attempts to reset its internal sleep clock. Bright light therapy, which is often used to help early morning wakers reset their natural sleep cycle, can also be used with sleep restriction therapy to reinforce a new wake schedule. Although applying this technique with consistency is difficult, it can have a positive effect on insomnia in motivated patients. Paradoxical intention is a cognitive reframing technique where the insomniac, instead of attempting to fall asleep at night, makes every effort to stay awake (i.e. essentially stops trying to fall asleep). One theory that may explain the effectiveness of this method is that by not voluntarily making oneself go to sleep, it relieves the performance anxiety that arises from the need or requirement to fall asleep, which is meant to be a passive act. This technique has been shown to reduce sleep effort and performance anxiety and also lower subjective assessment of sleep-onset latency and overestimation of the sleep deficit (a quality found in many insomniacs).[38] Meditation has been recommended for the treatment of insomnia. The renowned meditation teacher Siddhrtha Gautama, 'The Buddha', is recorded as having recommended the practice of 'loving-kindness' meditation, or mett bhvan as a way to produce relaxation and thereby, sound sleep putting it first in a list of the benefits of that meditation.[39] More recently, studies have concluded that: a mindfulness practice reduced mental and bodily restlessness before sleep and the subjective symptoms of insomnia;[40] and that mindfulness-based cognitive
Insomnia behavioural therapy reduced restlessness, sleep effort and dysfunctional sleep-related thoughts[41] including worry.[42] Cognitive Behavioral Therapy for Insomnia A recent study found that Cognitive Behavioral Therapy for Insomnia (CBT-I) is more effective than hypnotic medications in controlling insomnia.[43] In this therapy, patients are taught improved sleep habits and relieved of counter-productive assumptions about sleep. Common misconceptions and expectations that can be modified include: (1) unrealistic sleep expectations (e.g., I need to have 8 hours of sleep each night), (2) misconceptions about insomnia causes (e.g., I have a chemical imbalance causing my insomnia), (3) amplifying the consequences of insomnia (e.g., I cannot do anything after a bad night's sleep), and (4) performance anxiety after trying for so long to have a good night's sleep by controlling the sleep process. Numerous studies have reported positive outcomes of combining cognitive behavioral therapy for insomnia treatment with treatments such as stimulus control and the relaxation therapies. Hypnotic medications are equally effective in the short-term treatment of insomnia but their effects wear off over time due to tolerance. The effects of CBT-I have sustained and lasting effects on treating insomnia long after therapy has been discontinued.[44] [45] The addition of hypnotic medications with CBT-I adds no benefit in insomnia. The long lasting benefits of a course of CBT-I shows superiority over pharmacological hypnotic drugs. Even in the short term when compared to short-term hypnotic medication such as zolpidem (Ambien), CBT-I still shows significant superiority. Thus CBT-I is recommended as a first line treatment for insomnia.[46]
70
Medications
Many insomniacs rely on sleeping tablets and other sedatives to get rest, with research showing that medications are prescribed to over 95% of insomniac cases.[47] [48] Certain classes of sedatives such as benzodiazepines and newer nonbenzodiazepine drugs can also cause physical dependence, which manifests in withdrawal symptoms if the drug is not carefully tapered down. The benzodiazepine and nonbenzodiazepine hypnotic medications also have a number of side-effects such as day time fatigue, motor vehicle crashes, cognitive impairments and falls and fractures. Elderly people are more sensitive to these side-effects.[49] The non-benzodiazepines zolpidem and zaleplon have not adequately demonstrated effectiveness in sleep maintenance. Some benzodiazepines have demonstrated effectiveness in sleep maintenance in the short term but in the longer term are associated with tolerance and dependence. Drugs that may prove more effective and safer than existing drugs for insomnia are in development.[50] In comparing the options, a systematic review found that benzodiazepines and nonbenzodiazepines have similar efficacy that is not significantly more than for antidepressants.[51] Benzodiazepines did not have a significant tendency for more adverse drug reactions.[51] Chronic users of hypnotic medications for insomnia do not have better sleep than chronic insomniacs not taking medications. In fact, chronic users of hypnotic medications have more regular nighttime awakenings than insomniacs not taking hypnotic medications.[52] A further review of the literature regarding benzodiazepine hypnotic as well as the nonbenzodiazepines concluded that these drugs cause an unjustifiable risk to the individual and to public health and lack evidence of long-term effectiveness. The risks include dependence, accidents, and other adverse effects. Gradual discontinuation of hypnotics in long-term users leads to improved health without worsening of sleep. It is preferred that hypnotics be prescribed for only a few days at the lowest effective dose and avoided altogether wherever possible in the elderly.[53]
Insomnia Benzodiazepines The most commonly used class of hypnotics prescribed for insomnia are the benzodiazepines. Benzodiazepines all bind unselectively to the GABAA receptor.[51] But certain benzodiazepines (hypnotic benzodiazepines) have significantly higher activity at the 1 subunit of the GABAA receptor compared to other benzodiazepines (for example, triazolam and temazepam have significantly higher activity at the 1 subunit compared to alprazolam and Normison (temazepam) is a benzodiazepine commonly prescribed for insomnia diazepam, making them superior [54] and other sleep disorders. sedative-hypnotics alprazolam and diazepam in turn have higher activity at the 2 subunit compared to triazolam and temazepam, making them superior anxiolytic agents). Modulation of the 1 subunit is associated with sedation, motor-impairment, respiratory depression, amnesia, ataxia, and reinforcing behavior (drug-seeking behavior). Modulation of the 2 subunit is associated with anxiolytic activity and disinhibition. For this reason, certain benzodiazepines are better suited to treat insomnia than others. Hypnotic benzodiazepines include drugs such as temazepam, flunitrazepam, triazolam, flurazepam, midazolam, nitrazepam, and quazepam. These drugs can lead to tolerance, physical dependence, and the benzodiazepine withdrawal syndrome upon discontinuation, especially after consistent usage over long periods of time. Benzodiazepines, while inducing unconsciousness, actually worsen sleep as they promote light sleep while decreasing time spent in deep sleep.[55] A further problem is, with regular use of short-acting sleep aids for insomnia, daytime rebound anxiety can emerge.[56] Benzodiazepines can help to initiate sleep and increase sleep time, but they also decrease deep sleep and increase light sleep. Although there is little evidence for benefit of benzodiazepines in insomnia and evidence of major harm, prescriptions have continued to increase.[57] There is a general awareness that long-term use of benzodiazepines for insomnia in most people is inappropriate and that a gradual withdrawal is usually beneficial due to the adverse effects associated with the long-term use of benzodiazepines and is recommended whenever possible.[58] [59]
71
Non-benzodiazepines Nonbenzodiazepine sedative-hypnotic drugs, such as zolpidem, zaleplon, zopiclone, and eszopiclone, are a newer classification of hypnotic medications indicated for mild to moderate insomnia. They work on the benzodiazepine site on the GABAA receptor complex similarly to the benzodiazepine class of drugs. Some but not all of the nonbenzodiazepines are selective for the 1 subunit on GABAA receptors, which is responsible for inducing sleep and may therefore have a cleaner side-effect profile than the older benzodiazepines. Zopiclone and eszopiclone like benzodiazepine drugs bind unselectively to 1, 2, 3 and 5 GABAA benzodiazepine receptors.[60] Zolpidem is more selective and zaleplon is highly selective for the 1 subunit, thus giving them an advantage over benzodiazepines in terms of sleep architecture and a reduction in side-effects. The nonbenzodiazepine sedative-hypnotic drugs have milder activity at the 1 subunit on GABAA receptors compared to most benzodiazepines, rendering them ineffective for moderately severe to severe insomnia.[61] [62] However, there are controversies over whether these non-benzodiazepine drugs are superior to benzodiazepines. These drugs appear to cause both psychological dependence and physical dependence, though less than traditional benzodiazepines and can also cause the same memory and cognitive disturbances along with morning sedation.
Insomnia Alcohol Alcohol is often used as a form of self-treatment of insomnia to induce sleep. However, alcohol use to induce sleep can be a cause of insomnia. Long-term use of alcohol is associated with a decrease in NREM stage 3 and 4 sleep as well as suppression of REM sleep and REM sleep fragmentation. Frequent moving between sleep stages occurs, with awakenings due to headaches, the need to urinate, dehydration, and excessive sweating. Glutamine rebound also plays a role as when someone is drinking; alcohol inhibits glutamine, one of the body's natural stimulants. When the person stops drinking, the body tries to make up for lost time by producing more glutamine than it needs. The increase in glutamine levels stimulates the brain while the drinker is trying to sleep, keeping him/her from reaching the deepest levels of sleep.[63] Stopping chronic alcohol use can also lead to severe insomnia with vivid dreams. During withdrawal REM sleep is typically exaggerated as part of a rebound effect.[64] Opioids Opioid medications such as hydrocodone, oxycodone, and morphine are used for insomnia that is associated with pain due to their analgesic properties and hypnotic effects. Opioids can fragment sleep and decrease REM and stage 2 sleep. By producing analgesia and sedation, opioids may be appropriate in carefully selected patients with pain-associated insomnia.[24] Though, dependence on opium can lead to suffering from long time disturbance in sleep[65] . Antidepressants Some antidepressants such as amitriptyline, doxepin, mirtazapine, and trazodone can often have a very strong sedative effect, and are prescribed off label to treat insomnia.[66] The major drawback of these drugs is that they have properties that can lead to many side-effects; for example, amitriptyline and doxepin both have antihistaminergic, anticholinergic, and antiadrenergic properties, which contribute to their side-effect profile, while mirtazapines side-effects are primarily antihistaminergic, and trazadones side-effects are primarily antiadrenergic. Some also alter sleep architecture. As with benzodiazepines, the use of antidepressants in the treatment of insomnia can lead to withdrawal effects; withdrawal may induce rebound insomnia. Mirtazapine is known to decrease sleep latency, promoting sleep efficiency and increasing the total amount of sleeping time in patients suffering from both depression and insomnia.[67] [68] Melatonin and melatonin agonists The hormone melatonin, sold as a "dietary supplement" in some countries or as a slow-release prescription drug (Circadin) in Europe, is effective in several types of insomnia. Melatonin has demonstrated effectiveness equivalent to the prescription sleeping tablet zopiclone in inducing sleep and regulating the sleep/waking cycle.[69] One particular benefit of melatonin is that it can treat insomnia without altering the sleep pattern, which is altered by many prescription sleeping tablets. Another benefit is it does not impair performance related skills.[70] [71] Melatonin agonists, including ramelteon (Rozerem) and tasimelteon, seem to lack the potential for dependence.[72] This class of drugs has a relatively mild side-effect profile and low likelihood of causing morning sedation. While these drugs show good effect for the treatment of insomnia due to jet lag[73] and the chronic circadian rhythm disorders, the results for other forms of insomnia are less promising.[74]
72
Insomnia Antihistamines The antihistamine diphenhydramine is widely used in nonprescription sleep aids such as Benadryl. The antihistamine doxylamine is used in nonprescription sleep aids such as Unisom (USA) and Unisom 2 (Canada). In some countries, including Australia, it is marketed under the names Restavit and Dozile. It is the most effective over-the-counter sedative currently available in the United States, and is more sedating than some prescription hypnotics.[75] While the two drugs mentioned above are available over the counter in most countries, the effectiveness of these agents may decrease over time, and the incidence of next-day sedation is higher than for most of the newer prescription drugs. Anticholinergic side-effects may also be a draw back of these particular drugs. Dependence does not seem to be an issue with this class of drugs. Cyproheptadine is a useful alternative to benzodiazepine hypnotics in the treatment of insomnia. Cyproheptadine may be superior to benzodiazepines in the treatment of insomnia because cyproheptadine enhances sleep quality and quantity, whereas benzodiazepines tend to decrease sleep quality.[76] Atypical antipsychotics Low doses of certain atypical antipsychotics such as quetiapine, olanzapine, and risperidone are also prescribed for their sedative effect, but the danger of neurological, metabolic, and cognitive side-effects makes these drugs a poor choice to treat insomnia. Over time, quetiapine may lose its effectiveness as a sedative. The ability of quetiapine to produce sedation is determined by the dosage. Higher doses (300mg 900mg) are usually taken for its use as an antipsychotic, while lower doses (25mg 200mg) have a marked sedative effect; e.g., if a patient takes 300mg, he/she will more likely benefit from the drug's antipsychotic effects, but if the dose is brought down to 100mg, it will leave the patient feeling more sedated than at 300mg, because it works primarily as a sedative at lower doses. Eplivanserin is an investigational drug with a mechanism similar to antipsychotics.[72] Other substances Some insomniacs use herbs such as medical marijuana, valerian, chamomile, lavender, hops, and passion-flower. Valerian has undergone multiple studies and appears to be modestly effective.[77] [78] [79] Insomnia may be a symptom of magnesium deficiency, or low magnesium levels, but this has not yet been proven. A healthy diet containing magnesium can help to improve sleep in individuals without an adequate intake of magnesium.[80] L-Arginine L-aspartate, S-adenosyl-L-homocysteine, and Delta sleep-inducing peptide (DSIP) may be also helpful in alleviating insomnia.[81] There is some evidence showing that 3grams of L-Glycine before bedtime improves sleep quality.[82] Almorexant was an orexin antagonist undergoing clinical trials as a novel drug, but was dropped in January 2011 due to a poor side effect profile.[83]
73
Epidemiology
A survey of 1.1 million residents in the United States conducted by the American Cancer Society found that those that reported sleeping about 7 hours per night had the
Disability-adjusted life year for insomnia per 100,000inhabitants in 2002.no dataless than 252530.2530.25363641.541.5474752.552.5585863.563.5696974.574.580more than 80
Insomnia lowest rates of mortality, whereas those that slept for fewer than 6 hours or more than 8 hours had higher mortality rates. Getting 8.5 or more hours of sleep per night increased the mortality rate by 15%. Severe insomnia sleeping less than 3.5 hours in women and 4.5 hours in men also led to a 15% increase in mortality. However, most of the increase in mortality from severe insomnia was discounted after controlling for co-morbid disorders. After controlling for sleep duration and insomnia, use of sleeping pills was also found to be associated with an increased mortality rate.[84] The lowest mortality was seen in individuals who slept between six and a half and seven and a half hours per night. Even sleeping only 4.5 hours per night is associated with very little increase in mortality. Thus, mild to moderate insomnia for most people is associated with increased longevity and severe insomnia is associated only with a very small effect on mortality.[84] As long as a patient refrains from using sleeping pills, there is little to no increase in mortality associated with insomnia, but there does appear to be an increase in longevity. This is reassuring for patients with insomnia in that, despite the sometimes-unpleasantness of insomnia, insomnia itself appears to be associated with increased longevity.[84] It is unclear why sleeping longer than 7.5 hours is associated with excess mortality.[84] Insomnia is 40% more common in women than in men.[85]
74
Prevalence
The National Sleep Foundation's 2002 Sleep in America poll showed that 58% of adults in the U.S. experienced symptoms of insomnia a few nights a week or more.[86] Although insomnia was the most common sleep problem among about one half of older adults (48%), they were less likely to experience frequent symptoms of insomnia than their younger counterparts (45% vs. 62%), and their symptoms were more likely to be associated with medical conditions, according to the poll of adults between the ages of 55 and 84.[86] As explained by Thomas Roth,[10] estimates of the prevalence of insomnia depend on the criteria used as well as the population studied. About 30% of adults report at least one of the symptoms of insomnia. When daytime impairment is added as a criterion, the prevalence is about 10%. Primary insomnia persisting for at least one month yields estimates of 6%.
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[48] New clinical program addresses sleep problems and therapy options (http:/ / www. nps. org. au/ news_and_media/ media_releases/ repository/ New_clinical_program_addresses). nps.org.au. 3 February 2010 [49] Glass J, Lanctt KL, Herrmann N, Sproule BA, Busto UE (2005). "Sedative hypnotics in older people with insomnia: meta-analysis of risks and benefits". BMJ 331 (7526): 1169. doi:10.1136/bmj.38623.768588.47. PMC1285093. PMID16284208. [50] Rosenberg, RP. (2006). "Sleep maintenance insomnia: strengths and weaknesses of current pharmacologic therapies". Ann Clin Psychiatry 18 (1): 4956. doi:10.1080/10401230500464711. PMID16517453. [51] Buscemi N, Vandermeer B, Friesen C, Bialy L, Tubman M, Ospina M, Klassen TP, Witmans M. (2007). "The efficacy and safety of drug treatments for chronic insomnia in adults: a meta-analysis of RCTs". J Gen Intern Med 22 (9): 13351350. doi:10.1007/s11606-007-0251-z. PMC2219774. PMID17619935. [52] Ohayon MM, Caulet M (1995). "Insomnia and psychotropic drug consumption". Prog. Neuropsychopharmacol. Biol. Psychiatry 19 (3): 42131. doi:10.1016/0278-5846(94)00023-B. PMID7624493. [53] "What's wrong with prescribing hypnotics?" (http:/ / www. nelm. nhs. uk/ en/ NeLM-Area/ Evidence/ Drug-Class-Focused-Reviews/ 498264/ ). Drug Ther Bull 42 (12): 8993. 2004. doi:10.1136/dtb.2004.421289. PMID15587763. . [54] Definition of Temazepam (http:/ / www. websters-online-dictionary. org/ definitions/ Temazepam). Websters-online-dictionary.org. Retrieved on 2011-11-20. [55] Tsoi, Wf (1991). "Insomnia: drug treatment". Annals of the Academy of Medicine, Singapore 20 (2): 26972. PMID1679317. [56] Montplaisir J (2000). "Treatment of primary insomnia". CMAJ 163 (4): 38991. PMC80369. PMID10976252. [57] D. Maiuro PhD, Roland (13 December 2009). Handbook of Integrative Clinical Psychology, Psychiatry, and Behavioral Medicine: Perspectives, Practices, and Research (http:/ / books. google. com/ ?id=4Tkdm1vRFbUC). Springer. pp.128130. ISBN0-8261-1094-0. . [58] Lader, Malcolm Harold; P. Cardinali, Daniel; R. Pandi-Perumal, S. (22 March 2006). Sleep and sleep disorders: a neuropsychopharmacological approach. Georgetown, Tex.: Landes Bioscience/Eurekah.com. p.127. ISBN0-387-27681-5. [59] Authier, N.; Boucher, A.; Lamaison, D.; Llorca, PM.; Descotes, J.; Eschalier, A. (2009). "Second Meeting of the French CEIP (Centres d'Evaluation et d'Information sur la Pharmacodpendance). Part II: Benzodiazepine Withdrawal". Therapie 64 (6): 365370. doi:10.2515/therapie/2009051. PMID20025839. [60] WHO (2006). "World Health Organisation Assessment of Zopiclone" (http:/ / www. who. int/ medicines/ areas/ quality_safety/ 4. 6ZopicloneCritReview. pdf) (PDF). who.int. . [61] Rowlett JK, Woolverton WL (1996). "Assessment of benzodiazepine receptor heterogeneity in vivo: apparent pA2 and pKB analyses from behavioral studies". Psychopharmacology (Berl.) 128 (1): 116. doi:10.1007/s002130050103. PMID8944400. [62] Noguchi H; Kitazumi K, Mori M, Shiba T. (March 2004). "Electroencephalographic properties of zaleplon, a non-benzodiazepine sedative/hypnotic, in rats" (http:/ / www. jstage. jst. go. jp/ article/ jphs/ 94/ 3/ 246/ _pdf) (PDF). J Pharmacol Sci. 94 (3): 24651. doi:10.1254/jphs.94.246. PMID15037809. . [63] Perry, Lacy. (2004-10-12) HowStuffWorks "How Hangovers Work" (http:/ / health. howstuffworks. com/ hangover5. htm). Health.howstuffworks.com. Retrieved on 2011-11-20. [64] Lee-chiong, Teofilo (24 April 2008). Sleep Medicine: Essentials and Review (http:/ / books. google. com/ ?id=s1F_DEbRNMcC& pg=PT105). Oxford University Press, USA. p.105. ISBN0-19-530659-7. . [65] "Sleep profile in patients with chronic opioid abuse: A polysomnographic evaluation in an egyptian sample". Addictive Disorders & their Treatment 10 (1): 21-28. 2011. doi:10.1097/ADT.0b013e3181fb2847. [66] Bertschy G, Ragama-Pardos E, Muscionico M et al. (2005). "Trazodone addition for insomnia in venlafaxine-treated, depressed inpatients: a semi-naturalistic study". Pharmacol. Res. 51 (1): 7984. doi:10.1016/j.phrs.2004.06.007. PMID15519538. [67] Winokur, A; Demartinis Na, 3rd; McNally, DP; Gary, EM; Cormier, JL; Gary, KA (2003). "Comparative effects of mirtazapine and fluoxetine on sleep physiology measures in patients with major depression and insomnia". J Clin Psychiatry 64 (10): 12249. PMID14658972. [68] Schittecatte, Michel; Dumont, FranOise; Machowski, Robert; Cornil, Catherine; Lavergne, Francis; Wilmotte, Jean (2002). "Effects of mirtazapine on sleep polygraphic variables in major depression". Neuropsychobiology 46 (4): 197201. doi:10.1159/000067812. PMID12566938. [69] Paul MA, Gray G, Sardana TM, Pigeau RA (2004). "Melatonin and zopiclone as facilitators of early circadian sleep in operational air transport crews". Aviat Space Environ Med 75 (5): 43943. PMID15152897.
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[70] Paul MA, Gray G, Kenny G, Pigeau RA (2003). "Impact of melatonin, zaleplon, zopiclone, and temazepam on psychomotor performance". Aviat Space Environ Med 74 (12): 126370. PMID14692469. [71] Zhdanova IV, Tucci V (2003). "Melatonin, Circadian Rhythms, and Sleep". Curr Treat Options Neurol 5 (3): 225229. doi:10.1007/s11940-003-0013-0. PMID12670411. [72] Insomnia Treatment (http:/ / www. news-medical. net/ health/ Insomnia-Treatment. aspx). news-medical.net [73] Rajaratnam, SMW; Polymeropoulos MH, Fisher DM, Roth T, Scott C, Birznieks G, Klerman EB (2 December 2008). "Melatonin agonist tasimelteon (VEC-162) for transient insomnia after sleep-time shift: two randomised controlled multicentre trials". Lancet 373 (9662): 48291. doi:10.1016/S0140-6736(08)61812-7. PMID19054552. [74] Zammit G, Erman M, Wang-Weigand S, Sainati S, Zhang J, Roth T (2007). "Evaluation of the efficacy and safety of ramelteon in subjects with chronic insomnia". J Clin Sleep Med 3 (5): 495504. PMC1978328. PMID17803013. [75] DrugBank: DB00366 (Doxylamine) (http:/ / www. drugbank. ca/ cgi-bin/ getCard. cgi?CARD=DB00366. txt). Drugbank.ca. Retrieved on 2011-11-20. [76] Tokunaga S; Takeda Y, Shinomiya K, Hirase M, Kamei C. (2007). "Effects of some H1-antagonists on the sleep-wake cycle in sleep-disturbed rats" (http:/ / www. jstage. jst. go. jp/ article/ jphs/ 103/ 2/ 201/ _pdf) (PDF). J Pharmacol Sci. 103 (2): 2016. doi:10.1254/jphs.FP0061173. PMID17287588. . [77] Donath F, Quispe S, Diefenbach K, Maurer A, Fietze I, Roots I (2000). "Critical evaluation of the effect of valerian extract on sleep structure and sleep quality". Pharmacopsychiatry 33 (2): 4753. doi:10.1055/s-2000-7972. PMID10761819. [78] Morin CM, Koetter U, Bastien C, Ware JC, Wooten V (2005). "Valerian-hops combination and diphenhydramine for treating insomnia: a randomized placebo-controlled clinical trial". Sleep 28 (11): 146571. PMID16335333. [79] Meolie AL, Rosen C, Kristo D et al. (2005). "Oral nonprescription treatment for insomnia: an evaluation of products with limited evidence". Journal of Clinical Sleep Medicine 1 (2): 17387. PMID17561634. [80] Hornyak M, Voderholzer U, Hohagen F, Berger M, Riemann D (1998). "Magnesium therapy for periodic leg movements-related insomnia and restless legs syndrome: an open pilot study". Sleep 21 (5): 5015. PMID9703590. [81] Billiard, M, Kent, A (2003). Sleep: physiology, investigations, medicine (http:/ / books. google. com/ ?id=IorPrIY6dOYC& pg=PA275& lpg=PA275#v=onepage& q& f=false). pp.2757. ISBN9780306474064. . [82] Yamadera W, Inagawa K, Chiba S, Bannai M, Takahashi M, Nakayama K (2007). "Glycine ingestion improves subjective sleep quality in human volunteers, correlating with polysomnographic changes". Sleep and Biological rhythms 5 (2): 126131. doi:10.1111/j.1479-8425.2007.00262.x. [83] Actelion and GSK Discontinue Clinical Development of Almorexant (http:/ / www1. actelion. com/ en/ our-company/ news-and-events/ index. page?newsId=1483135). actelion.com (2011-01-28). Retrieved on 2011-11-20. [84] Kripke DF, Garfinkel L, Wingard DL, Klauber MR, Marler MR (2002). "Mortality associated with sleep duration and insomnia". Arch. Gen. Psychiatry 59 (2): 1316. doi:10.1001/archpsyc.59.2.131. PMID11825133. [85] <Please add first missing authors to populate metadata.> (2007). "Several Sleep Disorders Reflect Gender Differences" (http:/ / pn. psychiatryonline. org/ cgi/ content/ full/ 42/ 10/ 40). Psychiatric News 42 (8): 40. . [86] "2002 Sleep in America Poll" (http:/ / web. archive. org/ web/ 20080614221846/ http:/ / www. sleepfoundation. org/ site/ c. huIXKjM0IxF/ b. 2417355/ k. 143E/ 2002_Sleep_in_America_Poll. htm). National Sleep Foundation. Archived from the original (http:/ / www. sleepfoundation. org/ site/ c. huIXKjM0IxF/ b. 2417355/ k. 143E/ 2002_Sleep_in_America_Poll. htm) on June 14, 2008. . Retrieved 2008-08-13.
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Further reading
Summers-Bremner, Eluned. Insomnia: A Cultural History (University of Chicago Press, 2008) 176 pp.ISBN 978-1-86189-317-8 excerpt and text search (http://www.amazon.com/dp/1861896549/)
Psychosis
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Psychosis
Psychosis
Classification and external resources ICD-10 ICD-9 OMIM F20- F29 290 [2] [1] [3] [5] 603175 [6] 192430 [7]
-299 [4]
603342
608923
Psychosis (from the Greek "psyche", for mind/soul, and - "-osis", for abnormal condition) means abnormal condition of the mind, and is a generic psychiatric term for a mental state often described as involving a "loss of contact with reality". People suffering from psychosis are described as psychotic. Psychosis is given to the more severe forms of psychiatric disorder, during which hallucinations and delusions and impaired insight may occur.[10] Some professionals say that the term psychosis is not sufficient as some illnesses grouped under the term "psychosis" have nothing in common (Gelder, Mayou & Geddes 2005). People experiencing psychosis may report hallucinations or delusional beliefs, and may exhibit personality changes and thought disorder. Depending on its severity, this may be accompanied by unusual or bizarre behavior, as well as difficulty with social interaction and impairment in carrying out daily life activities. A wide variety of central nervous system diseases, from both external poisons and internal physiologic illness, can produce symptoms of psychosis.
Hallucinations
A hallucination is defined as sensory perception in the absence of external stimuli. Hallucinations are different from illusions, or perceptual distortions, which are the misperception of external stimuli.[11] Hallucinations may occur in any of the five senses and take on almost any form, which may include simple sensations (such as lights, colors, tastes, and smells) to experiences such as seeing and interacting with fully formed animals and people, hearing voices, and having complex tactile sensations. Auditory hallucinations, particularly experiences of hearing voices, are a common and often prominent feature of psychosis. Hallucinated voices may talk about, or to, the person, and may involve several speakers with distinct personas. Auditory hallucinations tend to be particularly distressing when they are derogatory, commanding or preoccupying. However, the experience of hearing voices need not always be a negative one. One research study has shown that the majority of people who hear voices are not in need of psychiatric help.[12] The Hearing Voices Movement has subsequently been created to support voice hearers, regardless of whether they are considered to have a mental illness or not.
Psychosis
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Delusions
Psychosis may involve delusional beliefs, some of which are paranoid in nature. Karl Jaspers has classified psychotic delusions into primary and secondary types. Primary delusions are defined as arising suddenly and not being comprehensible in terms of normal mental processes, whereas secondary delusions may be understood as being influenced by the person's background or current situation (e.g., ethnicity, religious beliefs, superstitious belief).[13]
Catatonia
Catatonia describes a profoundly agitated state in which the experience of reality is generally considered to be impaired. There are two primary manifestations of catatonic behavior. The classic presentation is a person who does not move or interact with the world in any way while awake. This type of catatonia presents with waxy flexibility. Waxy flexibility is when someone physically moves part of a catatonic person's body and the person stays in the position even if it is bizarre and otherwise nonfunctional (such as moving a person's arm straight up in the air and the arm stays there). The other type of catatonia is more of an outward presentation of the profoundly agitated state described above. It involves excessive and purposeless motor behavior as well as extreme mental preoccupation which prevents intact experience of reality. An example would be someone walking very fast in circles to the exclusion of anything else with a level of mental preoccupation (meaning not focused on anything relevant to the situation) that was not typical of the person prior to the symptom onset. In both types of catatonia there is generally no reaction to anything that happens outside of them. It is important to distinguish catatonic agitation from severe bipolar mania although someone could have both.
Thought disorder
Thought disorder describes an underlying disturbance to conscious thought and is classified largely by its effects on speech and writing. Affected persons show loosening of associations, that is, a disconnection and disorganization of the semantic content of speech and writing. In the severe form speech becomes incomprehensible and it is known as "word-salad".
Causes
Causes of symptoms of mental illness were customarily classified as "organic" or "functional." Organic disorders were those held to be caused by physical illness affecting the brain (that is, psychiatric disorders secondary to other conditions), while functional disorders were considered to be disorders of the functioning of the mind in the absence of physical disorders (that is, primary psychological or psychiatric disorders). The materialistic view of the mind-body problem holds that mental disorders arise from physical processes; in this view, the distinction between brain and mind, and therefore between organic and functional disease, is an artificial one. Subtle physical abnormalities have been found in illnesses traditionally considered functional, such as schizophrenia. The DSM-IV-TR avoids the functional/organic distinction, and instead lists traditional psychotic illnesses, psychosis due to general medical conditions, and substance-induced psychosis.
Psychiatric disorders
Primary psychiatric causes of psychosis include the following:[14] [15] [16] schizophrenia and schizophreniform disorder affective (mood) disorders, including severe depression, and severe depression or mania in bipolar disorder (manic depression). People experiencing a psychotic episode in the context of depression may experience persecutory or self-blaming delusions or hallucinations, while people experiencing a psychotic episode in the context of mania may form grandiose delusions. schizoaffective disorder, involving symptoms of both schizophrenia and mood disorders
Psychosis brief psychotic disorder, or acute/transient psychotic disorder delusional disorder (persistent delusional disorder) chronic hallucinatory psychosis Psychotic symptoms may also be seen in[16] schizotypal disorder certain personality disorders at times of stress (including paranoid personality disorder, schizoid personality disorder, and borderline personality disorder) major depressive disorder in its severe form although it is possible and more likely to have severe depression without psychosis bipolar disorder in severe mania and/or severe depression although it is possible to have severe mania and/or severe depression without psychosis as well, in fact that is more commonly the case post-traumatic stress disorder induced delusional disorder Sometimes in obsessive-compulsive disorder Stress is known to contribute to and trigger psychotic states. A history of psychologically traumatic events, and the recent experience of a stressful event, can both contribute to the development of psychosis. Short-lived psychosis triggered by stress is known as brief reactive psychosis, and patients may spontaneously recover normal functioning within two weeks.[17] In some rare cases, individuals may remain in a state of full-blown psychosis for many years, or perhaps have attenuated psychotic symptoms (such as low intensity hallucinations) present at most times.
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Normal states
Brief hallucinations are not uncommon in those without any psychiatric disease. Causes or triggers include[16] falling asleep and waking: hypnagogic and hypnopompic hallucinations, which are entirely normal[18] bereavement, in which hallucinations of a deceased loved one are common[16] severe sleep deprivation[19] [20] [21] sensory deprivation and sensory impairment Caffeine Intoxication
Medical conditions
A very large number of medical conditions can cause psychosis, sometimes called secondary psychosis.[16] Examples include: disorders causing delirium (toxic psychosis), in which consciousness is disturbed neurodevelopmental disorders and chromosomal abnormalities, including velocardiofacial syndrome neurodegenerative disorders, such as Alzheimer's disease,[22] dementia with Lewy bodies,[23] and Parkinson's disease[24] focal neurological disease, such as stroke, brain tumors,[25] multiple sclerosis,[26] and some forms of epilepsy malignancy (typically via masses in the brain, paraneoplastic syndromes, or drugs used to treat cancer) infectious and postinfectious syndromes, including infections causing delirium, viral encephalitis, HIV,[27] malaria,[28] Lyme disease,[29] [30] [31] syphilis[32] [33] endocrine disease, such as hypothyroidism, hyperthyroidism, adrenal failure, Cushing's syndrome, hypoparathyroidism and hyperparathyroidism; sex hormones also affect psychotic symptoms and sometimes childbirth can provoke psychosis, termed puerperal psychosis inborn errors of metabolism, such as porphyria and metachromatic leukodystrophy[34] [35] [36] nutritional deficiency, such as vitamin B12 deficiency[37] [38] other acquired metabolic disorders, including electrolyte disturbances such as hypocalcemia,[39] hypernatremia,[40] hyponatremia,[41] hypokalemia,[42] hypomagnesemia,[43] hypermagnesemia,[44]
Psychosis hypercalcemia,[45] and hypophosphatemia,[46] but also hypoglycemia,[47] hypoxia, and failure of the liver or kidneys autoimmune and related disorders, such as systemic lupus erythematosus (lupus, SLE),[48] sarcoidosis,[49] Hashimoto's encephalopathy,[50] [51] [52] and anti-NMDA-receptor encephalitis[53] poisoning, by therapeutic drugs (see below), recreational drugs (see below), and a range of plants, fungi, metals, organic compounds, and a few animal toxins[16] some sleep disorders, including hallucinations in narcolepsy (in which REM sleep intrudes into wakefulness)[16] Psychosis can even be caused by familiar ailments such as flu[54] [55] or mumps.[56]
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Recreational drugs
Various psychoactive substances (both legal and illegal) have been implicated in causing, exacerbating, and/or precipitating psychotic states and/or disorders in users. This may be upon intoxication, for a more prolonged period after use, or upon withdrawal. Drugs that can induce psychotic symptoms include amphetamine, caffeine (which can worsen psychotic symptoms in schizophrenia and produce olfactory hallucinations at very high doses in normal volunteers), cannabis, cocaine, desoxypipradrol, dimethyltryptamine, alcohol (ethanol), inhalants, gammahydroxybutyric acid (and its precursors gammabutyrolactone and 1,4-butanediol), ketamine, LSD, mephedrone and methcathinone, mescaline and other phenethylamine hallucinogens, methamphetamine, MDMA (very rarely), opiates such as heroin, phencyclidine, piperazine-based drugs, psilocybin, and anabolic steroids at high doses.[16] Frequent users of cannabis have twice the likelihood of developing both psychosis and schizophrenia.[57] Older studies indicate that certain strains containing large proportions of tetrahydrocannabinol and low proportions of cannabidiol[58] [59] merely lowers the threshold for psychosis, and thus helps to trigger full-blown psychosis in some people.[60] On the other hand, cannabis use has increased dramatically over the past few decades but declined in the last decade, whereas the rate of psychosis has not increased. This suggests cannabis generally only hastens the onset of psychosis in those who would otherwise only become psychotic at a later date.[61]
Medication
Administration, or sometimes withdrawal, of a large number of medications may provoke psychotic symptoms.[16] Drugs that can induce psychosis experimentally and/or in a significant proportion of patients include amphetamine and other sympathomimetics, dopamine agonists, ketamine, corticosteroids (often with mood changes in addition), and some anticonvulsants such as vigabatrin.[62] [16]
Pathophysiology
The first brain image of an individual with psychosis was completed as far back as 1935 using a technique called pneumoencephalography[63] (a painful and now obsolete procedure where cerebrospinal fluid is drained from around the brain and replaced with air to allow the structure of the brain to show up more clearly on an X-ray picture). The purpose of the brain is to collect information from the body (pain, hunger, etc.), and from the outside world, interpret it to a coherent world view, and produce a meaningful response. The information from the senses enter the brain in the primary sensory areas. They process the information and send it to the secondary areas where the information is interpreted. Spontaneous activity in the primary sensory areas may produce hallucinations which are misinterpreted by the secondary areas as information from the real world. For example, a PET or fMRI scan of a person who claims to be hearing voices may show activation in the primary auditory cortex, or parts of the brain involved in the perception and understanding of speech.[64] Tertiary brain cortex collects the interpretations from the secondary cortexes and creates a coherent world view of it. A study investigating structural changes in the brains of people with psychosis showed there was significant grey
Psychosis matter reduction in the right medial temporal, lateral temporal, and inferior frontal gyrus, and in the cingulate cortex bilaterally of people before and after they became psychotic.[65] Findings such as these have led to debate about whether psychosis itself causes excitotoxic brain damage and whether potentially damaging changes to the brain are related to the length of psychotic episode. Recent research has suggested that this is not the case[66] although further investigation is still ongoing. Studies with sensory deprivation have shown that the brain is dependent on signals from the outer world to function properly. If the spontaneous activity in the brain is not counterbalanced with information from the senses, loss from reality and psychosis may occur after some hours. A similar phenomenon is paranoia in the elderly when poor eyesight, hearing and memory causes the person to be abnormally suspicious of the environment. On the other hand, loss from reality may also occur if the spontaneous cortical activity is increased so that it is no longer counterbalanced with information from the senses. The 5-HT2A receptor seems to be important for this, since psychedelic drugs which activate them produce hallucinations. However, the main feature of psychosis is not hallucinations, but the inability to distinguish between internal and external stimuli. Close relatives to psychotic patients may hear voices, but since they are aware that they are unreal they can ignore them, so that the hallucinations do not affect their reality perception. Hence they are not considered to be psychotic. Psychosis has been traditionally linked to the neurotransmitter dopamine. In particular, the dopamine hypothesis of psychosis has been influential and states that psychosis results from an overactivity of dopamine function in the brain, particularly in the mesolimbic pathway. The two major sources of evidence given to support this theory are that dopamine receptor D2 blocking drugs (i.e., antipsychotics) tend to reduce the intensity of psychotic symptoms, and that drugs which boost dopamine activity (such as amphetamines and cocaine) can trigger psychosis in some people (see amphetamine psychosis).[67] However, increasing evidence in recent times has pointed to a possible dysfunction of the excitory neurotransmitter glutamate, in particular, with the activity of the NMDA receptor. This theory is reinforced by the fact that dissociative NMDA receptor antagonists such as ketamine, PCP and dextromethorphan/dextrorphan (at large overdoses) induce a psychotic state more readily than dopinergic stimulants, even at "normal" recreational doses. The symptoms of dissociative intoxication are also considered to mirror the symptoms of schizophrenia, including negative psychotic symptoms, more closely than amphetamine psychosis. Dissociative induced psychosis happens on a more reliable and predictable basis than amphetamine psychosis, which usually only occurs in cases of overdose, prolonged use or with sleep deprivation, which can independently produce psychosis. New antipsychotic drugs which act on glutamate and its receptors are currently undergoing clinical trials. The connection between dopamine and psychosis is generally believed to be complex. While dopamine receptor D2 suppresses adenylate cyclase activity, the D1 receptor increases it. If D2-blocking drugs are administered the blocked dopamine spills over to the D1 receptors. The increased adenylate cyclase activity affects genetic expression in the nerve cell, a process which takes time. Hence antipsychotic drugs take a week or two to reduce the symptoms of psychosis. Moreover, newer and equally effective antipsychotic drugs actually block slightly less dopamine in the brain than older drugs whilst also blocking 5-HT2A receptors, suggesting the 'dopamine hypothesis' may be oversimplified.[68] Soyka and colleagues found no evidence of dopaminergic dysfunction in people with alcohol-induced psychosis[69] and Zoldan et al. reported moderately successful use of ondansetron, a 5-HT3 receptor antagonist, in the treatment of levodopa psychosis in Parkinson's disease patients.[70] Psychiatrist David Healy has criticised pharmaceutical companies for promoting simplified biological theories of mental illness that seem to imply the primacy of pharmaceutical treatments while ignoring social and developmental factors which are known to be important influences in the aetiology of psychosis.[71] Some theories regard many psychotic symptoms to be a problem with the perception of ownership of internally generated thoughts and experiences.[72] For example, the experience of hearing voices may arise from internally generated speech that is mislabeled by the psychotic person as coming from an external source.
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Psychosis It has been suggested that persons with bipolar disorder may have increased activity of the left hemisphere compared to the right hemisphere of the brain, while persons with schizophrenia have increased activity in the right hemisphere.[73] Increased level of right hemisphere activation has also been found in people who have high levels of paranormal beliefs[74] and in people who report mystical experiences.[75] It also seems to be the case that people who are more creative are also more likely to show a similar pattern of brain activation.[76] Some researchers have been quick to point out that this in no way suggests that paranormal, mystical or creative experiences are in any way by themselves a symptom of mental illness, as it is still not clear what makes some such experiences beneficial and others distressing.
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Diagnosis
Diagnosing the presence and/or extent of psychosis may be distinguished from diagnosing the cause of psychosis.[16] The presence of psychosis is typically diagnosed by clinical interview, incorporating mental state examination.[14] [15] Its extent may be established by formal rating scales. The Brief Psychiatric Rating Scale (BPRS)[77] assesses the level of 18 symptom constructs of psychosis such as hostility, suspicion, hallucination, and grandiosity. It is based on the clinician's interview with the patient and observations of the patient's behavior over the previous 23 days. The patient's family can also provide the behavior report. During the initial assessment and the follow-up, both positive and negative symptoms of psychosis can be assessed using the 30 item Positive and Negative Symptom Scale (PANSS).[78] Establishing the cause of psychosis requires clinical examination, and sometimes special investigations, to diagnose or exclude secondary causes of psychosis; if these are excluded, a primary psychiatric diagnosis can be established.[16]
Treatment
The treatment of psychosis depends on the cause or diagnosis or diagnoses (such as schizophrenia, bipolar disorder and/ or substance intoxication). The first line treatment for many psychotic disorders is antipsychotic medication (oral or intramuscular injection), and sometimes hospitalization is needed. There is growing evidence that cognitive behavior therapy[79] and family therapy[80] can be effective in managing psychotic symptoms. When other treatments for psychosis are ineffective, electroconvulsive therapy or ECT (also known as shock treatment) is sometimes applied to relieve the underlying symptoms of psychosis due to depression. There is also increasing research suggesting that animal-assisted therapy can contribute to the improvement in general well-being of people with schizophrenia.[81]
Early intervention
Early intervention in psychosis is a relatively new concept based on the observation that identifying and treating someone in the early stages of a psychosis can significantly improve their longer term outcome.[82] This approach advocates the use of an intensive multi-disciplinary approach during what is known as the critical period, where intervention is the most effective, and prevents the long term morbidity associated with chronic psychotic illness. Newer research into the effectiveness of cognitive behavioural therapy during the early pre-cursory stages of psychosis (also known as the "prodrome" or "at risk mental state") suggests that such input can prevent or delay the onset of psychosis.[83]
Psychosis
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History
The word psychosis was first used by Ernst von Feuchtersleben in 1845[84] as an alternative to insanity and mania and stems from the Greek (psychosis), "a giving soul or life to, animating, quickening" and that from (psyche), "soul" and the suffix - (-osis), in this case "abnormal condition".[85] [86] The word was used to distinguish disorders which were thought to be disorders of the mind, as opposed to "neurosis", which was thought to stem from a disorder of the nervous system.[87] The psychoses thus became the modern equivalent of the old notion of madness, and hence there was much debate on whether there was only one (unitary) or many forms of the new disease.[88] The division of the major psychoses into manic depressive illness (now called bipolar disorder) and dementia praecox (now called schizophrenia) was made by Emil Kraepelin, who attempted to create a synthesis of the various mental disorders identified by 19th century psychiatrists, by grouping diseases together based on classification of common symptoms. Kraepelin used the term 'manic depressive insanity' to describe the whole spectrum of mood disorders, in a far wider sense than it is usually used today. In Kraepelin's classification this would include 'unipolar' clinical depression, as well as bipolar disorder and other mood disorders such as cyclothymia. These are characterised by problems with mood control and the psychotic episodes appear associated with disturbances in mood, and patients will often have periods of normal functioning between psychotic episodes even without medication. Schizophrenia is characterized by psychotic episodes which appear to be unrelated to disturbances in mood, and most non-medicated patients will show signs of disturbance between psychotic episodes. During the 1960s and 1970s, psychosis was of particular interest to counterculture critics of mainstream psychiatric practice, who argued that it may simply be another way of constructing reality and is not necessarily a sign of illness. For example, R. D. Laing argued that psychosis is a symbolic way of expressing concerns in situations where such views may be unwelcome or uncomfortable to the recipients. He went on to say that psychosis could be also seen as a transcendental experience with healing and spiritual aspects. Arthur J. Deikman suggested use of the term "mystical psychosis" to characterize first-person accounts of psychotic experiences that are similar to reports of mystical experiences. Thomas Szasz focused on the social implications of labeling people as psychotic, a label he argues unjustly medicalises different views of reality so such unorthodox people can be controlled by society. Psychoanalysis has a detailed account of psychosis which differs markedly from that of psychiatry. Freud and Lacan outlined their perspective on the structure of psychosis in a number of works. Since the 1970s, the introduction of a recovery approach to mental health, which has been driven mainly by people who have experienced psychosis (or whatever name is used to describe their experiences), has led to a greater awareness that mental illness is not a lifelong disability, and that there is an expectation that recovery is possible, and probable with effective support.
References
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Canadian Journal of Psychiatry 29 (7): 599600. PMID6391648. [47] Padder, Tanveer; Aparna Udyawar, Nouman Azhar, and Kamil Jaghab (December 2005). "Acute Hypoglycemia Presenting as Acute Psychosis" (http:/ / www. priory. com/ psych/ hypg. htm). Psychiatry online. . Retrieved 2006-09-27. [48] Robert, M.; R. Sunitha, and N. K. Thulaseedharan (1 March 2006). "Neuropsychiatric manifestations systemic lupus erythematosus: A study from South India" (http:/ / www. neurologyindia. com/ article. asp?issn=0028-3886;year=2006;volume=54;issue=1;spage=75;epage=77;aulast=Robert). Neurology India 54 (1): 757. doi:10.4103/0028-3886.24713. PMID16679649. . Retrieved 2006-09-29. [49] Bona, Joseph R.; Sondralyn M. Fackler, Morris J. Fendley and Charles B. Nemeroff (1 August 1998). "Neurosarcoidosis as a Cause of Refractory Psychosis: A Complicated Case Report" (http:/ / www. ajp. psychiatryonline. org/ cgi/ content/ full/ 155/ 8/ 1106). American Journal of Psychiatry 155 (8): 11068. PMID9699702. . 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The Positive and Negative Symptom Scale (PANNS) for schizophrenia. Schizophrenia Bulletin, 13, pp261-276 [79] Birchwood, M; Trower P (2006). "The future of cognitive-behavioural therapy for psychosis: not a quasi-neuroleptic". British Journal of Psychiatry 188: 108108. doi:10.1192/bjp.bp.105.014985. PMID16449695. [80] Haddock, G; Lewis S (2005). "Psychological interventions in early psychosis". Schizophrenia Bulletin 31 (3): 697704. doi:10.1093/schbul/sbi029. PMID16006594. [81] Nathans-Barel, I.; P. Feldman, B. Berger, I. Modai and H. Silver (2005). "Animal-assisted therapy ameliorates anhedonia in schizophrenia patients". Psychotherapy and Psychosomatics 74 (1): 3135. doi:10.1159/000082024. PMID15627854. [82] Birchwood, M; P. Todd, C. Jackson (1998). "Early Intervention in Psychosis: The Critical Period Hypothesis". British Journal of Psychiatry 172 (33): 5359. PMID9764127. [83] French, Paul; Anthony Morrison (2004). 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Further reading
Sims, A. (2002) Symptoms in the mind: An introduction to descriptive psychopathology (3rd edition). Edinburgh: Elsevier Science Ltd. ISBN 0-7020-2627-1
Personal accounts
Dick, P.K. (1981) VALIS. London: Gollancz. [Semi-autobiographical] ISBN 0-679-73446-5 Hinshaw, S.P. (2002) The Years of Silence are Past: My Father's Life with Bipolar Disorder. Cambridge: Cambridge University Press. Jamison, K.R. (1995) An Unquiet Mind: A Memoir of Moods and Madness. London: Picador. ISBN 0-679-76330-9 Schreber, Daniel Paul (2000) Memoirs of My Nervous Illness. New York: New York Review of Books. ISBN 0-940322-20-X McLean, R (2003) Recovered Not Cured: A Journey Through Schizophrenia. Allen & Unwin. Australia. ISBN 1-86508-974-5 The Eden Express by Mark Vonnegut James Tilly Matthews Saks, Elyn R. (2007) The Center Cannot HoldMy Journey Through Madness. New York: Hyperion. ISBN 978-1-4013-0138-5
External links
psychosis-bipolar.com - For persons afflicted, relatives and professionals: information, trialog, interactive therapy portal (http://www.psychosis-bipolar.com) Understanding psychotic experiences (http://www.mind.org.uk/help/diagnoses_and_conditions/ psychotic_experience) from mental health charity Mind
Racing thoughts
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Racing thoughts
Racing thoughts refers to the rapid thought patterns that often occur in manic, hypomanic, or mixed episodes. While racing thoughts are most commonly described in people with bipolar disorder, they are also common with anxiety disorders, such as OCD. Racing thoughts are also associated with use of amphetamines and sleep deprivation.[1] Racing thoughts may be experienced as background or take over a person's consciousness. Thoughts, music, and voices might be zooming through one's mind. There also might be a repetitive pattern of voice or of pressure without any associated "sound". It is a very overwhelming and irritating feeling, and can result in losing track of time. Generally, racing thoughts are described by an individual who has had an episode as an event where the mind uncontrollably brings up random thoughts and memories and switches between them very quickly. Sometimes they are related, as one thought leads to another; other times they are completely random. A person suffering from an episode of racing thoughts has no control over his or her train of thought and it stops them from focusing on one topic or prevents sleeping. Sleep deprivation can cause similar symptoms which can be described as racing thoughts or a racing mind. Chronic sleep apnea and prolonged disturbed sleep patterns may induce racing thoughts.[2] Treatment for racing thoughts is similar to treatments for Bipolar disorder; beginning with a healthy life style, sleeping regularly, eating healthy and staying away from drugs and alcohol.[3]
References
[1] Amphetamines (http:/ / www. dassa. sa. gov. au/ site/ page. cfm?u=126& print=1) [2] What Are Racing Thoughts? Bipolar Disorder Symptoms (http:/ / bipolar. about. com/ cs/ faqs/ f/ faq_racethought. htm) [3] smith, ma, melinda. Treatment for Bipolar Disorder.
External links
Racing Thoughts - Bipolar Disorder Symptoms (http://www.bipolardisordersymptoms.info/bipolar-symptoms/ racing-thoughts.htm)
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Bipolar spectrum
Bipolar spectrum
The bipolar spectrum (BS) refers to a category of mood disorders that feature abnormally elevated or depressed mood. These disorders range from bipolar I disorder, featuring full-blown manic episodes, to cyclothymia, featuring less prominent hypomanic episodes, to "subsyndromal" conditions where only some of the criteria for mania or hypomania are met. These disorders typically also involve depressive symptoms or episodes that alternate with the elevated mood states, or with mixed episodes that feature symptoms of both.[1] The concept of the bipolar spectrum is similar to that of Emil Kraepelin's original concept of manic depressive illness.[2] Currently, manic depressive illness is usually referred to as bipolar disorder or bipolar.
Referential nomenclature
A simple nomenclature system was introduced in 1978 by Angst, J., et al., to classify more easily individuals' affectedness within the spectrum, following a clinical study by the Psychiatric University Clinic of Zrich.[3] Points on the spectrum using this nomenclature are denoted using the following codes: Msevere mania Dsevere depression (unipolar depression) mless severe mania (hypomania) dless severe depression
Thus, mD represents a case with hypomania and major depression. A further distinction is sometimes made in the ordering of the letters, to represent the order of the episodes, where the patient's normal state is euthymic, interrupted by episodes of mania followed by depression (MD) or vice versa (DM). Employing this schema, major depression would be denoted D. Unipolar mania (M) is, depending on the authority cited, either very rare,[4] or nonexistent with such cases actually being Md. Unipolar hypomania (m) without accompanying depression has been noted in the medical literature.[5] There is speculation as to whether this condition may occur with greater frequency in the general, untreated population; successful social function of these potentially high-achieving individuals may lead to being labeled as normal, rather than as individuals suffering any substantial dysregulation.
References
[1] Diagnostic and Statistical Manual of Mental Disorders, 4th Edition (Text Revision). American Psychiatric Association. pp.2000. [2] Across the Bipolar Spectrum: From Practice to Research (http:/ / www. medscape. com/ viewarticle/ 441617) [3] Angst, J; Felder, W; Frey, R; Stassen, HH (1978). "The course of affective disorders. I. Change of diagnosis of monopolar, unipolar, and bipolar illness.". Archiv fur Psychiatrie und Nervenkrankheiten 226 (1): 5764. PMID708227. [4] Why No "Unipolar Mania" Listing in DSM-IV? | Serendip's Exchange (http:/ / serendip. brynmawr. edu/ bb/ neuro/ neuro00/ web3/ Wachterman. html) [5] Mood episodes and mood disorders: patterns of incidence and conversion in the first three decades of life, Katja Beesdo et al.,Bipolar Disorders Volume 11 Issue 6, Pages 637 - 64 http:/ / www3. interscience. wiley. com. ezp-prod1. hul. harvard. edu/ journal/ 122542146/ abstract
Bipolar I
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Bipolar I
Bipolar I disorder
Classification and external resources ICD-9 296.7 [7]
Bipolar I disorder is a mood disorder that is characterized by at least one manic or mixed episode. There may be episodes of hypomania or major depression as well.[1] It is a sub-diagnosis of bipolar disorder, and conforms to the classic concept of manic-depressive illness.[2]
Bipolar I disorder Single manic episode. Bipolar I disorder Most recent episode hypomanic Bipolar I disorder Most recent episode manic Bipolar I disorder Most recent episode mixed Bipolar I disorder Most recent episode depressed Bipolar I disorder Most recent episode unspecified
Treatment
Medical assessment
Routine medical assessments are often prescribed to rule-out or identify a somatic cause for bipolar I symptoms. These tests can include ultrasounds of the head, x-ray computed tomography (CAT scan), electroencephalogram, HIV test, full blood count, thyroid function test, liver function test, urea and creatinine levels and if patient is on lithium, lithium levels are taken. Drug screening includes recreational drugs, particularly cannabinoids, and exposure to toxins.
Medication
Mood stabilizers 1. Lithium carbonate, the mainstay in the management of bipolar disorder, but it has a narrow therapeutic range and typically requires monitoring
Bipolar I 2. Anticonvulsants, such as sodium valproate, carbamazepine or lamotrigine 3. Antipsychotics, such as quetiapine, risperidone, olanzapine or aripiprazole 4. Electroconvulsive therapy, a psychiatric treatment in which seizures are electrically induced in anesthetized patients for therapeutic effect Some antidepressants have been found to precipitate a manic episode.
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Patient education
Information on the condition, importance of regular sleep patterns, routines and eating habits and the importance of compliance with medication as prescribed. Behavior modification through counselling can have positive influence to help reduce the effects of risky behavior during the manic phase.
References
[1] "Bipolar Disorder: Whos at Risk?" (http:/ / www. webmd. com/ bipolar-disorder/ guide/ bipolar-disorder-whos-at-risk). . Retrieved 22 November 2011. [2] "What are the types of bipolar disorder?" (http:/ / www. medicinenet. com/ bipolar_disorder/ page2. htm#types). . Retrieved 22 November 2011.
External links
National Bipolar Foundation (http://www.nationalbipolarfoundation.org) Bipolar Test Online (http://bipolartestonline.com/) Advice for Bipolar Disorder Sufferers and Their Loved Ones (http://www.bipolaradviceguide.com/) Latest bipolar news and research via MedWorm (http://www.medworm.com/rss/search.php?qu=bipolar+ manic&kid=16&t=Bipolar&f=c&r=Any&o=d)
Bipolar II
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Bipolar II
This article needs more medical references for verification. [1] Please review the contents of the article and II disorder add the appropriate references if you can. Help may also be requested at Wikipedia:WikiProject Medicine. Please remove this message after the article has been corrected.
Bipolar II disorder
Classification and external resources ICD-10 F31.8 [2]
Bipolar II disorder is a bipolar spectrum disorder characterized by at least one hypomanic episode and at least one major depressive episode; with this disorder, depressive episodes can be more frequent and are more intense than hypomanic episodes.[3] [4] People with bipolar disorder type II have never experienced a full manic episode, although they can experience periods of high energy and impulsiveness similar to but not as extreme as mania. The hypomanic episodes associated with bipolar II disorder must last all day for a period of at least four days.[5] These periods alternate between episodes of depression.[6] Sometimes severe symptoms can make it extremely difficult or impossible to function in work, school, or at home. People with Bipolar Disorder may be depressed or irritable and violent.[7] Bipolar II is believed to be under-diagnosed because hypomanic behavior often presents as high-functioning behavior.[4] Those with bipolar II are at highest risk of suicide among the bipolar spectrum.[8] [9] Hypomania in bipolar II may manifest itself in disorganized racing thoughts, irritability, anxiety, insomnia, or all of the above combined. Because these agitated symptoms are negative, it may be difficult to distinguish a bipolar II hypomanic state from depression. Hypomania is often regarded as an elation of mood, however, mood may be negative in bipolar II hypomania. Mixed States and/or Rapid Cycling may also be present.[3] [10]
Bipolar II
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Depressive episodes
Low energy levels Cessation of usual activities Black and white thinking Unrealistic pessimism Overgeneralization Automatic thoughts Maladaptive assumptions Dysfunctional personal schemas[11]
Relapse
In the case of a relapse, the following symptoms often occur and are considered early warning signs:[12] Sleep disturbance: patient requires less sleep and does not feel tired Racing thoughts and/or speech Anxiety Irritability Emotional intensity Spending more money than usual Binge behavior, including food, drugs, and alcohol Arguments with family members and friends Taking on many projects at once
People with bipolar disorder may develop alternate identities to match each mood they experience. For some, this is done intentionally, as a means by which to escape trauma or pain from a depressive period, or simply to better organize one's life by setting boundaries for one's perceptions and behaviors.[13]
Causes
There have been very few studies conducted to examine the possible causes of Bipolar II. Those that have been done have not considered Bipolar I and Bipolar II separately and have had inconclusive results. Researchers have found that patients with either Bipolar I or II have increased levels of blood calcium concentrations and diminished size in the prefrontal and temporal regions of the brain. But these studies could not find a significant difference between those with Bipolar I or Bipolar II. There has been a study looking at genetics and Bipolar II disorder and the results are inconclusive; however, scientists did find that relatives of people with Bipolar II are more likely to develop the same bipolar disorder or major depression rather then developing Bipolar I disorder.[12]
Diagnosis
The Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) recognizes two types of bipolar disordersbipolar I and bipolar II. People with bipolar I disorder suffer from alterations of full manic episodes and major depressive episodes. On the contrary, as noted above, people with bipolar II disorder experience a milder form of a manic episode, known as a hypomanic episode as well as major depressive episodes. Although bipolar II is thought to be less severe than bipolar I in regards to symptom intensity, it is actually more severe and distressing with respect to episode frequency and overall course. Those with bipolar II often experience more frequent bouts of depressive episodes.[14] Specific criteria defined by the DSM-IV for a bipolar II diagnosis is as follows: The presence of a hypomanic or major depressive episode. If currently in major depressive episode, history of a hypomanic episode. If currently in a hypomanic episode, history of a major depressive episode. No history of a manic episode.
Bipolar II Significant stress or impairment in social, occupational, or other important areas of functioning.[15] When considering the possibility of bipolar II disorder, it is also important to utilize differential diagnosis methods, or methods to identify the presence of a particular disorder when other alternatives are possible. The DSM-IV notes that in the diagnosis of bipolar II disorder, the presence of mood symptoms like hypomanic and major depressive episodes cannot be better accounted for by Schizoaffective Disorder. Nor can it extend beyond Schizophrenia, Schizophreniform Disorder, Delusional Disorder, or Psychotic Disorder Not Otherwise Specified. Studies have identified major differences between bipolar I and bipolar II in regards to their clinical features, comorbidity rates and family histories. According Baek et al. (2011), during depressive episodes, bipolar II patients tend to show higher rates of psychomotor agitation, guilt, shame, suicide ideation, and suicide attempts. Bipolar II patients have shown higher lifetime comorbidity rates of DSM axis I diagnoses such as phobias, anxiety disorders, substance & alcohol abuse, and eating disorders and there is a higher correlation between bipolar II patients and family history of psychiatric illness, including major depression and substance-related disorders. The occurrence rate of psychiatric illness in first degree relatives of bipolar II patients was 26.5%, versus 15.4% in bipolar I patients.[14]
[16]
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Although the DSM-IV reports a bipolar II lifetime prevalence rate of 0.5%, recent epidemiological studies indicate a rate closer to 5% with one in two depressed outpatients suffering from this disorder.[17] There are several reasons for this increase in bipolar II diagnoses. New semi-structured interviews allow trained research clinicians to diagnose a patient on the bipolar spectrum more accurately, DSM-IV criteria has relaxed so that now the minimum duration of hypomania is less than four days, and a history of hypomania is now focused more on over-activity, especially in regards to goal-setting activity, than mood changes.[17] Screening instruments like the Mood Disorders Questionnaire (MDQ) are helpful tools in determining a patient's status on the bipolar spectrum and getting families involved can also improve chances of an accurate diagnosis and acknowledgment of hypomanic episodes. In addition, there are certain features that have been shown to increase the chances that depressed patients are suffering from a bipolar disorder including atypical symptoms of depression like hypersomnia and hyperphagia, a family history of bipolar disorder, medication-induced hypomania, recurrent or psychotic depression, antidepressant refractory depression, and early or postpartum depression.[16]
Treatments
The most common treatment for reducing bipolar II disorder symptoms is medication, usually in the form of mood stabilizers. However, treatment with mood stabilizers may produce a flat affect in the patient, which is dose dependent. Concurrent use of SSRI antidepressants may help some with bipolar II disorder, though these medications should be used with caution because it is believed that they may exacerbate manic symptoms in some people; moreover, even when used along with a mood stabilizer, SSRI antidepressants may induce rapid cycling. Lithium is considered the "gold standard" medication and is often individually used as first line treatment for bipolar II. The combination of lithium and lamotrigine can be prescribed when either one is not enough to either curb depression or hypomania. The combination is well tolerated and has been shown to be effective and safe in preventing mania, due to lithium's anti-manic properties, while keeping depression at bay with lamotrigine's anti-depressive properties. Non-pharmaceutical therapies can also help those with the illness. These include psychodynamic therapy, psychoanalysis, social rhythm therapy, interpersonal therapy, behavioral therapy, cognitive therapy, music therapy, psychoeducation, light therapy, and family-focused therapy. Relapses can still occur, even with continued medication and therapy.[18] Treatment for bipolar disorder mostly involves lithium or carbamazepine, and the effectiveness of both treatments are similar in patients of both bipolar I and bipolar II disorder. However, since there have not been many studies on the responsiveness to treatment between disorder types, more data is needed to make a more concise finding.[19] There is often failure to diagnose and treat bipolar disorder, more so amongst patients with type II. In a study on delayed treatment, it was found that women were given treatment much later than men were, starting lithium
Bipolar II treatment 11 years after the onset of the disorder compared to 6.9 years for men.[20] The management of bipolar II disorder is controversial. Some medications used are: Antipsychotics- there was a study done over a 6-month period that found there was a 60% response rate, however in this study there were some questions raised about whether the study actually was adequately testing the difference between the drugs being used and not being used. Dopamine Agonists- there was a recent study done, and it found that 60% of the patients taking the drug improved in their post-tests scores on the MADRS test by 50%. Antidepressants- most studies have shown that there is an association between stabilized moods and the antidepressants. They had improvements on their HDRS, MADRS, and CGI tests. Non-pharmaceutical therapies have not been well studied but include cognitive behavioral therapy (CBT) and interpersonal therapy, which seem to be effective in unipolar depression, which is believed to be able to expand to bipolar II disorder. Treatment typically includes three things: the treatment of acute hypomania, the treatment of acute depression, and the prevention of the relapse of either hypomania or depression. The main goal is to avoid causing harm to the patient.[21]
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Prognosis
There is evidence to suggest that Bipolar II Disorder has a more chronic course of illness than Bipolar I Disorder.[22] This constant and pervasive course of the illness leads to an increased risk in suicide and more hypomanic and major depressive episodes with shorter periods of time between episodes than Bipolar I patients experience.[22] The natural course of Bipolar II Disorder, when left untreated, leads to patients spending the majority of their lives unwell with much of their suffering stemming from depression.[16] Their recurrent depression results in personal suffering and disability.[16] This disability can present itself in the form of psychosocial impairment, which has been suggested to be worse in Bipolar II patients than in Bipolar I patients.[23] Another facet of this illness that is associated with a poorer prognosis is rapid cycling, which denotes the occurrence of four or more Major Depressive, Hypomanic, and/or mixed episodes in a twelve month period.[22] Rapid cycling is actually quite common in those with Bipolar II, much more so in women than in men (70% vs. 40%), and without treatment leads to added sources of disability and an increased risk of suicide.[16] In order to improve a patients prognosis, long term therapy is most favorably recommended for controlling symptoms, maintaining remission and preventing relapses.[24] With treatment, patients have been shown to present a decreased risk of suicide (especially when treated with Lithium) and a reduction of frequency and severity of their episodes, which in turns moves them toward a stable life and reduces the time they spend ill.[25] In order to maintain their state of balance, therapy is often continued indefinitely, as around 50% of the patients who discontinue it relapse quickly and experience either full-blown episodes or sub-syndromal symptoms that bring significant functional impairments.[24]
Functioning
The deficits in functioning associated with Bipolar II Disorder stem mostly from the recurrent depression that Bipolar II Patients suffer from. Depressive symptoms are much more disabling than hypomanic symptoms and are potentially as or more disabling than mania symptoms.[23] Functional impairment has been shown to be directly linked with increasing percentages of depressive symptoms, and because sub-syndromal symptoms are more commonand frequentin Bipolar II disorder, they have been implicated heavily as a major cause of psychosocial disability.[16] There is evidence that shows the mild depressive symptoms, or even sub-syndromal symptoms, are responsible for the non-recovery of social functioning, which furthers the idea that residual depressive symptoms are detrimental for functional recovery in patients being treated for Bipolar II.[26] It has been suggested that symptom interference in relation to social and interpersonal relationships in Bipolar II Disorder is worse than symptom interference in other chronic medical illnesses such as cancer.[26] This social impairment can last for years, even after
Bipolar II treatment that has resulted in a resolution of mood symptoms.[26] The factors related to this persistent social impairment are residual depressive symptoms, limited illness insight (a very common occurrence in patients with Bipolar II Disorder), and impaired executive functioning.[26] Impaired ability in regards to executive functions is directly tied to poor psychosocial functioning, a common side-effect in patients with Bipolar II.[27] The impact on a patients psychosocial functioning stems from the depressive symptoms (more common in Bipolar II than Bipolar I).[23] An increase in these symptoms severity seems to correlate with a significant increase in psychosocial disability.[27] Psychosocial disability can present itself in poor semantic memory, which in turn effects other cognitive domains like verbal memory and (as mentioned earlier) executive functioning leading to a direct and persisting impact on psychosocial functioning.[28] An abnormal semantic memory organization can manipulate thoughts and lead to the formation of delusions and possibly effect speech and communication problems, which can lead to interpersonal issues.[28] Bipolar II patients have also been shown to present worse cognitive functioning than those patients with Bipolar I, though they demonstrate about the same disability when it comes to occupational functioning, interpersonal relationships, and autonomy.[27] This disruption in cognitive functioning takes a toll on their ability to function in the work place, which leads to high rates of work loss in Bipolar II patient populations.[23] After treatment and while in remission, Bipolar II patients tend to report a good psychosocial functioning but they still score less in that department than normal patients without the disorder.[16] These lasting impacts further suggest that a prolonged exposure to an untreated Bipolar II disorder can lead to permanent adverse effects on functioning.[26]
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Bipolar II
98
Mortality
Several studies have shown that the risk of suicide is higher in patients who suffer from Bipolar II than those who suffer from Bipolar I, and especially higher than patients who suffer from Major Depressive Disorder.[16] In results of a summary of several lifetime study experiments, it was found that 24% of Bipolar II patients experienced suicidal ideation or suicide attempts compared to 17% in Bipolar I patients and 12% in Major Depressive Patients.[31] [16] The risk of suicide for Bipolar II patients is especially high; as many as 50% of them will attempt suicide at least once.[32] Bipolar Disorders in general are the 3rd leading cause of death in 1524 year olds.[32] Bipolar II patients were also found to employ more lethal means and have more complete suicides over all.[16] They had a higher rate of suicide attempts with a higher risk for death rather than just suicidal gestures that werent necessarily lethal (like self-harm).[23] Bipolar II patients have several risk factors that increase their risk of suicide. The illness is very recurrent and results in severe disabilities, interpersonal relationship problems, barriers to academic, financial, and vocational goals, and a loss of social standing in their community, all of which increase the likelihood of suicide.[33] Mixed symptoms and rapid-cycling, both very common in Bipolar II, are also associated with an increased risk of suicide.[16] The tendency for Bipolar II to be misdiagnosed and treated ineffectively, or not at all in some cases, also leads to an increased risk.[31] As a result of the high suicide risk for this group, reducing the risk and preventing attempts remains a main part of the treatment; a combination of self-monitoring, close supervision by a therapist, and faithful adherence to their medication regimen will help to reduce the risk and prevent the likelihood of a completed suicide.[33]
Specifiers
Chronic With catatonic features With melancholic features With psychotic features With atypical features With postpartum onset Longitudinal course specifiers (with and without inter-episode recovery) With seasonal pattern (applies only to the pattern of major depressive episodes) With rapid cycling
Bipolar II
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References
[1] http:/ / en. wikipedia. org/ wiki/ Bipolar [2] http:/ / apps. who. int/ classifications/ icd10/ browse/ 2010/ en#/ F31. 8 [3] "WebMD Rapid Cycling Bipolar Disorder" (http:/ / www. webmd. com/ bipolar-disorder/ guide/ rapid-cycling-bipolar-disorder). . Retrieved 22 November 2011. [4] "WebMD Bipolar II" (http:/ / www. webmd. com/ bipolar-disorder/ guide/ bipolar-2-disorder). . Retrieved 22 November 2011. [5] Buskist, W. & Davis, S.F., ed (2008). 21st Century Psychology: A Reference Handbook. Thousand Oaks, CA: Sage Publications Inc.. pp.290. ISBN978-1-4129-4968-2. [6] "Bipolar disorder" (http:/ / www. ncbi. nlm. nih. gov/ pubmedhealth/ PMH0001924/ ). . [7] "Bipolar Disorder" (http:/ / www. nimh. nih. gov/ health/ publications/ bipolar-disorder/ complete-index. shtml). National Institute of Mental Health. US Department of Health and Human Services. . Retrieved 30 September 2011. [8] David L. Dunner (2004). "Correlates of Suicidal Depression" (http:/ / www. psychiatrist. com/ supplenet/ v65s10/ v65s1002. pdf). Journal of Clinical Psychiatry. . Retrieved 2011-05-15. [9] Z. Rihmer & P. Pestality (1999-09-22). Bipolar II disorder and suicidal behavior. Psychiatric Clinics of North America. PMID10550861. [10] "Bipolar Disorder: Whos at Risk?" (http:/ / www. webmd. com/ bipolar-disorder/ guide/ bipolar-disorder-whos-at-risk). . Retrieved 22 November 2011. [11] Manicavasagar, Vijaya (2008). Gordan Parker. ed. Bipolar II Disorder: Modelling, Measuring, and Managing. Cambridge, England: Cambridge University Press. ISBN0521873142. [12] Orum, Margo (2008). Gordan Parker. ed. Bipolar II Disorder: Modelling, Measuring, and Managing. Cambridge, England: Cambridge University Press. ISBN0521873142. [13] Smith, Meg (2008). Gordan Parker. ed. Bipolar II Disorder: Modelling, Measuring, and Managing. Cambridge, England: Cambridge University Press. pp.195203. ISBN0521873142. [14] Baek, J. H., Park, D. Y., Choi, J., Kim, J. S., Choi, J. S., Ha, K., ... Hong, K. S. (2011). Differences between bipolar I and bipolar II in clinical features, comorbidity, and family history. Journal of Affective Disorders, 131, 5967. [15] American Psychiatric Association (2000). Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition Text Revision (DSM-IV-TR). [16] Hadjipavlou, George; Lakshmi N. Yatham (2008). Gordan Parker. ed. Bipolar II Disorder: Modelling, Measuring, and Managing. Cambridge, England: Cambridge University Press. p.65. ISBN0521873142. [17] Benazzi, F. (2007). Bipolar II disorder : epidemiology, diagnosis and management. CNS Drugs, 21(9), 727740. [18] "Understanding Bipolar Disorder -- Treatment" (http:/ / www. webmd. com/ bipolar-disorder/ guide/ understanding-bipolar-disorder-treatment?page=2). . Retrieved 22 November 2011. [19] MacQueen G.M., Young L.T. (2001). Bipolar II disorder: symptoms, course and response to treatment. American Psychiatric Association. Retrieved from http:/ / ps. psychiatryonline. org/ cgi/ content/ full/ 52/ 3/ 358#R52311648 [20] Baldessarini RJ, Tondo L, Hennen J. (1999). Effects of lithium treatment and its discontinuation on suicidal behavior in bipolar manic-depressive disorders. Journal of Clinical Psychiatry 60(suppl 2):7784 [21] El-Mallakh R, Weisler RH, Townsend MH, Ginsberg LD (2006). "Bipolar II disorder: current and future treatment options". Annals of Clinical Psychiatry : Official Journal of the American Academy of Clinical Psychiatrists 18 (4): 25966. doi:10.1080/10401230600948480. PMID17162626. [22] Randall, Carol (2010). "1" (http:/ / digitalcommons. library. unlv. edu/ thesesdissertations/ 843/ ). Neuropsychological emotion processing abnormalities in bipolar disorder I and II (Ph. D thesis). University of Nevada. . Retrieved 19 October 2011. [23] Ruggero, Camilo J.; Iwona Chelminski, Diane Young, Mark Zimmerman (December 1, 2007). "Psychosocial impairment associated with bipolar II disorder". Journal of Affective Disorders 104: 13. doi:10.1016/j.jad.2007.01.035. [24] McAllister-Williams, R. Hamish (January 1, 2006). "Relapse prevention in bipolar disorder: a critical review of current guidelines". Journal of Psychopharmacology 20 (2): 1216. doi:10.1177/1359786806063071. [25] Hadjipavlou, George (2008). Gordan Parker. ed. Bipolar II Disorder: Modelling, Measuring, and Managing. Cambridge, England: Cambridge University Press. pp.120132. ISBN0521873142. [26] Wingo, Aliza P.; Ross J. Baldessarini, Michael T. Compton, Philip D. Harvey (May 15, 2010). "Correlates of recovery of social functioning in types I and II bipolar disorder patients". Psychiatry Research 177: 131134. doi:10.1016/j.psychres.2010.02.020. [27] Rosa, A.R.; C.M. Bonnin, G.H. Vazquez, M. Reinares, B. Sole, R. Tabares-seisdedos, V. Balanza-Martinez, A. Gonzalez-Pinto, J. Sanchez-Moreno, E. Vieta (December 1, 2010). "Functional impairment in bipolar II disorder: Is it as disabling as bipolar I?". Journal of Affective Disorders 127: 7176. doi:10.1016/j.jad.2010.05.014. [28] Chang, Jae Seung; Sungwon Choi, Kyooseob Ha, Tae Hyon Ha, Hyun Sang Cho, Jung Eun Choi, Boseok Cha, Eunsoo Moon (June 1, 2011). "Differential pattern of semantic memory organization between bipolar I and II disorders". Progress in Neuro-Psychopharmacology & Biological Psychiatry 35: 10531058. doi:10.1016/j.pnpbp.2011.02.020. [29] Orum, Margo (2008). Gordan Parker. ed. Bipolar II Disorder: Modelling, Measuring, and Managing. Cambridge, England: Cambridge University Press. pp.177194. ISBN0521873142. [30] Benazzi, Franco (2008). Gordan Parker. ed. Bipolar II Disorder: Modelling, Measuring, and Managing. Cambridge, England: Cambridge University Press. pp.232236. ISBN0521873142.
Bipolar II
[31] MacQueen, Glenda M; L. Trevor Young (March 2001). "Bipolar II disorder: symptoms, course, and response to treatment". Psychiatric Services 52 (3): 358361. ISSN1075-2730. [32] Fieve, Ronald R. (2009). Bipolar Breakthrough: The Essential Guide to Going Beyond Moodswings to Harness Your Highs, Escape the Cycles of Recurrent Depression, and Thrive with Bipolar II. New York: Rodale. pp.232. ISBN978-1-60529-645-6. [33] Manicavasagar, Vijaya (2008). Bipolar II Disorder: Modelling, Measuring, and Managing. Cambridge, England: Cambridge University Press. pp.151176. ISBN0521873142. [34] http:/ / www. bbc. co. uk/ news/ uk-wales-13073676 [35] http:/ / www. usatoday. com/ news/ health/ spotlight/ 2002/ 05/ 29-fisher. htm
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External links
Latest bipolar news and research via MedWorm (http://www.medworm.com/rss/search.php?qu=bipolar+ manic&kid=16&t=Bipolar&f=c&r=Any&o=d) Bipolar Test Online (http://bipolartestonline.com/) http://www.dsm5.org/ProposedRevisions/Pages/proposedrevision.aspx?rid=426
Cyclothymia
101
Cyclothymia
Cyclothymia
Classification and external resources ICD-10 ICD-9 MeSH F34.0 [1] [2] [3]
301.13
D003527
Cyclothymia is a mood and mental disorder in the bipolar spectrum that causes both hypomanic and depressive episodes. It is defined medically within the bipolar spectrum and consists of recurrent disturbances between sudden hypomania and dysthymic episodes. The diagnosis of cyclothymic disorder is not made when there is a history of mania or major depressive episode or mixed episode. The lifetime prevalence of cyclothymic disorder is 0.4-1%. The rate appears equal in men and women, though women more often seek treatment. Unlike some other forms of bipolar disorder (to be specific, bipolar I disorder), people with cyclothymia are more often either somewhat or fully functioning, sometimes even hyper-productive. Cyclothymia is similar to bipolar II disorder in that it presents itself in signature hypomanic episodes. Because hypomania is often associated with exceptionally creative, outgoing, and high-functioning behavior, both conditions are often undiagnosed. As with most of the disorders in the bipolar spectrum, it is the depressive phase that leads most sufferers to get help. The term derives from the Greek (kuklos), "circle"[4] + (thumos), "temper".[5]
Differential diagnosis
This disorder is common in the relatives of patients with bipolar disorder, and some individuals with cyclothymia eventually develop bipolar disorder themselves. It may persist throughout adult life, cease temporarily or permanently, or develop into more severe mood swings, meeting the criteria for bipolar disorder or recurrent depressive disorder in rare cases.
Symptoms
Dysthymic phase Symptoms of the dysthymic phase include difficulty making decisions, problems concentrating, poor memory recall, guilt, self-criticism, low self-esteem, pessimism, self-destructive thinking, continuously feeling sad, apathy, hopelessness, helplessness, irritability, quick temper, poor judgment, lack of motivation, social withdrawal, appetite change, lack of sexual desire, self-neglect, fatigue, and insomnia.[6] Euphoric phase Symptoms of the euphoric phase include unusually good mood or cheerfulness (euphoria), extreme optimism, inflated self-esteem, rapid speech, racing thoughts, aggressive or hostile behavior, being inconsiderate of others, agitation, massively increased physical activity, risky behavior, spending sprees, increased drive to perform or achieve goals, increased sexual drive, decreased need for sleep, tendency to be easily distracted, and inability to concentrate.[7]
Cyclothymia
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Causes
There may be a genetic component to Cyclothymia. In one study, it was found that an individual is 2-3 times more likely to have the disorder if an identical twin is affected.[8]
Management
Medications
Anti-seizure medication/anticonvulsants (e.g., valproic acid, divalproex, and lamotrigine) are options. Seroquel Klonopin Lithium
Therapy
Cognitive behavioural therapy (CBT) Interpersonal psychotherapy (IT) Group therapy Integrative therapy Psychodynamic Therapy
References
[1] [2] [3] [4] [5] [6] [7] [8] http:/ / apps. who. int/ classifications/ icd10/ browse/ 2010/ en#/ F34. 0 http:/ / www. icd9data. com/ getICD9Code. ashx?icd9=301. 13 http:/ / www. nlm. nih. gov/ cgi/ mesh/ 2011/ MB_cgi?field=uid& term=D003527 (http:/ / www. perseus. tufts. edu/ hopper/ text?doc=Perseus:text:1999. 04. 0057:entry=ku/ klos), Henry George Liddell, Robert Scott, A Greek-English Lexicon, on Perseus (http:/ / www. perseus. tufts. edu/ hopper/ text?doc=Perseus:text:1999. 04. 0057:entry=qumo/ s), Henry George Liddell, Robert Scott, A Greek-English Lexicon, on Perseus "Dysthymic disorder and chronic depression" (http:/ / www. psychologyinfo. com/ depression/ dysthymic. htm). Psychologyinfo.com. . Retrieved 2010-11-18. "Cyclothymia (cyclothymic disorder): Symptoms" (http:/ / www. mayoclinic. com/ health/ cyclothymia/ DS00729/ DSECTION=symptoms). MayoClinic.com. . Retrieved 2010-11-18. Bartelsen, A; Harvald, B; and Hauge, M. "A Danish twin study of manic-depressive disorders." (http:/ / bjp. rcpsych. org/ content/ 130/ 4/ 330. full. pdf+ html). . Retrieved 6 September 2011.
External links
Cyclothymia Symptoms (http://www.counsellingresource.com/distress/mood-disorders/ cyclothymic-symptoms.html) from CounsellingResource.com Cyclothymia (http://www.psycom.net/depression.central.cyclothymia.html) from Psycom.net Cyclothymia (http://www.mcmanweb.com/article-93.htm) from McmanWeb What Is Cyclothymia? (http://www.mental-health-matters.com/disorders/mood-disorders/cyclothymia) from Mental Health Matters Cyclothymia Workbook (http://www.allaboutdepression.com/cyclothymia/about.shtml) from All About Depression (Commercial Link) What Is Cyclothymia? (http://bipolar.about.com/cs/faqs/f/faq_cyclothymia.htm) from About.com A Sudden Shift in Moods (http://www.washingtonpost.com/wp-dyn/content/article/2005/12/17/ AR2005121700892.html) from WashingtonPost.com
Dysthymia
103
Dysthymia
Dysthymic disorder
Classification and external resources ICD-10 ICD-9 MeSH F34.1 300.4 [1] [2] [3]
D019263
Dysthymia (English pronunciation: /ds.a.mi./, dis-theye-mee-, from Ancient Greek , "melancholy") is a mood disorder consisting of chronic depression, with less severe symptoms than major depressive disorder.[4] The concept was coined by Dr Robert Spitzer (an editor of the American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders (DSM-III)) as a replacement for the term "depressive personality" in the late 1970s.[5] According to the DSM's definition of dysthymia, it is a type of chronic mild depression.[6] As dysthymia is a chronic disorder, sufferers may experience symptoms for many years before it is diagnosed, if diagnosis occurs at all. As a result, they may believe that depression is a part of their character, so they may not even discuss their symptoms with doctors, family members, or friends.
Diagnostic criteria
The Diagnostic and Statistical Manual of Mental Disorders (DSM), published by the American Psychiatric Association, characterizes dysthymic disorder.[9] The essential symptom involves the individual feeling depressed for the majority of days and parts of the day for at least two years. Low energy, disturbances in sleep or in appetite, and low self-esteem typically contribute to the clinical picture as well. Sufferers have often experienced dysthymia for many years before it is diagnosed. People around them come to believe that the sufferer is 'just a moody person'. Note the following diagnostic criteria:[4] [10] 1. During a majority of days for two years or more, the adult patient reports depressed mood or appears depressed to others for most of the day. 2. When depressed, the patient has two or more of: 1. 2. 3. 4. 5. 6. decreased or increased appetite decreased or increased sleep (insomnia or hypersomnia) Fatigue or low energy Reduced self-esteem Decreased concentration or problems making decisions Feels hopeless or pessimistic
Dysthymia 3. 4. 5. 6. 7. 8. During this two-year period, the above symptoms are never absent longer than two consecutive months. During the first two years of this syndrome, the patient has not had a major depressive episode. The patient has not had any manic, hypomanic, or mixed episodes. The patient has never fulfilled criteria for cyclothymic disorder. The depression does not exist only as part of a chronic psychosis (such as schizophrenia or delusional disorder). The symptoms are often not directly caused by a medical illness or by substances, including drug abuse, or other medications. 9. The symptoms may cause significant problems or distress in social, work, academic, or other major areas of life functioning.[9] In children and adolescents, mood can be irritable, and duration must be at least one year, in contrast to two years needed for diagnosis in adults. Early onset (diagnosis before age 21) is associated with more frequent relapses, psychiatric hospitalizations, and more co-occurring conditions [8] . For younger adults with dysthymia, there is a higher co-occurrence in personality abnormalities and the symptoms are likely chronic and may result from personality. However, in older adults suffering from dysthymia the psychological symptoms are associated with medical conditions and/or stressful life events and losses. [11] Dysthymia can be contrasted with Major Depressive Disorder by assessing the acute nature of the symptoms. Dysthymia is far more chronic (long lasting) than Major Depressive Disorder, in which symptoms may be present for a little as 2 weeks. Also Dysthymia often presents itself at an earlier age than Major Depressive Disorder. [12]
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Biological Indicators
There is evidence indicating that there may be neurological indicators of early onset dysthymia. There are several brain structures (corpus callosum and frontal lobe) are different between women with dysthymia and normal individuals. This may indicate that there is a developmental difference between these two groups. [13] Another study, which used fMRI techniques to assess the differences between individuals with dysthymia and normal people found additional support for neurological indicators of the disorder. This study found several areas of the brain that function differently. The amygdala (associated with processing negative emotions such as fear) was more activated in dysthymia patients. The study also observed increased activity in the insula (which is associated with sad emotions). Finally, there was increased activity in the cingulate gyrus (which serves as the bridge between attention and emotion). [14] A study comparing healthy individuals to people with dysthymia indicates there are other biological indicators of the disorder. An anticipated result appeared as healthy individuals expected fewer negative adjectives to apply to them, whereas, people with dysthymia expected fewer positive adjectives to apply to them in the future. Biologically these groups are also differentiated in that healthy individuals showed greater neurological anticipation for all types of events (positive, neutral, or negative) than those with dysthymia. This provides neurological evidence toward the lack of emotion that individuals with dysthymia have compared to healthy people. [15] There is some evidence of a genetic basis for all types of depressions, including dysthymia. A study using identical and fraternal twins indicated that is a stronger likelihood of identical twins both having depression than fraternal twins. This provides support for the idea that dysthymia is in part caused by heredity. [16]
Dysthymia
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Prevalence
The lifetime prevalence rate of dysthymia in community settings appears to range from 3 to 6% in the United States. However, in primary care settings the rate is higher ranging from 5 to 15 percent. United States prevalence rates tend to be somewhat higher than rates in other countries. Finally, the rate is higher among women than men. [8]
Co-occurring conditions
"At least three-quarters of patients with dysthymia also have a chronic physical illness or another psychiatric disorder such as one of the anxiety disorders, cyclothymia, drug addiction, or alcoholism".[6] Common co-occurring conditions include: major depression (up to 75%), anxiety disorders (up to 50%), personality disorders (up to 40%), somatoform disorders (up to 45%) and substance abuse (up to 50%). [8] People with dysthymia have a higher-than-average chance of developing major depression. When an intense episode of depression occurs on top of dysthymia the state is called "double depression."[17]
Treatments
Often times, people with dysthymia will seek out treatment not necessarily because of depressed mood, but rather due to increasing levels of stress or because of personal difficulties that may be situationally-related. [18] This is hypothesized to be because of the chronic nature of the disorder, and how depressed mood is often times thought to be a characterological pattern for the individual with the condition. [19] It is usually through the administration of the Structured Clinical Interview for DSM-IV that dysthymia is first diagnosed. [18] At this point, with the help of a trained professional, a certain line of treatment is often discussed and then selected. It is important to consider all factors in the person's life that may be affected when deciding on a particular course of treatment. Additionally, if one method of treatment does not particularly work for a certain individual, it may be helpful to try something else.
Therapy
Psychotherapy is often effective in treating dysthymia. Different modalities have been shown to be beneficial. Empirically-based treatments, such as cognitive-behavioral therapy, have been researched to show that through the proper course of treatment, symptoms can dissipate over time. [18] Other forms of talk-therapy (e.g. psychodynamic psychotherapy, interpersonal psychotherapy) have also been said to be effective in treating the disorder. [20] It may be helpful for people diagnosed with dysthymia to develop better coping skills, search for the root cause of symptoms, and work on changing faulty beliefs (e.g. I am worthless). [18] In addition to individual psychotherapy, both group psychotherapy and self-help, or support groups, can be an effective line of treatment for dysthymia as well. [18] Through these treatment modalities, issues such as self-esteem, self-confidence, relationship issues/patterns, assertiveness skills, cognitive restructuring, etc., can be worked through and strengthened. [18]
Dysthymia
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Medications
SSRIs are usually the first line of treatment via pharmacotherapy due to its more tolerable nature and reduced side effects. [18] Studies have found that the mean response to antidepressant medications for people with dysthymia is 55% compared with a 31% response rate to a placebo. [20] The most commonly prescribed antidepressants/SSRIs for dysthymia are fluoxetine, paroxetine, sertraline, and fluvoxamine. These medications will often take an average of 6-8 weeks before the patient will begin to feel its therapeutic effects. [18] Additionally, STAR*D, a multi-clinic governmental study, found that people with overall depression will generally need to try different brands of medication before finding one that works specifically for them. [18] Of those who switch medications, about 1 in 4 have been found to get better regardless of whether or not the second medication is an SSRI or some other type of antidepressant. [18] Below is a list of particular antidepressant medications that are recommended by staff at the Mayo Clinic as listed online:[21] Selective serotonin reuptake inhibitors (SSRIs) Serotonin and norepinephrine reuptake inhibitors (SNRIs) Norepinephrine and dopamine reuptake inhibitors (NDRIs) Tetracyclic antidepressants (TeCAs) Tricyclic antidepressants (TCAs) Monoamine oxidase inhibitors (MAOIs)
Treatment Resistance
Because of dysthymia's chronic nature, treatment resistance can be somewhat common in dysthymic patients. [20] In such a case, augmentation is often recommended. Such treatment augmentations can include lithium pharmacology, thyroid hormone augmentation, buspirone, bupropion, stimulants, and mirtazapine. Additionally, if the personal also suffers from seasonal affective disorder, light therapy can be useful in helping augment therapeutic effects. [20]
References
[1] [2] [3] [4] http:/ / apps. who. int/ classifications/ icd10/ browse/ 2010/ en#/ F34. 1 http:/ / www. icd9data. com/ getICD9Code. ashx?icd9=300. 4 http:/ / www. nlm. nih. gov/ cgi/ mesh/ 2011/ MB_cgi?field=uid& term=D019263 Turner, Samuel M.; Hersen, Michel; Beidel, Deborah C., eds (2007). Adult Psychopathology and Diagnosis (5th ed.). Hoboken, New Jersey: John Wiley. ISBN9780471745846. OCLC427516745. [5] Brody, Jane (30 January 1995), "Help awaits those who live with sadness" (http:/ / news. google. com/ newspapers?id=NeopAAAAIBAJ& sjid=YdMEAAAAIBAJ& dq=dr-james-kocsis& pg=2251,6530609), The News-Journal (Daytona Beach, Florida): 54, [6] "Dysthymia" (http:/ / web. archive. org/ web/ 20100106064958/ http:/ / www. health. harvard. edu/ newsweek/ Dysthymia. htm), Harvard Health Publications (Harvard University), February 2005, archived from the original (http:/ / www. health. harvard. edu/ newsweek/ Dysthymia. htm) on 6 January 2010, , retrieved 12 December 2009 [7] Niculescu, A.B. and Akiskal, H.S. (2001). "Proposed Endophenotypes of Dysthymia: Evolutionary, Clinical, and Pharmacogenomic Considerations". Molecular Psychiatry 6: 363366.
Dysthymia
[8] Sansone, R. A. MD and Sansone, L. A. MD (2009). "Dysthymic Dosorder: Forlorn and Overlooked?". Psychiatry 6 (5): 4650. [9] American Psychiatric Association, ed (June 2000). Diagnostic and Statistical Manual of Mental Disorders DSM-IV-TR (http:/ / www. dsmivtr. org/ ) (4th ed.). American Psychiatric Publishing. ISBN978-0890420249. . [10] 300.4 (http:/ / www. icd9data. com/ getICD9Code. ashx?icd9=300. 4), ICD9, Accessed 2009 May 2 [11] Bellino, S., Patria, L., Ziero, S., Rocca, G., Bogetto, F. (2001). "Clinical Features of Dysthymia and Age: a Clinical Investigation". Psychiatry Review 103: 219228. [12] Goodman, S. H., Schwab-Stone, M., Lahey, B. B., Shaffer, D. and Jensen, P. S. (2000). "Major Depression and Dysthymia in Children and Adolescents: Discriminant Validity and Differential Consequences in a Community Sample". Journal of American Academy of Child and Adolescent Psychiatry 39 (6): 761771. [13] Lyoo, I.K., Kwon, J.S., Lee, S.J., Hann, M.H., Chang, C., Seo, Lee, S.I., and Renshaw, P.F. (2002). "Decrease in Genu of the Corpus Callosum in Medication-Nave, Early-Onset Dysthymia and Depressive Personality Disorder". Biological Psychiatry 52: 11341143. [14] Ravindran, A. V., Smith, A. Cameron, C., Bhatal, R., Cameron, I., Georgescu, T. M., Hogan, M. J. (2009). "Toward a Functional Neuroanatomy of Dysthymia: A Functional Magnetic Resonance Imaging Study". Journal of Affective Disorders 119: 915. [15] Casement, M. D., Shestyuk, A. Y., Best, J. L., Casas, B. R., Glezer, A., Segundo, M. A., Deldin, P. J. (2008). "Anticipation of Affect in Dysthymia: Behavioral and Neurophysiological Indicators". Biological Psychiatry 77: 197204. [16] Edvardsen, J., Torgersen, S., Roysamb, E., Lygren, S., Skre, I., Onstad, S., and Oien, A. (2009). "Unipolar Depressive Disorders have a Common Genotype". Journal of Affective Disorders 117: 3041. [17] Double Depression: Hopelessness Key Component Of Mood Disorder (http:/ / web. archive. org/ web/ 20080907155216/ http:/ / www. sciencedaily. com/ releases/ 2007/ 07/ 070723160142. htm), Science Daily, 26 July 2007, archived from the original (http:/ / www. sciencedaily. com/ releases/ 2007/ 07/ 070723160142. htm) on 7 September 2008, , retrieved 17 July 2008 [18] (http:/ / psychcentral. com/ lib/ 2008/ dysthymia-treatment/ ). [19] (http:/ / www. alternativedepressiontherapy. com/ symptoms-of-depression. html), Thus, it is only when the person experiences increasing stress that he or she thinks to go to some sort of trained professional for symptom relief. [20] (http:/ / emedicine. medscape. com/ article/ 290686-treatment) [21] Mayo Clinic Staff (26 August 2010), Treatment and drugs (http:/ / web. archive. org/ web/ 20101229143445/ http:/ / www. mayoclinic. com/ health/ dysthymia/ DS01111/ DSECTION=treatments-and-drugs), "Dysthymia", Health Information (Mayo Clinic), archived from the original (http:/ / www. mayoclinic. com/ health/ dysthymia/ DS01111/ DSECTION=treatments-and-drugs) on 29 December 2010, , retrieved 3 October 2011
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Further reading
Davidson JR, Abraham K, Connor KM, McLeod MN (February 2003). "Effectiveness of chromium in atypical depression: a placebo-controlled trial". Biol. Psychiatry 53 (3): 2614. doi:10.1016/S0006-3223(02)01500-7. PMID12559660.
External links
Depression patients helping community (http://www.aware.ie/) Video: How to Identify and Treat Depression (http://www.youtube.com/watch?v=dcAZRHnYIxc)
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Vincent van Gogh's 1890 painting At Eternity's Gate ICD-10 ICD-9 OMIM DiseasesDB MedlinePlus eMedicine MeSH F32 296 [1] [3] [4] , F33 [2]
608516 3589
003213
med/532 D003865
Major depressive disorder (MDD) (also known as recurrent depressive disorder, clinical depression, major depression, unipolar depression, or unipolar disorder) is a mental disorder characterized by an all-encompassing low mood accompanied by low self-esteem, and by loss of interest or pleasure in normally enjoyable activities. This cluster of symptoms (syndrome) was named, described and classified as one of the mood disorders in the 1980 edition of the American Psychiatric Association's diagnostic manual. The term "depression" is ambiguous. It is often used to denote this syndrome but may refer to other mood disorders or to lower mood states lacking clinical significance. Major depressive disorder is a disabling condition that adversely affects a person's family, work or school life, sleeping and eating habits, and general health. In the United States, around 3.4% of people with major depression commit suicide, and up to 60% of people who committed suicide had depression or another mood disorder.[9] The diagnosis of major depressive disorder is based on the patient's self-reported experiences, behavior reported by relatives or friends, and a mental status examination. There is no laboratory test for major depression, although physicians generally request tests for physical conditions that may cause similar symptoms. If depressive disorder is not detected in the early stages it may result in a slow recovery and affect or worsen the person's physical health. Standardized screening tools such as Major Depression Inventory can be used to detect major depressive disorder.[10]
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The most common time of onset is between the ages of 20 and 30 years, with a later peak between 30 and 40 years.[12] Typically, patients are treated with antidepressant medication and, in many cases, also receive psychotherapy or counseling, although the effectiveness of medication for mild or moderate cases is questionable. Hospitalization may be necessary in cases with associated self-neglect or a significant risk of harm to self or others. A minority are treated with electroconvulsive therapy (ECT), under a short-acting general anesthetic. The course of the disorder varies widely, from one episode lasting weeks to a lifelong disorder with recurrent major depressive episodes. Depressed individuals have shorter life expectancies than those without depression, in part because of greater susceptibility to medical illnesses and suicide. It is unclear whether or not medications affect the risk of suicide. Current and former patients may be stigmatized. The understanding of the nature and causes of depression has evolved over the centuries, though this understanding is incomplete and has left many aspects of depression as the subject of discussion and research. Proposed causes include psychological, psycho-social, hereditary, evolutionary and biological factors. Certain types of long-term drug use can both cause and worsen depressive symptoms. Psychological treatments are based on theories of personality, interpersonal communication, and learning. Most biological theories focus on the monoamine chemicals serotonin, norepinephrine and dopamine, which are naturally present in the brain and assist communication between nerve cells.
In children
Although it is common for most children and teenagers to feel down or sad sometimes, a smaller number of youth experience a more severe phenomenon known as depression. Such young people, who are often described as "clinically" depressed, feel sad, hopeless, or irritable for weeks or even months at a time. They may lose interest in activities that they used to enjoy (e.g., playing with friends); their sleeping and eating habits often change (i.e., they may eat or sleep either more or less than usual); and they may have trouble thinking or paying attention, even to TV
Major depressive disorder programs or games.[22] Depressed children may often display an irritable mood rather than a depressed mood,[15] and show varying symptoms depending on age and situation.[23] Most lose interest in school and show a decline in academic performance. They may be described as clingy, demanding, dependent, or insecure.[18] Diagnosis may be delayed or missed when symptoms are interpreted as normal moodiness.[15] Depression may also coexist with attention-deficit hyperactivity disorder (ADHD), complicating the diagnosis and treatment of both.[24] Of particular concern, youths who are clinically depressed may think or talk a lot about death and some depressed children have more specific thoughts about hurting or killing themselves. Often children and teenagers may have similar symptoms when they are grieving the loss of someone close to them. In clinical depression, however, these thoughts and feelings tend to appear even when the child has not experienced a loss or a sad event.[22]
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In the elderly
Older depressed people may have cognitive symptoms of recent onset, such as forgetfulness,[17] and a more noticeable slowing of movements.[25] Depression often coexists with physical disorders common among the elderly, such as stroke, other cardiovascular diseases, Parkinson's disease, and chronic obstructive pulmonary disease.[26]
Causes
The biopsychosocial model proposes that biological, psychological, and social factors all play a role in causing depression.[27] The diathesisstress model specifies that depression results when a preexisting vulnerability, or diathesis, is activated by stressful life events. The preexisting vulnerability can be either genetic,[28] [29] implying an interaction between nature and nurture, or schematic, resulting from views of the world learned in childhood.[30] These interactive models have gained empirical support. For example, researchers in New Zealand took a prospective approach to studying depression, by documenting over time how depression emerged among an initially normal cohort of people. The researchers concluded that variation among the serotonin transporter (5-HTT) gene affects the chances that people who have dealt with very stressful life events will go on to experience depression. To be specific, depression may follow such events, but seems more likely to appear in people with one or two short alleles of the 5-HTT gene.[28] In addition, a Swedish study estimated the heritability of depressionthe degree to which individual differences in occurrence are associated with genetic differencesto be around 40% for women and 30% for men,[31] and evolutionary psychologists have proposed that the genetic basis for depression lies deep in the history of naturally selected adaptations. A substance-induced mood disorder resembling major depression has been causally linked to long-term drug use or drug abuse, or to withdrawal from certain sedative and hypnotic drugs.[32] [33]
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Biological
Monoamine hypothesis Most antidepressant medications increase the levels of one or more of the monoamines the neurotransmitters serotonin, norepinephrine and dopamine in the synaptic cleft between neurons in the brain. Some medications affect the monoamine receptors directly. Serotonin is hypothesized to regulate other neurotransmitter systems; decreased serotonin activity may allow these systems to act in unusual and erratic ways.[35] According to this "permissive hypothesis", Of approx. 30 neurotransmitters that have been identified, depression arises when low serotonin levels promote researchers have discovered associations between clinical depression low levels of norepinephrine, another monoamine and the function of three major neurochemicals. These substances are neurotransmitter.[36] Some antidepressants enhance the serotonin, norepinephrine, and dopamine. Antidepressants influence levels of norepinephrine directly, whereas others raise the overall balance of these three neurotransmitters within structures of the brain that regulate emotion, reactions to stress, and the the levels of dopamine, a third monoamine [34] physical drives of sleep, appetite, and sexuality. neurotransmitter. These observations gave rise to the monoamine hypothesis of depression. In its contemporary formulation, the monoamine hypothesis postulates that a deficiency of certain neurotransmitters is responsible for the corresponding features of depression: "Norepinephrine may be related to alertness and energy as well as anxiety, attention, and interest in life; [lack of] serotonin to anxiety, obsessions, and compulsions; and dopamine to attention, motivation, pleasure, and reward, as well as interest in life."[37] The proponents of this theory recommend the choice of an antidepressant with mechanism of action that impacts the most prominent symptoms. Anxious and irritable patients should be treated with SSRIs or norepinephrine reuptake inhibitors, and those experiencing a loss of energy and enjoyment of life with norepinephrine- and dopamine-enhancing drugs.[37] Besides the clinical observations that drugs that increase the amount of available monoamines are effective antidepressants, recent advances in psychiatric genetics indicate that phenotypic variation in central monoamine function may be marginally associated with vulnerability to depression. Despite these findings, the cause of depression is not simply monoamine deficiency.[38] In the past two decades, research has revealed multiple limitations of the monoamine hypothesis, and its explanatory inadequacy has been highlighted within the psychiatric community.[39] A counterargument is that the mood-enhancing effect of MAO inhibitors and SSRIs takes weeks of treatment to develop, even though the boost in available monoamines occurs within hours. Another counterargument is based on experiments with pharmacological agents that cause depletion of monoamines; while deliberate reduction in the concentration of centrally available monoamines may slightly lower the mood of unmedicated depressed patients, this reduction does not affect the mood of healthy people.[38] An intact monoamine system is necessary for antidepressants to achieve therapeutic effectiveness,[40] but some medications like tianeptine and opipramol have antidepressant properties despite the fact that the former is a serotonin reuptake enhancer and the latter has no effect on the monoamine system. The monoamine hypothesis, already limited, has been further oversimplified when presented to the general public as a mass marketing tool, usually phrased as a "chemical imbalance".[41] In 2003 a gene-environment interaction (GxE) was hypothesized to explain why life stress is a predictor for depressive episodes in some individuals, but not in others, depending on an allelic variation of the serotonin-transporter-linked promoter region (5-HTTLPR);[42] a 2009 meta-analysis showed stressful life events were associated with depression, but found no evidence for an association with the 5-HTTLPR genotype.[43] Another 2009 meta-analysis agreed with the latter finding.[44] A 2010 review of studies in this area found a systematic
Major depressive disorder relationship between the method used to assess environmental adversity and the results of the studies; this review also found that both 2009 meta-analyses were significantly biased toward negative studies, which used self-report measures of adversity.[45] Other theories MRI scans of patients with depression have revealed a number of differences in brain structure compared to those who are not depressed. Recent meta-analyses of neuroimaging studies in major depression, reported that compared to controls, depressed patients had increased volume of the lateral ventricles and adrenal gland and smaller volumes of the basal ganglia, thalamus, hippocampus, and frontal lobe (including the orbitofrontal cortex and gyrus rectus). [46] [47] Hyperintensities have been associated with patients with a late age of onset, and have led to the development of the theory of vascular depression.[48] There may be a link between depression and neurogenesis of the hippocampus,[49] a center for both mood and memory. Loss of hippocampal neurons is found in some depressed individuals and correlates with impaired memory and dysthymic mood. Drugs may increase serotonin levels in the brain, stimulating neurogenesis and thus increasing the total mass of the hippocampus. This increase may help to restore mood and memory.[50] [51] Similar relationships have been observed between depression and an area of the anterior cingulate cortex implicated in the modulation of emotional behavior.[52] One of the neurotrophins responsible for neurogenesis is brain-derived neurotrophic factor (BDNF). The level of BDNF in the blood plasma of depressed subjects is drastically reduced (more than threefold) as compared to the norm. Antidepressant treatment increases the blood level of BDNF. Although decreased plasma BDNF levels have been found in many other disorders, there is some evidence that BDNF is involved in the cause of depression and the mechanism of action of antidepressants.[53] There is some evidence that major depression may be caused in part by an overactive hypothalamic-pituitary-adrenal axis (HPA axis) that results in an effect similar to the neuro-endocrine response to stress. Investigations reveal increased levels of the hormone cortisol and enlarged pituitary and adrenal glands, suggesting disturbances of the endocrine system may play a role in some psychiatric disorders, including major depression. Oversecretion of corticotropin-releasing hormone from the hypothalamus is thought to drive this, and is implicated in the cognitive and arousal symptoms.[54] The hormone estrogen has been implicated in depressive disorders due to the increase in risk of depressive episodes after puberty, the antenatal period, and reduced rates after menopause.[55] On the converse, the premenstrual and postpartum periods of low estrogen levels are also associated with increased risk.[55] Sudden withdrawal of, fluctuations in or periods of sustained low levels of estrogen have been linked to significant mood lowering. Clinical recovery from depression postpartum, perimenopause, and postmenopause was shown to be effective after levels of estrogen were stabilized or restored.[56] [57] Other research has explored potential roles of molecules necessary for overall cellular functioning: cytokines. The symptoms of major depressive disorder are nearly identical to those of sickness behavior, the response of the body when the immune system is fighting an infection. This raises the possibility that depression can result from a maladaptive manifestation of sickness behavior as a result of abnormalities in circulating cytokines.[58] The involvement of pro-inflammatory cytokines in depression is strongly suggested by a meta-analysis of the clinical literature showing higher blood concentrations of IL-6 and TNF- in depressed subjects compared to controls.[59] These immunological abnormalities may cause excessive prostaglandin E production and likely excessive COX-2 expression. Abnormalities in how indoleamine 2,3-dioxygenase enyme activates as well as the metabolism of tryptophan-kynurenine may lead to excessive metabolism of tryptophan-kynurenine and lead to increased production of the neurotoxin quinolinic acid, contributing to major depression. NMDA activation leading to excessive glutamatergic neurotransmission, may also contribute.[60] Finally, some relationships have been reported between specific subtypes of depression and climatic conditions. Thus, the incidence of psychotic depression has been found to increase when the barometric pressure is low, while
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Major depressive disorder the incidence of melancholic depression has been found to increase when the temperature and/or sunlight are low.[61]
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Psychological
Various aspects of personality and its development appear to be integral to the occurrence and persistence of depression,[62] with negative emotionality as a common precursor.[63] Although depressive episodes are strongly correlated with adverse events, a person's characteristic style of coping may be correlated with his or her resilience.[64] In addition, low self-esteem and self-defeating or distorted thinking are related to depression. Depression is less likely to occur, as well as quicker to remit, among those who are religious.[65] [66] [67] It is not always clear which factors are causes and which are effects of depression; however, depressed persons who are able to reflect upon and challenge their thinking patterns often show improved mood and self-esteem.[68] American psychiatrist Aaron T. Beck, following on from the earlier work of George Kelly and Albert Ellis, developed what is now known as a cognitive model of depression in the early 1960s. He proposed that three concepts underlie depression: a triad of negative thoughts composed of cognitive errors about oneself, one's world, and one's future; recurrent patterns of depressive thinking, or schemas; and distorted information processing.[69] From these principles, he developed the structured technique of cognitive behavioral therapy (CBT).[70] According to American psychologist Martin Seligman, depression in humans is similar to learned helplessness in laboratory animals, who remain in unpleasant situations when they are able to escape, but do not because they initially learned they had no control.[71] Attachment theory, which was developed by English psychiatrist John Bowlby in the 1960s, predicts a relationship between depressive disorder in adulthood and the quality of the earlier bond between the infant and the adult caregiver. In particular, it is thought that "the experiences of early loss, separation and rejection by the parent or caregiver (conveying the message that the child is unlovable) may all lead to insecure internal working models ... Internal cognitive representations of the self as unlovable and of attachment figures as unloving [or] untrustworthy would be consistent with parts of Becks cognitive triad".[72] While a wide variety of studies has upheld the basic tenets of attachment theory, research has been inconclusive as to whether self-reported early attachment and later depression are demonstrably related.[72] Depressed individuals often blame themselves for negative events,[73] and, as shown in a 1993 study of hospitalized adolescents with self-reported depression, those who blame themselves for negative occurrences may not take credit for positive outcomes.[74] This tendency is characteristic of a depressive attributional, or pessimistic explanatory style.[73] According to Albert Bandura, a Canadian social psychologist associated with social cognitive theory, depressed individuals have negative beliefs about themselves, based on experiences of failure, observing the failure of social models, a lack of social persuasion that they can succeed, and their own somatic and emotional states including tension and stress. These influences may result in a negative self-concept and a lack of self-efficacy; that is, they do not believe they can influence events or achieve personal goals.[75] An examination of depression in women indicates that vulnerability factorssuch as early maternal loss, lack of a confiding relationship, responsibility for the care of several young children at home, and unemploymentcan interact with life stressors to increase the risk of depression.[76] For older adults, the factors are often health problems, changes in relationships with a spouse or adult children due to the transition to a care-giving or care-needing role, the death of a significant other, or a change in the availability or quality of social relationships with older friends because of their own health-related life changes.[77] The understanding of depression has also received contributions from the psychoanalytic and humanistic branches of psychology. From the classical psychoanalytic perspective of Austrian psychiatrist Sigmund Freud, depression, or melancholia, may be related to interpersonal loss[78] [79] and early life experiences.[80] Existential therapists have connected depression to the lack of both meaning in the present[81] and a vision of the future.[82] [83] The founder of humanistic psychology, American psychologist Abraham Maslow, suggested that depression could arise when people are unable to attain their needs or to self-actualize (to realize their full potential).[84] [85]
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Social
Poverty and social isolation are associated with increased risk of mental health problems in general.[62] Child abuse (physical, emotional, sexual, or neglect) is also associated with increased risk of developing depressive disorders later in life.[86] Such a link has good face validity given that it is during the years of development that a child is learning how to become a social being. Abuse of the child by the caregiver is bound to distort the developing personality and create a much greater risk for depression and many other debilitating mental and emotional states. Disturbances in family functioning, such as parental (particularly maternal) depression, severe marital conflict or divorce, death of a parent, or other disturbances in parenting are additional risk factors.[62] In adulthood, stressful life events are strongly associated with the onset of major depressive episodes.[87] In this context, life events connected to social rejection appear to be particularly related to depression.[88] [89] Evidence that a first episode of depression is more likely to be immediately preceded by stressful life events than are recurrent ones is consistent with the hypothesis that people may become increasingly sensitized to life stress over successive recurrences of depression.[90] [91] The relationship between stressful life events and social support has been a matter of some debate; the lack of social support may increase the likelihood that life stress will lead to depression, or the absence of social support may constitute a form of strain that leads to depression directly.[92] There is evidence that neighborhood social disorder, for example, due to crime or illicit drugs, is a risk factor, and that a high neighborhood socioeconomic status, with better amenities, is a protective factor.[93] Adverse conditions at work, particularly demanding jobs with little scope for decision-making, are associated with depression, although diversity and confounding factors make it difficult to confirm that the relationship is causal.[94]
Evolutionary
From the standpoint of evolutionary theory, major depression is hypothesized, in some instances, to increase an individual's reproductive fitness. Evolutionary approaches to depression and evolutionary psychology posit specific mechanisms by which depression may have been genetically incorporated into the human gene pool, accounting for the high heritability and prevalence of depression by proposing that certain components of depression are adaptations,[95] such as the behaviors relating to attachment and social rank.[96] Current behaviors can be explained as adaptations to regulate relationships or resources, although the result may be maladaptive in modern environments.[97] From another viewpoint, a counseling therapist may see depression not as a biochemical illness or disorder but as "a species-wide evolved suite of emotional programmes that are mostly activated by a perception, almost always over-negative, of a major decline in personal usefulness, that can sometimes be linked to guilt, shame or perceived rejection".[98] This suite may have manifested in aging hunters in humans' foraging past, who were marginalized by their declining skills, and may continue to appear in alienated members of today's society. The feelings of uselessness generated by such marginalization could in theory prompt support from friends and kin. In addition, in a manner analogous to that in which physical pain has evolved to hinder actions that may cause further injury, "psychic misery" may have evolved to prevent hasty and maladaptive reactions to distressing situations.[99]
Major depressive disorder neurochemistry, such as decreased levels of serotonin and norepinephrine.[33] [103] Chronic use of benzodiazepines also can cause or worsen depression,[104] [105] or depression may be part of a protracted withdrawal syndrome.[33]
[106] [107] [108]
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Diagnosis
Clinical assessment
Further information: Rating scales for depression A diagnostic assessment may be conducted by a suitably trained general practitioner, or by a psychiatrist or psychologist,[13] who records the person's current circumstances, biographical history, current symptoms and family history. The broad clinical aim is to formulate the relevant biological, psychological and social factors that may be impacting on the individual's mood. The assessor may also discuss the person's current ways of regulating their mood (healthy or otherwise) such as alcohol and drug use. The assessment also includes a mental state examination, which is an assessment of the person's current mood and thought content, in particular the presence of themes of hopelessness or pessimism, self-harm or suicide, and an absence of positive thoughts or plans.[13] Specialist mental health services are rare in rural areas, and thus diagnosis and management is left largely to primary-care clinicians.[109] This issue is even more marked in developing countries.[110] The score on a rating scale alone is insufficient to diagnose depression to the satisfaction of the DSM or ICD, but it provides an indication of the severity of symptoms for a time period, so a person who scores above a given cut-off point can be more thoroughly evaluated for a depressive disorder diagnosis.[111] Several rating scales are used for this purpose.[111] Screening programs have been advocated to improve detection of depression, but there is evidence that they do not improve detection rates, treatment, or outcome.[112] Primary care physicians and other non-psychiatrist physicians have difficulty diagnosing depression, in part because they are trained to recognize and treat physical symptoms, and depression can cause a myriad of physical (psychosomatic) symptoms. Non-psychiatrists miss two-thirds of cases and unnecessarily treat other patients.[113]
[114]
Before diagnosing a major depressive disorder, in general a doctor performs a medical examination and selected investigations to rule out other causes of symptoms. These include blood tests measuring TSH and thyroxine to exclude hypothyroidism; basic electrolytes and serum calcium to rule out a metabolic disturbance; and a full blood count including ESR to rule out a systemic infection or chronic disease.[115] Adverse affective reactions to medications or alcohol misuse are often ruled out, as well. Testosterone levels may be evaluated to diagnose hypogonadism, a cause of depression in men.[116] Subjective cognitive complaints appear in older depressed people, but they can also be indicative of the onset of a dementing disorder, such as Alzheimer's disease.[117] [118] Cognitive testing and brain imaging can help distinguish depression from dementia.[119] A CT scan can exclude brain pathology in those with psychotic, rapid-onset or otherwise unusual symptoms.[120] No biological tests confirm major depression.[121] In general, investigations are not repeated for a subsequent episode unless there is a medical indication. Biomarkers of depression have been sought to provide an objective method of diagnosis. There are several potential biomarkers, including Brain-Derived Neurotrophic Factor and various functional MRI techniques. One study developed a decision tree model of interpreting a series of fMRI scans taken during various activities. In their subjects, the authors of that study were able to achieve a sensitivity of 80% and a sensitivity of 87%, corresponding to a negative predictive value of 98% and a positive predictive value of 32% (positive and negative likelihood ratios were 6.15, 0.23, respectively). However, much more research is needed before these tests could be used clinically.[122]
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Major depressive disorder Atypical depression is characterized by mood reactivity (paradoxical anhedonia) and positivity, significant weight gain or increased appetite (comfort eating), excessive sleep or sleepiness (hypersomnia), a sensation of heaviness in limbs known as leaden paralysis, and significant social impairment as a consequence of hypersensitivity to perceived interpersonal rejection.[141] Catatonic depression is a rare and severe form of major depression involving disturbances of motor behavior and other symptoms. Here the person is mute and almost stuporous, and either remains immobile or exhibits purposeless or even bizarre movements. Catatonic symptoms also occur in schizophrenia or in manic episodes, or may be caused by neuroleptic malignant syndrome.[142] Postpartum depression, or mental and behavioural disorders associated with the puerperium, not elsewhere classified,[143] refers to the intense, sustained and sometimes disabling depression experienced by women after giving birth. Postpartum depression has an incidence rate of 1015% among new mothers. The DSM-IV mandates that, in order to qualify as postpartum depression, onset occur within one month of delivery. It has been said that postpartum depression can last as long as three months.[144] Seasonal affective disorder (SAD) is a form of depression in which depressive episodes come on in the autumn or winter, and resolve in spring. The diagnosis is made if at least two episodes have occurred in colder months with none at other times, over a two-year period or longer.[145]
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Differential diagnoses
To confer major depressive disorder as the most likely diagnosis, other potential diagnoses must be considered, including dysthymia, adjustment disorder with depressed mood or bipolar disorder. Dysthymia is a chronic, milder mood disturbance in which a person reports a low mood almost daily over a span of at least two years. The symptoms are not as severe as those for major depression, although people with dysthymia are vulnerable to secondary episodes of major depression (sometimes referred to as double depression).[135] Adjustment disorder with depressed mood is a mood disturbance appearing as a psychological response to an identifiable event or stressor, in which the resulting emotional or behavioral symptoms are significant but do not meet the criteria for a major depressive episode.[139] Bipolar disorder, also known as manicdepressive disorder, is a condition in which depressive phases alternate with periods of mania or hypomania. Although depression is currently categorized as a separate disorder, there is ongoing debate because individuals diagnosed with major depression often experience some hypomanic symptoms, indicating a mood disorder continuum.[146] Other disorders need to be ruled out before diagnosing major depressive disorder. They include depressions due to physical illness, medications, and substance abuse. Depression due to physical illness is diagnosed as a mood disorder due to a general medical condition. This condition is determined based on history, laboratory findings, or physical examination. When the depression is caused by a substance abused including a drug of abuse, a medication, or exposure to a toxin, it is then diagnosed as a substance-induced mood disorder.[147] In such cases, a substance is judged to be etiologically related to the mood disturbance. Schizoaffective disorder is different from major depressive disorder with psychotic features because in the schizoaffective disorder at least two weeks of delusions or hallucinations must occur in the absence of prominent mood symptoms. Depressive symptoms may be identified during schizophrenia, delusional disorder, and psychotic disorder not otherwise specified, and in such cases those symptoms are considered associated features of these disorders, therefore, a separate diagnosis is not deemed necessary unless the depressive symptoms meet full criteria for a major depressive episode. In that case, a diagnosis of depressive disorder not otherwise specified may be made as well as a diagnosis of schizophrenia. Some cognitive symptoms of dementia such as disorientation, apathy, difficulty concentrating and memory loss may get confused with a major depressive episode in major depressive disorder. They are especially difficult to determine in elderly patients. In such cases, the premorbid state of the patient may be helpful to differentiate both disorders. In
Major depressive disorder the case of dementia, there tends to be a premorbid history of declining cognitive function. In the case of a major depressive disorder patients tend to exhibit a relatively normal premorbid state and abrupt cognitive decline associated with the depression.
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Prevention
Behavioral interventions, such as interpersonal therapy, are effective at preventing new onset depression.[148] Because such interventions appear to be most effective when delivered to individuals or small groups, it has been suggested that they may be able to reach their large target audience most efficiently through the Internet.[149] However, an earlier meta-analysis found preventive programs with a competence-enhancing component to be superior to behaviorally oriented programs overall, and found behavioral programs to be particularly unhelpful for older people, for whom social support programs were uniquely beneficial. In addition, the programs that best prevented depression comprised more than eight sessions, each lasting between 60 and 90 minutes, were provided by a combination of lay and professional workers, had a high-quality research design, reported attrition rates, and had a well-defined intervention.[150] The "Coping with Depression" course (CWD) is claimed to be the most successful of psychoeducational interventions for the treatment and prevention of depression (both for its adaptability to various populations and its results), with a risk reduction of 38% in major depression and an efficacy as a treatment comparing favorably to other psychotherapies.[151]
Management
The three most common treatments for depression are psychotherapy, medication, and electroconvulsive therapy. Psychotherapy is the treatment of choice for people under 18, while electroconvulsive therapy is used only as a last resort. Care is usually given on an outpatient basis, whereas treatment in an inpatient unit is considered if there is a significant risk to self or others. Treatment options are much more limited in developing countries, where access to mental health staff, medication, and psychotherapy is often difficult. Development of mental health services is minimal in many countries; depression is viewed as a phenomenon of the developed world despite evidence to the contrary, and not as an inherently life-threatening condition.[152] Physical exercise is recommended for management of mild depression,[153] but it has only a moderate, statistically insignificant effect on symptoms in most cases of major depressive disorder.[154]
Psychotherapy
Psychotherapy can be delivered, to individuals, groups, or families by mental health professionals, including psychotherapists, psychiatrists, psychologists, clinical social workers, counselors, and suitably trained psychiatric nurses. With more complex and chronic forms of depression, a combination of medication and psychotherapy may be used.[155] Cognitive behavioral therapy (CBT) currently has the most research evidence for the treatment of depression in children and adolescents, and CBT and interpersonal psychotherapy (IPT) are preferred therapies for adolescent depression.[22] In people under 18, according to the National Institute for Health and Clinical Excellence, medication should be offered only in conjunction with a psychological therapy, such as CBT, interpersonal therapy, or family therapy.[156] Psychotherapy has been shown to be effective in older people.[157] [158] Successful psychotherapy appears to reduce the recurrence of depression even after it has been terminated or replaced by occasional booster sessions. The most-studied form of psychotherapy for depression is CBT, which teaches clients to challenge self-defeating, but enduring ways of thinking (cognitions) and change counter-productive behaviors. Research beginning in the mid-1990s suggested that CBT could perform as well or better than antidepressants in patients with moderate to
Major depressive disorder severe depression.[159] [160] CBT may be effective in depressed adolescents,[161] although its effects on severe episodes are not definitively known.[162] Combining fluoxetine with CBT appeared to bring no additional benefit,[163] [164] or, at the most, only marginal benefit.[165] Several variables predict success for cognitive behavioral therapy in adolescents: higher levels of rational thoughts, less hopelessness, fewer negative thoughts, and fewer cognitive distortions.[166] CBT is particularly beneficial in preventing relapse.[167] [168] Several variants of cognitive behavior therapy have been used in depressed patients, the most notable being rational emotive behavior therapy,[169] and more recently mindfulness-based cognitive therapy.[170] Psychoanalysis is a school of thought, founded by Sigmund Freud, which emphasizes the resolution of unconscious mental conflicts.[171] Psychoanalytic techniques are used by some practitioners to treat clients presenting with major depression.[172] A more widely practiced, eclectic technique, called psychodynamic psychotherapy, is loosely based on psychoanalysis and has an additional social and interpersonal focus.[173] In a meta-analysis of three controlled trials of Short Psychodynamic Supportive Psychotherapy, this modification was found to be as effective as medication for mild to moderate depression.[174] Logotherapy, a form of existential psychotherapy developed by Austrian psychiatrist Viktor Frankl, addresses the filling of an "existential vacuum" associated with feelings of futility and meaninglessness. It is posited that this type of psychotherapy may be useful for depression in older adolescents.[175] Koreans use two different coping methods: emotion-focused coping and problem-focused coping. Emotion-focused coping decreases emotional distress through avoidance, distancing, and finding positive values in negative events. Problem-focused coping influences environmental conditions by altering the source of stress or changing one's self (example. finding alternative ways of gratification).[176]
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Antidepressants
The effectiveness of antidepressants is none to minimal in those with mild or moderate depression but significant in those with very severe disease.[178] The effects of antidepressants are somewhat superior to those of psychotherapy, especially in cases of chronic major depression, although in short-term trials more patients especially those with less serious forms of depression cease medication than cease psychotherapy, most likely due to adverse effects from the medication and to patients' preferences for psychological therapies over pharmacological [179] [180] treatments. To find the most effective antidepressant medication with minimal side-effects, the dosages can be adjusted, Zoloft (sertraline) is used primarily to treat major depression in adult and if necessary, combinations of different classes of outpatients. In 2007, it was the most prescribed antidepressant on the [177] U.S. retail market, with 29,652,000 prescriptions. antidepressants can be tried. Response rates to the first antidepressant administered range from 5075%, and it can take at least six to eight weeks from the start of medication to remission, when the patient is back to their normal self.[181] Antidepressant medication treatment is usually continued for 16 to 20 weeks after remission, to minimize the chance of recurrence,[181] and even up to one year of continuation is recommended.[182] People with chronic depression may need to take medication indefinitely to avoid relapse.[13] Selective serotonin reuptake inhibitors (SSRIs) are the primary medications prescribed owing to their effectiveness, relatively mild side-effects, and because they are less toxic in overdose than other antidepressants.[183] Patients who
Major depressive disorder do not respond to one SSRI can be switched to another antidepressant, and this results in improvement in almost 50% of cases.[184] Another option is to switch to the atypical antidepressant bupropion.[185] [186] [187] Venlafaxine, an antidepressant with a different mechanism of action, may be modestly more effective than SSRIs.[188] However, venlafaxine is not recommended in the UK as a first-line treatment because of evidence suggesting its risks may outweigh benefits,[189] and it is specifically discouraged in children and adolescents.[190] [191] For adolescent depression, fluoxetine[190] and escitalopram[192] are the two recommended choices. Antidepressants have not been found to be beneficial in children.[193] There is also insufficient evidence to determine effectiveness in those with depression complicated by dementia.[194] Any antidepressant can cause low serum sodium levels (also called hyponatremia);[195] nevertheless, it has been reported more often with SSRIs.[183] It is not uncommon for SSRIs to cause or worsen insomnia; the sedating antidepressant mirtazapine can be used in such cases.[196] [197] Irreversible monoamine oxidase inhibitors, an older class of antidepressants, have been plagued by potentially life-threatening dietary and drug interactions. They are still used only rarely, although newer and better tolerated agents of this class have been developed.[198] The safety profile is different with reversible monoamine oxidase inhibitor's such as moclobemide where the risk of serious dietary interactions is negligible and dietry restrictions are less 'strict'.[199] The terms "refractory depression" and "treatment-resistant depression" are used to describe cases that do not respond to adequate courses of at least two antidepressants.[200] In many major studies, only about 35% of patients respond well to medical treatment. It may be difficult for a doctor to decide when someone has treatment-resistant depression or whether the problem is due to coexisting disorders, which are common among patients with major depression.[201] A team of psychologists from multiple American universities found that antidepressant drugs hardly have better effects than a placebo in cases of mild or moderate depression. The study focused on paroxetine and imipramine.[202] For children, adolescents, and probably young adults between 18 and 24 years old, there is a higher risk of both suicidal ideations and suicidal behavior in those treated with SSRIs.[203] [204] [205] [206] [207] For adults, it is unclear whether or not SSRIs affect the risk of suicidality.[207] One review found no connection;[208] another an increased risk;[209] and a third no risk in those 2565 years old and a decrease risk in those more than 65.[210] Epidemiological data has found that the widespread use of antidepressants in the new SSRI-era is associated with a significant decline in suicide rates in most countries with traditionally high baseline suicide rates.[211] The causality of the relationship is inconclusive.[212] A black box warning was introduced in the United States in 2007 on SSRI and other antidepressant medications due to increased risk of suicide in patients younger than 24 years old.[213] Similar precautionary notice revisions were implemented by the Japanese Ministry of Health.[214] Fish oil supplements containing high levels of eicosapentaenoic acid to docosahexaenoic acid have been established as effective in major depression.[215] There is some preliminary evidence that COX-2 inhibitors have a beneficial effect on major depression.[60]
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Electroconvulsive therapy
Electroconvulsive therapy (ECT) is a procedure whereby pulses of electricity are sent through the brain via two electrodes, usually one on each temple, to induce a seizure while the patient is under a brief period of general anesthesia. Hospital psychiatrists may recommend ECT for cases of severe major depression that have not responded to antidepressant medication or, less often, psychotherapy or supportive interventions.[216] ECT can have a quicker effect than antidepressant therapy and thus may be the treatment of choice in emergencies such as catatonic depression where the patient has stopped eating and drinking, or where a patient is severely suicidal.[216] ECT is probably more effective than pharmacotherapy for depression in the immediate short-term,[217] although a landmark community-based study found much lower remission rates in routine practice.[218] When ECT is used on its own, the relapse rate within the first six months is very high; early studies put the rate at around 50%,[219] while a more recent controlled trial found rates of 84% even with placebos.[220] The early relapse rate may be reduced by the use of psychiatric medications or further ECT[221] [222] (although the latter is not recommended by some authorities)[223]
Major depressive disorder but remains high.[224] Common initial adverse effects from ECT include short and long-term memory loss, disorientation and headache.[225] Although memory disturbance after ECT usually resolves within one month, ECT remains a controversial treatment, and debate on its efficacy and safety continues.[226] [227]
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Prognosis
Major depressive episodes often resolve over time whether or not they are treated. Outpatients on a waiting list show a 1015% reduction in symptoms within a few months, with approximately 20% no longer meeting the full criteria for a depressive disorder.[228] The median duration of an episode has been estimated to be 23 weeks, with the highest rate of recovery in the first three months.[229] Studies have shown that 80% of those suffering from their first major depressive episode will suffer from at least 1 more during their life,[230] with a lifetime average of 4 episodes.[231] Other general population studies indicate around half those who have an episode (whether treated or not) recover and remain well, while the other half will have at least one more, and around 15% of those experience chronic recurrence.[232] Studies recruiting from selective inpatient sources suggest lower recovery and higher chronicity, while studies of mostly outpatients show that nearly all recover, with a median episode duration of 11 months. Around 90% of those with severe or psychotic depression, most of whom also meet criteria for other mental disorders, experience recurrence.[233] [234] Recurrence is more likely if symptoms have not fully resolved with treatment. Current guidelines recommend continuing antidepressants for four to sixmonths after remission to prevent relapse. Evidence from many randomized controlled trials indicates continuing antidepressant medications after recovery can reduce the chance of relapse by 70% (41% on placebo vs. 18% on antidepressant). The preventive effect probably lasts for at least the first 36months of use.[235] Those people who experience repeated episodes of depression require ongoing treatment in order to prevent more severe, long-term depression. In some cases, people need to take medications for long periods of time or for the rest of their lives.[236] Cases when outcome is poor are associated with inappropriate treatment, severe initial symptoms that may include psychosis, early age of onset, more previous episodes, incomplete recovery after 1 year, pre-existing severe mental or medical disorder, and family dysfunction as well.[237] Depressed individuals have a shorter life expectancy than those without depression, in part because depressed patients are at risk of dying by suicide.[238] However, they also have a higher rate of dying from other causes,[239] being more susceptible to medical conditions such as heart disease.[240] Up to 60% of people who commit suicide have a mood disorder such as major depression, and the risk is especially high if a person has a marked sense of hopelessness or has both depression and borderline personality disorder.[9] The lifetime risk of suicide associated with a diagnosis of major depression in the US is estimated at 3.4%, which averages two highly disparate figures of almost 7% for men and 1% for women[241] (although suicide attempts are more frequent in women).[242] The estimate is substantially lower than a previously accepted figure of 15%, which had been derived from older studies of hospitalized patients.[243] Depression is often associated with unemployment and poverty.[244] Major depression is currently the leading cause of disease burden in North America and other high-income countries, and the fourth-leading cause worldwide. In the year 2030, it is predicted to be the second-leading cause of disease burden worldwide after HIV, according to the World Health Organization.[245] Delay or failure in seeking treatment after relapse, and the failure of health professionals to provide treatment, are two barriers to reducing disability.[246]
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Epidemiology
Prevalence
Depression is a major cause of morbidity worldwide.[248] Lifetime prevalence varies widely, from 3% in Japan to 17% in the US. In most countries the number of people who would suffer from depression during their lives falls within an 812% range.[249] [250] In North America the probability of having a major depressive episode within a year-long period is 35% for males and 810% for females.[251] Age-standardised disability-adjusted life year (DALY) rates of [252] unipolar depressive disorders by country (per 100,000 inhabitants) in Population studies have consistently shown major [247] 2004. depression to be about twice as common in women as in men, although it is unclear why this is so, and whether factors unaccounted for are contributing to this.[253] The relative increase in occurrence is related to pubertal development rather than chronological age, reaches adult ratios between the ages of 15 and 18, and appears associated with psychosocial more than hormonal factors.[253] People are most likely to suffer their first depressive episode between the ages of 30 and 40, and there is a second, smaller peak of incidence between ages 50 and 60.[254] The risk of major depression is increased with neurological conditions such as stroke, Parkinson's disease, or multiple sclerosis and during the first year after childbirth.[255] It is also more common after cardiovascular illnesses, and is related more to a poor outcome than to a better one.[240] [256] Studies conflict on the prevalence of depression in the elderly, but most data suggest there is a reduction in this age group.[257] Depressive disorders are most common to observe in urban than in rural population and the prevalence is in groups with stronger socioeconomic factors i.e. homelessness [258]
Comorbidity
Major depression frequently co-occurs with other psychiatric problems. The 199092 National Comorbidity Survey (US) reports that 51% of those with major depression also suffer from lifetime anxiety.[259] Anxiety symptoms can have a major impact on the course of a depressive illness, with delayed recovery, increased risk of relapse, greater disability and increased suicide attempts.[260] American neuroendocrinologist Robert Sapolsky similarly argues that the relationship between stress, anxiety, and depression could be measured and demonstrated biologically.[261] There are increased rates of alcohol and drug abuse and particularly dependence,[262] and around a third of individuals diagnosed with ADHD develop comorbid depression.[263] Post-traumatic stress disorder and depression often co-occur.[13] Depression and pain often co-occur, especially if it is chronic or uncontrollable pain . This conforms with Seligman's theory of learned helplessness. One or more pain symptoms is present in 65% of depressed patients, and anywhere from five to 85% of patients with pain will be suffering from depression, depending on the setting; there is a lower prevalence in general practice, and higher in specialty clinics. The diagnosis of depression is often delayed or missed, and the outcome worsens. The outcome can also obviously worsen if the depression is noticed but completely misunderstood[264] Depression is also associated with a 1.5- to 2-fold increased risk of cardiovascular disease, independent of other known risk factors, and is itself linked directly or indirectly to risk factors such as smoking and obesity. People with major depression are less likely to follow medical recommendations for treating cardiovascular disorders, which further increases their risk. In addition, cardiologists may not recognize underlying depression that complicates a cardiovascular problem under their care.[265]
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History
The Ancient Greek physician Hippocrates described a syndrome of melancholia as a distinct disease with particular mental and physical symptoms; he characterized all "fears and despondencies, if they last a long time" as being symptomatic of the ailment.[266] It was a similar but far broader concept than today's depression; prominence was given to a clustering of the symptoms of sadness, dejection, and despondency, and often fear, anger, delusions and obsessions were included.[80] The term depression itself was derived from the Latin verb deprimere, "to press down".[267] From the 14thcentury, "to depress" meant to subjugate or to bring down in spirits. It was used in 1665 in English author Richard Baker's Chronicle to refer to someone having "a great depression of spirit", and by English author Samuel Johnson in a similar sense in 1753.[268] The term also came in to use in physiology and economics. An early usage referring to a psychiatric symptom was by French psychiatrist Louis Delasiauve in 1856, and by the 1860s it was appearing in medical dictionaries to refer to a physiological and metaphorical lowering of emotional function.[269] Since Aristotle, melancholia had been associated with men of learning and intellectual brilliance, a hazard of contemplation and creativity. The newer concept abandoned these associations and through the 19thcentury, became more associated with women.[80] Although melancholia remained the dominant diagnostic term, depression gained increasing currency in medical treatises and was a synonym by the end of the century; German psychiatrist Emil Kraepelin may have been the first to use it as the overarching term, referring to different kinds of melancholia as depressive states.[270] Sigmund Freud likened the state of melancholia to mourning in his 1917 paper Mourning and Melancholia. He theorized that objective loss, such as the loss of a valued relationship through death or a romantic break-up, results in subjective loss as well; the depressed individual has identified with the object of affection through an unconscious, narcissistic process called the libidinal cathexis of the ego. Such loss results in severe melancholic symptoms more profound than mourning; not only is the outside world viewed negatively but the ego itself is compromised.[78] The patient's decline of self-perception is revealed in his belief of his own blame, inferiority, and unworthiness.[79] He also emphasized early life experiences as a predisposing factor.[80] Meyer put forward a mixed social and biological framework emphasizing reactions in the context of an individual's life, and argued that the term depression should be used instead of melancholia.[271] The first version of the DSM (DSM-I, 1952) contained depressive reaction and the DSM-II (1968) depressive neurosis, defined as an excessive reaction to internal conflict or an identifiable event, and also included a depressive type of manic-depressive psychosis within Major affective disorders.[272] In the mid-20th century, researchers theorized that depression was caused by a chemical imbalance in neurotransmitters in the brain, a theory based on observations made in the 1950s of the effects of reserpine and isoniazid in altering monoamine neurotransmitter levels and affecting depressive symptoms.[273] The term Major depressive disorder was introduced by a group of US clinicians in the mid-1970s as part of proposals for diagnostic criteria based on patterns of symptoms (called the "Research Diagnostic Criteria", building on earlier Feighner Criteria),[274] and was incorporated in to the DSM-III in 1980.[275] To maintain consistency the ICD-10 used the same criteria, with only minor alterations, but using the DSM diagnostic threshold to mark a mild depressive episode, adding higher threshold categories for moderate and severe episodes.[275] [276] The ancient idea of melancholia still survives in the notion of a melancholic subtype. The new definitions of depression were widely accepted, albeit with some conflicting findings and views. There have been some continued empirically based arguments for a return to the diagnosis of melancholia.[277] [278] There has been some criticism of the expansion of coverage of the diagnosis, related to the development and promotion of antidepressants and the biological model since the late 1950s.[279]
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Major depressive disorder and reduce stigma from 1992 to 1996;[305] a MORI study conducted afterwards showed a small positive change in public attitudes to depression and treatment.[306]
125
Notes
References
[1] http:/ / apps. who. int/ classifications/ icd10/ browse/ 2010/ en#/ F32 [2] http:/ / apps. who. int/ classifications/ icd10/ browse/ 2010/ en#/ F33 [3] http:/ / www. icd9data. com/ getICD9Code. ashx?icd9=296 [4] http:/ / omim. org/ entry/ 608516 [5] http:/ / www. diseasesdatabase. com/ ddb3589. htm [6] http:/ / www. nlm. nih. gov/ medlineplus/ ency/ article/ 003213. htm [7] http:/ / www. emedicine. com/ med/ topic532. htm [8] http:/ / www. nlm. nih. gov/ cgi/ mesh/ 2011/ MB_cgi?field=uid& term=D003865 [9] Barlow 2005, pp.24849 [10] The sensitivity and specificity of the Major Depression Inventory, using the Present State Examination as the index of diagnostic validity.. Journal of affective disorders. 2001;66(23):15964. doi: 10.1016/S0165-0327(00)00309-8 (http:/ / dx. doi. org/ 10. 1016/ S0165-0327(00)00309-8). PMID 11578668. [11] The internal and external validity of the Major Depression Inventory in measuring severity of depressive states.. Psychological medicine. 2003;33(2):3516. doi: 10.1017/S0033291702006724 (http:/ / dx. doi. org/ 10. 1017/ S0033291702006724). PMID 12622314. [12] "Major Depressive Disorder" (http:/ / www. health. am/ psy/ major-depressive-disorder/ ). American Medical Network, Inc.. . Retrieved 2011-01-15. [13] Depression (http:/ / web. archive. org/ web/ 20110727123744/ http:/ / www. nimh. nih. gov/ health/ publications/ depression/ nimhdepression. pdf) [PDF]. National Institute of Mental Health (NIMH); [cited 2008-09-07]. [14] Hays RD, Wells KB, Sherbourne CD. Functioning and well-being outcomes of patients with depression compared with chronic general medical illnesses. Archives of General Psychiatry. 1995;52(1):1119. PMID 7811158. [15] American Psychiatric Association 2000a, p.349 [16] American Psychiatric Association 2000a, p.412 [17] Delgado PL and Schillerstrom J. Cognitive Difficulties Associated With Depression: What Are the Implications for Treatment? (http:/ / www. psychiatrictimes. com/ display/ article/ 10168/ 1387631). Psychiatric Times. 2009;26(3). [18] American Psychiatric Association 2000a, p.350 [19] "Bedfellows:Insomnia and Depression" (http:/ / www. psychologytoday. com/ articles/ 200307/ bedfellows-insomnia-and-depression). . Retrieved 2010-07-02. [20] Insomnia: Assessment and Management in Primary Care (http:/ / www. aafp. org/ afp/ 990600ap/ 3029. html), [21] Patel V, Abas M, Broadhead J. (fulltext) Depression in developing countries: Lessons from Zimbabwe (http:/ / www. bmj. com/ cgi/ content/ full/ 322/ 7284/ 482). BMJ. 2001 [cited 2008-10-05];322(7284):48284. doi: 10.1136/bmj.322.7284.482 (http:/ / dx. doi. org/ 10. 1136/ bmj. 322. 7284. 482). [22] Childhood Depression (http:/ / web. archive. org/ web/ 20110726055131/ http:/ / www. abct. org/ sccap/ ?m=sPublic& fa=pub_Depression). abct.org. Last updated: 30 July 2010 [23] American Psychiatric Association 2000a, p.354 [24] Brunsvold GL, Oepen G. Comorbid Depression in ADHD: Children and Adolescents (http:/ / www. psychiatrictimes. com/ adhd/ article/ 10168/ 1286863). Psychiatric Times. 2008;25(10). [25] Faculty of Psychiatry of Old Age, NSW Branch, RANZCP. Consensus Guidelines for Assessment and Management of Depression in the Elderly (http:/ / www. health. nsw. gov. au/ pubs/ 2001/ pdf/ depression_elderly. pdf) [PDF]. North Sydney, New South Wales: NSW Health Department; 2001. ISBN 0-7347-3341-0. p. 2. [26] Yohannes AM and Baldwin RC. Medical Comorbidities in Late-Life Depression (http:/ / www. psychiatrictimes. com/ depression/ article/ 10168/ 1358135). Psychiatric Times. 2008;25(14). [27] Department of Health and Human Services. The fundamentals of mental health and mental illness (http:/ / www. surgeongeneral. gov/ library/ mentalhealth/ pdfs/ c2. pdf) [PDF]; 1999 [cited 2008-11-11]. [28] Caspi A, Sugden K, Moffitt TE. Influence of life stress on depression: Moderation by a polymorphism in the 5-HTT gene. Science. 2003;301(5631):38689. doi: 10.1126/science.1083968 (http:/ / dx. doi. org/ 10. 1126/ science. 1083968). PMID 12869766. [29] Haeffel GJ; Getchell M; Koposov RA; Yrigollen CM; DeYoung CG; af Klinteberg B; et al.. Association between polymorphisms in the dopamine transporter gene and depression: Evidence for a geneenvironment interaction in a sample of juvenile detainees (http:/ / www. nd. edu/ ~ghaeffel/ Resources/ Haeffel et al. , 2008. pdf) [PDF]; 2008 [cited 2008-11-11]. [30] Slavich GM. Deconstructing depression: A diathesis-stress perspective (Opinion) (http:/ / www. psychologicalscience. org/ observer/ getArticle. cfm?id=1640); 2004 [cited 2008-11-11].
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Major depressive disorder Sadock, Virginia A.; Sadock, Benjamin J.; Kaplan, Harold I.. Kaplan & Sadock's synopsis of psychiatry: behavioral sciences/clinical psychiatry. Philadelphia: Lippincott Williams & Wilkins; 2003. ISBN 0-7817-3183-6.
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External links
Depression (http://www.dmoz.org/Health/Mental_Health/Disorders/Mood/Depression/) at the Open Directory Project NHS Evidence introduction and search results for Depression (http://www.evidence.nhs.uk/topic/ depression)
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Schizoaffective disorder
Schizoaffective disorder
Classification and external resources ICD-10 ICD-9 OMIM MeSH F25 [1] [2] [3] [4]
295.70 181500
D011618
Schizoaffective disorder is a psychiatric diagnosis that describes a mental disorder characterized by recurring episodes of elevated or depressed mood, or of simultaneously elevated and depressed mood, that alternate with, or occur together with, distortions in perception.[5] [6] Schizoaffective disorder most commonly affects cognition and emotion. Auditory hallucinations, paranoia, bizarre delusions, or disorganized speech and thinking with significant social and occupational dysfunction are typical. The division into depressive and bipolar types is based on whether the individual has ever had a manic, hypomanic or mixed episode. Symptoms usually begin in early adulthood, which makes diagnosis prior to age 13 rare. Schizoaffective disorder belongs to the "schizophrenia spectrum and other psychotic disorders"[7] proposed by the DSM-5 Workgroup, which includes schizophrenia, schizotypal personality disorder, schizophreniform disorder, brief psychotic disorder, delusional disorder, substance-induced psychotic disorder, both psychotic and catatonic disorders associated with a general medical condition, both unspecified psychotic and catatonic disorders and other unspecified psychotic disorder.[8] This spectrum of psychotic disorders is comparable to the bipolar spectrum in bipolar disorder. Each named disorder on this continuum shares symptoms with the others, and some professionals (including the working group for the DSM-5) contend that the boundaries are so unclear that separate labels are not necessarily warranted.
Overview
The lifetime prevalence of the disorder is probably less than 1 percent, in the range of 0.5 to 0.8 percent.[9] Diagnosis is based on the patient's self-reported experiences and observed behavior. No laboratory test for schizoaffective disorder currently exists, though extensive evidence exists for abnormalities in the metabolism of tetrahydrobiopterin (BH4), dopamine, and glutamate in people with schizophrenia and schizoaffective disorders. As a group, individuals with schizoaffective disorder have a more favorable prognosis than those with schizophrenia, but a worse prognosis than those with other mood disorders.[10] Genetics, early environment, neurobiology, psychological and social processes are important contributory factors. Some recreational and prescription drugs may cause or worsen symptoms. Current research is focused on the role of neurobiology, but no single organic cause has been found. The mainstay of treatment is antipsychotic medication combined with mood stabilizer medication or antidepressant medication, or both. Psychotherapy, vocational therapy and social/psychiatric rehabilitation are also important for recovery. In cases where there is risk to self and others, brief involuntary hospitalization may be necessary.[11] People with schizoaffective disorder are likely to have comorbid conditions, including anxiety disorders and substance abuse. Social problems, such as long-term unemployment, poverty and homelessness, are common. The average life expectancy of people with the disorder is shorter than those without, due to increased physical health problems and a higher suicide rate.
Schizoaffective disorder The diagnosis was introduced in 1933[12] and will be moderately amended[13] [14] in the next iteration of the American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders (DSM-5), because current diagnostic criteria are unreliable. The changes in the DSM-5 are intended to increase reliability and to reduce the frequency with which the diagnosis is used. The DSM-5 is scheduled to be published in May 2013.[15] [16]
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Schizoaffective disorder With comprehensive treatment, many individuals with schizoaffective disorder may recover much, most or even all of their functionality.
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Diagnosis
Diagnosis is based on the self-reported experiences of the person as well as abnormalities in behavior reported by family members, friends or co-workers to a psychiatrist, psychiatric nurse, social worker or psychologist in a clinical assessment. There is a list of criteria that must be met for someone to be so diagnosed. These depend on both the presence and duration of certain signs and symptoms. As discussed above, there are several psychiatric illnesses which may present with a similar range of psychotic symptoms; these include bipolar disorder with psychotic features, major depression with psychotic features, schizophrenia, drug intoxication, brief drug-induced psychosis, and schizophreniform disorder. These disorders need to be ruled out before a firm diagnosis of schizoaffective disorder can be made. An initial assessment includes a comprehensive history and physical examination by a physician. Although there are no biological tests which confirm schizoaffective disorder, tests are carried out to exclude medical illnesses which rarely may be associated with psychotic symptoms. These include blood tests measuring TSH to exclude hypo- or hyperthyroidism, basic electrolytes and serum calcium to rule out a metabolic disturbance, full blood count including ESR to rule out a systemic infection or chronic disease, and serology to exclude syphilis or HIV infection; two commonly ordered investigations are EEG to exclude epilepsy, and a CT scan of the head to exclude brain lesions. It is important to rule out a delirium which can be distinguished by visual hallucinations, acute onset and fluctuating level of consciousness and indicates an underlying medical illness. Investigations are not generally repeated for relapse unless there is a specific medical indication. These may include serum BSL if olanzapine has previously been prescribed, thyroid function if lithium has previously been taken to rule out hypothyroidism, liver function tests if chlorpromazine has been prescribed, and CPK levels to exclude neuroleptic malignant syndrome. Assessment and treatment are usually done on an outpatient basis; admission to an inpatient facility is considered if there is a risk to self or others. The most widely-used criteria for diagnosing schizoaffective disorder are from the American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders, the current version being DSM-IV-TR.
DSM-IV-TR criteria
The following are the revised criteria for a diagnosis of schizoaffective disorder from the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR): 1. Two (or more) of the following symptoms are present for the majority of a one-month period (or a shorter period of time if symptoms got better with treatment): delusions hallucinations disorganized speech (e.g., frequent derailment or incoherence) which is a manifestation of formal thought disorder grossly disorganized behavior (e.g. dressing inappropriately, crying frequently) or catatonic behavior negative symptomse.g., affective flattening (lack or decline in emotional response), alogia (lack or decline in speech), avolition (lack or decline in motivation), anhedonia (lack or decline in ability to experience pleasure), social withdrawal (sometimes called social anhedonia). Negative symptoms refers to symptoms that are not present or that are diminished in the affected persons but are normally found in healthy persons.[17] If the delusions are judged to be bizarre, or hallucinations consist of hearing one voice participating in a running commentary of the individual's actions or of hearing two or more voices conversing with each other, only that symptom is required to meet criterion A above. The speech disorganization criterion is only met if it is severe
Schizoaffective disorder enough to substantially impair communication. and at some time during the illness there is either one, two or all three of the following: major depressive episode manic episode mixed episode 2. During the illness, delusions or hallucinations were present for a minimum of two weeks, without major mood symptoms. 3. For a substantial part of the overall duration of both the active and residual period of the illness, symptoms meeting criteria for a mood episode are present. 4. Symptoms are not caused by drug abuse, medication or another medical condition.
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Subtypes
Two subtypes of schizoaffective disorder exist and may be noted in a diagnosis based on the mood component of the disorder: Bipolar type if the disturbance includes a manic episode a mixed episode Major depressive episodes usually, but not always, also occur in the bipolar subtype, however they are not required for DSM-IV diagnosis. Depressive type The depressive type is noted when the disturbance includes major depressive episodes exclusively. This subtype applies if major depressive episodes only (and no manic or mixed episodes) are part of the presentation.
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Cause
Although the causes of schizoaffective disorder are unknown, it is suspected that this diagnosis represents a heterogeneous group of individuals, some with aberrant forms of schizophrenia and some with very serious forms of mood disorders. There is little evidence that schizoaffective disorder is a distinct variety of psychotic illness. Consequently, the disorder appears to be comorbid or (co-occurring) schizophrenia and mood disorder. Schizoaffective disorder thus appears to exist on a continuum in-between schizophrenia and severe bipolar disorder and severe recurrent unipolar depression. It follows then that the etiology is probably more similar to that of schizophrenia in some cases and more similar to severe mood disorders in other cases. Many different genes may be contributing to the genetic risk of acquiring this illness. In addition, many different biological and environmental factors are believed to interact with the person's genes in ways which can increase or decrease the person's risk for developing schizoaffective disorder. Schizophrenia spectrum disorders (of which schizoaffective disorder is a part) have been marginally linked to advanced paternal age at the time of conception, a common cause of mutations.[22] The physiology of patients diagnosed with schizoaffective disorder appears to be similar but not identical to that of those diagnosed with schizophrenia and severe bipolar disorder.[23]
Substance abuse
A clear causal connection between drug use and psychotic spectrum disorders, including schizoaffective disorder, has been difficult to prove. The two most often used explanations for this are "substance use causes schizoaffective disorder" and "substance use is a consequence of schizoaffective disorder", and they both may be correct.[24] In the case of marijuana or cannabis, however, evidence is mounting that it can play a role in the development and morbidity of psychotic disorders, including schizoaffective disorder.[25] [26] For example, a 2007 meta-analysis showed that cannabis use is statistically associated with a dose-dependent increase in risk of development of psychotic disorders, including schizoaffective disorder.[25] Moreover, a 2005 meta-analysis found that cannabis use is a significant independent risk factor for developing psychotic symptoms and psychosis.[26] A 2009 Yale study stated that it is clear "that in individuals with an established psychotic disorder, cannabinoids can exacerbate symptoms, trigger relapse, and have negative consequences on the course of the illness."[27] On the other hand, a meta-analysis published in 2008 concluded that "Confidence that most associations reported were specifically due to cannabis is low. Despite clinical opinion, it remains important to establish whether cannabis is harmful, what outcomes are particularly susceptible, and how such effects are mediated."[28] However, despite increases in cannabis consumption in the 1960s and 1970s in western society, rates of psychotic disorders generally remained relatively stable.[29] [30] [31] Also, Sweden and Japan, where self-reported marijuana use is very low, do not have lower rates of psychosis than the U.S. and Canada do.[32] For the theory of causality to be correct, other factors which are thought to contribute to psychosis would have to have converged almost flawlessly to mask the effect of increased cannabis usage. However, there may be other confounding factors, including social structure, family structure, typical diet, and ethnic genetic makeup that preclude a clear 1:1 comparison either pro or con between populations from different countries. There is little evidence to suggest that other drugs including alcohol cause schizoaffective disorder, or that psychotic individuals choose specific drugs to self-medicate; there is some support for the theory that they use drugs to cope with unpleasant states such as depression, anxiety, boredom and loneliness.[33] However, regarding psychosis itself, it is well understood that methamphetamine and cocaine use can result in methamphetamine or cocaine-induced psychosis which presents very similar symptomatology and may persist even when users remain abstinent.[34] The same can also be said for alcohol-induced psychosis, though to a somewhat lesser extent.[35] [36] [37]
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Management
Treatment for schizoaffective disorder consists of a combination of medicine, psychotherapy and psychosocial rehabilitation focused on recovery or symptom management. A licensed psychiatrist will prescribe (usually combinations of) medicine for the individual. Each person responds differently to medication. The only medicine that is FDA-approved for Schizoaffective Disorder is paliperidone (Invega). For psychotic symptoms neuroleptic medications such as risperidone may be used. For manic symptoms, mood stabilizer medications may be prescribed along with a neuroleptic. Examples are: Lithium salt (Lithium) Valproate semisodium (Depakote ER)[38] Carbamazepine (Tegretol) For depression, antidepressant medications may be prescribed along with a neuroleptic. Examples are: SSRI antidepressants (includes Prozac and Zoloft among others) Lamotrigine (a mood stabilizer with antidepressant properties) In schizoaffective individuals with manic symptoms, combining lithium, carbamazepine, or valproate with a neuroleptic has been shown to be superior to neuroleptics alone. Lithium-neuroleptic combinations, however, may produce severe extrapyramidal reactions or confusion in some patients. When lithium is not effective or well tolerated in manic individuals with schizoaffective disorder, Tegretol or Depakote are frequently used. Granulocytopenia can occur during the first few weeks of carbamazepine treatment, and neuroleptic blood levels may be decreased substantially due to hepatic enzyme induction. Valproate can, in rare cases, cause liver toxicity and platelet dysfunction. Calcium channel blockers such as verapamil may also be an effective treatment for manic symptoms but are seldom prescribed for that purpose. The degree of benefit for an individual should be considered carefully, as each of these medications carries its own risks. Benzodiazepines such as Ativan and Klonopin are effective adjunctive treatment agents for acute manic symptoms, but long-term use may result in dependency. In schizoaffective individuals with depressive symptoms, an antidepressant (for example, Prozac or other SSRIs) may be prescribed with a neuroleptic. The SNRI antidepressants and Wellbutrin tend not to be prescribed in schizoaffective disorder because they may cause mixed episode symptoms and induce psychosis, respectively. The anticonvulsant Lamictal is gaining prominence in treating depressed schizoaffective individuals because antidepressants appear to increase the risk of mood cycling in some individuals, which is a safety concern. Often a sleeping pill will be prescribed initially to allow the individual rest from his or her anxiety, delusions or hallucinations. Long-term use of sleeping medications can, however, cause dependence and can also cause delusions and hallucinations thereby exacerbating psychosis.
Complications
Complications are similar to those for schizophrenia and major mood disorders. These include: Problems following medical treatment and therapy Use of unsanctioned drugs in an attempt to self-medicate Short-term side effects and problems arising from long-term use of prescribed medications, including drug interactions. Problems resulting from manic behavior (for example, spending sprees, sexual indiscretion) Suicidal behavior due to depressive or psychotic symptoms
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Epidemiology
Estimates of the prevalence of schizoaffective disorder vary widely, but schizoaffective manic patients appear to comprise 3-5% of psychiatric admissions to typical clinical centers. At one point it was widely believed that schizoaffective disorder was associated with increased risk of mood disorders in relatives. This may have been because of the number of patients with psychotic mood disorders who were included in schizoaffective study populations. The current diagnostic criteria define a group of individuals with a mixed genetic picture. They are more likely to have schizophrenic relatives than individuals with mood disorders but more likely to have relatives with mood disorders than individuals with schizophrenia.
History
The term schizoaffective psychosis was introduced by the American psychiatrist Jacob Kasanin in 1933[39] to describe an episodic psychotic illness with predominant affective symptoms, that was thought at the time to be a good-prognosis schizophrenia.[40] Kasanin's concept of the illness was influenced by the psychoanalytic teachings of Adolf Meyer and Kasanin postulated that schizoaffective psychosis was caused by "emotional conflicts" of a "mainly sexual nature" and that psychoanalysis "would help prevent the recurrence of such attacks."[41] He based his description on a case study of nine individuals.[41] Other psychiatrists, before and after Kasanin, have made scientific observations of schizoaffective disorder based on assumptions of a biological and genetic etiology of the illness. In 1863, German psychiatrist Karl Kahlbaum (18281899) described schizoaffective disorders as a separate group in his vesania typica circularis.[42] Kahlbaum distinguished between cross-sectional and longitudinal observations. (Cross-sectional refers to observation of a single, specific episode of the illness, for example, one episode of psychotic depression; while longitudinal refers to long-term observation of many distinct episodes [similar or different] often occurring over the span of years.) In 1920, psychiatrist Emil Kraepelin (18561926), the founder of contemporary scientific psychiatry, observed a "great number" of cases that had characteristics of both groups of psychoses that he originally posited were two distinct and separate illnesses, dementia praecox (now called schizophrenia) and manic depressive insanity (now called bipolar disorder and recurrent depression).[41] Kraeplin acknowledged that "there are many overlaps in this area", that is, the area between schizophrenia and severe mood disorders.[43] In 1959, psychiatrist Kurt Schneider (18871967) can be said to have been the first to begin to conceptualize the different forms that schizoaffective disorders can take since he observed "concurrent and sequential types".[41] (The concurrent type of illness he referred to is a longitudinal course of illness with episodes of mood disorder and psychosis occurring predominantly at the same time; while his sequential type refers to a longitudinal course predominantly marked by alternating mood and psychotic episodes.)[42] Schneider described schizoaffective disorders as "cases in-between" the traditional Kraepelinian dichotomy of schizophrenia and mood disorders.[42] The historical phenomenological observation that schizoaffective disorder is an overlap of schizophrenia and severe mood disorders has more recently been assumed to be explained by genes for both illnesses being present in individuals with schizoaffective disorder. But recent research shows that schizophrenia and severe mood disorders appear to share common genes and polygenic variations also.[20] [44] [45] [46] [47] Schizoaffective disorder was included as a subtype of schizophrenia in DSM-I and DSM-II, though research showed a schizophrenic cluster of symptoms in individuals with a family history of mood disorders whose illness course, other symptoms and treatment outcome were otherwise more akin to bipolar disorder than to schizophrenia. DSM-III placed schizoaffective disorder in "Psychotic Disorders Not Otherwise Specified" before being formally recognized in DSM-III-R.[48] DSM-III-R included its own diagnostic criteria as well as the subtypes, bipolar and depressive.[48] In DSM-IV, published in 1994, schizoaffective disorders belonged to the category "Other Psychotic Disorders" and
Schizoaffective disorder included almost the same criteria and the same subtypes of illness as DSM-III-R, with the addition of mixed bipolar symptomatology.[49]
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(http:/ / ndarc. med. unsw. edu. au/ NDARCWeb. nsf/ resources/ TR_18/ $file/ TR. 121. PDF). Technical Report No. 121.. Sydney: National Drug and Alcohol Research Centre.. . Retrieved 2006-08-19. [30] Martin Frisher, Ilana Crome, Orsolina Martino, and Peter Croft. (2009). "Assessing the impact of cannabis use on trends in diagnosed schizophrenia in the United Kingdom from 1996 to 2005" (http:/ / www. ukcia. org/ research/ keele_study/ Assessing-the-impact-of-cannabis-use-on-trend-in-diagnosed-schizophrenia. pdf). Schizophrenia Research 113 (2-3): 123128. doi:10.1016/j.schres.2009.05.031. PMID19560900. . [31] http:/ / www. nhsconfed. org/ Publications/ Documents/ MHN_factsheet_August_2009_FINAL_2. pdf Key facts and trends in mental health, National Health Service, 2009
Schizoaffective disorder
[32] "Interpreting hazy warnings about pot and mental illness" (http:/ / www. huffingtonpost. com/ paul-armentano-and-mitch-earleywine/ interpreting-hazy-warning_b_59543. html). Huffington Post. 2007-08-07. . Retrieved 2009-01-23. [33] Gregg L, Barrowclough C, Haddock G (May 2007). "Reasons for increased substance use in psychosis". Clinical Psychology Review 27 (4): 494510. doi:10.1016/j.cpr.2006.09.004. PMID17240501. [34] Mahoney JJ, Kalechstein AD, De La Garza R, Newton TF (2008). "Presence and persistence of psychotic symptoms in cocaine- versus methamphetamine-dependent participants". The American Journal on Addictions 17 (2): 8398. doi:10.1080/10550490701861201. PMID18393050. [35] Larson, Michael (2006-03-30). "Alcohol-Related Psychosis" (http:/ / www. emedicine. com/ med/ topic3113. htm). eMedicine. WebMD. . Retrieved September 27, 2006. [36] Soyka, Michael (March 1990). "Psychopathological characteristics in alcohol hallucinosis and paranoid schizophrenia". Acta Psychiatrica Scandinavica 81 (3): 2559. doi:10.1111/j.1600-0447.1990.tb06491.x. PMID2343749. [37] Gossman, William (November 19, 2005). "Delirium Tremens" (http:/ / www. emedicine. com/ EMERG/ topic123. htm). eMedicine. WebMD. . Retrieved October 16, 2006. [38] Flynn J, Grieger TA, Benedek DM (January 2002). "Pharmacologic treatment of hospitalized patients with schizoaffective disorder". Psychiatric Services (Washington, D.C.) 53 (1): 946. doi:10.1176/appi.ps.53.1.94. PMID11773657. [39] Lake CR, Hurwitz N (August 2006). "Schizoaffective disorders are psychotic mood disorders; there are no schizoaffective disorders". Psychiatry Research 143 (2-3): 25587. doi:10.1016/j.psychres.2005.08.012. PMID16857267. [40] Goodwin & Jamison. p. 102 [41] Goodwin & Marneros. p. 190 [42] Goodwin & Marneros. p189 [43] Marneros & Akiskal. pp. 3-4 [44] Van Snellenberg JX, de Candia T (July 2009). "Meta-analytic evidence for familial coaggregation of schizophrenia and bipolar disorder". Arch. Gen. Psychiatry 66 (7): 74855. doi:10.1001/archgenpsychiatry.2009.64. PMID19581566. [45] "Schizophrenia and bipolar disorder may share genetic origins". Harv Ment Health Lett 25 (12): 7. June 2009. PMID19582944. [46] Purcell SM, Wray NR, Stone JL, et al. (July 2009). "Common polygenic variation contributes to risk of schizophrenia and bipolar disorder". Nature 460 (7256): 74852. doi:10.1038/nature08185. PMID19571811. [47] Potash JB, Bienvenu OJ (June 2009). "Neuropsychiatric disorders: Shared genetics of bipolar disorder and schizophrenia". Nat Rev Neurol 5 (6): 299300. doi:10.1038/nrneurol.2009.71. PMID19498428. [48] Goodwin & Jamison. p. 96 [49] Goodwin & Marneros. p. 192
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Cited texts
Marneros A, Akiskal, HS (2007). The Overlap of Schizophrenic and Affective Spectra. New York: Cambridge University Press. ISBN0-521-85858-5. Goodwin FK, Jamison KR (2007). Manic-Depressive Illness: Bipolar Disorders and Recurrent Depression, 2nd Edition. New York: Oxford University Press. ISBN0-19-513579-2. Kaplan HI, Saddock VA (2007). Synopsis of Psychiatry. New York: Lippincott, Williams & Wilkins. ISBN978-0781773270. Murray WH (2006). Schizoaffective Disorders: New Research. New York: Nova Science Publishers, Inc. ISBN1-60021-030-9. Goodwin FK, Marneros, A (2005). Bipolar Disorders: Mixed States, Rapid Cycling and Atypical Forms. New York: Cambridge University Press. ISBN0-521-83517-8. Moore DP, Jefferson JW. Handbook of Medical Psychiatry. 2nd ed. St. Louis, Mo: Mosby; 2004:126-127. Goetz, CG. Textbook of Clinical Neurology. 2nd ed. St. Louis, Mo: WB Saunders; 2003: 48.
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Mania
Manic episode
Classification and external resources ICD-10 F30 [1] ICD-9 MeSH 296.0 [2] Single manic episode, 296.4 [14] [4] Most recent episode manic, 296.6 [6] Most recent episode mixed
D001714
Mania, the presence of which is a criterion for certain psychiatric diagnoses, is a state of abnormally elevated or irritable mood, arousal, and/ or energy levels.[2] In a sense, it is the opposite of depression. The word derives from the Greek "" (mania), "madness, frenzy"[3] and that from the verb "" (mainomai), "to be mad, to rage, to be furious".[4] In addition to mood disorders, individuals may exhibit manic behavior as a result of drug intoxication (notably stimulants such as cocaine or methamphetamine), medication side effects (notably steroids), or malignancy. However, mania is most often associated with bipolar disorder, where episodes of mania may alternate with episodes of major depression. Gelder, Mayou and Geddes (2005) suggests that it is vital that mania is predicted in the early stages because the patient becomes reluctant to comply to the treatment. The criteria for bipolar do not include depressive episodes and the presence of mania in the absence of depressive episodes is sufficient for a diagnosis. Regardless, even those who never experience depression experience cyclical changes in mood. These cycles are often affected by changes in sleep cycle (too much or too little), diurnal rhythms and environmental stressors. Mania varies in intensity, from mild mania known as hypomania to full-blown mania with psychotic features including hallucinations, delusion of grandeur, suspiciousness, catatonic behavior, aggression, and a preoccupation with thoughts and schemes that may lead to self neglect.[5] Standardized tools such as Altman Self-Rating Mania Scale [6] and Young Mania Rating Scale [7] can be used to measure severity of manic episode. Since mania and hypomania have also been associated with creativity and artistic talent,[8] it is not always the case that the clearly manic bipolar person will need or want medical assistance; such people will often either retain sufficient amount of control to function normally or be unaware that they have "gone manic" severely enough to be committed or to commit themselves ('commitment' means admission to a psychiatric facility). Manic individuals can often be mistaken for being on drugs or other mind-altering substances.
Classification
Mixed states
Mania can be experienced at the same time as depression, in a mixed episode. Dysphoric mania is primarily manic and agitated depression is primarily depressed. This has caused speculation amongst doctors that mania and depression are two independent axes in a bipolar spectrum, rather than opposites. There is an increased probability of suicide in the mixed state, as depressed individuals who are also manic have the energy needed to commit the act and the thoughts of depression that would lead them initially to suicide. Mania can be the result of using drugs. Quitting drugs can create situations in one's mind similar to the symptoms of mania, such as constant racing of the mind. A diagnosis of mania in these situations is often temporary.
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Hypomania
Hypomania is a lowered state of mania that does little to impair function or decrease quality of life.[9] In hypomania there is less need for sleep, and both goal-motivated behavior and metabolism increase. Though the elevated mood and energy level typical of hypomania could be seen as a benefit, mania itself generally has many undesirable consequences including suicidal tendencies.
Associated disorders
A single manic episode is sufficient to diagnose Bipolar I Disorder. Hypomania may be indicative of Bipolar II Disorder or Cyclothymia. However, if prominent psychotic symptoms are present for a duration significantly longer than the mood episode, a diagnosis of Schizoaffective Disorder is more appropriate. Several types of Mania such as kleptomania and pyromania are related more closely to OCD than to Bipolar Disorder, depending on the seriousness of these disorders. For instance, someone with kleptomania who suffers from impulses to steal things such as pencils, pens, and paperclips is better diagnosed with a form of OCD. B12 deficiency can also cause characteristics of mania and psychosis.[10] [11]
Mania thoughts. Racing thoughts also interfere with the ability to fall asleep. Mania is always relative to the normal rate of intensity of the person being diagnosed with it; therefore, an easily-angered person may exhibit mania by getting even angrier even more quickly, and an intelligent person may adopt seemingly "genius" characteristics and an ability to perform and to articulate thought beyond what they can do in a normal mood. But perhaps the easiest indicator of mania would be if a noticeably clinically depressed person becomes suddenly cheerful, optimistic, happy, and full of energy. Other elements of mania may include delusions (of grandeur, potential, or otherwise), hypersensitivity, hypersexuality, hyper-religiosity, hyperactivity, impulsiveness, talkativeness, an internal pressure to keep talking (over-explanation) or rapid speech, grandiose ideas and plans, and decreased need for sleep (e.g. feeling rested after 3 or 4 hours of sleep). In manic and hypomanic cases, the afflicted person may engage in out-of-character behavior, such as questionable business transactions, wasteful expenditures of money, risky sexual activity, recreational drug abuse, abnormal social interaction, or highly vocal arguments uncharacteristic of previous behaviors. These behaviors may increase stress in personal relationships, lead to problems at work and increase the risk of altercations with law enforcement. There is a high risk of impulsively taking part in activities potentially harmful to self and others. Although "severely elevated mood" sounds somewhat desirable and enjoyable, the experience of mania is ultimately often quite unpleasant and sometimes disturbing, if not frightening, for the person involved and for those close to them, and it may lead to impulsive behavior that may later be regretted. It can also often be complicated by the sufferer's lack of judgment and insight regarding periods of exacerbation of characteristic states. Manic patients are frequently grandiose, obsessive, impulsive, irritable, belligerent, and frequently deny anything is wrong with them. Because mania frequently encourages high energy and decreased perception of need or ability to sleep, within a few days of a manic cycle, sleep-deprived psychosis may appear, further complicating the ability to think clearly. Racing thoughts and misperceptions lead to frustration and decreased ability to communicate with others. There are different "stages" or "states" of mania. A minor state is essentially hypomania and, like hypomania's characteristics, may involve increased creativity, wit, gregariousness, and ambition. Full-blown mania will make a person feel elated, but perhaps also irritable, frustrated, and even disconnected from reality.
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Cause
Mania is a complex neurophysiological phenomenon. Predisposing factors to develop mania are primarily genetic and are no longer considered to be psychological, although stress triggers to a particular manic episode may include significant psychological and social conflicts. The primary trigger for (and the primary symptom of) acute mania is sleep deprivation. Social problems, medications, or illness may initiate manic hyperarousal but genetic predisposition or brain illnesses are most likely to be the main causations for classic and persistent manic symptoms. Some medications, including all stimulants, may mimic manic symptoms but differ substantially in duration and intensity compared with true manic episodes. The primary mediator of all mood disease is the brain's limbic system. A full description of the cause of mania is complex and should be referenced elsewhere. Some medications may cause symptoms that mimic mania. Some medications may trigger a manic episode through hyperarousal of the limbic system and subsequent sleep deprivation. These may include: amphetamines and other stimulants (Provigil, Nuvigil, Adipex), caffeine (caffeine/taurine energy drinks), cocaine and various illegal drugs, serotonin reuptake inhibitors (SSRI, SNRI), tricyclic compounds (TCA,excluding carbamazepine), steroid medications (Prednisone, oral cortisone), serotonin agonists, dopamine agonists (Mirapex, Sinemet), and several other groups of medicines. One common over the counter medication group that can be stimulating in large doses is cough and cold medications that contain agents meant to stimulate blood vessels which shrink nasal mucosa thereby enlarging space for nasal air flow (decongestants). For example, Phenylpropanolamine (PPA) is a sympathomimetic drug similar in structure to amphetamine which was formerly present in over 130 medications, primarily decongestants, cough/cold remedies, and anorectic agents.
Mania A report on PPA, from the Dept. of Psychiatry, F. Edward Hebert School of Medicine, Uniformed Services University of the Health Sciences, Bethesda, Maryland. Pharmacopsychiatry 1988 stated: We have reviewed 37 cases (published in North America and Europe since 1960) that received diagnoses of acute mania, paranoid schizophrenia, and organic psychosis and that were attributed to PPA product ingestion. Of the 27 North American case reports, more reactions followed the ingestion of combination products than preparations containing PPA alone; more occurred after ingestion of over-the-counter products than those obtained by prescription or on-the-street; and more of the cases followed ingestion of recommended doses rather than overdoses. Failure to recognize PPA as an etiological agent in the onset of symptoms usually led to a diagnosis of schizophrenia or mania, lengthy hospitalization, and treatment with substantial doses of neuroleptics or lithium. PPA is no longer available in any medication in the United States as of the year 2000.
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Treatment
Before beginning treatment for mania, careful differential diagnosis must be performed to rule out non-psychiatric causes. Acute mania in bipolar disorder is typically treated with mood stabilizers and/or antipsychotic medication. Note that these treatments need to be prescribed and monitored carefully to avoid harmful side-effects such as neuroleptic malignant syndrome with the antipsychotic medications. It may be necessary to temporarily admit the patient involuntarily until the patient is stabilized. Antipsychotics and mood stabilizers help stabilize mood of those with mania or depression. They work by blocking the receptor for the neurotransmitter dopamine and allowing serotonin to still work, but in diminished capacity. When the manic behaviours have gone, long-term treatment then focuses on prophylactic treatment to try to stabilize the patient's mood, typically through a combination of pharmacotherapy and psychotherapy. Lithium is the classic mood stabilizer to prevent further manic and depressive episodes. Anticonvulsants such as valproic acid and carbamazepine are also used for prophylaxis. More recent drug solutions include lamotrigine. Clonazepam (Rivotril, Ravotril or Rivatril) is also used. Verapamil, a calcium-channel blocker, is useful in the treatment of hypomania and in those cases where lithium and mood stabilizers are contraindicated or ineffective.[17] Verapamil is effective for both short-term and long-term treatment.[18]
Medications
The biological mechanism by which mania occurs is not yet known. One hypothesised cause of mania (among others), is that the amount of the neurotransmitter serotonin in the temporal lobe may be excessively high. Dopamine, norepinephrine, glutamate and gamma-aminobutyric acid also appear to play important roles. Imaging studies have shown that the left amygdala is more active in women who are manic and the orbitofrontal cortex is less active.[19] Antidepressant monotherapy is not recommended for the treatment of depression in patients with bipolar disorders I or II, and no benefit has been demonstrated by combining antidepressants with mood stabilizers in these patients.[20]
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References
[1] http:/ / apps. who. int/ classifications/ icd10/ browse/ 2010/ en#/ F30 [2] Berrios G.E. (2004). "Of mania". History of Psychiatry 15: 105124. [3] (http:/ / www. perseus. tufts. edu/ hopper/ text?doc=Perseus:text:1999. 04. 0057:entry=mani/ a1), Henry George Liddell, Robert Scott, A Greek-English Lexicon, on Perseus Digital Library [4] (http:/ / www. perseus. tufts. edu/ hopper/ text?doc=Perseus:text:1999. 04. 0057:entry=), Henry George Liddell, Robert Scott, A Greek-English Lexicon, on Perseus Digital Library [5] Semple, David. "Oxford Hand book of Psychiatry" Oxford press,2005. [6] Altman E, Hedeker D, Peterson JL, Davis JM (September 2001). "A comparative evaluation of three self-rating scales for acute mania" (http:/ / linkinghub. elsevier. com/ retrieve/ pii/ S0006322301010654). Biol. Psychiatry 50 (6): 46871. doi:10.1016/S0006-3223(01)01065-4. PMID11566165. . [7] Young RC, Biggs JT, Ziegler VE, Meyer DA (Nov 1978). "A rating scale for mania: reliability, validity and sensitivity" (http:/ / bjp. rcpsych. org/ cgi/ content/ abstract/ 133/ 5/ 429). Br J Psychiatry 133: 42935. doi:10.1192/bjp.133.5.429. PMID728692. . [8] Jamison, Kay R. (1996), Touched with Fire: Manic-Depressive Illness and the Artistic Temperament, New York: Free Press, ISBN 0-684-83183-X [9] NAMI (July 2007). "The many faces & facets of BP" (http:/ / www. nami. org/ Content/ ContentGroups/ bp_and_Schizophrenia_Digest/ The_Many_Faces_and_Facets_of_BP. htm). . Retrieved 2008-10-02. [10] Sethi NK, Robilotti E, Sadan Y (2005). "Neurological Manifestations Of Vitamin B-12 Deficiency". The Internet Journal of Nutrition and Wellness 2 (1). [11] Masalha R, Chudakov B, Muhamad M, Rudoy I, Volkov I, Wirguin I (2001). "Cobalamin-responsive psychosis as the sole manifestation of vitamin B12 deficiency" (http:/ / www. ima. org. il/ imaj/ dynamic/ web/ ArtFromPubmed. asp?year=2001& month=09& page=701). Israeli Medical Association Journal 3: 701703. . [12] "BehaveNet Clinical Capsule: Manic Episode" (http:/ / www. behavenet. com/ capsules/ disorders/ manicep. htm). . Retrieved 18 October 2010. [13] "ICD-10" (http:/ / apps. who. int/ classifications/ apps/ icd/ icd10online/ ). . Retrieved 18 October 2010. [14] DSM-IV [15] AJ Giannini. Biological Foundations of Clinical Psychiatry, NY Medical Examination Publishing Company, 1986. [16] Lakshmi N. Ytham, Vivek Kusumakar, Stanley P. Kutchar. (2002). Bipolar Disorder: A Clinician's Guide to Biological Treatments, page 3. [17] Giannini AJ, Houser WL Jr, Loiselle RH, Giannini MC, Price WA (1984). "Antimanic effects of verapamil". American Journal of Psychiatry 141: 1601604. PMID6439057. [18] Giannini AJ, Taraszewski RS, Loiselle RH (1987). "Verapamil and lithium in maintenance therapy of manic patients". Journal of Clinical Pharmacology 27: 980985. PMID3325531. [19] Altshuler L, Bookheimer S, Proenza MA, Townsend J, Sabb F, Firestine A, Bartzokis G, Mintz J, Mazziotta J, Cohen MS., L; Bookheimer, S; Proenza, MA; Townsend, J; Sabb, F; Firestine, A; Bartzokis, G; Mintz, J et al. (2005). "Increased Amygdala Activation During Mania: A Functional Magnetic Resonance Imaging Study" (http:/ / ajp. psychiatryonline. org/ cgi/ content/ full/ 162/ 6/ 1211). Am J Psychiatry 162 (6): 121113. doi:10.1176/appi.ajp.162.6.1211. PMID15930074. . [20] Nierenberg, A. (2010). "A critical appraisal of treatments for bipolar disorder". Primary care companion to the Journal of clinical psychiatry 12 (Suppl 1): 2329. doi:10.4088/PCC.9064su1c.04. PMC2902191. PMID20628503. [21] Behrman, Andy (2002). Electroboy: A Memoir of Mania. Random House Trade Paperbacks. pp.Preface: Flying High. ISBN978-0812967081.
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Further reading
Expert Opin Pharmacother. 2001 December;2(12):196373. Schizoaffective Disorder (http://www.mayoclinic.com/health/schizoaffective-disorder/DS00866). 2007 September Mayo Clinic. Retrieved October 1, 2007. Schizoaffective Disorder (http://allpsych.com/disorders/psychotic/schizoaffective.html). 2004 May. All Psych Online: Virtual Psychology Classroom. Retrieved October 2, 2007. Psychotic Disorders (http://allpsych.com/disorders/psychotic/index.html). 2004 May. All Psych Online: Virtual Psychology Classroom. Retrieved October 2, 2007. Increased concentrations and lateral asymmetry of amygdala dopamine in schizophrenia (http://www.nature. com/nature/journal/v305/n5934/abs/305527a0.html). 1983 October Nature. Retrieved October 2, 2007. Risperidone therapy in treatment refractory acute bipolar and schizoaffective mania (http://www.ncbi.nlm.nih. gov/sites/entrez?cmd=Retrieve&db=PubMed&list_uids=8927675&dopt=Citation). 1996 January Psychopharmacology Bulletin. Retrieved October 2, 2007.
External links
Bipolar Mania Symptoms (http://www.bipolardisordersymptoms.info/bipolar-symptoms/grandiosity.htm) Depression and Bipolar Support Alliance (http://www.dbsalliance.org) Manic Episode Symptoms (http://counsellingresource.com/distress/mood-disorders/manic-symptoms.html)
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Mixed state
This article is an expansion of a section titled Mixed State from the main article: Bipolar disorder
In the context of mental disorder, a mixed state (also known as dysphoric mania, agitated depression, or a mixed episode) is a condition during which symptoms of mania and depression occur simultaneously (e.g., agitation, anxiety, fatigue, guilt, impulsiveness, irritability, morbid or suicidal ideation, panic, paranoia, pressured speech and rage). Typical examples include tearfulness during a manic episode or racing thoughts during a depressive episode. One may also feel incredibly frustrated or be prone to fits of rage in this state, since one may feel like a failure and at the same time have a flight of ideas. Mixed states are often the most dangerous period of mood disorders, during which susceptibility to substance abuse, panic disorder, commission of violence, suicide attempts, and other complications increase greatly.
Diagnostic criteria
As affirmed by the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV), a mixed state must meet the criteria for a major depressive episode and a manic episode nearly every day for at least one week.[2] However, mixed episodes rarely conform to these qualifications; they may be described more practically as any combination of depressive and manic symptoms.[3] [4] [5] The Merck Manual of Diagnosis and Therapy (MMDT) splits the DSM-IV diagnosis into dysphoric mania and an agitated depression state. A dysphoric mania consists of a manic episode with depressive symptoms. Increased energy and some form of anger, from irritability to full blown rage, are the most common symptoms (MMDT). Symptoms may also include auditory hallucinations, confusion, insomnia, persecutory delusions, racing thoughts, restlessness, and suicidal ideation. Alcohol, drug abuse, and some antidepressant drugs may trigger dysphoric mania in susceptible individuals. An agitated depression is a "major depressive [episode] with superimposed hypomanic symptoms".[6] Mixed episodes in which major depression is the primary state, concurrent with atypical manic features have been described. A study by Goodwin and Ghaemi (2003) reported manic symptoms in two-thirds of patients with agitated depression, which they suggest calling "mixed-state agitated depression".[7]
Treatment
Treatment of mixed states is typically based upon administration of mood stabilizing medication, which may include anticonvulsants such as lamotrigine and valproic acid; atypical antipsychotics such as olanzapine, aripiprazole, and ziprasidone; or first-generation antipsychotics such as haloperidol. There is question of lithium's efficacy for treatment of mixed states due to conflicting conclusions drawn from various trials and research.[8] [9] Mood stabilizers work to reduce the manic symptoms associated with the mixed state, but they are not considered particularly effective for improving concurrent depressive symptoms.[10]
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References
[1] http:/ / apps. who. int/ classifications/ icd10/ browse/ 2010/ en#/ F38. 0 [2] American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 4th ed. Washington, DC: American Psychiatric Press, Inc., 1994. [3] Akiskal, H.S. Pinto, O. (1999). The evolving bipolar spectrum. Prototypes I, II, III, and IV. Psychiatr Clin North Am. 22(3):51734. [4] Goldman, E. (1999). Severe Anxiety, Agitation are Warning Signals of Suicide in Bipolar Patients. Clin Psychiatr News. pg 25. [5] Perugi, G. Toni, C. Akiskal, H.S. (1999). Anxious-bipolar comorbidity. Diagnostic and treatment therefore challenges. Psychiatr Clin North Am. 22(3):56583. [6] Benazzi, F. (2000). Depressive mixed states: unipolar and bipolar II (http:/ / www. ncbi. nlm. nih. gov/ entrez/ query. fcgi?cmd=Retrieve& db=PubMed& list_uids=11097167& dopt=Abstract) [Abstract]. Eur Arch Psychiatry Clin Neurosci. 250(5):24953. [7] Goodwin FK, Ghaemi SN (December 2003). "The course of bipolar disorder and the nature of agitated depression" (http:/ / ajp. psychiatryonline. org/ cgi/ pmidlookup?view=long& pmid=14638572). Am J Psychiatry 160 (12): 20779. PMID14638572. . [8] Pharmacotherapy of manic-depressive mixed States (http:/ / www. ncbi. nlm. nih. gov/ pubmed/ 16511729) [9] Muzina, D. J. (2009), Pharmacologic treatment of rapid cycling and mixed states in bipolar disorder: an argument for the use of lithium. Bipolar Disorders, 11: 8491. doi: 10.1111/j.1399-5618.2009.00713.x [10] Thase ME, Sachs GS. Bipolar depression: pharmacotherapy and related therapeutic strategies. Biol Psychiatry. 2000 Sep 15;48(6):558-572.
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Hypomania
This article is an expansion of a section titled Hypomania from within the main article: Bipolar disorder.
Hypomania
Classification and external resources ICD-10 F30.0 [1]
Hypomania (literally, "below mania") is a mood state characterized by persistent and pervasive elevated (euphoric) or irritable mood, as well as thoughts and behaviors that are consistent with such a mood state. Many people also experience signature hypersexuality.
Presentation
Individuals in a hypomanic state have a decreased need for sleep, are extremely outgoing and competitive, and have a great deal of energy. However, unlike with full mania, those with hypomanic systems are fully functioning, and are often more productive than usual.
Distinctive markers
Specifically, hypomania is distinguished from mania by the absence of psychotic symptoms and grandiosity, and by its lesser degree of impact on functioning. Hypomania is a feature of bipolar II disorder and cyclothymia, but can also occur in schizoaffective disorder. Hypomania is also a feature of bipolar I disorder as it arises in sequential procession as the mood disorder fluctuates between normal mood and mania. Some individuals with bipolar I disorder have hypomanic as well as manic episodes. Hypomania can also occur when moods progress downwards from a manic mood state to a normal mood. Hypomania is sometimes credited with increasing creativity and productive energy. A significant number of people with creative talents have reportedly experienced hypomania or other symptoms of bipolar disorder and attribute their success to it. Classic symptoms of hypomania include mild euphoria, a flood of ideas, endless energy, and a desire and drive for success. A lesser form of hypomania is called hyperthymia.
Definitions
Hypomania is also a side effect of numerous medications, oftenthough not alwaysthose used in psychopharmacotherapy. Patients suffering from severe depression who experience hypomania as a side effect of antidepressants (for example), may prove to have a form of bipolar disorder that has previously gone unrecognized. However, drug-induced hypomania is not invariably indicative of bipolar affective disorders. The difference between uni- and bi-polar disorders is essential for analysis of switches (mood changes). Consequently, it is important for researchers and mental health professionals to distinguish drug-induced hypomania in bipolar patients from drug-induced hypomania in unipolar (non-bipolar) depressives. Nevertheless, if antidepressants trigger the first episode of hypomania, it is strongly suggestive of an underlying diagnosis of bipolar disorder, particularly if the manic symptoms (mild, moderate or severe) last for a lengthy period of time after they start. In cases of true drug-induced hypomania, cessation of the antidepressant or whichever drug has triggered this mood statefor example steroid therapy or stimulants such as amphetamineusually causes a fairly swift return to normal mood. It is far less likely to be a side effect in those with pure Clinical Unipolar Depression, unless for example tricyclic antidepressants are given in very high doses. SSRIs are less likely to trigger manic symptoms except in those individuals where there is an underlying bipolar disorder, particularly if administered without a mood stabilizer.
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Occurrence
Often in those who have experienced their first episode of hypomania (which is a level of mild to moderate mania) generally without psychotic features - there will have been a long or recent history of depression prior to the emergence of manic symptoms, and commonly this surfaces in the mid to late teens. Due to this being an emotionally charged time, it is not unusual for mood swings to be passed off as hormonal or teenage ups and downs and for a diagnosis of Bipolar Disorder to be missed until there is evidence of an obvious manic/hypomanic phase.[2] Hypomania may also occur as a side effect of pharmaceuticals prescribed for conditions/diseases other than psychological states or mood disorders. In those instances, as in cases of drug-induced hypomanic episodes in unipolar depressives, the hypomania can almost invariably be eliminated by lowering medication dosage, withdrawing the drug entirely, or changing to a different medication if discontinuation of treatment is not possible.[3] Some, such as Johns Hopkins psychologist John Gartner, argue that hypomania is better understood as a stable non-pathological temperament rather than an episode of mental illness[4] The DSM however clearly defines hypomania as an aberrant state, not a stable trait.
Symptomatic recognition
The DSM-IV-TR defines a hypomanic episode as including, over the course of at least four days, elevated mood plus three of the following symptoms OR irritable mood plus four of the following symptoms: pressured speech inflated self-esteem or grandiosity decreased need for sleep flight of ideas or the subjective experience that thoughts are racing easy distractibility and attention-deficit similar to attention deficit hyperactivity disorder increase in psychomotor agitation involvement in pleasurable activities that may have a high potential for negative psycho-social or physical consequences (e.g., the person engages in unrestrained buying sprees, sexual indiscretions, reckless driving, or foolish business investments).[5]
Possible benefits
Some commentators believe that hypomania actually has an evolutionary advantage.[6] People with hypomania are generally perceived as being energetic, euphoric, visionary, overflowing with new ideas, and sometimes over-confident and very charismatic, yetunlike those with full-blown maniaare sufficiently capable of coherent thought and action to participate in everyday activities. Like mania, there seems to be a significant correlation between hypomania and creativity. A person in the state of hypomania might be immune to fear and doubt and have little social and sexual inhibition. People experiencing hypomania are often the "life of the party." They may talk to strangers easily, offer solutions to problems, and find pleasure in small activities. Such advantages may render them unwilling to submit to treatment, especially when disadvantages are minimal.
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Treatment
Medications typically prescribed for hypomania include mood stabilizers such as valproic acid and lithium carbonate as well as atypical antipsychotics such as olanzapine and quetiapine.
References
[1] http:/ / apps. who. int/ classifications/ icd10/ browse/ 2010/ en#/ F30. 0 [2] Drug-Induced Dysfunction in Psychiatry. Matcheri S. Keshavan and John S. Kennedy, Editors (Taylor & Francis, 1992). [3] Bipolar Disorder: A Summary of Clinical Issues and Treatment Options. Bipolar Disorder Sub-Committee, Canadian Network for Mood and Anxiety Treatments (CANMAT). April 1997 [4] http:/ / johngartner. com [5] "Hypomanic Episode" (http:/ / www. behavenet. com/ capsules/ disorders/ hypomanicep. htm). BehaveNet Clinical Capsules. . Retrieved 2008-01-03. [6] Fieve, Ronald R. Bipolar II: Enhance Your Highs, Boost Your Creativity, and Escape the Cycles of Recurrent Depression--The Essential Guide to Recognize and Treat the Mood Swings of This Increasingly Common Disorder (http:/ / www. amazon. com/ dp/ 1594862249). ISBN978-1594862243. . [7] "Cyclothymia" (http:/ / www. behavenet. com/ capsules/ path/ cyclothymia. htm). BehaveNet Clinical Capsules. . Retrieved 2008-01-03. [8] If the depressive episodes are routinely during the winter and the hypomania presents in the spring/summer it is possible that the person may be diagnosed with Seasonal Affective Disorder instead of bipolar II disorder. "Bipolar II Disorder" (http:/ / www. behavenet. com/ capsules/ disorders/ bip2dis. htm). BehaveNet Clinical Capsules. . Retrieved 2008-01-03. [9] Robert M. Post, Kindling and sensitization as models for affective episode recurrence, cyclicity, and tolerance phenomena, Neuroscience & Biobehavioral Reviews, Volume 31, Issue 6, Animal Models of Bipolar Disorder and Mood Stabilizer Efficacy, 2007, Pages 858873, ISSN 01497634, DOI: 10.1016/j.neubiorev.2007.04.003. (http:/ / www. sciencedirect. com/ science/ article/ B6T0J-4NJWNTB-2/ 2/ 528f428f1551fd5248570dd7cf7d0a07) [10] The Hypomanic Edge: The Link Between (A Little) Craziness and (A Lot of) Success in America, Gartner, John D. (Simon & Schuster, New York, 2005) http:/ / hypomanicedge. com [11] E.g. review by Nassir Ghaemi, M.D., M.A., M.P.H. at Mentalhealth.net (http:/ / www. mentalhelp. net/ poc/ view_doc. php?id=2913& type=book& cn=4).
Hypomania
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External links
Hypomanic Episode - Bipolar Disorder (http://www.bipolardisordersymptoms.info/hypomanic-episode.htm) Depression and Bipolar Support Alliance (http://www.dbsalliance.org) - Depression and Bipolar Support Alliance Advice for Bipolar Disorder Sufferers and Their Loved Ones (http://www.bipolaradviceguide.com/)
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A major depressive episode is the cluster of symptoms of major depressive disorder. The description has been formalised in psychiatric diagnostic criteria such as the DSM-IV and ICD-10, and is characterized by severe, highly persistent depression, and a loss of interest or pleasure in everyday activities, which is often manifested by lack of appetite, chronic fatigue, and sleep disturbances (somnipathy). The individual may think about suicide, and indeed an increased risk of actual suicide is present.[4] In addition to the emotional pain endured by those suffering from depression, significant economic costs are associated with depression. In fact, American and Canadian studies have indicated that the costs associated with depression are greater than those associated with hypertension, and equal to those of heart disease, diabetes, and back problems.[5]
Criteria
The criteria below are based on the formal DSM-IV criteria for a Major Depressive Episode. A diagnoses of major depressive episode requires that the patient hasover a two-week periodexperienced five or more of the symptoms below, and these must be outside the patient's normal behaviour. Either depressed mood or decreased interest or pleasure must be one of the five (although both are frequently concomitant).
Mood
For the better part of nearly every day, the patient reports a depressed mood or appears depressed to others.[6] The patient may state that he or she has been feeling sad, depressed, blue, empty, "down in the dumps," hopeless, etc. If the patient is in denial about these feelings, yet appears to be on the verge of tearfulness, manifests a depressed facial expression and disposition, or appears to be overly irritable, these may also indicate the presence of depressed mood. Some people may report physical complaints (i.e., aches, pains, headaches) rather than depressed mood, and physical symptoms without physical cause are sometimes indicators of depression. (See Myalgia and Neuralgia.[7] )
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Sleep
Nearly every day the patient sleeps excessively, known as hypersomnia, or not enough, known as insomnia.[6] Insomnia is the most common type of sleep disturbance for people who are clinically depressed. Waking in the middle of the night and being unable to go back to sleep is known as "middle insomnia"; waking too early as "terminal insomnia", and; having difficulty falling asleep at night is "initial" insomnia. Insomnia is often associated with a melancholic type of depression. A less frequent sleeping problem is oversleeping (called "hypersomnia"). This may occur in the form of sleeping for prolonged periods at night or increased sleeping during the daytime. Even with excess sleep, a person may still feel tired and sluggish during the day. People with seasonal affective disorder (SAD) may sleep longer during the winter months. Hypersomnia is often associated with an atypical depression.[7]
Motor activity
Nearly every day others can see that the patient's activity is agitated or slow.[6] People suffering from depression may be either quite agitated (psychomotor agitation), or very lethargic (psychomotor retardation) in their mannerisms and behavior. If a person is agitated, he or she may find it difficult to sit still, may pace the room, wring his/her hands, or fidget with clothes or objects. Someone with psychomotor retardation tend to move sluggishly, may move across a room very slowly, avert his/her eyes, sit slumped in a chair and speak slowly, saying little. In terms of diagnosis, the agitation or slowing down of one's demeanor must be to the degree that it can be observed by others.[7]
Fatigue
Nearly every day the person experiences extreme fatigue.[6] A decrease in energy and feeling fatigued are very common symptoms for those who are clinically depressed. A person may feel tired without having engaged in any physical activity, and day-to-day tasks become difficult, including getting washed and dressed in the morning. Job tasks or housework become very tiring, and the person finds that his/her work at home, school, or on the job suffers.[7]
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Self-worth
Nearly every day the patient feels worthless or inappropriately guilty. These feelings are not just about being depressed, they may be delusional.[6] Depressed people may think of themselves in very negative, unrealistic ways such as manifesting a preoccupation with past "failures", personalisation of trivial events, or believing that minor mistakes prove their inadequacy. They also may have an unrealistic sense of personal responsibility and see things beyond their control as being their fault. Additionally, self-loathing is common in clinical depression, and can lead to a downward spiral when combined with other symptoms.[7]
Concentration
Noted by the patient or by others, nearly every day the patient is indecisive or has trouble thinking or concentrating.[6] A person with depression frequently experiences negative and pessimistic thoughts, and reports that his/her ability to think, concentrate, or make decisions becomes impaired. Memory and distraction problems are common. This problem can be notably pronounced, causing significant difficulty in functioning for those involved in intellectually demanding activities.[7]
Thoughts of death
The patient has had repeated thoughts about death (other than the fear of dying), suicide (with or without a plan) or has made a suicide attempt.[6] The frequency and intensity of thoughts about suicide can range from believing that friends and family would be better off if one were dead, to frequent thoughts about committing suicide (generally related to wishing to stop the emotional pain), to detailed plans about how the suicide would be carried out. Less severely suicidal people may have regular thoughts of suicide, while those who are more severely suicidal may have made specific plans and decided upon a day and location for the suicide attempt.[7] Thoughts of suicide occur mostly when triggered. Thoughts of suicide happen more frequently than normal.
Diagnostic caveats
In diagnosing the symptoms a trained therapist must take the following into account: These symptoms must cause clinically important distress, or impair work, social or personal functioning, and they should not fulfil the criteria for Mixed Episode. The symptoms are not due to the direct physiological effects of a substance (e.g., abuse of a drug or medication) or a general medical condition (e.g., hypothyroidism).[4] Other than in the case of severe symptoms (severely impaired functioning, severe preoccupation with worthlessness, ideas of suicide, delusions or hallucinations or psychomotor retardation), the episode should not have begun within two months of the loss of a loved one. (See Bereavement.[6] )
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Treatment
If left untreated, a typical major depressive episode may last for about six months, while about 20% of these episodes can last two years or more, with 50% of depressive episodes ending spontaneously. However, even after the major depressive episode is over, 20% to 30% of patients have residual symptoms, which can be distressing and associated with disability.[5] Regarding the treatment of major depressive episodes of severe intensity (multiple symptoms, minimal mood reactivity, severe functional impairment), combined psychotherapy plus antidepressant medications are more effective than psychotherapy alone.
Demographics
Estimates of the numbers of people suffering from major depressive episodes and Major Depressive Disorder (MDD) vary significantly. Between 10% and 25% of women, and between 5% and 12% of men will suffer a major depressive episode. Fewer people, between 5% and 9% of women and between 2% and 3% of men, will have MDD, or full-blown depression. Depression occurs nearly twice as often in adolescent and adult females as in males, and the peak period of development is between the ages of 25 and 44 years. Onset of major depressive episodes or MDD often occurs to people in their mid-20s, and less often to those over 65. Prepubescent girls and boys are affected equally. Additionally, socio-economic or environmental factors do not appear to have any bearing on the incidence of a major depressive episode or MDD.[5]
External links
Depression and Bipolar Support Alliance [8] - Depression and Bipolar Support Alliance National Institutes of Health [9]
Notes
[1] [2] [3] [4] [5] [6] [7] [8] [9] http:/ / apps. who. int/ classifications/ icd10/ browse/ 2010/ en#/ F32. 2 http:/ / apps. who. int/ classifications/ icd10/ browse/ 2010/ en#/ F32. 3 http:/ / www. icd9data. com/ getICD9Code. ashx?icd9=296. 2 Diagnostic and Statistical Manual of Mental Disorders, fourth Edition. (http:/ / www. medscape. com/ viewarticle/ 467185_2) Medscape (http:/ / faculty. winthrop. edu/ DaughertyT/ dep. htm) Winthrop.edu (http:/ / www. allaboutdepression. com/ dia_12. html#7) All About Depression http:/ / www. dbsalliance. org http:/ / health. nih. gov/ result. asp?disease_id=183
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Treatment
Treatment of bipolar disorder
This article is an expansion of a section entitled Treatment from within the main article: Bipolar disorder The emphasis of the treatment of bipolar disorder is on effective management of the long-term course of the illness, which can involve treatment of emergent symptoms. Treatment methods include pharmacological and psychological techniques. A variety of medications are used to treat bipolar disorder; most people with bipolar disorder require combinations of medications.
Principles
The primary treatment for bipolar disorder consists of medications called mood stabilizers, which are used to prevent or control episodes of mania or depression. Proven mood stabilizers include lithium, and anticonvulsants such as Valproic acid (Depakote), carbamazepine (Tegretol), and lamotrigine (Lamictal). The atypical antipsychotics are all FDA approved for acute treatment of mania; these include quetiapine (Seroquel), olanzapine (Zyprexa), and risperidone (Risperdal). Generally speaking, mood stabilizers are more effective at treating or preventing manic episodes; however, some medications (i.e. lamotrigine, quetiapine) have been shown to be effective for the treatment of bipolar depression.In particular, lamotrigine is often the first-line treatment for bipolar II, where depression, rather than mania, tends to be the dominant symptom. . Antidepressants are often prescribed to treat depressive symptoms, however the role of antidepressants remains controversial because antidepressants have been known to induce mania, and some researchers believe that they can worsen the course of the disease (see below). Medications are not the only available treatment for bipolar disorder; other treatments include omega 3 fatty acids, therapy such as psychotherapy and cognitive behavioral therapy, and exercise. Stress, alcohol abuse, and drug abuse can all cause bipolar disorder to worsen, and so effective treatment may require management of stress and moderation or elimination of alcohol and drug use. The goal of treatment is not to cure the disorder but rather to control the symptoms and the course of the disorder. Generally speaking, maintenance treatment of bipolar disorder continues long after symptoms have been brought under control. Drugs used for bipolar disorder sometimes have significant side effects, which vary from drug to drug. Lithium may be associated with gastrointestinal upset (e.g. nausea, diarrhea), memory problems, weight gain and other side effects. Higher doses equal more side effects, but lower doses (within the therapeutic window) have little to no side effects. Anticonvulsant medications commonly cause sedation, weight gain, electrolyte disturbances, or other side effects. If one cannot tolerate one of the anticonvulsants, it's advisable to try another anticonvulsant. Two or more anticonvulsants in combination can often result in a lower effective dose of each and lower side effects. The side effect profile of the atypical antipsychotics vary widely between agents. Generally speaking, the most common side effects of the atypicals are sedation and metabolic disturbances (i.e. weight gain, dyslipidemia, hyperglycemia). Atypical antipsychotics may also cause extrapyramidal side effects and restlessness. Atypical antipsychotics also carry a risk of causing tardive dyskinesia; however, the risk with the newer atypical agents is much less than the risk associated with older antipsychotics (e.g. haloperidol). The risk of TD is thought to be proportionate to the duration of neuroleptic/antipsychotic use (roughly 5% per year in non-elderly patients treated with older antipsychotics). Patients and physicians need to be careful to watch for symptoms of this side effect carefully so that an antipsychotic can be reduced in dosage, or changed to another medication, before the condition progresses. The physician should, of course, be consulted about any change in dosage.
Treatment of bipolar disorder A recent large-scale study [1] found that severe depression in patients with bipolar disorder responds no better to a combination of antidepressant medications and mood stabilizers than it does to mood stabilizers alone. Furthermore, this federally funded study found that antidepressant use does not hasten the emergence of manic symptoms in patients with bipolar disorder. Medications work differently in each person, and it takes considerable time to determine in any particular case whether a given drug is effective at all, since bipolar disorder is by nature episodic, and patients may experience remissions whether or not they receive treatment. For this reason, neither patients nor their doctors should expect immediate relief, although psychosis with mania can respond quickly to anti psychotics, and bipolar depression can be alleviated quickly with electroconvulsive therapy (ECT). Many doctors emphasize that patients should not expect full stabilization for at least 34 weeks (some antidepressants, for example, take 46 weeks to take effect), and should not give up on a medication prematurely,[2] nor should they discontinue medication with the disappearance of symptoms as the depression may return. Compliance with medications can be a major problem. Some people, as they become manic, may lose the awareness of having an illness, and they therefore discontinue medications. Patients also often quit taking medication when symptoms disappear, erroneously thinking themselves "cured", and some people enjoy the effects of unmedicated hypomania. Other reasons cited by individuals for discontinuing medication are side effects, expense, and the stigma of having a psychiatric disorder. In a relatively small number of cases stipulated by law (varying by locality but typically, according to the law, only when a patient poses a threat to himself or others), patients who do not agree with their psychiatric diagnosis and treatment can legally be required to have treatment without their consent. Throughout North America and the United Kingdom, involuntary treatment or detention laws exist for severe cases of bipolar disorder and other mental illnesses where there is a potential for harm to oneself or others.
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Mood Stabilizers
Lithium salts
The use of lithium salts as a treatment of bipolar disorder was first discovered by Dr. John Cade, an Australian psychiatrist who published a paper on the use of lithium in 1949. Lithium salts had long been used as a first-line treatment for bipolar disorder. In ancient times, doctors would send their mentally ill patients to drink from "alkali springs" as a treatment. They did not know it, but they were really prescribing lithium, which was present in high concentration in the waters. The therapeutic effect of lithium salts appears to be entirely due to the lithium ion, Li+. The two lithium salts used for bipolar therapy are lithium carbonate (mostly) and lithium citrate (sometimes). Approved for the treatment of acute mania in 1970 by the Food and Drug Administration (FDA), lithium has been an effective mood-stabilizing medication for many people with bipolar disorder. Lithium is also noted for reducing the risk of suicide.[3] Although lithium is among the most effective mood stabilizers, persons taking it may experience side effects similar to the effects of ingesting too much table salt, such as high blood pressure, water retention, and constipation. Regular blood testing is required when taking lithium to determine the correct lithium levels since the therapeutic dose is close to the toxic dose. The mechanism of lithium salt treatment is believed to work as follows: some symptoms of bipolar disorder appear to be caused by the enzyme inositol monophosphatase (IMPase), an enzyme that splits inositol monophosphate into free inositol and phosphate. It is involved in signal transduction and is believed to create an imbalance in neurotransmitters in bipolar patients. The lithium ion is believed to produce a mood stabilizing effect by inhibiting IMPase by substituting for one of two magnesium ions in IMPase's active site, slowing down this enzyme. Lithium orotate is used as an alternative treatment to lithium carbonate by some individuals with bipolar disorder, mainly because it is available without a doctor's prescription. It is sometimes sold as "organic lithium" by nutritionists, as well as under a wide variety of brand names. There seems to be little evidence for its use in clinical
Treatment of bipolar disorder treatment in preference to lithium carbonate. Individuals with bipolar disorder have complained that it is much weaker than lithium carbonate and, therefore, less effective. Lithium has problems with its side effects, including hand trembling and intolerance of hot weather. Benztropine is sometimes used to control the trembling, but itself causes sedation. Lithium has a very narrow window of effectiveness. Below that level it has no effect, and above it is toxic. For that reason blood must be sampled frequently to determine if the proper blood level is currently present.
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Anticonvulsants
Anticonvulsant medications, particularly valproate and carbamazepine, are often used instead of, or along with, lithium. Valproate (Depakote, Epival) was FDA approved for the treatment of acute mania in 1995, and is now considered by some doctors to be the first line of therapy for bipolar disorder. A similar medication, valproic acid (Depakene) is also used. For some, it is preferable to lithium because its side effect profile seems to be less severe, compliance with the medication is better, and fewer breakthrough manic episodes occur. However, valproate is not as effective as lithium in preventing or managing depressive episodes,[4] so patients taking valproate may also need an antidepressant as an adjunct medicinal therapy. New research suggests that different combinations of lithium and anticonvulsants may be helpful. Anticonvulsants are also used in combination with antipsychotics. Newer anticonvulsant medications, including lamotrigine and oxcarbazepine, are also effective as mood stabilizers in bipolar disorder. Lamotrigine is particularly promising, as it alleviates bipolar depression and prevents recurrence at higher rates. Lamotrigine is also well tolerated by many patients. [5] ,[6] Zonisamide (trade name Zonegran), another anticonvulsant, also may show promise in treating bipolar depression according to Frederick K. Goodwin M.D. on a recent Medscape webcast titled "The Accurate Diagnosis and Long-Term Treatment of Bipolar Depression" to view the webcast click here [7]. (free reg required). Topiramate has not done well in clinical trials; it seems to help a few patients very much but most not at all. It appears to be useful in some treatment resistant cases and for anxiety issues when clonazepam cannot be prescribed. Gabapentin has failed to distinguish itself from placebo as a mood stabilizer. According to studies conducted in Finland in patients with epilepsy, valproate may increase testosterone levels in teenage girls and produce polycystic ovary syndrome in women who began taking the medication before age 20. Increased testosterone can lead to polycystic ovary syndrome with irregular or absent menses, obesity, and abnormal growth of hair. Therefore, young female patients taking valproate should be monitored carefully by a physician. However, the therapeutic dose for a patient taking valproate for epilepsy is much higher than the therapeutic dose of valproate for an individual with bipolar disorder. Other anticonvulsants effective in some cases and being studied closer include phenytoin, levetiracetam, pregabalin and valnoctamide.[8]
Treatment of bipolar disorder Symbyax, a combination of olanzapine and fluoxetine.[12] In addition, quetiapine (Seroquel and Seroquel XR) has been approved for the treatment of bipolar mania, bipolar depression, and for long-term maintenance treatment of bipolar disorder when used in conjunction with lithium or divalproex.[13] Ziprasidone (Geodon) and aripiprazole (Abilify) also show promise according to Gary Sachs M.D. of Harvard's Massachusetts General Hospital Bipolar Clinic and Research Program. (View the webcast above at the Bipolar Clinic and Research Program link). The atypical antipsychotics have some potential for causing weight gain and diabetes, and in larger doses over long periods may sometimes create tardive dyskinesia, though with much lesser probability than with the typical antipsychotics, such as Thorazine, Stelazine, or Haloperidol (Haldol.)
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New treatments
Modafinil (Provigil) and Pramipexole (Mirapex) show promise in treating the cognitive deterioration related to bipolar depression. In addition Riluzole, an ALS treatment, has been shown to be effective treatment. The breast cancer medicine tamoxifen has shown quick response to manic phases.[14]
Antidepressants
Depression is one of the major symptoms of bipolar disorder (indeed, in bipolar II it is frequently the dominant symptom) and so antidepressants are often used to treat the disorder. Antidepressants are typically administered along with a mood stabilizer rather than as the primary treatment for bipolar disorder. Antidepressants include seratonin reuptake inhibitors (SSRIs) such as Prozac and Paxil, the seratonin-norepinephrine reuptake inhibitor Effexor, and the dopamine reuptake inhibitor Wellbutrin. Older antidepressants include the monoamine oxidase inhibitors (MAOIs). The herbal supplement Saint John's Wort has also been shown to be an effective antidepressant in a number of clinical studies, although the precise mechanism of action remains unclear. The concurrent use of an antidepressant and a mood stabilizer, instead of monotherapy with a mood stabilizer, may lower the risk of further bipolar depression in patients whose most recent depressive episode has been resolved.[15] However, some studies have also found that antidepressants pose a risk of inducing hypomania or mania [16], sometimes in individuals with no prior history of mania. Saint John's Wort, although a naturally occurring compound, is thought to function in a fashion similar to man-made antidepressants, and so unsurprisingly, there are reports that suggest that it can also induce mania [17]. For these reasons, some psychiatrists are hesitant to prescribe antidepressants for the treatment bipolar disorder unless mood stabilizers have failed to have an effect, however, others feel that antidepressants still have an important role to play in treatment of bipolar disorder.
Dissociative anasthetics
One dosage of intravenous ketamine has been shown to produce "robust and rapid" relief of bipolar depression not alleviated by conventional treatments, often in less than one hour.[18]
Treatment of bipolar disorder Although medication and psychotherapy cannot cure the illness, therapy can often be valuable in helping to address the effects of disruptive manic or depressive episodes that have hurt a patient's career, relationships or self-esteem. Therapy is available not only from psychiatrists but from social workers, psychologists and other licensed counselors.
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Lifestyle Changes
Understanding One's Symptoms
Understanding the symptoms, when they occur and ways to control them using appropriate medications and psychotherapy has given many people diagnosed with bipolar disorder a chance at a better life. Technically this is called prodrome detection and this is partly what is meant by becoming an expert on one's illness.
Stress reduction
Forms of stress may include having too much to do, too much complexity and conflicting demands among others. There are also stresses that come from the absence of elements such as human contact, a sense of achievement, constructive creative outlets, and occasions or circumstances that will naturally elicit positive emotions. Stress reduction will involve reducing things that cause anxiety and increasing those that generate happiness. It is not enough to just reduce the anxiety.
Other Treatments
Omega-3 fatty acids
Omega-3 fatty acids may also be used as a treatment for bipolar disorder, particularly as a supplement to medication. An initial clinical trial by Stoll et al. produced positive results.[24] However, since 1999 attempts to confirm this finding of beneficial effects of omega-3 fatty acids in several larger double-blind clinical trials have produced inconclusive results. It was hypothesized that the therapeutic ingredient in omega-3 fatty acid preparations is eicosapentaenoic acid (EPA) and that supplements should be high in this compound to be beneficial.[25] Omega-3 fatty acids may be found in fish, fish oils, algae, and to a lesser degree in other foods such as flaxseed, flaxseed oil and walnuts. Although the benefits of Omega-3 fatty acids remain debated, they are readily available at drugstores and supermarkets, relatively inexpensive, and have no known side effects.
Exercise
Exercise has also been shown to have antidepressant effects. Its major advantages are that it appears to provide lasting improvement in mood, has no side effects, and is free.
Electroconvulsive therapy
Electroconvulsive therapy (ECT) is sometimes used to treat severe bipolar depression in cases where other treatments have failed. Although it has proved to be an effective treatment, ECT produces significant and long-lasting cognitive impairment, anterograde amnesia, and retrograde amnesia.[26]
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Ketogenic diet
A ketogenic diet similar to the diet used for pediatric epilepsy was thought to have mood stabilizing and antidepressant effects.[27] Stanford University Medical School attempted a study [28] using a ketogenic diet protocol on bipolar patients. However due to the lack of ability to attract subjects the trial was never started. Studies have shown it to have anti-depressant properties in rats.
Cannabinoids
While some reports indicate that cannabis can lessen the severity of mania and depression symptoms, others indicate cannabis can trigger mania and has been noted to have "a detrimental and potentially causative role in the development of psychosis."[29] However, a recent study noted neurocognitive functioning improved in bipolar patients who used cannabis.[30] The study added that further research was needed. Side effects Acute cannabis intoxication produces anterograde amnesia[31] , perceptual distortions[32] , and impairs the ability to safely operate a motor vehicle[33] .
References
[1] Sachs, G. et al. (2007). "Effectiveness of Adjunctive Antidepressant Treatment for Bipolar Depression" (http:/ / content. nejm. org/ cgi/ content/ abstract/ 356/ 17/ 1711). New England Journal of Medicine 356 (17): 171122. doi:10.1056/NEJMoa064135. PMID17392295. . (Abstract freely available; Subscription required for full text) [2] Fawcett, J., Golden, B., & Rosenfeld, N. (2000). New Hope for People with Bipolar Disorder. Roseville, CA: Prima Health. [3] Baldessarini RJ, Tondo L, Hennen J. (2003). "Lithium treatment and suicide risk in major affective disorders: update and new findings" (http:/ / www. psychiatrist. com/ privatepdf/ 2003/ v64s05/ v64s0506. pdf) (PDF). Journal of Clinical Psychiatry 64 (Suppl 5): 4452. PMID12720484. . (Subscription required) [4] Kessing, L. V.; Hellmund, G.; Geddes, J. R.; Goodwin, G. M.; Andersen, P. K. (2011). "Valproate v. Lithium in the treatment of bipolar disorder in clinical practice: Observational nationwide register-based cohort study". The British Journal of Psychiatry 199: 5763. doi:10.1192/bjp.bp.110.084822. PMID21593515. [5] Epilepsy Drug Lamictal Appears Effective For Bipolar Depression (http:/ / www. pslgroup. com/ dg/ eb8ea. htm) [6] Lamotrigine for Bipolar Disorder (http:/ / www. psycheducation. org/ depression/ meds/ lamotrigine. htm) PsychEducation.org [7] http:/ / www. medscape. com/ viewprogram/ 4509 [8] RH Belmaker, Yuly Bersudsky, Alex Mishory and Beersheva Mental Health Center (2005). "Valnoctamide in Mania" (http:/ / www. clinicaltrials. gov/ ct/ gui/ show/ NCT00140179?order=213). ClinicalTrials.gov. United States National Institutes of Health. . Retrieved 25 February 2006. [9] Belmaker, R. H. (July 29, 2004). "Bipolar Disorder" (http:/ / content. nejm. org/ cgi/ content/ full/ 351/ 5/ 476). The New England Journal of Medicine 351 (5): 476486. doi:10.1056/NEJMra035354. PMID15282355. . [10] Now Approved: ZYPREXA for maintenance therapy for bipolar disorder. (http:/ / www. zyprexa. com/ common_pages/ hcp_maintenance. jsp) Official Zyprexa Website. [11] Tohen, Mauricio; Waldemar Greil, Joseph R. Calabrese, Gary S. Sachs, Lakshmi N. Yatham, Bruno Mller Oerlinghausen, Athanasios Koukopoulos, Giovanni B. Cassano, Heinz Grunze, Rasmus W. Licht, Liliana DellOsso, Angela R. Evans, Richard Risser, Robert W. Baker, Heidi Crane, Martin R. Dossenbach and Charles L. Bowden (July 2005). "Olanzapine Versus Lithium in the Maintenance Treatment of Bipolar Disorder: A 12-Month, Randomized, Double-Blind, Controlled Clinical Trial" (http:/ / ajp. psychiatryonline. org/ cgi/ content/ full/ 162/ 7/ 1281). American Journal of Psychiatry 162 (7): 128190. doi:10.1176/appi.ajp.162.7.1281. PMID15994710. . [12] Long-term antidepressant efficacy and safety of olanzapine/fluoxetine combination: a 76-week open-label study (http:/ / www. biopsychiatry. com/ symbyax. htm) Biopsychiatry. [13] SEROQUEL XR (quetiapine fumarate) for Bipolar Disorder and Bipolar Depression (http:/ / www. seroquelxr. com/ seroquel-xr-bipolar-disorder. aspx) Official Seroquel XR Website. [14] Zarate CA Jr, Singh JB (2007). "Efficacy of a protein kinase C inhibitor (tamoxifen) in the treatment of acute mania: a pilot study.". Bipolar Disord. 9 (6): 56170. doi:10.1111/j.1399-5618.2007.00530.x. PMID17845270. [15] Impact of Antidepressant Discontinuation After Acute Bipolar Depression Remission on Rates of Depressive Relapse at 1-Year Follow-Up (http:/ / ajp. psychiatryonline. org/ article. aspx?articleID=176319) Am J Psychiatry 2003;160:1252-1262. [16] http:/ / www. ncbi. nlm. nih. gov/ pubmed/ 17960960 [17] http:/ / www. biologicalpsychiatryjournal. com/ article/ S0006-3223(99)00233-4/ abstract [18] A Randomized Add-on Trial of an N-methyl-D-aspartate Antagonist in Treatment-Resistant Bipolar Depression (http:/ / archpsyc. ama-assn. org/ cgi/ content/ full/ 67/ 8/ 793) Arch Gen Psychiatry. 2010;67(8):793-802.
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External links
International Society for Bipolar Disorders " Major advances in bipolar disorder (http://www.mja.com.au/public/issues/181_04_160804/mit10278_fm. html)", Medical Journal of Australia, 2004 " Bipolar Family Treatment Center (http://www.bpfamily.org)" Helping patients and families affected by Bipolar Mood Disorder, Associated with Beth Israel Medical Center in New York City
Carbamazepine
170
Carbamazepine
Carbamazepine
5H-dibenzo[b,f]azepine-5-carboxamide
Clinical data Trade names Tegretol
AHFS/Drugs.com monograph [1] MedlinePlus Pregnancy cat. Legal status Routes a682237 D(US) POM (UK) -only (US) Oral Pharmacokinetic data Bioavailability Protein binding Metabolism Half-life Excretion 80% 76% Hepaticby CYP3A4, to active epoxide form (carbamazepine-10,11 epoxide) 2565 hours (after several doses 12-17 hours) 23% excreted unchanged in urine Identifiers CAS number ATC code PubChem DrugBank ChemSpider 298-46-4
[3] [2]
85756-57-6
[4]
[5]
[6] [7]
Carbamazepine
[9]
171
UNII KEGG ChEBI ChEMBL
33CM23913M D00252
[10]
CHEBI:3387
[11]
CHEMBL108
[12]
& PubChem
[14]
[15]
Carbamazepine (CBZ) is an anticonvulsant and mood-stabilizing drug used primarily in the treatment of epilepsy and bipolar disorder, as well as trigeminal neuralgia. It is also used off-label for a variety of indications, including attention-deficit hyperactivity disorder (ADHD), schizophrenia, phantom limb syndrome, complex regional pain syndrome, paroxysmal extreme pain disorder, neuromyotonia, intermittent explosive disorder, borderline personality disorder and post-traumatic stress disorder. It has been seen as safe for pregnant women to use carbamazepine as a mood stabilizer,[16] but, like other anticonvulsants, intrauterine exposure is associated with spina bifida[17] and neurodevelopmental problems.[18]
Medical uses
Carbamazepine is typically used for the treatment of seizure disorders and neuropathic pain.[19] It may be used as a second line treatment for bipolar disorder and along with antipsychotic agents in schizophrenia.[19] In the United States, the FDA-approved indications are epilepsy (including partial seizures and tonic-clonic seizures), trigeminal neuralgia, and manic and mixed episodes of bipolar I disorder.[] Although data are still lacking, carbamazepine appears to be as effective and safe as lithium for the treatment of bipolar disorder, both in the acute and maintenance phase.[20]
Adverse effects
Common adverse effects may include drowsiness, headaches and migraines, motor coordination impairment, and/or upset stomach. Carbamazepine preparations typically greatly decrease a person's alcohol tolerance. Less common side-effects may include cardiac arrhythmias, blurry or double vision and/or the temporary loss of blood cells or platelets and in rare cases can cause aplastic anemia. With normal use, small reductions in white cell count and serum sodium are common; however, in rare cases, the loss of platelets may become life-threatening. In this case a doctor may recommend frequent blood tests during the first few months of use, followed by three to four tests per year for established patients. Additionally, carbamazepine may possibly exacerbate preexisting cases of hypothyroidism, so yearly thyroid function tests are advisable for persons taking the drug. There are also rare reports of an auditory side-effect for carbamazepine use, whereby patients perceive sounds about a semitone lower than previously.[21] [22] [23] Thus, middle C would be heard as the note B3 just below it, and so on. The inverse effect (that is, notes sounding higher) has also been recorded.[24] [25] This unusual side-effect is usually not noticed by most people, and quickly disappears after the person stops taking carbamazepine. Carbamazepine increases the risk of developing lupus by 88% (odds ratio of 1.88), with the effect possibly restricted to women.[26] Oxcarbazepine, a derivative of carbamazepine, reportedly has fewer and less serious side-effects.
Carbamazepine Carbamazepine may cause Syndrome of inappropriate antidiuretic hormone (SIADH), since it both increases the release and potentiates the action of ADH (vasopressin). Carbamazepine may aggravate juvenile myoclonic epilepsy, so it is important to uncover any history of jerking, especially in the morning, before starting the drug. It may also aggravate other types of generalized seizure disorder, particularly absence seizures.[27] In addition, carbamazepine has been linked to serious adverse cognitive anomalies, including EEG slowing[28] and apoptosis of cultured cerebellar neurons.[29] The FDA informed health care professionals that dangerous or even fatal skin reactions (StevensJohnson syndrome and toxic epidermal necrolysis), that can be caused by carbamazepine therapy, are significantly more common in patients with a particular human leukocyte antigen (HLA) allele, HLA-B*1502. This allele occurs almost exclusively in patients with ancestry across broad areas of Asia, including South Asian Indians.[30] In Europeans a large proportion of sensitivity is associated with HLA-B58.Researchers have also identified another genetic variant, HLA-A*3101 which has been shown to be a strong predictor of both mild and severe adverse reactions to carbamazepine among Japanese[31] and Europeans.[32]
172
Interactions
Carbamazepine has a potential for drug interactions; caution should be used in combining other medicines with it, including other antiepileptics and mood stabilizers.[33] Lower levels of carbamazepine are seen when administrated with phenobarbital, phenytoin (Dilantin), or primidone (Mysoline). Carbamazepine, as a CYP450 inducer, may increase clearance of many drugs, decreasing their blood levels.[34] Drugs that are more rapidly metabolized with carbamazepine include warfarin (Coumadin), phenytoin (Dilantin), theophylline, and valproic acid (Depakote, Depakote ER, Depakene, Depacon).[] Drugs that decrease the metabolism of carbamazepine or otherwise increase its levels include erythromycin,[35] cimetidine (Tagamet), propoxyphene (Darvon), and calcium channel blockers.[] Carbamazepine also increases the metabolism of the hormones in birth control pills and can reduce their effectiveness, potentially leading to unexpected pregnancies.[] Valproic acid and valnoctamide both inhibit microsomal epoxide hydrolase (mEH), the enzyme responsible for the breakdown of carbamazepine-10,11 epoxide into inactive metabolites.[36] By inhibiting mEH, valproic acid and valnoctamide cause a buildup of the active metabolite, prolonging the effects of carbamazepine and delaying its excretion. Grapefruit juice raises the bioavailability of carbamazepine by inhibiting CYP3A4 enzymes in the gut wall and in the liver.
Pharmacokinetics
Carbamazepine exhibits autoinduction: it induces the expression of the hepatic microsomal enzyme system CYP3A4, which metabolizes carbamazepine itself. Upon initiation of carbamazepine therapy, concentrations are predictable and follow their respective baseline clearance/half-life values that have been established for the specific patient. However, after enough carbamazepine has been presented to the liver tissue, the CYP3A4 activity increases, speeding up drug clearance and shortening the half-life. Autoinduction will continue with subsequent increases in dose but will usually reach a plateau within 57 days of a maintenance dose. Increases in dose at a rate of 200mg every 12 weeks may be required to achieve a stable seizure threshold. Stable carbamazepine concentrations occur usually within 23 weeks after initiation of therapy.[37]
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Mechanism of action
The mechanism of action of carbamazepine and its derivatives is relatively well understood. Voltage-gated sodium channels are the molecular pores that allow brain cells (neurons) to generate action potentials, the electrical events that allow neurons to communicate over long distances. After the sodium channels open to start the action potential, they inactivate, in essence closing the channel. Carbamazepine stabilizes the inactivated state of sodium channels, meaning that fewer of these channels are available to subsequently open, making brain cells less excitable (less likely to fire). Carbamazepine has also been shown to potentiate GABA receptors made up of alpha1, beta2, gamma2 subunits.[38]
History
Carbamazepine was discovered by chemist Walter Schindler at J.R. Geigy AG (now part of Novartis) in Basel, Switzerland, in 1953.[39] Schindler then synthesized the drug in 1960, before its anti-epileptic properties had been discovered. Carbamazepine was first marketed as a drug to treat trigeminal neuralgia (formerly known as tic douloureux) in 1962. It has been used as an anticonvulsant in the UK since 1965, and has been approved in the U.S. since 1974. In 1971, Drs. Takezaki and Hanaoka first used carbamazepine to control mania in patients refractory to antipsychotics (Lithium was not available in Japan at that time). Dr. Okuma, working independently, did the same thing with success. As they were also epileptologists, they had some familiarity with the anti-aggression effects of this drug. Carbamazepine would be studied for bipolar disorder throughout the 1970s.[40]
Brand names
Carbamazepine has been sold under the names Biston, Calepsin, Carbatrol, Epitol, Equetro, Finlepsin, Sirtal, Stazepine, Telesmin, Tegretol, Teril, Timonil, Trimonil, Epimaz, Carbama/Carbamaze (New Zealand), Amizepin (Poland),Carzine (Kolkata), Karbapin (Serbia), Hermolepsin (Sweden), Degranol (South Africa).,[41] and Tegretal (Chile, Germany).[42]
Chemistry
Carbamazepine
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References
[44] [45] [1] http:/ / www. drugs. com/ monograph/ carbamazepine. html [2] http:/ / www. nlm. nih. gov/ medlineplus/ druginfo/ meds/ a682237. html [3] http:/ / www. nlm. nih. gov/ cgi/ mesh/ 2009/ MB_cgi?term=298-46-4& rn=1 [4] http:/ / toolserver. org/ ~magnus/ cas. php?language=en& cas=85756-57-6& title= [5] http:/ / www. whocc. no/ atc_ddd_index/ ?code=N03AF01 [6] http:/ / pubchem. ncbi. nlm. nih. gov/ summary/ summary. cgi?cid=2554 [7] http:/ / www. drugbank. ca/ drugs/ DB00564 [8] http:/ / www. chemspider. com/ Chemical-Structure. 2457 [9] http:/ / fdasis. nlm. nih. gov/ srs/ srsdirect. jsp?regno=33CM23913M [10] http:/ / www. kegg. jp/ entry/ D00252 [11] https:/ / www. ebi. ac. uk/ chebi/ searchId. do?chebiId=CHEBI:3387 [12] https:/ / www. ebi. ac. uk/ chembldb/ index. php/ compound/ inspect/ CHEMBL108 [13] http:/ / www. emolecules. com/ cgi-bin/ search?t=ex& q=c1ccc2c%28c1%29C%3DCc3ccccc3N2C%28%3DO%29N [14] http:/ / pubchem. ncbi. nlm. nih. gov/ search/ ?smarts=c1ccc2c%28c1%29C%3DCc3ccccc3N2C%28%3DO%29N [15] http:/ / en. wikipedia. org/ wiki/ Special%3Acomparepages?rev1=451682337& page2=%3ACarbamazepine [16] Gelder, M., Mayou, R. and Geddes, J. 2005. Psychiatry. 3rd ed. New York: Oxford. pp250. [17] Jentink, J; Dolk, H, Loane, MA, Morris, JK, Wellesley, D, Garne, E, de Jong-van den Berg, L, EUROCAT Antiepileptic Study Working, Group (2010-12-02). "Intrauterine exposure to carbamazepine and specific congenital malformations: systematic review and case-control study". BMJ (Clinical research ed.) 341: c6581. doi:10.1136/bmj.c6581. PMC2996546. PMID21127116. [18] Cummings, C; Stewart, M, Stevenson, M, Morrow, J, Nelson, J (2011-03-17). "Neurodevelopment of children exposed in utero to lamotrigine, sodium valproate and carbamazepine". Archives of disease in childhood 96 (7): 6437. doi:10.1136/adc.2009.176990. PMID21415043. [19] "Carbamazepine" (http:/ / www. drugs. com/ monograph/ carbamazepine. html). The American Society of Health-System Pharmacists. . Retrieved 3 April 2011. [20] Ceron-Litvoc D, Soares BG, Geddes J, Litvoc J, de Lima MS (January 2009). "Comparison of carbamazepine and lithium in treatment of bipolar disorder: a systematic review of randomized controlled trials". Hum Psychopharmacol 24 (1): 1928. doi:10.1002/hup.990. PMID19053079. [21] Yoshikawa H, Abe T (March 2003). "Carbamazepine-induced abnormal pitch perception" (http:/ / linkinghub. elsevier. com/ retrieve/ pii/ S0387760402001559). Brain Dev. 25 (2): 1279. doi:10.1016/S0387-7604(02)00155-9. PMID12581810. . [22] Konno S, Yamazaki E, Kudoh M, Abe T, Tohgi H (September 2003). "Half pitch lower sound perception caused by carbamazepine" (http:/ / joi. jlc. jst. go. jp/ JST. Journalarchive/ internalmedicine1992/ 42. 880?from=PubMed). Intern. Med. 42 (9): 8803. doi:10.2169/internalmedicine.42.880. PMID14518681. . [23] Kashihara K, Imai K, Shiro Y, Shohmori T (September 1998). "Reversible pitch perception deficit due to carbamazepine" (http:/ / joi. jlc. jst. go. jp/ JST. Journalarchive/ internalmedicine1992/ 37. 774?from=PubMed). Intern. Med. 37 (9): 7745. doi:10.2169/internalmedicine.37.774. PMID9804087. . [24] Miyaoka T, Seno H, Itoga M, Horiguchi J (2000). "Reversible pitch perception deficit caused by carbamazepine" (http:/ / meta. wkhealth. com/ pt/ pt-core/ template-journal/ lwwgateway/ media/ landingpage. htm?issn=0362-5664& volume=23& issue=4& spage=219). Clin Neuropharmacol 23 (4): 21921. doi:10.1097/00002826-200007000-00010. PMID11020128. Archived (http:/ / www. webcitation. org/ 5uKvSxCd4) from the original on 2010-11-18. . [25] Wakamoto H, Kume A, Nakano N (June 2004). "Elevated pitch perception owing to carbamazepine-activating effect on the peripheral auditory system: auditory brainstem response study" (http:/ / jcn. sagepub. com/ cgi/ pmidlookup?view=long& pmid=15446396). J. Child Neurol. 19 (6): 4535. PMID15446396. Archived (http:/ / www. webcitation. org/ 5uKvULlsv) from the original on 2010-11-18. . [26] Schoonen, W. Marieke; Thomas, Sara L.; Somers, Emily C.; Smeeth, Liam; Kim, Joseph; Evans, Stephen; Hall, Andrew J. (2010). "Do selected drugs increase the risk of lupus? A matched case-control study". British Journal of Clinical Pharmacology 70 (4): 588596. doi:10.1111/j.1365-2125.2010.03733.x. PMC2950993. PMID20840450. [27] Lige Liu, Thomas Zheng, Margaret J. Morris, Charlott Wallengren, Alison L. Clarke, Christopher A. Reid, Steven Petrou and Terence J. O'Brien (2006). "The Mechanism of Carbamazepine Aggravation of Absence Seizures" (http:/ / jpet. aspetjournals. org/ content/ 319/ 2/ 790. abstract). JPET 319 (2): 790798. doi:10.1124/jpet.106.10496. PMID16895979. . [28] Salinsky MC, Binder LM, Oken BS, Storzbach D, Aron CR, Dodrill CB (2002). "Effects of gabapentin and carbamazepine on the EEG and cognition in healthy volunteers" (http:/ / www. blackwell-synergy. com/ doi/ full/ 10. 1046/ j. 1528-1157. 2002. 22501. x?cookieSet=1). Epilepsia 43 (5): 48290. doi:10.1046/j.1528-1157.2002.22501.x. PMID12027908. Archived (http:/ / www. webcitation. org/ 5uKvX3m5E) from the original on 2010-11-18. . [29] Gao XM, Margolis RL, Leeds P, Hough C, Post RM, Chuang DM (1995). "Carbamazepine induction of apoptosis in cultured cerebellar neurons: effects of N-methyl-D-aspartate, aurintricarboxylic acid and cycloheximide". Brain Res. 703 (12): 6371. doi:10.1016/0006-8993(95)01066-1. PMID8719616.
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[30] MedWatch (2007-12-12). "Carbamazepine" (http:/ / www. fda. gov/ medwatch/ safety/ 2007/ safety07. htm#carbamazepine). 2007 Safety Alerts for Drugs, Biologics, Medical Devices, and Dietary Supplements. FDA. Archived (http:/ / www. webcitation. org/ 5uKvY37EY) from the original on 2010-11-18. . [31] Ozeki T, Mushiroda T, Yowang A, Takahashi A, Kubo M, Shirakata Y, Ikezawa Z, Iijima M, Shiohara T, Hashimoto K, Kamatani N, Nakamura Y. (March 2011). "Genome-wide association study identifies HLA-A*3101 allele as a genetic risk factor for carbamazepine-induced cutaneous adverse drug reactions in Japanese population". Hum Mol Genet 20 (5): 10341041. doi:10.1093/hmg/ddq537. PMID21149285. [32] (http:/ / www. epilepsysociety. org. uk/ WhatWeDo/ News/ Reactiontodruglinkedtogeneticvariant), Epilepsy Society: genome-wide association study of Europeans with adverse reaction to carbamazepine. [33] Lexi-Comp (February 2009). "Carbamazepine" (http:/ / www. merck. com/ mmpe/ lexicomp/ carbamazepine. html). The Merck Manual Professional. Archived (http:/ / www. webcitation. org/ 5uKvOP99i) from the original on 2010-11-18. . Retrieved on May 3, 2009. [34] "eMedicine - Toxicity, Carbamazepine" (http:/ / www. emedicine. com/ emerg/ topic77. htm). Archived (http:/ / www. webcitation. org/ 5ZpbVBsOJ) from the original on 2008-08-04. . [35] Stafstrom CE, Nohria V, Loganbill H, Nahouraii R, Boustany RM, DeLong GR (January 1995). "Erythromycin-induced carbamazepine toxicity: a continuing problem" (http:/ / archpedi. ama-assn. org/ cgi/ pmidlookup?view=long& pmid=7827672). Arch Pediatr Adolesc Med 149 (1): 99101. PMID7827672. Archived (http:/ / www. webcitation. org/ 5uKvQB98w) from the original on 2010-11-18. . [36] Gonzalez, Frank J.; Robert H. Tukey (2006). "Drug Metabolism". In Laurence Brunton, John Lazo, Keith Parker (eds.). Goodman & Gilman's The Pharmacological Basis of Therapeutics (11th ed.). New York: McGraw-Hill. p.79. ISBN978-0-07-142280-2. [37] Bauer, Larry A. (2008). Applied Clinical Pharmacokinetics (2nd ed.). McGraw-Hill. ISBN978-0-8385-0388-1. [38] Granger, P. et al. Modulation of the gamma-aminobutyric acid type A receptor by the antiepileptic drugs carbamazepine and phenytoin. Mol. Pharmacol. 47, 11891196 (1995). [39] Schindler W, Hfliger F (1954). "ber Derivate des Iminodibenzyls". Helvetica Chimica Acta 37 (2): 47283.. doi:10.1002/hlca.19540370211. [40] Okuma T, Kishimoto A (February 1998). "A history of investigation on the mood stabilizing effect of carbamazepine in Japan". Psychiatry Clin. Neurosci. 52 (1): 312. doi:10.1111/j.1440-1819.1998.tb00966.x. PMID9682927. [41] Degranol Tablets (http:/ / www. intekom. com/ pharm/ lennon/ degranol. html) [42] http:/ / www. farmaciasahumada. cl/ fasaonline/ fasa/ MFT/ PRODUCTO/ P1163. HTM [43] http:/ / www. google. com/ patents?vid=2,948,718 [44] Hung SI, Chung WH, Chen YT et al. Common risk allele in aromatic antiepileptic-drug induced StevensJohnson syndrome and toxic epidermal necrolysis in Han Chinese. Pharmacogenomics.2010 Mar;11(3):349-56. [45] Carbamazepine-Induced Toxic Effects and HLA-B*1502 Screening in Taiwan, New England Journal of Medicine, March 2010. http:/ / www. nejm. org/ doi/ full/ 10. 1056/ NEJMoa1009717
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External links
Carbatrol website (http://www.carbatrol.com) Equetro website (http://www.equetro.com) Carbamazepine Pharmacokinetics - PubPK (http://www.pubpk.org/index.php?title=Carbamazepine) TA warning (http://www.rxlist.com/cgi/generic/carbam.htm) Carbamazepine overview (http://www.psycheducation.org/depression/meds/carbamazepine.htm) from PsychEducation.org Extensive review of the effects of carbamazepine in pregnancy and breastfeeding (http://www.medscape.com/ viewarticle/410736_4) (free full text with registration) U.S. Patent 2,948,718, August 1960 (http://patimg1.uspto.gov/.piw?Docid=02948718&homeurl=http://patft. uspto.gov/netacgi/nph-Parser?Sect1=PTO1%26Sect2=HITOFF%26d=PALL%26p=1%26u=/netahtml/ srchnum.htm%26r=1%26f=G%26l=50%26s1=2,948,718.WKU.%26OS=PN/2,948,718%26RS=PN/ 2,948,718&PageNum=&Rtype=&SectionNum=&idkey=2A0649DBED16)
Gabapentin
176
Gabapentin
Gabapentin
2-[1-(aminomethyl)cyclohexyl]acetic acid
Clinical data Licence data Pregnancy cat. Legal status Routes USFDA: link
[1]
B1(AU) C(US) POM (UK) -only (US) Prescription only Oral Pharmacokinetic data
Bioavailability
Protein binding Less than 3% Metabolism Half-life Excretion Not appreciably metabolized 5 to 7 hours Renal Identifiers CAS number ATC code PubChem DrugBank ChemSpider UNII KEGG ChEMBL 60142-96-3 N03 AX12 CID 3446
[2]
[3]
[4] [5]
APRD00015 3328
[6]
6CW7F3G59X D00332
[8]
[7]
CHEMBL940
[9]
Gabapentin
177
Mol. mass SMILES 171.237 g/mol eMolecules
[10]
& PubChem
[11]
[12]
Gabapentin (brand names Fanatrex, Gabarone, Gralise, Neurontin, Nupentin) is a pharmaceutical drug, specifically a GABA analogue. It was originally developed for the treatment of epilepsy, and currently is also used to relieve neuropathic pain. There are, however, concerns regarding the quality of the trials conducted.
Medical uses
Gabapentin is used primarily for the treatment of seizures, neuropathic pain, and hot flashes.[13] There are, however, concerns regarding the quality of the research on its use to treat migraines, bipolar disorders, and pain.[14]
Pain
Gabapentin provides significant pain relief in about a third of people who take it for fibromyalgia or chronic neuropathic pain.[15] It is also effective in reducing narcotic [16] usage post operatively and is helpful in neuropathic pain due to cancer.[17] It has not been shown to be useful for HIV associated sensory neuropathy.[18] When used for neuropathic pain it does not appear superior to carbamazepine.[19] Further evidence is needed to determine if it is effective for migraine prevention.[20] It appears to be equally effective as pregabalin and is of lower cost.[21] It does not appear to be of benefit in treating complex regional pain syndrome.[22]
A capsule of gabapentin
Seizures
Gabapentin is approved for treatment of focal seizures in a number of countries[23] and evidence supports it use for treating partial and mixed seizure disorders however there is insufficient evidence for it use in generalized epilepsy.[24] There is little data to support its initial use over older anticonvulsant medication for any type of seizure disorder.[25]
Other
There is some evidence of benefit in acquired pendular nystagmus and infantile nystagmus but not in periodic alternating nystagmus.[26] [27] Gabapentin may help with menopausal symptoms.[28] [29] It may be effective in reducing pain and spasticity in multiple sclerosis.[30] Gabapentin has been used to treat some symptoms of opiate withdrawal,[31] but tests for smoking cessation treatment have had mixed results.[32] [33]
Negative
Gabapentin has been prescribed in the mental health context. Numerous trials show that it is not effective as a mood-stabilizing treatment for bipolar disorder and so has no therapeutic advantage in having fewer side-effects over better established bipolar drugs such as lithium and valproic acid. Gabapentin has limited usefulness in the treatment of anxiety disorders such as social anxiety disorder and obsessive-compulsive disorder, in treatment-resistant depression, and for insomnia.[34] [35] Gabapentin can also cause weight gain.[36] A double blind, randomized controlled trial found gabapentin ineffective for the treatment of idiopathic subjective tinnitus.[37]
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Adverse effects
Gabapentin's most common side effects in adult patients include dizziness, drowsiness, and peripheral edema (swelling of extremities);[38] these mainly occur at higher doses in the elderly. Also, children 312 years of age were observed to be susceptible to mild-to-moderate mood swings, hostility, concentration problems, and hyperactivity. Although rare, there are several cases of hepatotoxicity reported in the literature.[39] [40] Gabapentin should be used carefully in patients with renal impairment due to possible accumulation and toxicity.[41] [42] An increase in formation of adenocarcinomas was observed in rats during preclinical trials; however, the clinical significance of these results remains undetermined. Gabapentin is also known to induce pancreatic acinar cell carcinomas in rats through an unknown mechanism, perhaps by stimulation of DNA synthesis; these tumors did not affect the lifespan of the rats and did not metastasize.[43]
Suicide
Gabapentin has been associated with an increased risk of suicidal acts or violent deaths.[44] In 2009, the FDA issued a warning of an increased risk of depression and suicidal thoughts and behaviors in patients taking gabapentin, along with other anticonvulsant drugs[45] modifying the packaging insert to reflect this.[38] In July 2009, the manufacturer of gabapentin (Pfizer) went to trial regarding the association between gabapentin and the increased risk of suicide.[46]
Withdrawal
Gabapentin should not be discontinued abruptly after long term use. Abrupt or over rapid withdrawal may provoke a withdrawal syndrome reminiscent to alcohol or benzodiazepine withdrawal.[47] [48] Gradual reduction over a period of weeks or months helps minimize or prevents the withdrawal syndrome.[47] Side effects upon discontinuation of gabapentin that have been reported in medical literature include insomnia, restlessness, agitation, anxiety, disorientation, confusion, light sensitivity, diaphoresis, headaches, palpitations, hypertension, chest pain, and flu-like symptoms.[47] [49] [50] [51] In at least one case, abrupt cessation of a high dose of gabapentin triggered a seizure in an individual with no history of epilepsy.[50]
Overdosage
Persons who accidentally or intentionally ingested overdoses have manifested drowsiness, blurred vision, slurred speech and somnolence or coma. Serum gabapentin concentrations may be measured to confirm diagnosis.[36] [52]
Pharmacology
Gabapentin was initially synthesized to mimic the chemical structure of the neurotransmitter gamma-aminobutyric acid (GABA), but is not believed to act on the same brain receptors. One possible mechanism of action, reported by Ben Barres of Stanford University and colleagues in Cell in 2009, was that gabapentin halts the formation of new synapses.[53] Gabapentin binds to the 2 subunit (1 and 2) and has been found to reduce calcium currents after chronic but not acute application via an effect on trafficking[54] of voltage-dependent calcium channels in the central nervous system.[55] This effect on calcium channel trafficking is another possible mechanism of action of gabapentin, but the exact mechanism remains in dispute.
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Related drugs
Parke-Davis developed a drug called pregabalin to be a successor of gabapentin.[56] Pregabalin was brought to market by Pfizer as Lyrica after the company acquired Warner-Lambert. Pregabalin is related in structure to gabapentin and is approved for treatment of epilepsy, neuropathic pain associated with diabetes, fibromyalgia, post-herpetic neuralgia, and generalized anxiety disorder. Compared to gabapentin, pregabalin is more potent, absorbs faster and has greater bioavailability. Higher potency means that less of the medication is required for the same effect. This does not necessarily result in fewer side effects.[57] [58] Another new drug atagabalin has been trialled by Pfizer as a treatment for insomnia.[59] One must remain skeptical of industry run trials[60] as, despite significant monetary damages awarded in trials discussed below, there is no certainty the company is not still suppressing negative or equivocal data and news reports indicate this may be the case with pregabalin as well.[61]
FDA approval
Gabapentin was originally approved by the U.S. Food and Drug Administration (FDA) in 1994 for use as an adjunctive medication to control partial seizures (effective when added to other antiseizure drugs). In 2002, an indication was added for treating postherpetic neuralgia (neuropathic pain following shingles).[65]
Legal action
Numerous cases have been brought against the makers of Neurontin, with convictions arising not only for the illegal promotion of off-label uses. Much of the popular use of Neurontin among physicians stems from the widespread illicit marketing that Pfizer was convicted of, which was communicated via promotional messages through advisory boards, consultants meetings, and accredited continuing medical education events posing as independent third-party organizations, co-opting opinion leaders, educational enterprises and academia in their marketing campaign.[66] The convictions for fraud set a new standard that goes beyond scientific misconduct and elevates the seriousness of the suppression of negative or unsupportive evidence as a form of fraud. As part of a case (CIVIL ACTION NO. 04-cv-10739-PBS) brought by Kaiser Foundation Health Plan against Pfizer, it was noted that "The general neuropathic pain indication cannot be granted for Neurontin based on the clinical trials in painful diabetic peripheral neuropathy (DPN) and postherpetic neuralgia (PHN)."[67] While it is often prescribed off-label (that is, at the discretion of a physician) for various conditions, this use is probably frequently due to the widespread illicit marketing Pfizer was convicted of, which was communicated via promotional messages through advisory boards, consultants meetings, and accredited continuing medical education events posing as independent third-party organizations, co-opting opinion leaders, educational enterprises and academia in their marketing campaign.[66]
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Recreational use
Although gabapentin is not a controlled substance, it does produce psychoactive effects that cause it to have potential for recreational use. Even in low doses, gabapentin causes sensations of reduced acute pain, reduced anxiety and even a tendency to become overly social and talkative. Larger doses can cause the user to become numb and even fully insensate. Tolerance to gabapentin occurs extremely rapidly with recreational use, with the user often needing to double the dosage within a day or two of misuse. Although it is widely regarded as having little or no potential for misuse, it is often a misused drug in Canadian Northern communities and among inmates in California State prisons. However, Pregabalin, a subsequent Pfizer spin-off, is a controlled substance under Schedule V of the United States'
Gabapentin Controlled Substances Act. Staggering Because of perceived low bioavaliablity, a commonly reported method of Gabapentin usage is "staggering", as reported on drug-experience sharing websites such as Bluelight and Erowid[77] 1. Staggering involves taking more than the prescribed daily amount of drug, often over an interval of half hours or longer. The method sometimes include food with the repeated dosings. Users have reported mixed feelings; ranging from euphoria to nausea and chest tension.[78] . Gastrointestinal side effects of very high doses of gabapentin are extremely common. Profuse diarrea is common with doses of gabapentin exceeding 4800mg at a time, or perhaps more over the course of a day. It is likely that the large quantities of binders and fillers in gabapentin tablets cause diarrea, although the sheer volume of the alkaloid itself needed to produce recreational effects may irritate the GI tract causing the diarreah. The effects of staggering are intended to maximize the saturation along its main transporter. Because Gabapentin's mechanism for action remains relatively unknown, especially because additional research is needed into its effects on bipolar and psychological disorders, the tendency of users to experiment and self-regulate the acceptable levels of gabapentin in them should be considered when examining its adverse effects[79] . It is actively absorbed via the L amino acid transporter system[80] . Because it is a non-plasma-bound renally excreted drug, it is entirely eliminated by the kidneys[81] . Other methods of recreational Gabapentin abuse are chewing the time-released pills into a powder that can be absorbed through swallowing or absorption into the lining of the mouth. Snorting a powdery residue of chopped-up Gabapentin is reported as well, although highly ill-advised[82] . Such abuse led to the removal of gabapentin in certain California correctional facilities [83] ,[84] . Neurocognitive Effects with Other Interactions Alcohol Dependence While symptoms of abrupt gabapentin withdrawal are many-fold, a study has combined gabapentin and flumazenil, a benzodiapazine antagonist, in order to measure cognitive performance on individual's in the beginning stages of alcohol withdrawal. The research impetus came from the GABA and glutamate signaling that occurs during alcohol withdrawal. The study observed for improvement of response inhibitions between subjects that had received treatment versus a group receiving a placebo; over 60 alcohol-dependent participants were evaluated. The results were moderate; the gabapentin and flumazenil treatment slightly improved response inhibition task during the early phases of abstinence, and this corresponds to many self-testimonials. However the quality of the overall impact was mixed and the medication cannot be said to improve alcoholic relapse; however it has the potential to subdue early withdrawal discomforts when combined with the benzodiapazine receptor antagonist[85] . Cocaine Frequently mentioned online in drug-experience sharing websites, Gabapentin has been considered for reducing cocaine use or assisting in cocaine withdrawal because of its GABAergic feedback properties. One study chose nine individuals with cocaine withdrawal symptoms from a clincial setting. Gabapentin presence was tested over a 24-week trial; the study concluded that Gabapentin may be a useful medicine for reducing cocaine usage in addicted patients, especially during the early weeks of any attempt to come clean[86] .
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Gabapentin
182
Veterinary use
Gabapentin is also used for some animal treatments, but formulations (especially liquid forms) for human use may contain the sweetener Xylitol which is toxic to dogs, so care must be taken if the human version is used for veterinary purposes.
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Gabapentin
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[55] Davies, A; Hendrich, J; Van Minh, AT; Wratten, J; Douglas, L; Dolphin, AC (May 2007). "Functional biology of the alpha(2)delta subunits of voltage-gated calcium channels". Trends Pharmacol Sci 28 (5): 2208. doi:10.1016/j.tips.2007.03.005. PMID17403543. [56] Baillie, JK; Power, I (January 2006). "The mechanism of action of gabapentin in neuropathic pain". Curr Opin Investig Drugs 7 (1): 339. ISSN1472-4472. PMID16425669. [57] David F. McAuley, Pharm.D. How does pregabalin compare to gabapentin in the treatment of neuropathic pain? (http:/ / www. globalrph. com/ pregabalin. htm) GlobalRPh Inc. [58] Jensen B, Regier LD, editors. RxFiles : Drug comparison charts. 7th ed. Saskatoon, SK: RxFiles, 2010; p.78 [59] Kjellsson MC, Ouellet D, Corrigan B, Karlsson MO (June 2011). "Modeling Sleep Data for a New Drug in Development using Markov Mixed-Effects Models". Pharmaceutical Research. doi:10.1007/s11095-011-0490-x. PMID21681607. [60] Sotelo J. 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[65] Pfizer: Product Monograph Neurontin (http:/ / www. pfizer. com/ pfizer/ download/ uspi_neurontin. pdf)PDF(251KB) Retrieved 14 August 2006 [66] Steinman, MA; Bero LA, Chren MM, Landefeld CS. (2006-08-15). "Narrative review: the promotion of gabapentin: an analysis of internal industry documents.". Ann Intern Med. 145 (4): 284293.. PMID16908919. [67] [lieffcabraser.com/media/pnc/0/media.750.pdf Saris Decision]. lieffcabraser.com/media/pnc/0/media.750.pdf. [68] Pande, AC; Crockatt JG, Janney CA, Werth JL, Tsaroucha G. (2000). "Gabapentin in bipolar disorder: a placebo-controlled trial of adjunctive therapy" (Abstract). Bipolar Disorders 2 (3 Pt 2): 24955. doi:10.1034/j.1399-5618.2000.20305.x. PMID11249802. [69] http:/ / www. accessdata. fda. gov/ scripts/ cder/ drugsatfda/ index. cfm?fuseaction=Search. Label_ApprovalHistory [70] Baldessarini, Ross J.; Leahy L, Arcona S, Gause D, Zhang W, Hennen J. (2007). 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Journal of Clinical Psychiatry 2004 Jan;65(1):84-6 ( http:/ / www. ncbi. nlm. nih. gov/ pubmed/ 14744174 )
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185
External links
Gabapentin information from MedlinePlus (http://www.nlm.nih.gov/medlineplus/druginfo/meds/a694007. html) Gabapentin (http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0000940/) PubMed Health. National Center for Biotechnology Information (NCBI) News Article regarding Neurontin settlement and off-label marketing/use (http://www.legalnewswatch.com/ news_351.html) Website for the pending Class Action Lawsuit against Pfizer (http://www.adrugrecall.com/neurontin/ class-action.html) U.S. FDA information on safety of antiepileptics (http://www.fda.gov/Drugs/DrugSafety/ PostmarketDrugSafetyInformationforPatientsandProviders/ucm100190.htm) Bloomberg News on Neurontin lawsuit (http://www.bloomberg.com/apps/news?pid=20601127& sid=a1CYnBA5tGV4) U.S. National Library of Medicine: Drug Information Portal - Gabapentin (http://druginfo.nlm.nih.gov/ drugportal/dpdirect.jsp?name=Gabapentin) Erowid Gabapentin Vault (http://www.erowid.org/pharms/gabapentin/gabapentin.shtml)
Lamotrigine
186
Lamotrigine
Lamotrigine
6-(2,3-dichlorophenyl)-1,2,4-triazine-3,5-diamine
Clinical data Trade names Lamictal
AHFS/Drugs.com monograph [1] MedlinePlus Pregnancy cat. Legal status Routes a695007 C(US) POM (UK) -only (US) Oral Pharmacokinetic data Bioavailability Protein binding Metabolism Half-life Excretion 98% 55% Hepatic (mostly UGT1A4-mediated) 2434 hours (healthy adults) Renal Identifiers CAS number ATC code PubChem DrugBank ChemSpider UNII KEGG 84057-84-1 N03 AX09 CID 3878 DB00555 3741
[7] [8] [3] [2]
[4]
[5] [6]
U3H27498KS D00354
[9]
Lamotrigine
[10]
187
ChEBI ChEMBL
CHEBI:6367
CHEMBL741
[11]
Chemical data Formula Mol. mass SMILES C9H7Cl2N5 256.091 g/mol eMolecules
[12]
& PubChem
[14]
[13]
Lamotrigine, marketed in the US and most of Europe as Lamictal ( /lmktl/) by GlaxoSmithKline, is an anticonvulsant drug used in the treatment of epilepsy and bipolar disorder. It is also used as an adjunct in treating depression, though this is considered off-label usage. For epilepsy, it is used to treat partial seizures, primary and secondary tonic-clonic seizures, and seizures associated with Lennox-Gastaut syndrome. Like many other anticonvulsant medications, Lamotrigine also seems to act as an effective mood stabilizer, and in fact has been the only U.S. Food and Drug Administration (FDA)-approved drug for this purpose since lithium, a drug approved almost 30 years earlier. It is approved for the maintenance treatment of bipolar type I. Chemically unrelated to other anticonvulsants (due to lamotrigine's being a phenyltriazine), lamotrigine has many possible side-effects. Lamotrigine is generally accepted to be a member of the sodium channel blocking class of antiepileptic drugs,[15] but it could have additional actions inasmuch as it has a broader spectrum of action than other sodium channel antiepileptic drugs such as phenytoin and carbamazepine and is effective in the treatment of the depressed phase of bipolar disorder, whereas other sodium channel blocking antiepileptic drugs are not. In addition, lamotrigine shares few side-effects with other, unrelated anticonvulsants known to inhibit sodium channels, which further emphasizes its unique properties.[16] Lamotrigine is inactivated by hepatic glucuronidation.
Medical uses
Epilepsy and seizures
Lamotrigine is approved in the US for the treatment of partial seizures.[17] Lamotrigine is one of a small number of FDA-approved therapies for seizures associated with Lennox-Gastaut syndrome, a severe form of epilepsy. Typically developing before four years of age, LGS is associated with developmental delays. There is no cure, treatment is often complicated, and complete recovery is rare. Symptoms include the atonic seizure (also known as a "drop attack"), during which brief loss of muscle tone and consciousness cause abrupt falls. Lamotrigine significantly reduces the frequency of LGS seizures, and is one of two medications known to decrease the severity of drop attacks.[18] Combination with valproate is common, but this increases the risk of lamotrigine-induced rash, and necessitates reduced dosing due to the interaction of these drugs.[19]
Bipolar disorder
While traditional anticonvulsant drugs are predominantly antimanics, the best evidence for lamotrigines effectiveness is in the prophylaxis of bipolar depression. As a consequence, it is approved in the US for maintenance treatment of Bipolar I disorder.[20] The drug seems ineffective in the maintenance of rapid cycling bipolar disorder.[21] According to studies in 2007, Lamotrigine may treat bipolar depression without triggering mania, hypomania, mixed states, or rapid-cycling.[22] The evidence for lamotrigines effectiveness in treating a preexisting mood episode is weaker. It has not demonstrated efficacy in the treatment of acute mania[23] and there is controversy regarding the drugs effectiveness in treating acute bipolar depression. The 2002 American Psychiatric Association (APA) guidelines recommend
Lamotrigine lamotrigine as a first-line treatment for acute depression in Bipolar II disorder.[24] In light of the guidelines being more than five years old, the APAs website notes that the guidelines can no longer be assumed to be current."[25] A paper written in 2008 by Nasser et al. reviewed evidence from trials that were unpublished and not referenced in the 2002 APA guidelines and concludes that lamotrigine has very limited, if any, efficacy in the treatment of acute bipolar depression.[21] A 2008 paper by Calabrese et al. examined much of the same data and found that in four out of five placebo controlled studies, lamotrigine was ineffective in treating acute bipolar depression.[26] However, in a meta-analysis of the studies conducted in 2008, Calabrese found that patients who suffered from severe depression (as opposed to mild to moderate) did benefit in the use of lamotrigine vs. a placebo.[27] At doses considered sub-therapeutic, lamotrigine is thought to have a mild anti-depressant effect, leading some to question its safety for use in bipolar disorder, as partial remediation of cyclically depressed individuals (especially teens and young adults) has an elevated correlation to suicide until remission attains therapeutically acceptable levels.
188
Other uses
Off-label uses include the treatment of peripheral neuropathy, trigeminal neuralgia, cluster headaches, migraines, and reducing neuropathic pain. [28] [29] [30] Off-label psychiatric usage includes the treatment of depersonalization disorder, bipolar II disorder and other bipolar disorders, schizoaffective disorder, borderline personality disorder and post-traumatic stress disorder. Lamotrigine has been studied as an adjunctive therapy for treatment of refractory unipolar depression, attaining efficacy on the secondary metric for treatment outcomes (Clinical Global Impressions), but not the primary metrics (Montgomery-sberg Depression Rating Scale and Hamilton Rating Scale for Depression).[31]
Mechanism of action
Lamotrigine is a member of the sodium channel blocking class of antiepileptic drugs.[32] Early studies of lamotrigine's mechanism of action examined its effects on the release of endogenous amino acids from rat cerebral cortex slices in vitro. As is the case for antiepileptic drugs that act on voltage-dependent sodium channels, lamotrigine inhibited the release of glutamate and aspartate evoked by the sodium-channel activator veratrine and was less effective in the inhibition of acetylcholine or GABA release. At high concentrations, it Lamotrigine, 150mg tablet. had no effect on spontaneous or potassium evoked amino acid release. These studies suggested that lamotrigine acts presynaptically on voltage-gated sodium channels to decrease glutamate release. Several electrophysiological studies have investigated the effects of lamotrigine on voltage-dependent sodium channels. For example, lamotrigine blocked sustained repetitive firing in cultured mouse spinal cord neurons in a concentration-dependent manner at concentrations therapeutic in the treatment of human seizures. In cultured hippocampal neurons, lamotrigine reduced sodium currents in a voltage-dependent manner, and at depolarized potentials showed a small frequency-dependent inhibition. These and a variety of other results indicate that the antiepileptic effect of lamotrigine, like that of phenytoin and carbamazepine, is at least in part due to use- and voltage-dependent modulation of fast voltage-dependent sodium currents. However, lamotrigine has a broader clinical spectrum of activity than phenytoin and carbamazepine and is recognized to be protective against generalized absence epilepsy and other generalized epilepsy syndromes, including primary generalized tonicclonic seizures, juvenile myoclonic epilepsy, and Lennox-Gastaut syndrome. The basis for the broader spectrum of activity of lamotrigine is unknown, but could relate
Lamotrigine to actions of the drug on voltage-activated calcium channels. Lamotrigine blocks T-type calcium channels weakly, if at all. However, it does inhibit native and recombinant high-voltageactivated calcium channels (N- and P/Q/R-types) at therapeutic concentrations. Whether this activity on calcium channels accounts for lamotrigine's broader clinical spectrum of activity in comparison with phenytoin and carbamazepine remains to be determined.
189
Pharmacokinetics
The pharmacokinetics of lamotrigine follow first-order kinetics, with a half-life of 13.5 hours and volume of distribution of 1.36l/kg.[33] Lamotrigine has fewer drug interactions than many anticonvulsant drugs, although pharmacokinetic interactions with carbamazepine, phenytoin and other hepatic enzyme inducing medications may shorten half-life. Dose adjustments should be made on clinical response, but monitoring may be of benefit in assessing compliance.
Dosage
Lamotrigine must be dose titrated carefully. Different doctors will proscribe different titration policies based on their experience and the specific condition of the patient. For this reason the titration information must be viewed purely as an example -and never to be adopted directly. Any proposal to take Lamotrogine must be discussed with a suitably qualified doctor, and their prescriptions followed -and any warning signs -such as a rash- responded to immediately. The normal starting dose is 25mg a day week 1-2, which may be increased 50mg a day a week 2-3, 100mg week 5 and 200mg week 6.[34] If the patient also takes valproate the dosage should be halved; if taken with carbamazepine the dosage needs to be doubled since they both interfere with lamotrigine's metabolism. The normal maintenance dose for bipolar depression is 200mg, but some patients may require up to 600mg a day. Some patients who cannot tolerate 200mg have to take a lower dose. In clinical trials doses up to 400mg for bipolar disorder and 500mg but it's common that higher doses are prescribed. Too high starting doses and fast dose increase increases the risk of developing serious rashes and in worst case StevensJohnson syndrome Pediatric patients have a higher risk of developing rashes and bad skin reactions.[35] The consensus is that the dose titration should be taken slow in small steps. Many patients develop benign rashes when starting treatment but the patient doesn't have to stop take lamotrigine if the same dose is withheld for some time the rash usually goes away and then the dose can be increased again. If a patient has stopped taking lamotrigine for a period of more than 5 times the half life of its metabolism (approximately two-and-a-half days), the dose titration has to start over again from zero.[36] As stopping any anti-epilepsy drug may trigger seizures, this implies that stopping taking lamotrogine is a serious action. Reducing dosage of the drug must also be performed after consultation with a suitably qualified doctor -and their prescriptions strictly followed.
Side-effects
Lamotrigine prescribing information has a black box warning about life-threatening skin reactions, including StevensJohnson syndrome, DRESS syndrome and toxic epidermal necrolysis.[37] The manufacturer states that nearly all cases appear in the first 2 to 8 weeks of therapy and if medication is suddenly stopped then resumed at the normal dosage. Patients should seek medical attention for any unexpected skin rash, as its presence is an indication of a possible serious or even deadly side-effect of the drug. Not all rashes that occur while taking lamotrigine progress to SJS or TEN. Between 5 to 10% of patients will develop a rash, but only one in a thousand patients will develop a serious rash. It is thought that one in 50,000 exposed patients may die from the rash. As of December 2010, lamotrigine carries an FDA black box warning for aseptic meningitis.[38]
Lamotrigine Side-effects include loss of balance or coordination, double vision, crossed eyes, blurred vision, dizziness and lack of coordination, drowsiness, insomnia, anxiety, vivid dreams or nightmares, dry mouth, mouth ulcers, memory and cognitive problems, mood changes, runny nose, cough, nausea, indigestion, abdominal pain, weight loss, missed or painful menstrual periods, and vaginitis. The side-effect profile is different for different patient populations.[38] Side-effects such as rash, fever, and fatigue are very serious, as they may indicate incipient StevensJohnson syndrome, toxic epidermal necrolysis, DRESS syndrome or aseptic meningitis.[38] In rare cases, lamotrigine has been known to cause the dangerous drug eruptions DRESS syndrome, StevensJohnson syndrome (SJS) and toxic epidermal necrolysis (TEN). The rash is more common in children, so this medication is often reserved for adults. There is also an increased incidence of these eruptions in patients who are currently on, or recently discontinued a valproate-type anticonvulsant drug, as these medications interact in such a way that the clearance of both is decreased and the effective dose of lamotrigine is increased. The rash often appears in the first month of treatment and is even more likely to appear if dosage is started too high, but it can appear at any time and at any dosage. Lamotrigine has been associated with a decrease in white blood cell count (leucopenia).[39] Lamotrigine does not prolong QT/QTc in TQT studies in healthy subjects [40]
190
Effects in women
In clinical trials women were more likely than men to have side-effects. This is the opposite of most other anticonvulsants and antipsychotics. There is evidence showing interactions between lamotrigine and female hormones, which can be of particular concern for women on estrogen-containing hormonal contraceptives. Ethinyl estradiol, the ingredient of such contraceptives, has been shown to decrease serum levels of lamotrigine.[41] Women starting an estrogen-containing oral contraceptive may need to increase the dosage of lamotrigine to maintain its level of efficacy. Likewise, women may experience an increase in lamotrigine side-effects upon discontinuation of the pill. This may include the "pill free" week where lamotrigine serum levels have been shown to increase twofold.[37] Another study showed a significant increase in follicle stimulating hormone (FSH) and luteinizing hormone (LH) in women taking lamotrigine with oral contraceptive compared to women taking oral contraceptives alone.[42] However, these increases were not in conjunction with increased progesterone, indicating that oral contraceptives maintained suppression of ovulation.[42]
Lamotrigine
191
History
December 1994 Lamotrigine was approved for the treatment of partial seizures.[17] August 1998 for use as adjunctive treatment of Lennox-Gastaut syndrome in pediatric and adult patients, new dosage form: chewable dispersible tablets. December 1998 for use as monotherapy for treatment of partial seizures in adult patients when converting from a single enzyme-inducing anti-epileptic drug (EIAED). January 2003 for use as adjunctive therapy for partial seizures in pediatric patients as young as 2 years of age. June 2003 Lamotrigine approved for maintenance treatment of Bipolar I disorder; the first since lithium.[20] January 2004 for use as monotherapy for treatment of partial seizures in adult patients when converting from the anti-epileptic drug valproate (including valproic acid (Depakene); sodium valproate (Epilim) and divalproex sodium (Depakote)).
Availability
GlaxoSmithKline's trademarked brand of lamotrigine, Lamictal, is manufactured in scored tablets (25mg, 50mg, 100mg, 150mg and 200mg) and chewable dispersible tablets (2mg, 5mg and 25mg). Five-week sample kits are also available; these include titration instructions and scored tablets (25mg for patients taking valproate, 25mg and 100mg for patients not taking valproate). Lamotrigine is also available in un-scored tablet form. In 2005, Teva Pharmaceutical Industries Ltd. began selling generic lamotrigine in the United States, but only in 5mg and 25mg chewable dispersible tablets.[55] On 23 July 2008 Teva began
Lamotrigine offering the full line of generic lamotrigine in the US.[56] Lamotrigine is also available in generic form[57] in the United States, the United Kingdom, Canada and Australia. It should be noted that brand name Lamictal is not available in 200mg tablets in Canada, at all registered pharmacies (while 25, 100, and 150mg are all offered). Starter kits are also not available in Canada. GlaxoSmithKline has also recently received FDA Approval for an extended-release version of lamotrigine called Lamictal XR.[58] Lamotrigine is marketed as Lamictin in South Africa, ( 'Lamogine)[59] in Israel, and in South Korea and generally named as Lamitor.
192
Chemistry
References
[1] http:/ / www. drugs. com/ monograph/ lamotrigine. html [2] http:/ / www. nlm. nih. gov/ medlineplus/ druginfo/ meds/ a695007. html [3] http:/ / www. nlm. nih. gov/ cgi/ mesh/ 2009/ MB_cgi?term=84057-84-1& rn=1 [4] http:/ / www. whocc. no/ atc_ddd_index/ ?code=N03AX09 [5] http:/ / pubchem. ncbi. nlm. nih. gov/ summary/ summary. cgi?cid=3878 [6] http:/ / www. drugbank. ca/ drugs/ DB00555 [7] http:/ / www. chemspider. com/ Chemical-Structure. 3741 [8] http:/ / fdasis. nlm. nih. gov/ srs/ srsdirect. jsp?regno=U3H27498KS [9] http:/ / www. kegg. jp/ entry/ D00354 [10] https:/ / www. ebi. ac. uk/ chebi/ searchId. do?chebiId=CHEBI:6367 [11] https:/ / www. ebi. ac. uk/ chembldb/ index. php/ compound/ inspect/ CHEMBL741 [12] http:/ / www. emolecules. com/ cgi-bin/ search?t=ex& q=Clc2c%28Cl%29c%28c1nnc%28nc1N%29N%29ccc2 [13] http:/ / pubchem. ncbi. nlm. nih. gov/ search/ ?smarts=Clc2c%28Cl%29c%28c1nnc%28nc1N%29N%29ccc2 [14] http:/ / en. wikipedia. org/ wiki/ Special%3Acomparepages?rev1=420280917& page2=%3ALamotrigine [15] Rogawski MA, Lscher W (Jul 2004). "The neurobiology of antiepileptic drugs". Nat Rev Neurosci 5 (7): 553564. doi:10.1038/nrn1430. PMID15208697. [16] Lees G, Leach MJ (May 1993). "Studies on the mechanism of action of the novel anticonvulsant lamotrigine (Lamictal) using primary neurological cultures from rat cortex". Brain Research 612 (1-2): 1909. doi:10.1016/0006-8993(93)91660-K. PMID7687190. [17] anonymous (19 March 2004). "EFFICACY SUPPLEMENTS APPROVED IN CALENDAR YEAR 2003" (http:/ / www. fda. gov/ cder/ rdmt/ ESCY03AP. HTM). FDA/Center for Drug Evaluation and Research. . Retrieved 2008-04-09. [18] French JA, Kanner AM, Bautista J, et al. (April 2004). "Efficacy and tolerability of the new antiepileptic drugs II: treatment of refractory epilepsy: report of the Therapeutics and Technology Assessment Subcommittee and Quality Standards Subcommittee of the American Academy of Neurology and the American Epilepsy Society" (http:/ / www. neurology. org/ cgi/ content/ full/ 62/ 8/ 1261). Neurology 62 (8): 126173. doi:10.1212/01.WNL.0000123695.22623.32. PMID15111660. .
Lamotrigine
[19] Pellock JM (November 1999). "Managing pediatric epilepsy syndromes with new antiepileptic drugs" (http:/ / pediatrics. aappublications. org/ cgi/ content/ full/ 104/ 5/ 1106). Pediatrics 104 (5 Pt 1): 110616. doi:10.1542/peds.104.5.1106. PMID10545555. . [20] GlaxoSmithKline, 2003 [21] Ghaemi, S.N., Shirzadi, A.A., Filkowski, M. (2008). "Publication Bias and the Pharmaceutical Industry: The Case of Lamotrigine in Bipolar Disorder". Medscape J Med 10 (9): 211. PMC2580079. PMID19008973. [22] Goldberg JF, Calabrese JR, Saville BR, Frye MA, Ketter TA, Suppes T, Post RM, Goodwin FK. (2009). "Mood stabilization and destabilization during acute and continuation phase treatment for bipolar I disorder with lamotrigine or placebo.". Clinical Psychiatry 70 (9): 127380. doi:10.4088/JCP.08m04381. PMID19689918. [23] Goldsmith DR, Wagstaff AJ, Ibbotson T, Perry CM (2003). "Lamotrigine: a review of its use in bipolar disorder". Drugs 63 (19): 202950. PMID12962521. [24] "Acute Treatment Formula and Implementation of a Treatment Plan" (http:/ / www. psychiatryonline. com/ content. aspx?aID=50136). Practice Guideline for the Treatment of Patients With Bipolar Disorder Second Edition. American Psychiatric Association. . Retrieved 15 August 2010. [25] "Main page" (http:/ / www. psychiatryonline. com/ pracGuide/ pracGuideTopic_8. aspx). Practice Guideline for the Treatment of Patients With Bipolar Disorder Second Edition. American Psychiatric Association. . Retrieved 15 August 2010. [26] Calabrese JR, Huffman RF, White RL, Edwards S, Thompson TR, Ascher JA, Monaghan ET, Leadbetter RA (2008). "Lamotrigine in the acute treatment of bipolar depression: results of five double-blind, placebo-controlled clinical trials". Bipolar disorders 10 (2): 323333. doi:10.1111/j.1399-5618.2007.00500.x. PMID18271912. [27] Calabrese JR, Geddes JR, Goodwin GM (2009). "Lamotrigine for treatment of bipolar depression: independent meta-analysis and meta-regression of individual patient data from five randomised trials". Psychiatry 194 (1): 49. [28] Backonja M (June 2004). "Neuromodulating drugs for the symptomatic treatment of neuropathic pain". Curr Pain Headache Rep 8 (3): 2126. doi:10.1007/s11916-004-0054-4. PMID15115640. [29] Jensen TS (2002). "Anticonvulsants in neuropathic pain: rationale and clinical evidence" (http:/ / linkinghub. elsevier. com/ retrieve/ pii/ S1090-3801(01)90324-6). Eur J Pain 6 (Suppl A): 618. doi:10.1053/eujp.2001.0324. PMID11888243. . [30] Pappagallo M (October 2003). "Newer antiepileptic drugs: possible uses in the treatment of neuropathic pain and migraine" (http:/ / linkinghub. elsevier. com/ retrieve/ pii/ S0149291803803144). Clin Ther 25 (10): 250638. doi:10.1016/S0149-2918(03)80314-4. PMID14667954. . [31] Barbosa L, Berk M, Vorster M (April 2003). "A double-blind, randomized, placebo-controlled trial of augmentation with lamotrigine or placebo in patients concomitantly treated with fluoxetine for resistant major depressive episodes" (http:/ / www. psychiatrist. com/ privatepdf/ 2003/ v64n04/ v64n0407. pdf). J Clin Psychiatry 64 (4): 4037. doi:10.4088/JCP.v64n0407. PMID12716240. . [32] Rogawski, M (2002). "Chapter 1: Principles of antiepileptic drug action". In Levy RH, Mattson RH, Meldrum BS, Perucca E. Antiepileptic Drugs, Fifth Edition. Lippincott Williams & Wilkins. pp.322. ISBN10781723213. [33] Ramsay RE, Pellock JM, Garnett WR, et al. (1991). "Pharmacokinetics and safety of lamotrigine (Lamictal) in patients with epilepsy". Epilepsy Res. 10 (2-3): 191200. doi:10.1016/0920-1211(91)90012-5. PMID1817959. [34] http:/ / professionals. epilepsy. com/ medications/ p_lamictal_dosage. html [35] http:/ / www. drugs. com/ pro/ lamotrigine. html [36] http:/ / www. ncbi. nlm. nih. gov/ pubmed/ 18845017 [37] "Lamictal Prescribing Information" (http:/ / us. gsk. com/ products/ assets/ us_lamictal. pdf) (PDF). GlaxoSmithKline.. May 2007. . Retrieved 2008-04-09. [38] http:/ / www. drugs. com/ monograph/ lamotrigine. html [39] Nicholson, R J; Kelly, K P; Grant, I S (25 February 1995). "Leucopenia associated with lamotrigine" (http:/ / www. bmj. com/ cgi/ content/ full/ 310/ 6978/ 504/ b). BMJ. . Retrieved 16 June 2010. [40] Lamotrigine does not prolong QTc in a thorough QT/QTc study in healthy subjects (http:/ / www. richmondpharmacology. com/ downloads/ Publications/ Lamotrigine does not prolong QTc in a thorough QTQTc study in healthy subjects. pdf)Dixon, Ruth; Job, S., Oliver, R., Tompson, D., Wright, J. G., Maltby, K., Lorch, U. and Taubel, J. (2008). (July 2008). "Lamotrigine does not prolong QTc in a thorough QT/QTc study in healthy subjects.". Br J Clin Pharmacol 2008 66 (3): 396404. doi:10.1111/j.1365-2125.2008.03250.x. [41] Reimers A, A; Helde G, Brodtkorb E (September 2005). "Ethinyl estradiol, not progestogens, reduces lamotrigine serum concentrations". Epilepsia (Blackwell Science) 46 (9): 14147. doi:10.1111/j.1528-1167.2005.10105.x. PMID16146436. [42] Sidhu J, J; Job S, Singh S, Philipson R (February 2006). "The pharmacokinetic and pharmacodynamic consequences of the co-administration of lamotrigine and a combined oral contraceptive in healthy female subjects.". Br J Clin Pharmacol. 61 (2): 1919. doi:10.1111/j.1365-2125.2005.02539.x. PMC1885007. PMID16433873. [43] FDA: Safety Alerts: Lamotrigine (http:/ / www. fda. gov/ Safety/ MedWatch/ SafetyInformation/ SafetyAlertsforHumanMedicalProducts/ ucm150637. htm) [44] Berwaerts, K; Sienaert P, De Fruyt J (2009). "Teratogenic effects of lamotrigine in women with bipolar disorder." (in Dutch). Tijdschr Psychiatr 51 (10): 74150. PMID19821242. [45] Prakash; Prabhu LV, Nasar MA et al. (October 2007). "Lamotrigine in pregnancy: safety profile and the risk of malformations.". Singapore Med J 48 (10): 8803. PMID17909669. [46] McVearry, KM; Gaillard WD, VanMeter J, Meador KJ (December 2009). "A prospective study of cognitive fluency and originality in children exposed in utero to carbamazepine, lamotrigine, or valproate monotherapy.". Epilepsy Behav 16 (4): 60916.
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doi:10.1016/j.yebeh.2009.09.024. PMID19892603. [47] Hale, TW (2008). Medications and Mothers' Milk (13th ed.). Hale Publishing. p.532. ISBN978-0-9815257-2-3. [48] anonymous. "Lamictal, Warnings & Precautions" (http:/ / www. rxlist. com/ cgi/ generic/ lamotrigine_wcp. htm). RxList Inc.. . Retrieved 2008-04-09. [49] anonymous. "lamotrigine studies" (http:/ / ctr. gsk. co. uk/ Summary/ lamotrigine/ studylist. asp). GlaxoSmithKline. . Retrieved 2008-04-09. [50] Foldvary, N; Perry M, Lee J et al. (December 2001). "The effects of lamotrigine on sleep in patients with epilepsy.". Epilepsia 42 (12): 156973. doi:10.1046/j.1528-1157.2001.46100.x. PMID11879368. [51] Bonanni, E; Galli R, Gori S et al. (June 2001). "Neurophysiological evaluation of vigilance in epileptic patients on monotherapy with lamotrigine.". Clin Neurophysiol 112 (6): 101822. doi:10.1016/S1388-2457(01)00537-5. PMID11377260. [52] Placidi, F; Marciani MG, Diomedi M et al. (August 2000). "Effects of lamotrigine on nocturnal sleep, daytime somnolence and cognitive functions in focal epilepsy.". Acta Neurol Scand 102 (2): 816. doi:10.1034/j.1600-0404.2000.102002081.x. PMID10949523. [53] Sadler, M (March 1999). "Lamotrigine associated with insomnia.". Epilepsia 40 (3): 3225. doi:10.1111/j.1528-1157.1999.tb00712.x. PMID10080513. [54] http:/ / www. ehealthme. com/ ds/ lamictal/ myoclonic+ jerks Retrieved August 19, 2010. Myoclonic Jerk in the use of Lamictal. [55] anonymous (17 February 2005). "Press Release, Teva Announces Settlement Of Lamictal Litigation With Glaxosmithkline" (http:/ / www. tevapharm. com/ pr/ 2005/ pr_513. asp). Teva Pharmaceutical Industries Ltd.. . Retrieved 2008-04-09. [56] http:/ / www. tevapharm. com/ pr/ 2008/ pr_779. asp [57] anonymous (2 March 2005). "Treatment for epilepsy: generic lamotrigine" (http:/ / www. dh. gov. uk/ en/ Healthcare/ Medicinespharmacyandindustry/ Prescriptions/ DH_4104966). Department of Health (UK). . Retrieved 2008-04-09. [58] Waknine Y (2009). "FDA Approves Extended-Release Lamotrigine for Adjunctive Treatment of Epilepsy" (http:/ / www. medscape. com/ viewarticle/ 703853). MedScape. . Retrieved 2010-05-18. [59] anonymous (2007). "LAMOTRIGINE" (http:/ / www. drug. co. il/ bygeneric. asp?gen_id=775& drugID=7007& wel=). www.drug.co.il. . Retrieved 2008-04-14. [60] http:/ / www. google. com/ patents?vid=4,560,687
194
External links
FAQ: Psychiatric Uses of Lamotrigine (Lamictal) (http://www.psycom.net/depression.central.lamotrigine. html), by Ivan K. Goldberg, MD. Includes many references from the medical literature. Center for Drug Evaluation and Research: Lamictal (http://www.accessdata.fda.gov/scripts/cder/drugsatfda/ index.cfm?fuseaction=Search.Label_ApprovalHistory) documents related to the FDA approval process, including medical reviews and correspondence letters. Epilepsy South Africa: MEDICATION FOR EPILEPSY (http://www.epilepsy.org.za/faq.php) an Epilepsy FAQ with a list of medicines for treatment thereof, includes Lamotrigine with South African trade name Lamictin. Adverse Reactions (http://www.druglib.com/adverse-reactions_side-effects/lamictal/) Reported adverse reactions and side-effects. U.S. National Library of Medicine: Drug Information Portal Lamotrigine (http://druginfo.nlm.nih.gov/ drugportal/dpdirect.jsp?name=Lamotrigine)
Oxcarbazepine
195
Oxcarbazepine
Oxcarbazepine
[4] [5]
[6]
Oxcarbazepine
[7]
196
ChemSpider UNII KEGG ChEMBL
31608
[8]
VZI5B1W380 D00533
[9]
[10]
& PubChem
[12]
[13]
Oxcarbazepine (ox-kar-BAY-zih-peen) is a anticholinergic [14] anticonvulsant and mood stabilizing drug, used primarily in the treatment of epilepsy. It is also used to treat anxiety and mood disorders, and benign motor tics. Oxcarbazepine is marketed as Trileptal by Novartis and available in some countries as a generic drug.
Uses
In treatment of epilepsy, oxcarbazepine has recently been found to be associated with a greater enhancement in mood and reduction in anxiety symptoms than other drugs employed to treat epilepsy.[15] It also appears to be effective in approximately half of patients with bipolar disorder and is well tolerated.[16]
Structure pharmacology
Oxcarbazepine is a structural derivative of carbamazepine, with a ketone in place of the carbon-carbon double bond on the dibenzazepine ring. This difference helps reduce the impact on the liver of metabolizing the drug, and also prevents the serious forms of anemia or agranulocytosis occasionally associated with carbamazepine. Aside from this reduction in side effects, it is thought to have the same mechanism as carbamazepine - sodium channel inhibition (presumed to be the main mechanism of action) - and is generally used to treat the same conditions. Oxcarbazepine is a prodrug which is activated to eslicarbazepine in the liver.[17]
Oxcarbazepine
197
History
First synthesized in 1965, it was patent protected by Geigy in 1969 through DE 2011087 [18]. It was approved for use as an anticonvulsant in Denmark in 1990, Spain in 1993, Portugal in 1997, and eventually for all other EU countries in 1999. It was approved in the US in 2000. In September 2010, Novartis pleaded guilty of marketing Trileptal for the unapproved uses of neuropathic pain and bipolar disorder during 2000 and 2001.[19]
Side effects
Oxcarbazepine causes dizziness, drowsiness, blurred or double vision, fatigue and may cause headaches, nausea, and vomiting. There is also evidence of difficulty in concentration and mental sluggishness. It can also cause hyponatremia (2.7% of patients), so blood sodium levels should be tested if the patient complains of severe fatigue. Some of these side effects (such as headache) are more pronounced shortly after a dose is taken and tend to fade with the passage of time (generally 60 300mg Trileptal tablets to 90 minutes). A craving for salty foods (such as potato chips) and increased impulsiveness have also been noted. Other side effects include stomach pain; tremor; rash; diarrhea, constipation, decreased appetite; and dry mouth. Skin sensitivity to sunlight also may increase, and patients could experience severe sunburns as a result of sun exposure. The frequency of adverse effects rises above a daily dosage of 1200mg. Some patients reported a sensation of incontinence after taking the drug, although the sensation was false.
Nursing mothers
Oxcarbazepine and its active metabolite MHD are excreted in human breast milk. Because of the potential for serious adverse reactions to oxcarbazepine in nursing infants, a decision should be made about whether to discontinue nursing or to discontinue the drug in nursing women.
References
[1] [2] [3] [4] http:/ / www. drugs. com/ monograph/ oxcarbazepine. html http:/ / www. nlm. nih. gov/ medlineplus/ druginfo/ meds/ a601245. html http:/ / www. nlm. nih. gov/ cgi/ mesh/ 2009/ MB_cgi?term=28721-07-5& rn=1 http:/ / www. whocc. no/ atc_ddd_index/ ?code=N03AF02
[5] http:/ / pubchem. ncbi. nlm. nih. gov/ summary/ summary. cgi?cid=34312 [6] http:/ / www. drugbank. ca/ drugs/ DB00776 [7] http:/ / www. chemspider. com/ Chemical-Structure. 31608 [8] http:/ / fdasis. nlm. nih. gov/ srs/ srsdirect. jsp?regno=VZI5B1W380
Oxcarbazepine
[9] http:/ / www. kegg. jp/ entry/ D00533 [10] https:/ / www. ebi. ac. uk/ chembldb/ index. php/ compound/ inspect/ CHEMBL1068 [11] http:/ / www. emolecules. com/ cgi-bin/ search?t=ex& q=O%3DC3c1c%28cccc1%29N%28c2ccccc2C3%29C%28%3DO%29N [12] http:/ / pubchem. ncbi. nlm. nih. gov/ search/ ?smarts=O%3DC3c1c%28cccc1%29N%28c2ccccc2C3%29C%28%3DO%29N [13] http:/ / en. wikipedia. org/ wiki/ Special%3Acomparepages?rev1=445068911& page2=%3AOxcarbazepine [14] University of East Anglia. "Drugs on the Anticholinergic Burden (ACB) scale" (http:/ / www. uea. ac. uk/ mac/ comm/ media/ press/ 2011/ June/ Anticholinergics+ study+ drug+ list) [15] Mazza M, Della Marca G, Di Nicola M, et al. (May 2007). "Oxcarbazepine improves mood in patients with epilepsy". Epilepsy Behav 10 (3): 397401. doi:10.1016/j.yebeh.2007.01.003. PMID17300991. [16] Ghaemi SN, Berv DA, Klugman J, Rosenquist KJ, Hsu DJ (August 2003). "Oxcarbazepine treatment of bipolar disorder". J Clin Psychiatry 64 (8): 9435. doi:10.4088/JCP.v64n0813. PMID12927010. [17] Dulsat, C., Mealy, N., Castaner, R., Bolos, J. (2009). "Eslicarbazepine acetate". Drugs of the Future 34 (3): 189. doi:10.1358/dof.2009.034.03.1352675. [18] http:/ / worldwide. espacenet. com/ textdoc?DB=EPODOC& IDX=DE2011087 [19] U.S. District Court for the Eastern District of Pennsylvania. "Governments memorandum for entry of plea and sentencing" (http:/ / www. justice. gov/ usao/ pae/ News/ Pr/ 2010/ Sept/ novartis_entryofplea. pdf). .
198
ChemicalLand21.com: Oxcarbazepine (http://www.chemicalland21.com/lifescience/phar/ OXCARBAZEPINE.htm) Trileptal Story (http://www.trileptal.info/media_center/content/pages/media_center/story.htm) Trileptal.com(Novartis) (http://www.trileptal.com/) Prescribing Information(PDF) (http://www.pharma.us.novartis.com/product/pi/pdf/trileptal.pdf) psychatlanta.com (http://www.psychatlanta.com/documents/trileptal.pdf)
External links
RxList entry (http://www.rxlist.com/cgi/generic3/oxcarbazepine.htm) http://www.psycheducation.org/depression/meds/moodstabilizers.htm http://www.psycheducation.org/depression/meds/trileptal.htm DrugBank entry (http://redpoll.pharmacy.ualberta.ca/drugbank/cgi-bin/getCard.cgi?CARD=APRD01308) http://www.konduskarlabs.com
Topiramate
199
Topiramate
Topiramate
2,3:4,5-Bis-O-(1-methylethylidene)-beta-D-fructopyranose sulfamate
Clinical data Trade names AHFS/Drugs.com MedlinePlus Pregnancy cat. Legal status Routes Topamax monograph a697012
[2] [1]
80% 30% hepatic, 70% is excreted unchanged 19 to 23 hours 70% renal (in urine) in unchanged form Identifiers
[3]
[4] [5]
[7]
0H73WJJ391
[8]
Topiramate
[9]
200
KEGG ChEMBL
D00537
[10]
& PubChem
[12]
[13]
Topiramate (brand name Topamax) is an anticonvulsant (antiepilepsy) drug. It was originally produced by Ortho-McNeil Neurologics and Noramco, Inc., both divisions of the Johnson & Johnson Corporation. This medication was discovered in 1979 by Bruce E. Maryanoff and Joseph F. Gardocki during their research work at McNeil Pharmaceutical.[14] [15] [16] Generic versions are available in Canada and these were approved by the Food and Drug Administration (FDA) in September 2006. Mylan Pharmaceuticals was recently granted final approval for generic topiramate 25, 100, and 200mg tablets and sprinkle capsules by the FDA for sale in the United States. 50mg tablets were granted tentative approval.[17] The last patent for topiramate in the U.S. was for pediatric use; this patent expired on February 28, 2009.[18] On May 21, 2010, Ortho-McNeil pled guilty and was fined $6.14 million by the FDA for promoting Topamax to treat psychiatric disorders, without applying for any Federal government approval. Also, there was no data from any well-controlled clinical trial to demonstrate that Topamax was safe and/or effective to treat any psychiatric conditions at all.[19]
Medical uses
Topiramate is used to treat epilepsy in children and adults, and it was originally used as an anticonvulsant. In children, it is indicated for the treatment of Lennox-Gastaut syndrome, a disorder that causes seizures and developmental delay. It is also Food and Drug Administration (FDA) approved for, and most frequently prescribed for, the prevention of migraines. Psychiatrists have used topiramate to treat bipolar disorder,[20] and they sometimes use topiramate to augment psychotropics, or to counteract the weight gain associated with numerous antidepressants. In 2006, a Cochrane review concluded that there is insufficient evidence on which to base any recommendations regarding the use of topiramate in any phase of bipolar illness.[21] However, a more recent Cochrane review, published in 2010, concluded that there was evidence for the efficacy of topiramate in the treatment of symptoms of borderline personality disorder, including mood instability. [22] This drug has been investigated for use in treating alcoholism[23] eating.[27] [28]
[24]
and obesity,[25]
[26]
The drug is also used in clinical trials to treat posttraumatic stress disorder.[29] A pilot study suggested that topiramate is effective against infantile spasms.[30] Another study recommends topiramate as an effective treatment in the prevention of periventricular leukomalacia in preterm infants after an hypoxic-ischemic injury.[31]
Other
Recent clinical reports indicate that it may have mood stabilizing properties.[32] Other off-label and investigational uses of topiramate include the treatment of essential tremor, bulimia nervosa,[33] obsessive-compulsive disorder, alcoholism,[24] smoking cessation,[34] idiopathic intracranial hypertension,[35] neuropathic pain,[36] cluster headache,[37] migraine headache, cocaine dependence, and Borderline Personality Disorder. [38] [39] Topiramate is also being studied with a mixture of phentermine to form a drug called Qnexa for the treatment of obesity.
Topiramate
201
Adverse effects
A GlaxoSmithKline-sponsored Phase IV study suggested that cognitive side effects may be more common with topiramate than with lamotrigine.[40] In studies of healthy volunteers, therapeutic doses of topiramate for bipolar disorder produced greater cognitive deficits than lamotrigine, including short term memory loss and word-finding difficulty. The side-effects reported by > 10% of subjects in at least one clinical study[41] Listed by prevalence: paresthesia (numbness & tingling) (23.7%) upper respiratory tract infection (17.5%) diarrhea (16.8%) nausea (15.4%) anorexia (loss of appetite) (13.3%) memory problems (11.2%)
The side-effects most frequently leading to discontinuation of therapy with topiramate were: psychomotor slowing (4.1%) memory problems (3.3%) fatigue (3.3%) confusion (3.2%) somnolence (3.2%) That same study also reported that in adult patients with Bipolar 1 disorder who were already receiving either lithium or valproate, the addition of topiramate did not produce a statistically-significant improvement versus placebo, while adding the above adverse reactions. Rarely, the inhibition of carbonic anhydrase may be strong enough to cause metabolic acidosis of clinical importance.[42] The U.S. Food and Drug Administration (FDA) has notified prescribers that topiramate can cause acute myopia and secondary angle closure glaucoma in a small subset of people who take topiramate regularly. The symptoms, which typically begin in the first month of use, include blurred vision and eye pain. Discontinuation of topiramate may halt the progression of the ocular damage, and may reverse the visual impairment. Preliminary data suggests that, as with several other anti-epileptic drugs, topiramate carries an increased risk of congenital malformations.[43] This might be particularly important for women who take topiramate to prevent migraine attacks. Topiramate has been associated with a statistically significant increase in suicidality.[44] In March 2011 the FDA notified healthcare professionals and patients of an increased risk of development of cleft lip and/or cleft palate (oral clefts) in infants born to women treated with Topamax (topiramate) during pregnancy.[45] =
Interactions
Topiramate has many drug-drug interactions. Some of the most common are listed below: As topiramate inhibits carbonic anhydrase, use with other inhibitors of carbonic anhydrase (e.g. acetazolamide) increases the risk of kidney stones. Enzyme inducers (e.g. carbamazepine) can increase the elimination of topiramate, possibly necessitating dose escalations of topiramate. Topiramate may increase the plasma-levels of phenytoin. Topiramate itself is a weak inhibitor of CYP2C19 and induces CYP3A4; a decrease in plasma levels of estrogens and digoxin has been noted during topiramate therapy. This can reduce the effectiveness of oral contraceptives (the pill); use of alternative birth control methods is recommended.[46] Neither intrauterine devices (IUDs) nor
Topiramate Depo-Provera are affected by topiramate.[46] Alcohol may cause increased sedation or drowsiness, and increase the risk of having a seizure. As listed in the 06/29/2005 label posted at the Drugs@FDA website page 14,'conditions or therapies that predispose to acidosis may be additive to the bicarbonate lowering effects of Topiramate'.[47] Oligohidrosis and hyperthermia were reported in post-marketing reports about topiramate; antimuscarinic drugs (like trospium) can aggravate these disorders.
202
Overdose
Overdose is rare. In most cases, acute exposure produced only minimal to moderate effects. Fatalities have occurred, but were the result of polydrug exposure. Symptoms of overdose may include but are not limited to:[48] Agitation Depression Speech problems Blurred vision, double vision Troubled thinking Loss of coordination Inability to respond to things around you Loss of consciousness Confusion and coma Fainting Upset stomach and stomach pain Loss of appetite and vomiting Shortness of breath; fast, shallow breathing Pounding or irregular heartbeat Muscle weakness Bone pain Seizures
Warnings
People taking topiramate should be aware of the following risks: Avoid activities requiring mental alertness and coordination until drug effects are realized Topiramate may impair heat regulation, especially in children. Use caution with activities leading to an increased core temperature, such as strenuous exercise, exposure to extreme heat, or dehydration Topiramate may decrease effectiveness of estrogen-containing oral contraceptives Topiramate should not be suddenly discontinued, as this may cause increased seizure activity.[52] Avoid evening primrose (seizure threshold decreased) [53]
Topiramate
203
Pharmacology
Chemically, topiramate is a sulfamate-substituted monosaccharide, related to fructose, a rather unusual chemical structure for an anticonvulsant. Topiramate is quickly absorbed after oral use. Most of the drug (70%) is excreted in the urine unchanged. The remainder is extensively metabolized by hydroxylation, hydrolysis, and glucuronidation. Six metabolites have been identified in humans, none of which constitutes more than 5% of an administered dose. The exact mechanism of action is unknown,[52] but four properties that may contribute to topiramate's antiepileptic and antimigraine efficacy include a blockage of voltage-dependent sodium channels, an augmentation of gamma-aminobutyrate acid activity at some subtypes of the GABA- A receptors, antagonism of AMPA/kainate subtype of the glutamate receptor, and inhibition of the carbonic anhydrase enzyme, particularly isozymes II and IV . Its possible effect as a mood stabilizer seems to occur before anticonvulsant qualities at lower dosages. Topiramate inhibits maximal electroshock and pentylenetetrazol-induced seizures as well as partial and secondarily generalized tonic-clonic seizures in the kindling model, findings predictive of a broad spectrum of activities clinically. Its action on mitochondrial permeability transition pores has been proposed as a mechanism.[54] While many anticonvulsants have been associated with apoptosis in young animals, animal experiments have found that topiramate is the only anticonvulsant that does not induce apoptosis in young animals at doses needed to produce an anticonvulsant effect.[55]
References
[1] http:/ / www. drugs. com/ monograph/ topiramate. html [2] http:/ / www. nlm. nih. gov/ medlineplus/ druginfo/ meds/ a697012. html [3] http:/ / www. nlm. nih. gov/ cgi/ mesh/ 2009/ MB_cgi?term=97240-79-4& rn=1 [4] http:/ / www. whocc. no/ atc_ddd_index/ ?code=N03AX11 [5] http:/ / pubchem. ncbi. nlm. nih. gov/ summary/ summary. cgi?cid=5284627 [6] http:/ / www. drugbank. ca/ drugs/ DB00273 [7] http:/ / www. chemspider. com/ Chemical-Structure. 4447672 [8] http:/ / fdasis. nlm. nih. gov/ srs/ srsdirect. jsp?regno=0H73WJJ391 [9] http:/ / www. kegg. jp/ entry/ D00537 [10] https:/ / www. ebi. ac. uk/ chembldb/ index. php/ compound/ inspect/ CHEMBL220492 [11] http:/ / www. emolecules. com/ cgi-bin/ search?t=ex& q=O%3DS%28%3DO%29%28OC%5BC%40%40%5D21OC%28O%5BC%40H%5D1%5BC%40%40H%5D3OC%28O%5BC%40%40H%5D3CO2%29%28C% [12] http:/ / pubchem. ncbi. nlm. nih. gov/ search/ ?smarts=O%3DS%28%3DO%29%28OC%5BC%40%40%5D21OC%28O%5BC%40H%5D1%5BC%40%40H%5D3OC%28O%5BC%40%40H%5D3CO2%29% [13] http:/ / en. wikipedia. org/ wiki/ Special%3Acomparepages?rev1=408971931& page2=%3ATopiramate [14] Maryanoff, BE; Nortey, SO; Gardocki, JF; Shank, RP; Dodgson, SP (1987). "Anticonvulsant O-alkyl sulfamates. 2,3:4,5-Bis-O-(1-methylethylidene)-beta-D-fructopyranose sulfamate and related compounds". Journal of medicinal chemistry 30 (5): 8807. doi:10.1021/jm00388a023. PMID3572976. [15] Maryanoff, BE; Costanzo, MJ; Nortey, SO; Greco, MN; Shank, RP; Schupsky, JJ; Ortegon, MP; Vaught, JL (1998). "Structure-activity studies on anticonvulsant sugar sulfamates related to topiramate. Enhanced potency with cyclic sulfate derivatives". Journal of medicinal chemistry 41 (8): 131543. doi:10.1021/jm970790w. PMID9548821. [16] B. E. Maryanoff and J. F. Gardocki, "Anticonvulsant sulfamate derivatives", U.S. Patent number 4,513,006 (1985) [17] http:/ / www. medscape. com/ viewarticle/ 544994 [18] http:/ / www. accessdata. fda. gov/ scripts/ cder/ ob/ docs/ patexclnew. cfm?Appl_No=020844& Product_No=002& table1=OB_Rx [19] "Ortho-McNeil Pharmaceutical, LLC Pleads Guilty to Illegal Promotion of Topamax" (http:/ / www. fda. gov/ ICECI/ CriminalInvestigations/ ucm213163). FDA website. 2010-05-21. . Retrieved 2010-05-25. [20] Arnone, D (2005). "Review of the use of Topiramate for treatment of psychiatric disorders". Annals of general psychiatry 4 (1): 5. doi:10.1186/1744-859X-4-5. PMC1088011. PMID15845141. [21] Vasudev, Kamini; MacRitchie, Karine; Geddes, John; Watson, Stuart; Young, Allan H; Young, Allan H (2006). Young, Allan H. ed. "Topiramate for acute affective episodes in bipolar disorder". Cochrane database of systematic reviews (Online) (1): CD003384. doi:10.1002/14651858.CD003384.pub2. PMID16437453. [22] Leib, Klaus; Vllm, Birgit; Rcker, Gerta; Timmer, Antje; Stoffers, Jutta M (2010). "Pharmacotherapy for borderline personality disorder: Cochrane systematic review of randomised trials". British Journal of Psychiatry 196 (1): 4-12. doi:10.1192/bjp.bp.108.062984.
Topiramate
[23] Johnson, BA; Ait-Daoud, N; Bowden, CL; Diclemente, CC; Roache, JD; Lawson, K; Javors, MA; Ma, JZ (2003). "Oral topiramate for treatment of alcohol dependence: a randomised controlled trial". Lancet 361 (9370): 167785. doi:10.1016/S0140-6736(03)13370-3. PMID12767733. [24] Johnson, BA; Rosenthal, N; Capece, JA; Wiegand, F; Mao, L; Beyers, K; McKay, A; Ait-Daoud, N et al. (2007). "Topiramate for treating alcohol dependence: a randomized controlled trial". JAMA : the journal of the American Medical Association 298 (14): 164151. doi:10.1001/jama.298.14.1641. PMID17925516. [25] Van Ameringen, M; Mancini, C; Pipe, B; Campbell, M; Oakman, J (2002). "Topiramate treatment for SSRI-induced weight gain in anxiety disorders". The Journal of clinical psychiatry 63 (11): 9814. doi:10.4088/JCP.v63n1104. PMID12444810. [26] Wilding, J; Van Gaal, L; Rissanen, A; Vercruysse, F; Fitchet, M; Obes-002 Study, Group (2004). "A randomized double-blind placebo-controlled study of the long-term efficacy and safety of topiramate in the treatment of obese subjects". International journal of obesity and related metabolic disorders : journal of the International Association for the Study of Obesity 28 (11): 1399410. doi:10.1038/sj.ijo.0802783. PMID15486569. [27] Shapira, NA; Goldsmith, TD; McElroy, SL (2000). "Treatment of binge-eating disorder with topiramate: a clinical case series". The Journal of clinical psychiatry 61 (5): 36872. doi:10.4088/JCP.v61n0508. PMID10847312. [28] McElroy, SL; Arnold, LM; Shapira, NA; Keck Jr, PE; Rosenthal, NR; Karim, MR; Kamin, M; Hudson, JI (2003). "Topiramate in the treatment of binge eating disorder associated with obesity: a randomized, placebo-controlled trial". The American journal of psychiatry 160 (2): 25561. doi:10.1176/appi.ajp.160.2.255. PMID12562571. [29] Berlant, J; Van Kammen, DP (2002). "Open-label topiramate as primary or adjunctive therapy in chronic civilian posttraumatic stress disorder: a preliminary report". The Journal of clinical psychiatry 63 (1): 1520. doi:10.4088/JCP.v63n0104. PMID11838620. [30] Glauser, TA; Clark, PO; Strawsburg, R (1998). "A pilot study of topiramate in the treatment of infantile spasms". Epilepsia 39 (12): 13248. doi:10.1111/j.1528-1157.1998.tb01331.x. PMID9860068. [31] Follett, PL; Deng, W; Dai, W; Talos, DM; Massillon, LJ; Rosenberg, PA; Volpe, JJ; Jensen, FE (2004). "Glutamate receptor-mediated oligodendrocyte toxicity in periventricular leukomalacia: a protective role for topiramate". Journal of Neuroscience 24 (18): 441220. doi:10.1523/JNEUROSCI.0477-04.2004. PMID15128855. [32] Letmaier, M; Schreinzer, D; Wolf, R; Kasper, S (2001). "Topiramate as a mood stabilizer". International clinical psychopharmacology 16 (5): 2958. doi:10.1097/00004850-200109000-00008. PMID11552774. [33] Hoopes, SP; Reimherr, FW; Hedges, DW; Rosenthal, NR; Kamin, M; Karim, R; Capece, JA; Karvois, D (2003). "Treatment of bulimia nervosa with topiramate in a randomized, double-blind, placebo-controlled trial, part 1: improvement in binge and purge measures". The Journal of clinical psychiatry 64 (11): 133541. doi:10.4088/JCP.v64n1109. PMID14658948. [34] Khazaal, Y; Cornuz, J; Bilancioni, R; Zullino, DF (2006). "Topiramate for smoking cessation". Psychiatry and clinical neurosciences 60 (3): 3848. doi:10.1111/j.1440-1819.2006.01518.x. PMID16732758. [35] Celebisoy, N; Gkay, F; Sirin, H; Akyrekli, O (2007). "Treatment of idiopathic intracranial hypertension: topiramate vs acetazolamide, an open-label study". Acta neurologica Scandinavica 116 (5): 3227. doi:10.1111/j.1600-0404.2007.00905.x. PMID17922725. [36] Chong, MS; Libretto, SE (2003). "The rationale and use of topiramate for treating neuropathic pain". The Clinical journal of pain 19 (1): 5968. doi:10.1097/00002508-200301000-00008. PMID12514458. [37] Linez, MJ; Pascual, J; Pascual, AM; Santonja, JM; Ponz, A; Salvador, A (2003). "Topiramate in the prophylactic treatment of cluster headache". Headache 43 (7): 7849. doi:10.1046/j.1526-4610.2003.03137.x. PMID12890134. [38] . PMID16635055. [39] ClinicalTrials.gov NCT00685178 Clinical Trial of Topiramate for Cocaine Addiction (http:/ / www. clinicaltrials. gov/ show/ NCT00685178) [40] Blum, D; Meador, K; Biton, V; Fakhoury, T; Shneker, B; Chung, S; Mills, K; Hammer, A et al. (2006). "Cognitive effects of lamotrigine compared with topiramate in patients with epilepsy". Neurology 67 (3): 4006. doi:10.1212/01.wnl.0000232737.72555.06. PMID16894098. [41] Roy Chengappa, KN; Schwarzman, LK; Hulihan, JF; Xiang, J; Rosenthal, NR; Clinical Affairs Product Support Study-168 Investigators (2006). "Adjunctive topiramate therapy in patients receiving a mood stabilizer for bipolar I disorder: a randomized, placebo-controlled trial". The Journal of clinical psychiatry 67 (11): 1698706. doi:10.4088/JCP.v67n1105. PMID17196048. [42] Mirza, Nasir; Marson, Anthony G.; Pirmohamed, Munir (2009). "Effect of topiramate on acid-base balance: extent, mechanism and effects". British Journal of Clinical Pharmacology 68 (5): 65561. doi:10.1111/j.1365-2125.2009.03521.x. PMC2791971. PMID19916989. [43] Hunt, S; Russell, A; Smithson, WH; Parsons, L; Robertson, I; Waddell, R; Irwin, B; Morrison, PJ et al. (2008). "Topiramate in pregnancy: preliminary experience from the UK Epilepsy and Pregnancy Register". Neurology 71 (4): 2726. doi:10.1212/01.wnl.0000318293.28278.33. PMID18645165. [44] http:/ / www. fda. gov/ ohrms/ dockets/ ac/ 08/ slides/ 2008-4344s1_09_01_Trileptal%20slides. pdf [45] http:/ / www. drugs. com/ fda/ topamax-topiramate-label-change-risk-development-cleft-lip-cleft-palate-newborns-12916. html [46] Sweetman, Sean C., ed (2009). "Sex hormones and their modulators". Martindale: The complete drug reference (36th ed.). London: Pharmaceutical Press. p.2068. ISBN978-0-85369-840-1. [47] FDA.gov (http:/ / www. fda. gov/ cder/ foi/ label/ 2005/ 020505s018lbl. pdf) [48] http:/ / dailymed. nlm. nih. gov/ dailymed/ drugInfo. cfm?id=7412 [49] Goswami D, Kumar A, Khuroo AH, et al. Bioanalytical LC-MS/MS method validation for plasma determination of topiramate in healthy Indian volunteers. Biomed. Chromatogr. 23: 1227-1241, 2009.
204
Topiramate
[50] Brandt C, Elsner H, Fratsch N et al. (2010). "Topiramate overdose: a case report of a patient with extremely high topiramate serum concentrations and nonconvulsive status epilepticus". Epilepsia 51 (6): 10901093. doi:10.1111/j.1528-1167.2009.02395.x. PMID19889015. [51] R. Baselt, Disposition of Toxic Drugs and Chemicals in Man, 8th edition, Biomedical Publications, Foster City, CA, 2008, pp. 1567-1569. [52] http:/ / www. rxlist. com/ topamax-drug. htm [53] Lexi-Comp Online, Lexi-Drugs Online, Hudson, Ohio: Lexi-Comp, Inc.; 2011; February 18, 2011. [54] Kudin, AP; Debska-Vielhaber, G; Vielhaber, S; Elger, CE; Kunz, WS (2004). "The mechanism of neuroprotection by topiramate in an animal model of epilepsy". Epilepsia 45 (12): 147887. doi:10.1111/j.0013-9580.2004.13504.x. PMID15571505. [55] Czuczwar, K; Czuczwar, M; Cieszczyk, J; Gawlik, P; Luszczki, JJ; Borowicz, KK; Czuczwar, SJ (2004). "Neuroprotective activity of antiepileptic drugs". Przeglad lekarski 61 (11): 126871. PMID15727029.
205
External links
Topamax (topiramate): Treatment for Migraine Prevention (http://www.topamax.com) Topamax: Treatment for Epilepsy (http://www.topamax-epilepsy.com) Currently listed clinical trials related to topiramate (http://www.clinicaltrials.gov/ct/gui/ search?term=topiramate&submit=Search) FDA topiramate safety (http://www.fda.gov/medwatch/safety/2001/topamax.htm) MSN article (http://content.health.msn.com/content/article/70/81128.htm) Effects of topiramate (http://www.mdsupport.org/library/effects.html) MedlinePlus: Topiramate (http://www.nlm.nih.gov/medlineplus/druginfo/medmaster/a697012.html) FAQ: Topiramate (Topamax), Mood Disorders and PTSD (http://www.psycom.net/depression.central. topiramate.html) RxList.com: Topiramate (http://www.rxlist.com/cgi/generic2/topiram_cp.htm) Focus on Topiramate - a new anti-epileptic (http://www.priory.com/focus7.htm), Ben Green, Priory Lodge Education Ltd., 1997-99. Version 1.1
Valproic acid
206
Valproic acid
Valproic acid
2-propylpentanoic acid
Clinical data AHFS/Drugs.com monograph [1] MedlinePlus Licence data Pregnancy cat. Legal status Routes a682412
[2] [3]
USFDA: link
Rapid absorption Concentration-dependent, from 90% at 40g/mL to 81.5% at 130g/mL Hepaticglucuronide conjugation 3050%, mitochondrial -oxidation over 40% 916 h Less than 3% excreted unchanged in urine. Identifiers
99-66-1
[4]
[5]
[6] [7]
Valproic acid
[9]
207
UNII KEGG ChEBI ChEMBL
614OI1Z5WI D00399
[10]
CHEBI:39867 CHEMBL109
[11] [12]
Chemical data Formula Mol. mass SMILES C8H16O2 144.211 g/mol eMolecules
[13]
& PubChem
[14]
[15]
Valproic acid (VPA) is a chemical compound that has found clinical use as an anticonvulsant and mood-stabilizing drug, primarily in the treatment of epilepsy, bipolar disorder, and, less commonly, major depression. It is also used to treat migraine headaches and schizophrenia. VPA is a liquid at room temperature, but it can be reacted with a base such as sodium hydroxide to form the salt sodium valproate which is a solid. The acid, salt or a mixture of the two (valproate semisodium) are marketed under the various brand names Depakote, Depakote ER, Depakene, Depacon, Depakine, Valparin and Stavzor. Approved uses of the various formulations vary by country, e.g. valproate semisodium is used as a mood stabilizer and additionally in the U.S. as an anticonvulsant. VPA is a histone deacetylase inhibitor and is under investigation for treatment of HIV and various cancers.
History
Valproic acid (systematic name 2-propylpentanoic acid and historical name 2-propylvaleric acid) was first synthesized in 1882 by B.S. Burton as an analogue of valeric acid, found naturally in valerian.[16] Names are given to organic acids in the following way. Each organic acid containing only one chain with a specific number of carbon atoms was given the name of the natural (organic) substance from which it was first isolated, e.g. caproic acid (goat). The many historical names became too difficult to memorize. So systematic names were given based on Greek numbers starting from 5, pentanoic acid (valeric acid), then 6, hexanoic acid (caproic acid), etc. Each carbon atom in the chain can then have a group of atoms bonded to it. The name of this group and the number of the carbon atom to which it is attached is then prefixed to the root name of the acid, thus 2-propylpentanoic acid. (propyl is the name of a three carbon atom chain.) As are many organic acids with eight or fewer carbon atoms, valproic acid is a fatty acid that is a clear liquid at room temperature. For many decades its only use was in laboratories as a "metabolically inert" solvent for organic compounds. In 1962, the French researcher Pierre Eymard serendipitously discovered the anticonvulsant properties of valproic acid while using it as a vehicle for a number of other compounds that were being screened for antiseizure activity. He found it prevented pentylenetetrazol-induced convulsions in laboratory rats.[17] It was approved as an antiepileptic drug in 1967 in France and has become the most widely prescribed antiepileptic drug worldwide.[18] Valproic acid has also been used for migraine prophylaxis and bipolar disorder.[19]
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Mechanism of Action
Valproate is believed to affect the function of the neurotransmitter GABA in the human brain, making it an alternative to lithium salts in treatment of bipolar disorder. Its mechanism of action includes enhanced neurotransmission of GABA (by inhibiting GABA transaminase, then GABA would increase in concentration). However, several other mechanisms of action in neuropsychiatric disorders have been proposed for valproic acid in recent years.[20] Valproic acid also blocks the voltage-gated sodium channels and T-type calcium channels. These mechanisms make valproic acid a broad spectrum anticonvulsant drug. Valproic acid is an inhibitor of the enzyme histone deacetylase 1 (HDAC1), hence it is a histone deacetylase inhibitor.
Indications
As an anticonvulsant, valproic acid is used to control absence seizures, tonic-clonic seizures (grand mal), complex partial seizures, juvenile myoclonic epilepsy and the seizures associated with Lennox-Gastaut syndrome. It is also used in treatment of myoclonus. In some countries, parenteral preparations of valproate are used also as second-line treatment of status epilepticus, as an alternative to phenytoin. Valproate is one of the most common drugs used to treat posttraumatic epilepsy.[21] Valproic acid is also FDA approved for the treatment of manic episodes associated with bipolar disorder, adjunctive therapy in multiple seizure types (including epilepsy), and prophylaxis of migraine headaches.[22] It is more recently being used to treat neuropathic pain, as a second line agent, particularly lancinating pain from A delta fibers.
Investigational
HIV Histone deacetylase HDAC1 is needed for HIV to remain latent, or dormant, in infected cells. When the virus is latent it cannot be destroyed by anti-HIV drugs. A study published in August 2005 found that three of four patients treated with valproic acid in addition to highly active antiretroviral therapy (HAART) showed a mean 75% reduction in latent HIV infection.[23] The idea was that valproic acid, by inhibiting HDAC1, forced HIV out of latency (reactivation) and into its replicative cycle. The highly-active antiretroviral drugs could then stop the virus, whilst the immune system could destroy the infected cell. Flushing out all latent virus in this manner would potentially cure HIV patients. Subsequent trials, however, found no long-term benefits of valproic acid in HIV infection.[24] Cancers According to the U.S. National Institutes of Health and others, valproic acid appears to have wide implications in the treatment of various cancers,[25] including multiple myeloma (bone marrow cancer),[26] glioma (an aggressive type of brain tumor),[27] and melanoma.[28] Valproic acid is cytotoxic to many different cancer types through its action as a histone deacetylase inhibitor. A phase I trial showed the maximum tolerated dose was 60mg/kg limited by neurotoxicity.[29] Another potential indication may be leukemia in juvenile patients. Studies conducted by several European centres are ongoing. Although it is too early to make a definitive statement, preliminary results are encouraging. Valproic acid has given encouraging results for breast cancer when used alongside a standard chemotherapy in a phase I/II trial (44+10 patients).[30] As of January 2011 the salt magnesium valproate is in phase III trials for cervical cancer[31] and ovarian cancer.[32]
Valproic acid Other diseases Three distinct formulations of valproic acid have been investigated in clinical trials for the treatment of colorectal polyps in familial adenomatous polyposis patients; treatment of hyperproliferative skin diseases (e.g. basal cell carcinoma); and treatment of inflammatory skin diseases (e.g. acne) by TopoTarget. The current names for these therapeutics are Savicol, Baceca and Avugane, respectively.[33] In October, 2008, a research team at the University of British Columbia in Vancouver, Canada announced that in a study doses of valproic acid reversed the early stages of Alzheimer's disease in mice. Human trials are underway. Stem cells Valproic acid's function as an HDAC inhibitor has also led to its use in direct reprogramming in generation of induced pluripotent stem (iPS) cells, where it has been shown that addition of VPA allows for reprogramming of human fibroblasts to iPS cells without addition of genetic factors Klf4 and c-myc.[34] This function has also been investigated as an epigenetic therapy for treatment of lupus.[35]
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Contraindications
Safety in pregnancy
Valproate causes birth defects: exposure during pregnancy is associated with about three times as many major anomalies as usual, mainly spina bifida and, more rarely, with several other defects, possibly including a "valproate syndrome".[36] Characteristics of this valproate syndrome include facial features that tend to evolve with age, including trigonocephaly, tall forehead with bifrontal narrowing, epicanthic folds, medial deficiency of eyebrows, flat nasal bridge, broad nasal root, anteverted nares, shallow philtrum, long upper lip and thin vermillion borders, thick lower lip and small downturned mouth.[37] Women who intend to become pregnant should switch to a different drug if possible. Women who become pregnant while taking valproate should be warned that it causes birth defects and cognitive impairment in the newborn, especially at high doses (although vaproate is sometimes the only drug that can control seizures, and seizures in pregnancy would have even worse consequences.) They should take high dose folic acid and be offered antenatal screening (alpha-fetoprotein and second trimester ultrasound scans), although screening and scans do not find all birth defects.[38] Valproate is a known folate antagonist, which can cause neural tube defects. Thus, folic acid supplements may alleviate the teratogenic problems. A recent study showed children of mothers taking valproate during pregnancy are at risk for significantly lower IQs.[39] [40] Risk of autism Exposure of the human embryo to valproic acid is associated with risk of autism, and it is possible to duplicate features characteristic of autism by exposing rat embryos to valproic acid at the time of neural tube closure.[41] One study found valproate exposure on embryonic day 11.5 led to significant local recurrent connectivity in the juvenile rat neocortex, consistent with the underconnectivity theory of autism.[42] A 2009 study demonstrated children of pregnant women taking valproate had an IQ nine points lower than a well-matched control group.[43] [44] [45] [46]
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Adverse effects
The foremost and most severe concern for anyone taking valproic acid is its potential for sudden and severe, possibly fatal, fulminating impairments in liver, hematopoietic and/or pancreatic function, especially in those just starting the medication. This particular warning is the first one listed on any drug adverse effect listing when one receives the drug at the pharmacy. There are rare reports of individuals who have used valproic acid for a long time (chronic users) who have suffered renal impairment, usually as a result of having been injured or ill or on a drug regimen already and so having been overwhelmed. Valproate is also cautioned against in many patients because it can cause weight gain.[47] Preexisting severe hepatic (liver) and/or renal (kidney) damage and certain cases of metastatic cancer, severe hepatitis or pancreatitis, end-stage AIDS HIV infection, marked bone marrow depression, urea cycle disorders, and coagulation hematological disorders that have caused impairment are absolute contraindications. Some patients with symptomatic but manageable AIDS, cancer, hepatic or renal disease are kept on the medication (usually at a reduced dose with more frequent blood tests) to avoid having to manipulate the drug regimen for as long as possible. Common side effects are dyspepsia and/or weight gain. Less common are fatigue, peripheral edema, acne, dizziness, drowsiness, hair loss, headaches, nausea, sedation and tremors. Valproic acid also causes hyperammonemia, an increase of ammonia levels in the blood, which can lead to vomiting and sluggishness, and ultimately to mental changes and brain damage.[48] Valproate levels within the normal range are capable of causing hyperammonemia and ensuing encephalopathy. There have been reports of brain encephalopathy developing without hyperammonemia or elevated valproate levels.[49] Rarely, valproic acid can cause blood dyscrasia, impaired liver function, jaundice, thrombocytopenia, and prolonged coagulation (clotting) times due to a lack of blood cells. In about 5% of pregnant users, valproic acid will cross the placenta and cause congenital anomalies that resemble fetal alcohol syndrome, and there is a possibility of cognitive impairment. Due to these side effects most doctors will try to continue the medication, but will ask for blood tests, initially as often as once a week and then once every 2 months (those taking it for a long period may go 6 months before being retested; if a pregnant woman and her doctor decide to keep using the drug and to keep the pregnancy, then frequent blood testing, and possibly a higher frequency of diagnostic ultrasounds to identify fetal problems, is a must). Temporary liver enzyme increase has been reported in 20% of cases during the first few months of taking the drug. Inflammation of the liver (hepatitis), the first symptom of which is jaundice, is found in rare cases. Valproic acid may also cause acute hematological toxicities, especially in children, including rare reports of myelodysplasia and acute leukemia-like syndrome.[50] [51] There have also been reports of cognitive dysfunction, Parkinsonian symptoms,[52] and even (reversible) pseudoatrophic brain changes[53] in long-term treatment with valproic acid. According to the prescription information that comes with a prescription of this drug, some individuals have become depressed or had a suicidal ideation while on the drug; those taking it should be monitored for this side effect. Also, the statement goes on to say that the drug can alter the findings of tests for urine ketones, though because of the potentially serious consequences, the dose should never be unilaterally altered by the patient without medical and pharmacological advice.
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Overdosage
Excessive amounts of valproic acid can result in tremor, stupor, respiratory depression, coma, metabolic acidosis and death. Overdosage in children is usually of an accidental nature, whereas with adults it is more likely to be an intentional act. Serum or plasma valproic acid concentrations are generally in a range of 20100mg/L during controlled therapy, but may reach 1501500mg/L following acute poisoning. Monitoring of the serum level is often accomplished using commercial immunoassay techniques, although some laboratories employ gas or liquid chromatography. In severe intoxication, hemoperfusion or hemofiltration can be an effective means of hastening elimination of the drug from the body.[54] [55] [56]
Interactions
Valproic acid may interact with carbamazepine, as valproates inhibit microsomal epoxide hydrolase (mEH), the enzyme responsible for the breakdown of carbamazepine-10,11 epoxide (the main active metabolite of carbamazepine) into inactive metabolites.[57] By inhibiting mEH, valproic acid causes a buildup of the active metabolite, prolonging the effects of carbamazepine and delaying its excretion. Valproic acid also decreases the clearance of amitriptyline and nortriptyline.[58] Aspirin may decrease the clearance of valproic acid, leading to higher than intended serum levels of the anticonvulsant. Also, combining valproic acid with the benzodiazepine clonazepam can lead to profound sedation and increases the risk of absence seizures in patients susceptible to them.[58] Valproic acid and sodium valproate reduce the apparent clearance of lamotrigine (lamictal), in most patients the lamotrigine dosage for coadministration with valproate must be reduced to half the monotherapy dosage. Valproic acid is contraindicated in pregnancy as it decreases the intestinal reabsorption of folate (folic acid) which leads to neural tube defects. Because of a decrease in folate, megaloblastic anemia may also result. Phenytoin also decreases folate absorption which may lead to the same adverse effects as valproic acid.
Formulations
Branded products include: Convulex (Pfizer in the UK and Byk Madaus in South Africa) Depakene (Abbott Laboratories in U.S. & Canada) Depakine (Sanofi Aventis French) Depakine (Sanofi Synthelabo Romania) Deprakine (Sanofi Aventis Finland) Encorate (Sun Pharmaceuticals India) Epival (Abbott Laboratories U.S. & Canada) Epilim (Sanofi Synthelabo Australia) Stavzor (Noven Pharmaceuticals Inc.) Valcote (Abbott Laboratories Argentina)
Chemistry
Valproic acid, 2-propylvaleric acid, is synthesized by the alkylation of cyanoacetic ester with two moles of propylbromide, to give dipropylcyanoacetic ester. Hydrolysis and decarboxylation of the carboethoxy group gives dipropylacetonitrile, which is hydrolyzed into valproic acid.
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M. Chignac, C. Grain, U.S. Patent 4155929 [59] (1979). H.E.J.-M. Meunier, GB 980279 [60] (1963). H.E.J.-M. Meunier, U.S. Patent 3325361 [61] (1967). M. Chignac, C. Grain, Ch. Pigerol, GB 1522450 [62] (1977).
References
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[31] http:/ / clinicaltrials. gov/ ct2/ show/ NCT00532818 [32] http:/ / clinicaltrials. gov/ ct2/ show/ NCT00533299 [33] "Annual Report 2007" (http:/ / www. topotarget. com/ multimedia/ Topotarget_rapport_web_2007_UK_final. pdf) (PDF). TopoTarget. 14 March 2008. . Retrieved 2008-11-23. [34] Huangfu D, Osafune K, Maehr R, Guo W, Eijkelenboom A, Chen S, Muhlestein W, Melton DA (2008). Induction of pluripotent stem cells from primary human fibroblasts with only Oct4 and Sox2. Nature Biotechnology, 26, 1269 - 1275. [35] http:/ / sexualhealth. e-healthsource. com/ index. php?p=news1& id=529147 [36] Ornoy A (2009). "Valproic acid in pregnancy: how much are we endangering the embryo and fetus?". Reprod Toxicol 28 (1): 110. doi:10.1016/j.reprotox.2009.02.014. PMID19490988. [37] Kulkarni ML, Zaheeruddin M, Shenoy N, Vani HN (October 2006). "Fetal valproate syndrome" (http:/ / medind. nic. in/ icb/ t06/ i10/ icbt06i10p937. pdf). Indian J Pediatr 73 (10): 9379. doi:10.1007/BF02859291. PMID17090909. . [38] British National Formulary (March 2003) 45 [39] Cassels, Caroline (December 8, 2006). "NEAD: In Utero Exposure To Valproate Linked to Poor Cognitive Outcomes in Kids" (http:/ / www. medscape. com/ viewarticle/ 549073). Medscape. . Retrieved 2007-05-23. [40] Meador KJ, Baker GA, Finnell RH, et al. (2006). "In utero antiepileptic drug exposure: Fetal death and malformations". Neurology 67 (3): 40712. doi:10.1212/01.wnl.0000227919.81208.b2. PMC1986655. PMID16894099. [41] Arndt TL, Stodgell CJ, Rodier PM (2005). "The teratology of autism". Int J Dev Neurosci 23 (23): 18999. doi:10.1016/j.ijdevneu.2004.11.001. PMID15749245. [42] Rinaldi T, Silberberg G, Markram H (2007). "Hyperconnectivity of local neocortical microcircuitry induced by prenatal exposure to valproic acid". Cereb Cortex 18 (4): 76370. doi:10.1093/cercor/bhm117. PMID17638926. [43] I.Q. Harmed by Epilepsy Drug in Utero (http:/ / www. nytimes. com/ 2009/ 04/ 16/ health/ research/ 16child. html) By RONI CARYN RABIN, New York Times, April 15, 2009 [44] Cognitive function at 3 years of age after fetal exposure to antiepileptic drugs (http:/ / content. nejm. org/ cgi/ content/ full/ 360/ 16/ 1597), Kimford J. Meador et al. for the NEAD Study Group, N Engl J Med 360:1597 April 16, 2009 [45] Meador KJ, Baker GA, Browning N et al. (2009). "Cognitive Function at 3 Years of Age after Fetal Exposure to Antiepileptic Drugs". New England Journal of Medicine 360 (16): 1597605. doi:10.1056/NEJMoa0803531. PMC2737185. PMID19369666. [46] http:/ / www. drugs. com/ fda/ valproate-products-safety-communication-risk-impaired-cognitive-development-children-exposed-utero-12994. html [47] "Highlights of Prescribing Information" (http:/ / www. rxabbott. com/ pdf/ dep3. pdf). . [48] Wadzinski J, Franks R, Roane D, Bayard M (2007). "Valproate-associated Hyperammonemic Encephalopathy". The Journal of the American Board of Family Medicine 20 (5): 499502. doi:10.3122/jabfm.2007.05.070062. PMID17823470. [49] Gerstner T, Bsing D, Longin E et al. (2007). "Valproic Acid associated encephalopathy -19 new cases in Germany from 1994 to 2003- a side effect associated to VPA-therapy not only in young children". Neuropediatrics 37 (6). doi:10.1055/s-2006-973995. [50] Williams DC Jr, Massey GV, Russell EC, Riley RS, Ben-Ezra J. (2007). "Translocation positive acute myeloid leukemia associated with valproic acid therapy". Pediatric Blood and Cancer. Mar 29 (3): 6413. doi:10.1002/pbc.21149. PMID17262798. [51] Coyle TE, Bair AK, Stein C, Vajpayee N, Mehdi S, Wright J. (2005). "Acute leukemia associated with valproic acid treatment: a novel mechanism for leukemogenesis?". Pediatric Blood and Cancer Apr (78): 25660. doi:10.1002/ajh.20273. PMID15795916. [52] Ricard C, Martin K, Tournier M, Bgaud B, Verdoux H (2005). "[A case of Parkinsonian syndrome, cognitive impairment and hyperammonemia induced by divalproate sodium prescribed for bipolar disorder]" (in French). L'Encphale 31 (1 Pt 1): 98101. doi:10.1016/S0013-7006(05)82378-4. PMID15971646. [53] McLachlan RS (1987). "Pseudoatrophy of the brain with valproic acid monotherapy". The Canadian journal of neurological sciences. Le journal canadien des sciences neurologiques 14 (3): 2946. PMID3117347. [54] Sztajnkrycer MD. Valproic acid toxicity: overview and management. Clin. Toxicol. 40: 789-801, 2002. [55] Thanacoody RH. Extracorporeal elimination in acute valproic acid poisoning. Clin. Toxicol. 47: 609-616, 2009. [56] R. Baselt, Disposition of Toxic Drugs and Chemicals in Man, 8th edition, Biomedical Publications, Foster City, CA, 2008, pp. 1622-1626. [57] Gonzalez, Frank J.; Robert H. Tukey (2006). "Drug Metabolism". In Laurence Brunton, John Lazo, Keith Parker (eds.). Goodman & Gilman's The Pharmacological Basis of Therapeutics (11th ed.). New York: McGraw-Hill. pp.79. ISBN978-0071422802. [58] "Depakene side effects (Valproic Acid) and drug interactions" (http:/ / www. rxlist. com/ cgi/ generic/ depakene_ad. htm). RxList.com. 2007. . Retrieved 2007-06-07. [59] http:/ / www. google. com/ patents?vid=4155929 [60] http:/ / worldwide. espacenet. com/ textdoc?DB=EPODOC& IDX=GB980279 [61] http:/ / www. google. com/ patents?vid=3325361 [62] http:/ / worldwide. espacenet. com/ textdoc?DB=EPODOC& IDX=GB1522450
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Further reading
T.R. Henry, "The History of Valproate in Clinical Neuroscience." Psychopharmacology bulletin (2003) 37 (Suppl 2):5-16 (http://www.medworksmedia.com/psychopharmbulletin/pdf/19/1-PB_VOL 37 SUPPL 2.pdf) (More details on history)
External links
The Lundbeck Institute Guide to Psychotropics - Valproic acid (http://www.psychotropics.dk/moleculeView/ default.aspx) http://www.psycheducation.org/depression/meds/moodstabilizers.htm http://www.psycheducation.org/depression/meds/valproate.htm The Comparative Toxicogenomics Database:Valproic Acid (http://ctdbase.org/detail.go?type=chem& acc=D014635) Chemical Land21: Valproic Acid (http://www.chemicalland21.com/lifescience/phar/VALPROIC ACID.htm) RXList.com: Depakene (Valproic Acid) (http://www.rxlist.com/cgi/generic2/depakene.htm) (U.S.) South African Electronic Package Inserts: Convulex (http://home.intekom.com/pharm/byk/convulex.html) Med Broadcast.com: Valproic Acid (http://www.medbroadcast.com/drug_info_list. asp?search_letter=VALPROIC ACID) (Canadian)
Sodium valproate
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Sodium valproate
Sodium valproate
sodium 2-propylpentanoate
Clinical data AHFS/Drugs.com monograph [1] MedlinePlus Pregnancy cat. Legal status Routes a682412
[2]
Pharmacokinetic data Protein binding Metabolism Half-life Excretion 9095% 75% by CYP enzymes 918 hours 20% excreted as glucuronide Identifiers CAS number ATC code PubChem ChemSpider UNII KEGG ChEBI ChEMBL 1069-66-5
[2]
[5] [3]
5VOM6GYJ0D D00710
[6] [7]
[5]
CHEBI:9925
[8]
C H NaO
8 15
& PubChem
[11]
[10]
Sodium valproate Sodium valproate (INN) or valproate sodium (USAN) is the sodium salt of valproic acid and is an anticonvulsant used in the treatment of epilepsy, anorexia nervosa, panic attack, anxiety disorder, posttraumatic stress disorder, migraine and bipolar disorder, as well as other psychiatric conditions requiring the administration of a mood stabilizer. Sodium valproate can be used to control acute episodes of mania and acute stress reaction. Side effects can include tiredness, tremors, nausea, vomiting and sedation.[12] The intravenous formulations are used when oral administration is not possible. In pregnancy, valproate has the highest risk of birth defects of any of the commonly-used antiepilepsy drugs. However, some epilepsy can only be controlled by valproate, and seizures also pose grave risk to mother and child. Some of the common adverse effects include: tiredness, tremor, sedation and gastrointestinal disturbances. In addition, about 10% of the users experience reversible hair loss. [13]
216
Formulations
Trade names are in bold, followed by the manufacturer.
U.S.
Intravenous injection Depacon by Abbott Laboratories. Syrup Depakene by Abbott Laboratories. (Note Depakene capsules are valproic acid). Depakote tablets are a mixture of sodium valproate and valproic acid.
Australia
Epilim Crushable Tablets Sanofi-Aventis Epilim Sugar Free Liquid Sanofi-Aventis Epilim Syrup Sanofi-Aventis Epilim Tablets Sanofi-Aventis Sodium Valproate Sandoz Tablets Sanofi-Aventis Valpro Tablets Alphapharm Valproate Winthrop Tablets Sanofi-Aventis
UK
Tablets Orlept by Wockhardt and Epilim by Sanofi-Aventis. Oral solution Orlept Sugar Free by Wockhardt and Epilim by Sanofi-Aventis. Syrup Epilim by Sanofi-Aventis. Intravenous injection Epilim Intravenous by Sanofi-Aventis. Extended release tablets Epilim Chrono by Sanofi-Aventis. A combination of sodium valproate and valproic acid in a 2.3:1 ratio. Enteric-coated tablets Epilim EC200 by Sanofi-synthlabo. A 200mg sodium valproate enteric-coated tablet.
Sodium valproate UK only Capsules Episenta prolonged release by Beacon. Sachets Episenta prolonged release by Beacon. Intravenous solution for injection Episenta solution for injection by Beacon.
217
South Africa
Syrup Convulex by Byk Madaus Tablets Epilim by sanofi~synthelabo
Canada
Intravenous injection Epival or Epiject by Abbott Laboratories. Syrup Depakene by Abbott Laboratories. Generic formulations include Apo-Valproic [14] and ratio-Valproic [15] .
Japan
Tablets Depakene by Kyowa Hakko Kirin. Extended release tablets Depakene-R by Kyowa Hakko Kogyo and Selenica-R by Kowa. Syrup Depakene by Kyowa Hakko Kogyo.
Europe
In much of Europe, Depakine and Depakine Chrono (tablets) are equivalent to Epilim and Epilim Chrono above.
Taiwan
Tablets (white round tablet) Depakine (Chinese: ; pinyin: di-ba-dian) by Sanofi Winthrop Industrie (France).
Safety in pregnancy
The risk of birth defects with valproate is two to five times higher than other frequently-used anti-epileptic drugs (absolute rates of birth defects 6-11%). Children born to mothers using valproate have significantly lower I.Q. scores (9 points). However, some epilepsy can only be controlled by valproate, and seizures during pregnancy can have grave consequences for both mother and child. Doctors recommend that women who intend to become pregnant should be switched to a different drug using combined therapy if possible, which takes several months. Women who are already pregnant and taking a high dose of valproate should try to lower their dose.[16] [17] [18] All antiepileptic medications have been shown to be associated with higher risks of fetal abnormalities (mostly for spina bifida) since at least 1983 with the risks being related to the strength of medication used and use of more than one drug[19] [20] Valproate has also been recognised as sometimes causing a specific facial changes ("facial phenotype") termed "fetal valproate syndrome".[21] Sodium valproate has been associated with the rare condition paroxysmal tonic upgaze of childhood, also known as Ouvrier-Billson syndrome, from childhood or fetal exposure (this condition resolved after discontinuing valproate therapy.[22] [23]
Sodium valproate While developmental delay is usually associated with altered physical characteristics (dysmorphic features), this is not always the case.[24] A 2005 study found rates of autism among children exposed to sodium valproate before birth in the cohort studied were 8.9%.[25] The normal incidence for autism in the general population is estimated at less than one percent.[26] It has been suggested that Valproate may best be avoided in women with localisation epilepsy, where there are more effective and less risky alternatives such as carbamazepine.[24] A 2008 study [27] also suggested a correlation between higher rates of autism in children whose mothers were treated for seizure disorders during pregnancy using sodium valproate (less than 1% for children who didn't receive the drug in vitro vs. 6.3% for children who did). However, only 632 children were followed in this study, prompting criticism that this study was too small to rely on to say whether there was a definitive correlation between the use of sodium valproate in pregnant mothers and higher autism rates in their children, or whether other anti-seizure medications used during pregnancy don't cause this effect. One multi-centre trial in the UK and US looked at cognitive function in 309 children born to mothers with epilepsy and found that sodium valproate-use was associated with an IQ level eight points lower in children born to mothers taking sodium valproate than mothers taking other anti-epileptic drugs.[28] The authors of the study attempted to correct for confounding factors, but this is an observational study, and therefore cannot prove a causal link. It should be noted, however, that to prove a causal link requires a randomised-controlled trial, which is not possible to perform.[29] It is therefore unlikely that any stronger evidence will become available. A class action is currently underway in the United Kingdom regarding the claim that the drug used in pregnancy caused a range of problems in children, including autism, learning and social difficulties, ADHD, spinal stenosis, facial abnormalities, vision defects, dyslexia, dyspraxia, delayed speech and motor development.[30] [31] [32]
218
References
[1] http:/ / www. drugs. com/ monograph/ valproate-sodium. html [2] http:/ / www. nlm. nih. gov/ cgi/ mesh/ 2009/ MB_cgi?term=1069-66-5& rn=1 [3] http:/ / pubchem. ncbi. nlm. nih. gov/ summary/ summary. cgi?cid=14047 [4] http:/ / www. chemspider. com/ Chemical-Structure. 13428 [5] http:/ / fdasis. nlm. nih. gov/ srs/ srsdirect. jsp?regno=5VOM6GYJ0D [6] http:/ / www. kegg. jp/ entry/ D00710 [7] https:/ / www. ebi. ac. uk/ chebi/ searchId. do?chebiId=CHEBI:9925 [8] https:/ / www. ebi. ac. uk/ chembldb/ index. php/ compound/ inspect/ CHEMBL433 [9] http:/ / www. emolecules. com/ cgi-bin/ search?t=ex& q=%5BNa%2B%5D. %5BO-%5DC%28%3DO%29C%28CCC%29CCC [10] http:/ / pubchem. ncbi. nlm. nih. gov/ search/ ?smarts=%5BNa%2B%5D. %5BO-%5DC%28%3DO%29C%28CCC%29CCC [11] http:/ / en. wikipedia. org/ wiki/ Special%3Acomparepages?rev1=464404696& page2=%3ASodium+ valproate [12] Gelder, M., Mayou, R., Geddes, J. (2006) Psychiarty. 3rd edition. Oxford: Oxford University Press [13] Gelder, M, Mayou, R. and Geddes, J. 2005. Psychiatry. 3rd ed. New York: Oxford. pp250. [14] http:/ / www. apotex. ca/ Products/ EN/ Detail. asp?MaterialNumber=000000000000042290 [15] http:/ / www. ratiopharm. ca/ e/ Products/ productSearch. asp?Cap=V [16] I.Q. Harmed by Epilepsy Drug in Utero (http:/ / www. nytimes. com/ 2009/ 04/ 16/ health/ research/ 16child. html) By RONI CARYN RABIN, New York Times, April 15, 2009 [17] Cognitive function at 3 years of age after fetal exposure to antiepileptic drugs (http:/ / content. nejm. org/ cgi/ content/ full/ 360/ 16/ 1597), Kimford J. Meador et al. for the NEAD Study Group, N Engl J Med 360:1597 April 16, 2009 [18] Which drug for the pregnant woman with epilepsy? (http:/ / content. nejm. org/ cgi/ content/ full/ 360/ 16/ 1667) Torbjorn Tomson, N Engl J Med 360:1597 April 16, 2009 [19] Koch S, Gpfert-Geyer I, Jger-Roman E, et al. (February 1983). "[Anti-epileptic agents during pregnancy. A prospective study on the course of pregnancy, malformations and child development]" (in German). Dtsch. Med. Wochenschr. 108 (7): 2507. doi:10.1055/s-2008-1069536. PMID6402356. [20] Moore SJ, Turnpenny P, Quinn A, et al. (July 2000). "A clinical study of 57 children with fetal anticonvulsant syndromes" (http:/ / jmg. bmj. com/ cgi/ pmidlookup?view=long& pmid=10882750). J. Med. Genet. 37 (7): 48997. doi:10.1136/jmg.37.7.489. PMC1734633. PMID10882750. . [21] DiLiberti JH, Farndon PA, Dennis NR, Curry CJ (November 1984). "The fetal valproate syndrome". Am. J. Med. Genet. 19 (3): 47381. doi:10.1002/ajmg.1320190308. PMID6439041.
Sodium valproate
[22] Epileptic Disord. 2007 Sep; 9(3):332-6 [23] J Child Neurol. 1988 Jul;3(3):177-80 [24] Adab N, Kini U, Vinten J, et al. (November 2004). "The longer term outcome of children born to mothers with epilepsy" (http:/ / jnnp. bmj. com/ cgi/ content/ full/ 75/ 11/ 1575). J. Neurol. Neurosurg. Psychiatr. 75 (11): 157583. doi:10.1136/jnnp.2003.029132. PMC1738809. PMID15491979. . "This argues that the fetal valproate syndrome constitutes a real clinical entity that includes developmental delay and cognitive impairments, but that some children might exhibit some developmental delay without marked dysmorphism." [25] Rasalam AD, Hailey H, Williams JH, et al. (August 2005). "Characteristics of fetal anticonvulsant syndrome associated autistic disorder" (http:/ / www. blackwell-synergy. com/ openurl?genre=article& sid=nlm:pubmed& issn=0012-1622& date=2005& volume=47& issue=8& spage=551). Dev Med Child Neurol 47 (8): 5515. doi:10.1017/S0012162205001076. PMID16108456. . [26] Autism Society of America: About Autism (http:/ / www. autism-society. org/ site/ PageServer?pagename=about_home) [27] Bromley L, Mawer G, Clayton-Smith J, Baker GA, et al. (December 2008). "Autism spectrum disorders following in utero exposure to antiepileptic drugs" (http:/ / www. neurology. org/ cgi/ content/ full/ 71/ 23/ 1923). Neurology 71 (23): 19234. doi:10.1212/01.wnl.0000339399.64213.1a. PMID19047565. . [28] Meador KJ, Baker GA, Browning N, et al. (2009). "Cognitive function at 3 years of age after fetal exposure to antiepileptic drugs" (http:/ / content. nejm. org/ cgi/ content/ abstract/ 360/ 16/ 1597?ijkey=40a3bc71b9fbaf20b868a2f9bff104523ac6b696& keytype2=tf_ipsecsha). N Engl J Med 360 (16): 15971605. doi:10.1056/NEJMoa0803531. PMC2737185. PMID19369666. . [29] Tomson T (2009). "Which drug for the pregnant woman with epilepsy?" (http:/ / content. nejm. org/ cgi/ content/ full/ 360/ 16/ 1667). N Engl J Med 360 (16): 16671669. doi:10.1056/NEJMe0901550. PMID19369673. . [30] Families Sue Europes Largest Drug Company Over Anti-Convulsant Drug as Deadline Is Given By High Court (http:/ / web. archive. org/ web/ 20060722003428/ http:/ / www. irwinmitchell. com/ PressOffice/ PressReleases/ epilepsy-drug-claims. htm) [31] "Legal action over Epilim" (http:/ / www. epilepsy. org. uk/ node/ 1149). Epilepsy Action. 24 April 2007. . Retrieved 15 April 2009. [32] Brimelow A (1 October 2004). "Women sue over epilepsy drug risk" (http:/ / news. bbc. co. uk/ 2/ hi/ health/ 3705384. stm). BBC News. . Retrieved 15 April 2009.
219
External links
Chemical Land21: Sodium Valproate (http://www.chemicalland21.com/lifescience/phar/SODIUM VALPORATE.htm) RXList.com: Depacon (Sodium Valproate) (http://www.rxlist.com/cgi/generic/valproate.htm) British National Formulary Edition 58 (http://www.bnf.org/bnf/bnf/current/noframes/index.htm) Med Broadcast.com: Epival (http://www.medbroadcast.com/drug_info_details.asp?brand_name_id=547) Drugs.com: Depaken Syrup (http://www.drugs.com/PDR/Depakene_Syrup.html)
Valproate semisodium
220
Valproate semisodium
Valproate semisodium (INN) or divalproex sodium (USAN) consists of a compound of sodium valproate and valproic acid in a 1:1 molar relationship in an enteric coated form. It is used in the United Kingdom, Canada, and United States for the treatment of the manic episodes of bipolar disorder. In rare cases, it is also used as a treatment for major depressive disorder, and increasingly taken long-term for prevention of both manic and depressive phases of bipolar disorder, especially the rapid-cycling variant. It is also used in the US for the treatment of epilepsy, certain side effects of autism, chronic pain associated with neuropathy, and migraine headaches. Its chemical name is sodium hydrogen bis(2-propylpentanoate). The extended release formulation allows for a single daily dose. In the UK semisodium valproate has been sold for a few years as the proprietary drug Depakote and marketed for psychiatric conditions only. It is about five times the price of sodium valproate, which has been marketed for around 30 years as Epilim by the same company for epilepsy and is also available from other manufacturers as a generic product.
Side effects
The most severe side effect is a ten times higher-than-average incidence rate of serious, irreversible birth defects (teratogenic) such as births of brainless babies (anencephaly). Risk of birth defects such as spina bifida has been demonstrated among populations of female patients who took the medicine in childbearing age. Otherwise, people who take this drug can experience a variety of side effects, some of which may require immediate medical attention. Mild side effects include: dizziness decreased coordination misbalance Especially dangerous side effects include: vomiting loss of appetite fever dark urine jaundice
The above side effects suggest a possibility of liver damage. People taking this drug should also call their doctor if they experience other serious side effects. Some serious side effects include: unusual bleeding (especially in the urine) hallucinations drowsiness Some people also experience: constipation diarrhea 1% to 10% of people report: weight gain increased appetite abnormal dreams[1]
Valproate semisodium
221
Branded formulations
Brazil Depakote by Abbott Laboratories Canada Epival by Abbott Laboratories. Mexico Epival and Epival ER (Extended Release) by Abbott Laboratories. United Kingdom Depakote by Sanofi-Aventis United States Depakote and Depakote ER (Extended Release) by Abbott Laboratories and generics India Valance and Valance OD by Abbott Healthcare Pvt Ltd Germany Ergenyl Chrono by Sanofi-Aventis and generics Chile Valcote and Valcote ER by Abbott Laboratories France and other European countries Dpakine Chrono and generics
Additional brand names for this medication include Depacon, Depakene and Zalkote[2] In the United States, generic versions of Depakote became available on July 29, 2008.[3]
References
Notes
[1] Drug Information Handbook, 15th ed. [2] http:/ / ssl. search. live. com/ health/ article. aspx?id=articles%2fgs%2fpages%2f2%2f637-122. htm& q=Depakote [3] http:/ / fdanews. com/ newsletter/ article?issueId=11836& articleId=109236
External links
RXList.com: Depakote (Divalproex sodium) (http://www.rxlist.com/cgi/generic/dival.htm) British National Formulary Edition 50 (http://www.bnf.org/bnf/bnf/current/noframes/index.htm) Drugs.com Advanced Consumer Info: Valproic Acid (http://www.drugs.com/cons/valproic_acid.html) Depakote (Official) - Abbott Laboratories (http://rxabbott.com/pdf/depakote.pdf) Drug Information Online (http://www.drugs.com/depakote.html) Mayo Clinic drug information (http://www.mayoclinic.com/health/drug-information/DR602951)
Lithium pharmacology
222
Lithium pharmacology
Lithium pharmacology refers to use of the lithium ion, Li+, as a drug. A number of chemical salts of lithium are used medically as a mood stabilizing drug, primarily in the treatment of bipolar disorder, where they have a role in the treatment of depression and particularly of mania, both acutely and in the long term. As a mood stabilizer, lithium is probably more effective in preventing mania than depression, and may reduce the risk of suicide in certain bipolar patients.[1] In depression alone (unipolar disorder) lithium can be used to augment Lithium citrate other antidepressants. Lithium carbonate (Li2CO3), sold under several trade names, is the most commonly prescribed, while the citrate salt lithium citrate (Li3C6H5O7) is also used in conventional pharmacological treatments. The sulfate salt lithium sulfate (Li2SO4) has been presented as an alternative. Lithium orotate (orotic acid) is sometimes marketed as a "safe" natural alternative with fewer side-effects than conventional lithium, yet caution must be taken with all of the active lithium salts. Upon ingestion, lithium becomes widely distributed in the central nervous system and interacts with a number of neurotransmitters and receptors, decreasing norepinephrine release and increasing serotonin synthesis.
Medical uses
Lithium treatment is used to treat mania in bipolar disorder. Initially, lithium is often used in conjunction with antipsychotic drugs as it can take up to a month for lithium to have an effect. Lithium is also used as prophylaxis for depression and mania in bipolar disorder. It is sometimes used for other psychiatric disorders such as cycloid psychosis and major depressive disorder.[2] [3] Lithium possesses a very important antisuicidal effect not shown in other stabilizing medications such as antiseizures drugs.[4] [4] [5] Non-psychiatric applications are limited; however, its use is well established in the prophylaxis of some headaches related to cluster headaches (trigeminal autonomic cephalgias), particularly hypnic headache. An Italian pilot study in humans conducted in 200506 suggested that lithium may improve outcomes in the neurodegenerative disease amyotrophic lateral sclerosis.[6] [7] However, a randomised, double-blind, placebo-controlled trial comparing the safety and efficacy of lithium in combination with riluzole for treatment of amyotrophic lateral sclerosis failed to demonstrate any benefit from a combination therapy over riluzole alone.[8] Lithium is sometimes used as an augmenting agent to increase the benefits of standard drugs used for unipolar depression. Lithium treatment was previously considered to be unsuitable for children; however, more recent studies show its effectiveness for treatment of early-onset bipolar disorder in children as young as eight. The required dosage (1520mg per kg of body weight) is slightly less than the toxic level, requiring blood levels of lithium to be monitored closely during treatment. To prescribe the correct dosage, the patient's entire medical history, both physical and psychological, is sometimes taken into consideration. The starting dosage of lithium should be 400600mg given at night and increased weekly depending on serum monitoring.[9] Those who use lithium should receive regular serum level tests and should monitor thyroid and kidney function for abnormalities. As it interferes with the regulation of sodium and water levels in the body, lithium can cause dehydration. Dehydration, which is compounded by heat, can result in increasing lithium levels. The reason why water is lost is because Lithium inhibits the action of antidiuretic hormone (ADH) which enables the kidney to reabsorb water from urine. This causes an inability to concentrate urine leading to consequent loss of body water and thirst.[10]
Lithium pharmacology High doses of haloperidol, fluphenazine, or flupenthixol may be hazardous when used with lithium; irreversible toxic encephalopathy has been reported. Lithium salts have a narrow therapeutic/toxic ratio and should therefore not be prescribed unless facilities for monitoring plasma concentrations are available. Patients should be carefully selected. Doses are adjusted to achieve plasma concentrations of 0.4[11] [12] to 1.2mmol Li+/L (lower end of the range for maintenance therapy and elderly patients, higher end for pediatric patients) on samples taken 12 hours after the preceding dose. Overdosage, usually with plasma concentrations over 1.5mmol Li+/L, may be fatal, and toxic effects include tremor, ataxia, dysarthria, nystagmus, renal impairment, confusion, and convulsions. If these potentially hazardous signs occur, treatment should be stopped, plasma lithium concentrations redetermined, and steps taken to reverse lithium toxicity. The most common side effects are an overall dazed feeling and a fine hand tremor. These side effects are generally present during the length of the treatment, but can sometimes disappear in certain patients. Other common side effects, such as nausea and headache, can be generally remedied by a higher intake of water. Lithium unbalances electrolytes; to counteract this, increased water intake is suggested. Lithium toxicity is compounded by sodium depletion. Concurrent use of diuretics that inhibit the uptake of sodium by the distal tubule (e.g. thiazides) is hazardous and should be avoided. In mild cases, withdrawal of lithium and administration of generous amounts of sodium and fluid will reverse the toxicity. Plasma concentrations in excess of 2.5mmol Li+/L are usually associated with serious toxicity requiring emergency treatment. When toxic concentrations are reached, there may be a delay of 1 or 2 days before maximum toxicity occurs. In long-term use, therapeutic concentrations of lithium have been thought to cause histological and functional changes in the kidney. The significance of such changes is not clear, but is of sufficient concern to discourage long-term use of lithium unless it is definitely indicated. Doctors may change a bipolar patient's medication from lithium to another mood stabilizing drug, such as valproate (Depakote), if problems with the kidneys arise. An important potential consequence of long-term lithium usage is the development of renal diabetes insipidus (inability to concentrate urine). Patients should therefore be maintained on lithium treatment after 35 years only if, on assessment, benefit persists. Conventional and sustained-release tablets are available. Preparations vary widely in bioavailability, and a change in the formulation used requires the same precautions as initiation of treatment. There are few reasons to prefer any one simple salt of lithium; the carbonate has been the more widely used, but the citrate is also available. Lithium may be used as a treatment of seborrhoeic dermatitis (Lithium gluconate 8% gel). In addition, lithium has been shown to increase production of white blood cells in the bone marrow and might be indicated in patients suffering from leukopenia.[13] A limited amount of evidence suggests that lithium may contribute to treatment of substance abuse for some dual-disorder patients.[14] [15] [16]
223
Side effects
The average developmental score for the lithium-exposed group of children was 78 points lower than the control group (siblings), but well within the normal range of 10015.[17] Cognitive depression in adults is disputed. Lithium is known to be responsible for significant amounts of weight gain.[18] It increases the appetite and thirst ("polydypsia", potentially causing nephrogenic diabetes insipidus), may cause more depression than before with suicidal thoughts and actions, and reduces the activity of thyroid hormone (hypothyroidism).[19] [20] [21] [22] [23] It is also believed to affect renal function.[24] Lithium is a well known cause of downbeat nystagmus.[25] The nystagmus may be permanent or require several months of abstinence for improvement.[26] Lithium is also a teratogen causing birth defects in a small number of new born babies.[27] If taken during a woman's pregnancy can cause her child to develop Ebstein's anomaly, a heart defect.
Lithium pharmacology
224
Dehydration
Dehydration in patients taking Lithium salts can be very hazardous especially when combined with nephrogenic diabetes insipidus and thus polyuria. Low sodium in water they drink may very quickly produce hyponatremia with its danger of toxic Lithium concentrations in plasma. Situation such as: preoperative fluid regimen (ECT) or otherwise fluid unaccessibility, warm water conditions, sporting events, hiking.
Overdose
Lithium toxicity may occur in persons taking excessive amounts either accidentally or intentionally on an acute basis or in patients who accumulate high levels during ongoing chronic therapy. The manifestations include nausea, emesis, diarrhea, asthenia, ataxia, confusion, lethargy, polyuria, seizures and coma. Other toxic effects of lithium also include coarse tremor, muscle twitching, convulsions and renal failure.[28] Persons who survive a poisoning episode may develop persistent neurotoxicity.
Mechanism of action
Unlike other psychoactive drugs, Li+ typically produces no obvious psychotropic effects (such as euphoria) in normal individuals at therapeutic concentrations. The precise mechanism of action of Li+ as a mood-stabilizing agent is currently unknown. It is possible that Li+ produces its effects by interacting with the transport of monovalent or divalent cations in neurons. However, because it is a poor substrate at the sodium pump, it cannot maintain a membrane potential and only sustains a small gradient across biological membranes. Li+ is similar enough to Na+ that under experimental conditions, Li+ can replace Na+ for production of a single action potential in neurons. Recent research suggests three different mechanisms which may or may not act together to deliver the mood-stabilizing effect of this ion.[31] The excitatory neurotransmitter glutamate could be involved in the effect of lithium as other mood stabilizers such as valproate and lamotrigine exert influence over glutamate, suggesting a possible biological explanation for mania. The other mechanisms by which lithium might help to regulate mood include the alteration of gene expression.[32] An unrelated mechanism of action has been proposed in which lithium deactivates the GSK3 enzyme.[33] This enzyme normally phosphorylates the Rev-Erb transcription factor protein stabilizing it against degradation. Rev-Erb in turn represses BMAL1, a component of the circadian clock. Hence lithium by inhibiting GSK3 causes the degradation of Rev-Erb and increases the expression of BMAL which dampens the circadian clock[34] Through this mechanism, lithium is able to block the resetting of the "master clock" inside the brain; as a result, the body's natural cycle is disrupted. When the cycle is disrupted, the routine schedules of many functions (metabolism, sleep, body temperature) are disturbed. Lithium may thus restore normal brain function after it is disrupted in some people. Another mechanism proposed in 2007 is that lithium may interact with nitric oxide (NO) signalling pathway in the central nervous system, which plays a crucial role in the neural plasticity. Ghasemi et al. (2008, 2009) have shown that the NO system could be involved in the antidepressant effect of lithium in the Porsolt forced swimming test in mice.[35] [36] It was also reported that NMDA receptor blockage augments antidepressant-like effects of lithium in the mouse forced swimming test,[37] indicating the possible involvement of NMDA receptor/NO signaling in the
Lithium pharmacology action of lithium in this animal model of learned helplessness. Lithium treatment has been found to inhibit the enzyme inositol monophosphatase, leading to higher levels of inositol triphosphate.[38] This effect was enhanced further with an inositol triphosphate reuptake inhibitor. Inositol disruptions have been linked to memory impairment and depression.
225
History
Lithium was first used in the nineteenth century as a treatment for gout after scientists discovered that, at least in the laboratory, lithium could dissolve uric acid crystals isolated from the kidneys. The levels of lithium needed to dissolve urate in the body, however, were toxic.[39] Because of prevalent theories linking excess uric acid to a range of disorders, including depressive and manic disorders, Carl Lange in Denmark[40] and William Alexander Hammond in New York[41] used lithium to treat mania from the 1870s onwards though there are reports of its use in the form of spring waters to treat mania in Roman and Greek times. By the turn of the century, this use of lithium was largely abandoned, according to Susan Greenfield due to the reluctance of the pharmaceutical industry to invest in a drug that could not be patented.[42] As accumulating knowledge indicated a role for excess sodium intake in hypertension and heart disease, lithium salts were prescribed to patients for use as a replacement for dietary table salt (sodium chloride). This practise was discontinued in 1949 when reports of side effects and deaths were published, leading to a ban of lithium sales.[39] The use of lithium salts to treat mania was rediscovered by the Australian psychiatrist John Cade in 1949. Cade was injecting rodents with urine extracts taken from schizophrenic patients, in an attempt to isolate a metabolic compound which might be causing mental symptoms. Since uric acid in gout was known to be psychoactive (adenosine receptors on neurons are stimulated by it; caffeine blocks them), Cade needed soluble urate for a control. He used lithium urate, already known to be the most soluble urate compound, and observed that this caused the rodents to be tranquilized. Cade traced the effect to the lithium ion itself. Soon, Cade proposed lithium salts as tranquilizers, and soon succeeded in controlling mania in chronically hospitalized patients with them. This was one of the first successful applications of a drug to treat mental illness, and it opened the door for the development of medicines for other mental problems in the next decades.[43] The rest of the world was slow to adopt this treatment, largely because of deaths which resulted from even relatively minor overdosing, including those reported from use of lithium chloride as a substitute for table salt. Largely through the research and other efforts of Denmark's Mogens Schou and Paul Baastrup in Europe,[39] and Samuel Gershon and Baron Shopsin in the U.S., this resistance was slowly overcome. The application of lithium for mania in manic illness was approved by the United States Food and Drug Administration in 1970.[44] In 1974 this application was extended to the use of lithium as a preventive agent for manic-depressive illness. In 2009, Japanese researchers at Oita University reported that low levels of naturally-occurring lithium in drinking water supplies reduced suicide rates.[45] A previous report had found similar data in the American state of Texas.[46] In response, psychiatrist Peter Kramer raised the hypothetical possibility of adding lithium to drinking water.[47] Lithium has become a part of Western popular culture. Characters in Pi, Premonition, Stardust Memories, American Psycho, and An Unmarried Woman all take lithium. Sirius XM Satellite Radio in North America has a 1990s alternative rock station called Lithium, and several songs refer to the use of lithium as a mood stabilizer. These include: "Lithium Lips" by Mac Lethal, "Equilibrium met Lithium" by South African artist Koos Kombuis, "Lithium" by Evanescence, "Lithium" by Nirvana, "Lithium and a Lover" by Sirenia, "Lithium Sunset", from the album Mercury Falling by Sting,[48] "Tea and Thorazine" by Andrew Bird, and "Lithium" by Thin White Rope.
Lithium pharmacology
226
Use in 7 Up
As with cocaine in Coca-Cola, lithium was widely marketed as one of a number of patent medicine products popular in the late-19th and early-20th centuries, and was the medicinal ingredient of a refreshment beverage, 7 Up. Charles Leiper Grigg, who launched his St. Louis-based company The Howdy Corporation in 1920, invented a formula for a lemon-lime soft drink in 1929. The product, originally named "Bib-Label Lithiated Lemon-Lime Soda", was launched two weeks before the Wall Street Crash of 1929.[49] It contained the mood stabiliser lithium citrate and was one of a number of patent medicine products popular in the late-19th and early-20th centuries.[50] Its name was soon changed to 7 Up; all American beverage makers were forced to remove lithium in 1948.
References
[1] Baldessarini RJ, Tondo L, Davis P, Pompili M, Goodwin FK, Hennen J (2006). "Decreased risk of suicides and attempts during long-term lithium treatment: a meta-analytic review.". Bipolar disorders 8 (5 Pt 2): 62539. doi:10.1111/j.1399-5618.2006.00344.x. PMID17042835. [2] Mash, Eric J.; Russell A. Barkley (2006). Treatment of childhood disorders (http:/ / books. google. com/ ?id=KCZqs_NlfmQC). Guilford Press. p.443. ISBN1572309210. . [3] Schatzberg, Alan F.; Jonathan O. Cole, Charles DeBattista (2007). Manual of clinical psychopharmacology (http:/ / books. google. com/ ?id=NvT0l6iL5IQC). American Psychiatric Publishing. p.267. ISBN1585623172. . [4] Mller-Oerlinghausen, B; Berghfer, A; Ahrens, B (2003). "The Antisuicidal and Mortality-Reducing Effect of Lithium Prophylaxis: Consequences for Guidelines in Clinical Psychiatry" (https:/ / ww1. cpa-apc. org/ Publications/ Archives/ CJP/ 2003/ august/ muller. asp). Canadian Journal of Psychiatry 48 (7): 4339. PMID12971012. . [5] Kovacsics, Colleen E.; Gottesman, Irving I.; Gould, Todd D. (2009). "Lithium's Antisuicidal Efficacy: Elucidation of Neurobiological Targets Using Endophenotype Strategies". Annual Review of Pharmacology and Toxicology 49: 175198. doi:10.1146/annurev.pharmtox.011008.145557. PMID18834309. [6] "Lithium Slows ALS Progression In Study" (http:/ / www. als-mda. org/ research/ news/ 080204Lithium_slows_ALS. html). Muscular Dystrophy Association. 2008-02-04. . Retrieved 2009-06-23. [7] Fornai, F.; Longone, P.; Cafaro, L.; Kastsiuchenka, O.; Ferrucci, M.; Manca, M. L.; Lazzeri, G.; Spalloni, A. et al. (2008). "Lithium delays progression of amyotrophic lateral sclerosis". Proceedings of the National Academy of Sciences 105 (6): 20522057. doi:10.1073/pnas.0708022105. [8] Aggarwal, SP; Zinman L, Simpson E, McKinley J, Jackson KE, Pinto H, Kaufman P, Conwit RA, Schoenfeld D, Shefner J, Cudkowicz M (2010). "Safety and efficacy of lithium in combination with riluzole for treatment of amyotrophic lateral sclerosis: a randomised, double-blind, placebo-controlled trial". Lancet Neurology 9 (5): 4818. doi:10.1016/S1474-4422(10)70068-5. PMC3071495. PMID20363190. [9] Semple, David"oxford hand book of psychiatry" oxford press. 2005. [10] Healy D. 2005. Psychiatric Drugs Explained. 4th ed. Churchhill Livingstone: London. [11] The UK Electronic Medical Compendium recommends 0.40.8 mmol/L plasma lithium level in adlults for Prophylaxis of recurrent affective bipolar manic-depressive illness Camcolit 250 mg Lithium Carbonate (http:/ / www. medicines. org. uk/ emc/ document. aspx?documentId=1239) Revision 2 December 2010, Retrieved 5 May 2011 [12] One study (Solomon, D.; Ristow, W.; Keller, M.; Kane, J.; Gelenberg, A.; Rosenbaum, J.; Warshaw, M. (1996). "Serum lithium levels and psychosocial function in patients with bipolar I disorder". The American journal of psychiatry 153 (10): 13011307. PMID8831438.) concluded that a "low" dose of 0.40.6 mmol/L serum lithium treatment for patients with bipolar 1 disorder had less side effects, but a higher rate of relapse, than a "standard" dose of 0.81.0 mmol/L. However, a re-analysis of the same experimental data (Perlis, R.; Sachs, G.; Lafer, B.; Otto, M.; Faraone, S.; Kane, J.; Rosenbaum, J. (2002). "Effect of abrupt change from standard to low serum levels of lithium: A reanalysis of double-blind lithium maintenance data". The American journal of psychiatry 159 (7): 11551159. PMID12091193.) concluded that the higher rate of relapse for the "low" dose was due to abrupt changes in the lithium serum levels [13] Vieweg, W. V. R.; Yank, Rowe, Hovermale, Clayton (Fall 1986). "Increase in White Blood Cell Count and Serum Sodium Level Following the Addition of Lithium to Carbamazephine Treatment among three chronically Psychotic male Patients with disturbed Affective States" (http:/ / resources. metapress. com/ pdf-preview. axd?code=u11w152782481762& size=largest). Psychiatric Quarterly 583: 213. . Retrieved 2010-04-20. [14] Rosenberg, J.; Salzman, C. (2007). "Update: New uses for lithium and anticonvulsants". CNS spectrums 12 (11): 831841. PMID17984856. [15] Frye, M. A.; Salloum, I. M. (2006). "Bipolar disorder and comorbid alcoholism: Prevalence rate and treatment considerations". Bipolar Disorders 8 (6): 677685. doi:10.1111/j.1399-5618.2006.00370.x. PMID17156154. [16] Vornik, L.; Brown, E. (2006). "Management of comorbid bipolar disorder and substance abuse". The Journal of clinical psychiatry 67 Suppl 7: 2430. PMID16961421. [17] Neurobehavioral Outcome following Lithium Exposure (http:/ / www. womensmentalhealth. org/ resources/ PDFs/ LandL2006. pdf) [18] Sperner-Unterweger, Barbara; W. Wolfgang Fleischhacker, Wolfgang P. Kaschka (2001). Psychoneuroimmunology (http:/ / books. google. com/ ?id=Q0xJfkY5VRUC). Karger Publishers. p.22. ISBN380557262X. . [19] Keshavan, Matcheri S.; John S. Kennedy (2001). Drug-induced dysfunction in psychiatry (http:/ / books. google. com/ ?id=pol0204fqjIC). Taylor & Francis. p.305. ISBN089116961X. .
Lithium pharmacology
[20] Side Effects Lithium / Various Brand Names Bipolar Disorder Medications (http:/ / bipolar. about. com/ cs/ sfx/ a/ sfx_lithium. htm) [21] Bipolar Medications and Weight Gain (http:/ / www. psycheducation. org/ hormones/ Insulin/ weightgain. htm) [22] Nutrition Articles The Relationship between Weight Gain and Medications for Depression and Seizures (http:/ / www. netnutritionist. com/ fa12. htm) [23] Safer lithium therapy (http:/ / www. nrls. npsa. nhs. uk/ resources/ patient-safety-topics/ medication-safety/ ?entryid45=65426). NHS National Patient Safety Agency. Issue date: 1 December 2009 [24] Bendz, Hans; Schn, Attman, Aurell (February 1, 2010). "Renal failure occurs in chronic lithium treatment but is uncommon". Kidney International 77 (3): 219. doi:10.1038/ki.2009.433. PMID19940841. [25] Lee, Michael S.; Lessell, Simmons (January 28, 2003). "Lithium-induced periodic alternating nystagmus". Neurology (journal) 60 (2): 344. doi:10.1212/01.WNL.0000042787.51461.D1. PMID12552061. [26] Williams, Douglas P.; Jack Rogers and B. Todd Troost (September 1988). "Lithium-Induced Downbeat Nystagmus". Archives of Neurology 45 (9): 10221023. doi:10.1212/01.WNL.0000042787.51461.D1. PMID12552061. [27] Shepard, TH.; Brent, RL.; Friedman, JM.; Jones, KL.; Miller, RK.; Moore, CA.; Polifka, JE. (2002). "Update on new developments in the study of human teratogens". Teratology 65 (4): 15361. doi:10.1002/tera.10032. PMID11948561. [28] Gelder, M., Mayou, R. and Geddes, J. 2005. Psychiatry. 3rd ed. New York: Oxford. pp249. [29] Amdisen A. (1978). "Clinical and serum level monitoring in lithium therapy and lithium intoxication". J. Anal. Toxicol. 2: 193202. [30] R. Baselt, Disposition of Toxic Drugs and Chemicals in Man, 8th edition, Biomedical Publications, Foster City, CA, 2008, pp. 851854. [31] Jope RS (1999). "Anti-bipolar therapy: mechanism of action of lithium". Mol. Psychiatry 4 (2): 117128. doi:10.1038/sj.mp.4000494. PMID10208444. [32] Lenox RH, Wang L (February 2003). "Molecular basis of lithium action: integration of lithium-responsive signaling and gene expression networks". Mol. Psychiatry 8 (2): 13544. doi:10.1038/sj.mp.4001306. PMID12610644. [33] Klein PS, Melton DA (August 1996). "A molecular mechanism for the effect of lithium on development". Proc. Natl. Acad. Sci. U.S.A. 93 (16): 84559. doi:10.1073/pnas.93.16.8455. PMC38692. PMID8710892. [34] Yin L, Wang J, Klein PS, Lazar MA (February 2006). "Nuclear receptor Rev-erbalpha is a critical lithium-sensitive component of the circadian clock". Science 311 (5763): 10025. doi:10.1126/science.1121613. PMID16484495. Lay summary (http:/ / www. the-scientist. com/ news/ display/ 23129/ )The Scientist. [35] Ghasemi M, Sadeghipour H, Mosleh A, Sadeghipour HR, Mani AR, Dehpour AR (May 2008). "Nitric oxide involvement in the antidepressant-like effects of acute lithium administration in the mouse forced swimming test". Eur Neuropsychopharmacol 18 (5): 32332. doi:10.1016/j.euroneuro.2007.07.011. PMID17728109. [36] Ghasemi M, Sadeghipour H, Poorheidari G, Dehpour AR (June 2009). "A role for nitrergic system in the antidepressant-like effects of chronic lithium treatment in the mouse forced swimming test". Behav. Brain Res. 200 (1): 7682. doi:10.1016/j.bbr.2008.12.032. PMID19166880. [37] Ghasemi M, Raza M, Dehpour AR (April 2010). "NMDA receptor antagonists augment antidepressant-like effects of lithium in the mouse forced swimming test". J. Psychopharmacol. (Oxford) 24 (4): 58594. doi:10.1177/0269881109104845. PMID19351802. [38] Einat H, Kofman O, Itkin O, Lewitan RJ, Belmaker RH (1998). "Augmentation of lithium's behavioral effect by inositol uptake inhibitors". J Neural Transm 105 (1): 318. doi:10.1007/s007020050035. PMID9588758. [39] Marmol, F. (2008). "Lithium: bipolar disorder and neurodegenerative diseases Possible cellular mechanisms of the therapeutic effects of lithium". Progress in neuro-psychopharmacology & biological psychiatry 32 (8): 17611771. doi:10.1016/j.pnpbp.2008.08.012. PMID18789369. [40] Lenox, RH; Watson, DG (1994). "Lithium and the brain: a psychopharmacological strategy to a molecular basis for manic depressive illness". Clinical chemistry 40 (2): 30914. PMID8313612. [41] Mitchell, PB; Hadzi-Pavlovic, D (2000). "Lithium treatment for bipolar disorder" (https:/ / www. who. int/ entity/ bulletin/ archives/ 78(4)515. pdf). Bulletin of the World Health Organization 78 (4): 5157. PMC2560742. PMID10885179. . [42] Greenfield, Susan: "Brain Power: Working out the Human Mind", page 91. Element Books Limited, 1999 [43] Cade J. F. J. (1949). "Lithium salts in the treatment of psychotic excitement" (http:/ / www. who. int/ docstore/ bulletin/ pdf/ 2000/ issue4/ classics. pdf) (PDF). Medical Journal of Australia 2 (10dfbnm): 34952. PMID18142718. . [44] P. B. Mitchell, D. Hadzi-Pavlovic (2000). "Lithium treatment for bipolar disorder" (http:/ / www. who. int/ docstore/ bulletin/ pdf/ 2000/ issue4/ classics. pdf) (PDF). Bulletin of the World Health Organization 78 (4): 5157. PMC2560742. PMID10885179. . [45] Ohgami H. Terao T. et al, Lithium levels in drinking water and risk of suicide. British Journal of Psychiatry. 194(5):4645; discussion 446, May 2009 [46] Gonzalez R. Bernstein I., et al. An investigation of water lithium concentrations and rates of violent acts in 11 Texas counties: can an association be easily shown? Journal of Clinical Psychiatry. 69(2):3256, 2008 Feb. [47] Listening to Lithium (http:/ / www. doublex. com/ section/ health-science/ listening-lithium) Sept 9. 2009 [48] Agassi, Tirzah (1996-03-12). "Sting is now older, wiser and duller" (http:/ / pqasb. pqarchiver. com/ jpost/ access/ 62551750. html?dids=62551750:62551750& FMT=ABS& FMTS=ABS:FT& date=Mar+ 12,+ 1996& author=TIRZAH+ AGASSI& pub=Jerusalem+ Post& desc=Sting+ is+ now+ older,+ wiser+ and+ duller). The Jerusalem Post. . Retrieved 2009-06-25. [49] " 7 UP: The Making of a Legend (http:/ / web. archive. org/ web/ 20080430022917/ http:/ / www. brandspeoplelove. com/ csab/ ?TabId=148)". Cadbury Schweppes: America's Beverages. [50] "Urban Legends Reference Pages: 7Up" (http:/ / www. snopes. com/ business/ names/ 7up. asp). . Retrieved 2007-11-13.
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External links
Official FDA information (http://www.drugs.com/pro/lithium-carbonate.html) published by Drugs.com "Exposing lithium's circadian action" (http://www.the-scientist.com/news/display/23129/) http://www.psycheducation.org/depression/meds/moodstabilizers.htm http://www.psycheducation.org/depression/meds/lithium.html SID 685039 PubChem Substance Summary (Lithium Oxybutyrate) (http://pubchem.ncbi.nlm.nih.gov/ summary/summary.cgi?sid=685039) N05 AN01 (http://www.whocc.no/atc_ddd_index/?code=N05AN01)
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Lithium carbonate
Lithium carbonate
Identifiers CAS number PubChem ChemSpider UNII KEGG ChEBI ChEMBL RTECS number Jmol-3D images 554-13-2 11125 10654
[2] [3] [4] [1]
2BMD2GNA4V D00801
[5] [6]
CHEBI:6504
[7]
Molecular formula Molar mass Appearance Density Melting point Boiling point Solubility in water
Li2CO3 73.891 g/mol Odorless white powder 2.11 g/cm3 723C, 996K, 1333F 1310C, 1583K, 2390F (decomp.) 15.4 g/L (0 C) 13.2 g/L (20 C) 7.2 g/L (100 C) insoluble in acetone and ethanol
D
1.428
[9]
16.46 kJ/g
298
Lithium carbonate
[10]
230
MSDS EU Index Main hazards Flash point LD50
Other cations
(what is: / ?) Except where noted otherwise, data are given for materials in their standard state (at 25C, 100kPa)
Infobox references
Lithium carbonate is a chemical compound of lithium, carbon, and oxygen with the formula Li2CO3. This colorless salt is widely used in the processing of metal oxides and has received attention for its use in psychiatry. It is found in nature as the rare mineral zabuyelite.[12]
Properties
Like almost all other lithium compounds, Li2CO3 is polymeric. It is an ionic compound. Lithium carbonate is soluble in water, and thus can be used either as a source of the lithium ion or the carbonate ion, but it is not that soluble, which is rare, given that lithium compounds typically have exceptional aqueous solubility. The isolation of lithium from aqueous extracts of its ores capitalizes on this poor solubility. Its apparent solubility increases tenfold under a mild pressure of carbon dioxide; this effect is due to the formation of the metastable bicarbonate: Li2CO3 + CO2 + H2O 2 LiHCO3 Lithium carbonate, and other carbonates of Group 1, do not decompose readily, unlike other carbonates. Li2CO3 decomposes at temperatures >1300 C.
Applications
Lithium carbonate is an important industrial chemical. It forms low-melting fluxes with silica and other materials. Glasses derived from lithium carbonate are useful in ovenware. Lithium carbonate is a common ingredient in both low-fire and high-fire ceramic glaze. Its alkaline properties are conducive to changing the state of metal oxide colorants in glaze particularly red iron oxide (Fe2O3). Cement sets more rapidly when prepared with lithium carbonate, and is useful for tile adhesives. When added to aluminium trifluoride, it forms LiF which gives a superior electrolyte for the processing of aluminium.[13] Lithium carbonate is used as an active material of carbon dioxide sensors.[14] It is also used in the manufacture of most lithium-ion battery cathodes, which are made of lithium cobalt oxide.
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Medical uses
In 1843, lithium carbonate was used as a new solvent for stones in the bladder. In 1859, some doctors recommended a therapy with lithium salts for a number of ailments including gout, urinary calculi, rheumatism, mania, depression and headache. In 1949, Cade discovered the anti-manic effects of lithium ions. This knowledge led lithium, specifically lithium carbonate to be used to treat mania associated with bipolar disorder. Lithium carbonate is used to treat mania, the elevated phase of bipolar disorder. Lithium ions interfere with ion transport processes (see sodium pump) that relay and amplify messages carried to the cells of the brain.[15] In mania there is an observed irregular increase in protein kinase C (PKC) activity within the brain. A recent study has shown that lithium carbonate and sodium valproate, another drug traditionally used to treat the disorder, act in the brain by inhibiting PKCs activity and help to create other compounds that also inhibit the PKC.[16] Additionally, daily doses of lithium have been found to delay progression of amyotrophic lateral sclerosis (ALS) in an Italian study of 44 people with the disorder. No other treatment to date has shown such a dramatic effect on ALS.[17] Despite these findings, a great deal remains unknown regarding lithium's mood controlling properties. Recently, topical lithium has been utilized in dermatological disorders, such as herpes viral infections. It is hoped that lithium will be used in the future as an anti-inflammatory, antiviral, anti-fungal, and anti-tumor agent. Lithium salts when used at low doses do not cause addiction, but do have a number of risks and side effects associated with their use, especially at higher doses. Lithium intoxication affects the central nervous system and renal system and is potentially lethal.[18]
Pyrotechnics
Lithium carbonate is found in fireworks, because lithium imparts a deep red to flames.
References
[1] http:/ / www. commonchemistry. org/ ChemicalDetail. aspx?ref=554-13-2 [2] http:/ / pubchem. ncbi. nlm. nih. gov/ summary/ summary. cgi?cid=11125 [3] http:/ / www. chemspider. com/ 10654 [4] http:/ / fdasis. nlm. nih. gov/ srs/ srsdirect. jsp?regno=2BMD2GNA4V [5] http:/ / www. kegg. jp/ entry/ D00801 [6] https:/ / www. ebi. ac. uk/ chebi/ searchId. do?chebiId=6504 [7] https:/ / www. ebi. ac. uk/ chembldb/ index. php/ compound/ inspect/ CHEMBL1200826 [8] http:/ / chemapps. stolaf. edu/ jmol/ jmol. php?model=%5BLi%2B%5D. %5BLi%2B%5D. %5BO-%5DC%28%5BO-%5D%29%3DO [9] Pradyot Patnaik. Handbook of Inorganic Chemicals. McGraw-Hill, 2002, ISBN 0070494398 [10] http:/ / www. inchem. org/ documents/ icsc/ icsc/ eics1109. htm [11] http:/ / en. wikipedia. org/ wiki/ Special%3Acomparepages?rev1=462092421& page2=%3ALithium+ carbonate [12] David Barthelmy. "Zabuyelite Mineral Data" (http:/ / webmineral. com/ data/ Zabuyelite. shtml). Mineralogy Database. . Retrieved 2010-02-07. [13] Ulrich Wietelmann, Richard J. Bauer "Lithium and Lithium Compounds" in Ullmann's Encyclopedia of Industrial Chemistry 2005, Wiley-VCH: Weinheim. [14] Technical Information for Carbon Dioxide Sensors (http:/ / www. figarosensor. com/ products/ 4161Dtl. pdf) [15] Medical use (http:/ / www. medicinenet. com/ lithium/ article. htm) [16] Yildiz, A; Guleryuz, S; Ankerst, DP; Ongr, D; Renshaw, PF (2008). "Protein kinase C inhibition in the treatment of mania: a double-blind, placebo-controlled trial of tamoxifen". Archives of general psychiatry 65 (3): 25563. doi:10.1001/archgenpsychiatry.2007.43. PMID18316672. [17] MDA Research|Lithium Slows ALS Progression In Study (http:/ / www. als-mda. org/ research/ news/ 080204Lithium_slows_ALS. html) [18] Simard, M; Gumbiner, B; Lee, A; Lewis, H; Norman, D (1989). "Lithium carbonate intoxication. A case report and review of the literature" (http:/ / archinte. highwire. org/ cgi/ reprint/ 149/ 1/ 36. pdf). Archives of internal medicine 149 (1): 3646. doi:10.1001/archinte.149.1.36. PMID2492186. .
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Lithium citrate
Lithium citrate
Identifiers CAS number ChemSpider ChEMBL RTECS number Jmol-3D images 919-16-4 12932
[2] [1] [3]
(what is: / ?) Except where noted otherwise, data are given for materials in their standard state (at 25C, 100kPa)
Infobox references
Lithium citrate (Li3C6H5O7) is a chemical compound of lithium and citrate that is used as a mood stabilizer in psychiatric treatment of manic states and bipolar disorder.[6] For the medical aspects of lithium citrate, see lithium pharmacology. Hundreds of soft drinks included lithium salts or lithia water (naturally occurring mineral waters with higher lithium amounts). An early version of Coca-Cola available in pharmacies' soda fountains called Lithia Coke was a mixture of Coca-Cola syrup and lithia water.[7] The soft drink 7Up was originally named "Bib-Label Lithiated Lemon-Lime Soda" when it was formulated in 1929 because it contained lithium citrate. The beverage was a patent medicine
Lithium citrate marketed as a cure for hangover. Lithium citrate was removed from 7Up in 1948.[8] Lithium citrate is sold as Litarex and Demalit.
233
References
[1] [2] [3] [4] [5] [6] [7] [8] http:/ / www. commonchemistry. org/ ChemicalDetail. aspx?ref=919-16-4 http:/ / www. chemspider. com/ 12932 https:/ / www. ebi. ac. uk/ chembldb/ index. php/ compound/ inspect/ CHEMBL1201170 http:/ / chemapps. stolaf. edu/ jmol/ jmol. php?model=%5BLi%2B%5D. %5BLi%2B%5D. %5BLi%2B%5D. O%3DC%28%5BO-%5D%29CC%28O%29%28C%28%5BO-%5D%29%3DO%29CC%28%3DO%29%5BO-%5D http:/ / en. wikipedia. org/ wiki/ Special%3Acomparepages?rev1=400144718& page2=%3ALithium+ citrate Medical use (http:/ / www. nami. org/ Template. cfm?Section=About_Medications& Template=/ TaggedPage/ TaggedPageDisplay. cfm& TPLID=51& ContentID=20820) And Now Lithium in Water (http:/ / www. scribd. com/ doc/ 14956227/ And-Now-Lithium-in-Water-Curbs-Suicide) Gielen, Marcel; Edward R. T. Tiekink (2005). Metallotherapeutic drugs and metal-based diagnostic agents: The use of metals in medicine. John Wiley and Sons. p.3. ISBN0470864036.
Lithium sulfate
234
Lithium sulfate
Lithium sulfate
OJ6419000 Properties
[3]
Li2SO4 109.94 g/mol White crystalline solid, hygroscopic 2.221 g/cm (anhydrous) 3 2.06 g/cm (monohydrate) 859 C 1377 C monohydrate: 34.9 g/100 mL (25 C) 29.2 g/100 mL (100 C) insoluble in absolute ethanol, acetone and pyridine
D 3
1436.37 kJ/mol
298
Not listed
(what is: / ?) Except where noted otherwise, data are given for materials in their standard state (at 25C, 100kPa)
Infobox references
Lithium sulfate Lithium sulfate is a white inorganic salt with the formula Li2SO4. It is the lithium salt of sulfuric acid.
235
Properties
Lithium sulfate is soluble in water, though it does not follow the usual trend of solubility versus temperature its solubility in water decreases with increasing temperature, as its dissolution is an endothermic process. This property is shared with few inorganic compounds, such as the lanthanoid sulfates. Lithium sulfate crystals, being piezoelectric, are also used in ultrasound-type non-destructive testing because they are very efficient sound generators. However, they do suffer in this application because of their water solubility.
Uses
Lithium sulfate is used to treat bipolar disorder (see lithium pharmacology).
References
[1] http:/ / www. commonchemistry. org/ ChemicalDetail. aspx?ref=10377-48-7 [2] http:/ / pubchem. ncbi. nlm. nih. gov/ summary/ summary. cgi?cid=66320 [3] Patnaik, Pradyot (2002). Handbook of Inorganic Chemicals. McGraw-Hill. ISBN0070494398. [4] http:/ / en. wikipedia. org/ wiki/ Special%3Acomparepages?rev1=450706600& page2=%3ALithium+ sulfate
236
Non-pharmaceutical treatment
Clinical psychology
Clinical psychology is an integration of science, theory and clinical knowledge for the purpose of understanding, preventing, and relieving psychologically-based distress or dysfunction and to promote subjective well-being and personal development.[1] [2] Central to its practice are psychological assessment and psychotherapy, although clinical psychologists also engage in research, teaching, consultation, forensic testimony, and program development and administration.[3] In many countries, clinical psychology is a regulated mental health profession. The field is often considered to have begun in 1896 with the opening of the first psychological clinic at the University of Pennsylvania by Lightner Witmer. In the first half of the 20th century, clinical psychology was focused on psychological assessment, with little attention given to treatment. This changed after the 1940s when World War II resulted in the need for a large increase in the number of trained clinicians. Since that time, two main educational models have developedthe Ph.D. scientistpractitioner model (requiring a doctoral dissertation and therefore research as well as clinical expertise); and the Psy.D. practitionerscholar model (in which a doctoral level dissertation is not required). Clinical psychologists are now considered experts in providing psychotherapy, psychological testing, and in diagnosing mental illness. They generally train within four primary theoretical orientationspsychodynamic, humanistic, behavior therapy/cognitive behavioral, and systems or family therapy. Many continue clinical training in post-doctoral programs in which they might specialize more intensively in disciplines such as psychoanalytic approaches, or child and adolescent treatment modalities.
History
Further information: Eastern philosophy and clinical psychologyandIslamic psychology Although modern, scientific psychology is often dated at the 1879 opening of the first psychological laboratory by Wilhelm Wundt, attempts to create methods for assessing and treating mental distress existed long before. The earliest recorded approaches were a combination of religious, magical and/or medical perspectives.[4] Early examples of such physicians included Patajali, Padmasambhava,[5] Rhazes, Avicenna,[6] and Rumi.[7] In the early 19th century, one could have his or her head examined, literally, using phrenology, the study of personality by the shape of the skull. Other popular treatments included physiognomythe study of the shape of the faceand mesmerism, Mesmer's treatment by the use of magnets. Spiritualism and Phineas Quimby's "mental healing" were also popular.[8] While the scientific community eventually came to reject all of these methods, academic psychologists also were not concerned with serious forms of mental illness. That area was already being addressed by the developing fields of psychiatry and neurology within the asylum movement.[4] It was not until the end of the 19th century, around the time when Sigmund Freud was first developing his "talking cure" in Vienna, that the first scientifically clinical application of psychology began.
Many 18th c. treatments for psychological distress were based on pseudo-scientific ideas, such as phrenology.
Clinical psychology
237
Even as clinical psychology was growing, working with issues of serious mental distress remained the domain of psychiatrists and neurologists.[12] However, clinical psychologists continued to make inroads into this area due to their increasing skill at psychological assessment. Psychologists' reputation as assessment experts became solidified during World War I with the development of two intelligence tests, Army Alpha and Army Beta (testing verbal and nonverbal skills, respectively), which could be used with large groups of recruits.[8] [9] Due in large part to the success of these tests, assessment was to become the core discipline of clinical psychology for the next quarter century, when another war would propel the field into treatment.
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A changing profession
Since the 1970s, clinical psychology has continued growing into a robust profession and academic field of study. Although the exact number of practicing clinical psychologists is unknown, it is estimated that between 1974 and 1990, the number in the US grew from 20,000 to 63,000.[20] Clinical psychologists continue to be experts in assessment and psychotherapy while expanding their focus to address issues of gerontology, sports, and the criminal justice system to name a few. One important field is health psychology, the fastest-growing employment setting for clinical psychologists in the past decade.[8] Other major changes include the impact of managed care on mental health care; an increasing realization of the importance of knowledge relating to multicultural and diverse populations; and emerging privileges to prescribe psychotropic medication. Approximately 20% of clinical health
Clinical psychology psychologists identify themselves as counseling psychologists as well.[21] In the UK psychology is now one of the most popular degree subjects, and over 15,000 people graduate in psychology each year, many with the hope of developing this into a career, although only around 600 places for doctoral training in clinical psychology means there is intense competition for these places.[22] [23] There is also fierce competition to get into US Ph.D. programs in clinical psychology, with an average acceptance rate of 8%.[24]
239
Professional practice
Clinical psychologists can offer a range of professional services, including:[10] Administer and interpret psychological assessment and testing Conduct psychological research Consultation (especially with schools and businesses) Development of prevention and treatment programs Program administration Provide expert testimony (forensic psychology) Provide psychological treatment (psychotherapy) Teach
In practice, clinical psychologists may work with individuals, couples, families, or groups in a variety of settings, including private practices, hospitals, mental health organizations, schools, businesses, and non-profit agencies. Most clinical psychologists who engage in research and teaching do so within a college or university setting. Clinical psychologists may also choose to specialize in a particular fieldcommon areas of specialization, some of which can earn board certification,[25] include: Child and adolescent Family and relationship counseling Forensic Health Neuropsychological disorders Organization and business School Specific disorders (e.g. trauma, addiction, eating, sleep, sex, clinical depression, anxiety, or phobias) Sport
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Clinical psychology In the UK, registration as a clinical psychologist with the Health Professions Council (HPC) is necessary. The HPC is the statutory regulator for practitioner psychologists in the UK. In the UK the following titles are restricted by law: "registered psychologist" and "practitioner psychologist"; in addition, the specialist title "clinical psychologist" is also restricted by law.
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Assessment
An important area of expertise for many clinical psychologists is psychological assessment, and there are indications that as many as 91% of psychologists engage in this core clinical practice.[38] Such evaluation is usually done in service to gaining insight into and forming hypotheses about psychological or behavioral problems. As such, the results of such assessments are usually used to create generalized impressions (rather than diagnoses) in service to informing treatment planning. Methods include formal testing measures, interviews, reviewing past records, clinical observation, and physical examination.[2] There exist literally hundreds of various assessment tools, although only a few have been shown to have both high validity (i.e., test actually measures what it claims to measure) and reliability (i.e., consistency). These measures generally fall within one of several categories, including the following: Intelligence & achievement tests These tests are designed to measure certain specific kinds of cognitive functioning (often referred to as IQ) in comparison to a norming-group. These tests, such as the WISC-IV, attempt to measure such traits as general knowledge, verbal skill, memory, attention span, logical reasoning, and visual/spatial perception. Several tests have been shown to predict accurately certain kinds of performance, especially scholastic.[38] Personality tests Tests of personality aim to describe patterns of behavior, thoughts, and feelings. They generally fall within two categories: objective and projective. Objective measures, such as the MMPI, are based on restricted answerssuch as yes/no, true/false, or a rating scalewhich allow for computation of scores that can be compared to a normative group. Projective tests, such as the Rorschach inkblot test, allow for open-ended answers, often based on ambiguous stimuli, presumably revealing non-conscious psychological dynamics. Neuropsychological tests Neuropsychological tests consist of specifically designed tasks used to measure psychological functions known to be linked to a particular brain structure or pathway. They are typically used to assess impairment after an injury or illness known to affect neurocognitive functioning, or when used in research, to contrast neuropsychological abilities across experimental groups. Clinical observation Clinical psychologists are also trained to gather data by observing behavior. The clinical interview is a vital part of assessment, even when using other formalized tools, which can employ either a structured or unstructured format. Such assessment looks at certain areas, such as general appearance and behavior, mood and affect, perception, comprehension, orientation, insight, memory, and content of communication. One psychiatric example of a formal interview is the mental status examination, which is often
Clinical psychology used in psychiatry as a screening tool for treatment or further testing.[38]
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Diagnostic impressions
After assessment, clinical psychologists often provide a diagnostic impression. Many countries use the International Statistical Classification of Diseases and Related Health Problems (ICD-10) while the US most often uses the Diagnostic and Statistical Manual of Mental Disorders (the DSM version IV-TR). Both assume medical concepts and terms, and state that there are categorical disorders that can be diagnosed by set lists of descriptive criteria.[39] Several new models are being discussed, including a "dimensional model" based on empirically validated models of human differences (such as the five factor model of personality[39] [40] ) and a "psychosocial model," which would take changing, intersubjective states into greater account.[41] The proponents of these models claim that they would offer greater diagnostic flexibility and clinical utility without depending on the medical concept of illness. However, they also admit that these models are not yet robust enough to gain widespread use, and should continue to be developed. Some clinical psychologists do not tend to diagnose, but rather use formulationan individualized map of the difficulties that the patient or client faces, encompassing predisposing, precipitating and perpetuating (maintaining) factors.[42]
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Clinical psychology Multiple assessment techniques have come from this approach including functional analysis (psychology), which has found a strong focus in the school system. In addition, multiple intervention programs have come from this tradition including community reinforcement and family training for treating addictions, acceptance and commitment therapy, functional analytic psychotherapy, integrative behavioral couples therapy including dialectical behavior therapy and behavioral activation. In addition, specific techniques such as contingency management and exposure therapy have come from this tradition. Systems or family therapy Systems or family therapy works with couples and families, and emphasizes family relationships as an important factor in psychological health. The central focus tends to be on interpersonal dynamics, especially in terms of how change in one person will affect the entire system.[51] Therapy is therefore conducted with as many significant members of the "system" as possible. Goals can include improving communication, establishing healthy roles, creating alternative narratives, and addressing problematic behaviors. Contributors include John Gottman, Jay Haley, Sue Johnson, and Virginia Satir.
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Other perspectives
Multiculturalism Although the theoretical foundations of psychology are rooted in European culture, there is a growing recognition that there exist profound differences between various ethnic and social groups and that systems of psychotherapy need to take those differences into greater consideration.[44] Further, the generations following immigrant migration will have some combination of two or more cultureswith aspects coming from the parents and from the surrounding societyand this process of acculturation can play a strong role in therapy (and might itself be the presenting problem). Culture influences ideas about change, help-seeking, locus of control, authority, and the importance of the individual versus the group, all of which can potentially clash with certain givens in mainstream psychotherapeutic theory and practice.[57] As such, there is a growing movement to integrate knowledge of various cultural groups in order to inform therapeutic practice in a more culturally sensitive and effective way.[58] Feminism Feminist therapy is an orientation arising from the disparity between the origin of most psychological theories (which have male authors) and the majority of people seeking counseling being female. It focuses on societal, cultural, and political causes and solutions to issues faced in the counseling process. It openly encourages the client to participate in the world in a more social and political way.[59] Positive psychology Positive psychology is the scientific study of human happiness and well-being, which started to gain momentum in 1998 due to the call of Martin Seligman,[60] then president of the APA. The history of psychology shows that the field has been primarily dedicated to addressing mental illness rather than mental wellness. Applied positive psychology's main focus, therefore, is to increase one's positive experience of life and ability to flourish by promoting such things as optimism about the future, a sense of flow in the present, and personal traits like courage, perseverance, and altruism.[61] [62] There is now preliminary empirical evidence to show that by promoting Seligman's three components of happinesspositive emotion (the pleasant life), engagement (the engaged life), and meaning (the meaningful life)positive therapy can decrease clinical depression.[63]
Integration
In the last couple of decades, there has been a growing movement to integrate the various therapeutic approaches, especially with an increased understanding of cultural, gender, spiritual, and sexual-orientation issues. Clinical psychologists are beginning to look at the various strengths and weaknesses of each orientation while also working with related fields, such as neuroscience, genetics, evolutionary biology, and psychopharmacology. The result is a growing practice of eclecticism, with psychologists learning various systems and the most efficacious methods of therapy with the intent to provide the best solution for any given problem.[64]
Professional ethics
The field of clinical psychology in most countries is strongly regulated by a code of ethics. In the US, professional ethics are largely defined by the APA Code of Conduct, which is often used by states to define licensing requirements. The APA Code generally sets a higher standard than that which is required by law as it is designed to guide responsible behavior, the protection of clients, and the improvement of individuals, organizations, and society.[65] The Code is applicable to all psychologists in both research and applied fields. The APA Code is based on five principles: Beneficence and Nonmaleficence, Fidelity and Responsibility, Integrity, Justice, and Respect for People's Rights and Dignity.[65] Detailed elements address how to resolve ethical issues, competence, human relations, privacy and confidentiality, advertising, record keeping, fees, training, research, publication, assessment, and therapy.
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Fluoxetine hydrochloride, branded by Lilly as Prozac, is a common antidepressant drug prescribed by psychiatrists. There is a small but growing movement to give prescription privileges to qualified psychologists.
Clinical psychologists generally do not prescribe medication, although there is a growing movement for psychologists to have prescribing privileges.[67] These medical privileges require additional training and education. To date, medical psychologists may prescribe psychotropic medications in Guam, New Mexico, and Louisiana and military psychologists.[68]
Counseling psychology
Counseling psychologists study and use many of the same interventions and tools as clinical psychologists, including psychotherapy and assessment. Traditionally, counseling psychologists help people with what might be considered normal or moderate psychological problemssuch as the feelings of anxiety or sadness resulting from major life changes or events.[3] [10] Many counseling psychologists also receive specialized training in career assessment, group therapy, and relationship counseling, although some counseling psychologists also work with the more serious problems that clinical psychologists are trained for, such as dementia or psychosis. There are fewer counseling psychology graduate programs than those for clinical psychology and they are more often housed in departments of education rather than psychology. The two professions can be found working in all the same settings but counseling psychologists are more frequently employed in university counseling centers compared to hospitals and private practice for clinical psychologists.[69]
School psychology
Clinical psychology
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Comparison of mental health professionals in USA Occupation Degree Common Licenses Prescription Privilege Ave. 2004 Income (USD) Psychologist MFT/LPC MFT/LPC/LPA Psychologist Psychiatrist LCSW Mostly no No No No Yes No No Yes (Varies by state) No $75,000 $65,000 $49,000 $78,000 $145,600 $36,170 $53,450 $75,711 $45,000
Clinical Psychologist Counseling Psychologist (Doctorate) Counseling Psychologist (Master's) School Psychologist Psychiatrist Clinical Social Worker Psychiatric Nurse
Sources:
School psychologists are primarily concerned with the academic, social, and emotional well-being of children and adolescents within a scholastic environment. In the UK, they are known as "educational psychologists." Like clinical psychologists and counselling psychologists, school psychologists with doctoral degrees are eligible for licensure as health service psychologists, and many work in private practice. Unlike clinical psychologists, they receive much more training in education, child development and behavior, and the psychology of learning. Common degrees include the Educational Specialist Degree (Ed.S.), Doctor of Philosophy (Ph.D.), and Doctor of Education (Ed.D.). Traditional job roles for school psychologists employed in school settings have focused mainly on assessment of students to determine their eligibility for special education services in schools, and on consultation with teachers and other school professionals to design and carry out interventions on behalf of students. Other major roles also include offering individual and group therapy with children and their families, designing prevention programs (e.g. for reducing dropout), evaluating school programs, and working with teachers and administrators to help maximize teaching efficacy, both in the classroom and systemically.[76] [77]
Occupational therapy
Occupational therapyoften abbreviated OTis the "use of productive or creative activity in the treatment or rehabilitation of physically, cognitively, or emotionally disabled people."[79] Most commonly, occupational therapists work with people with disabilities to enable them to maximize their skills and abilities. Occupational therapy practitioners are skilled professionals whose education includes the study of human growth and development with specific emphasis on the physical, emotional, psychological, sociocultural, cognitive and environmental components of illness and injury. They commonly work alongside clinical psychologists in settings such as inpatient and outpatient mental health, pain management clinics, eating disorder clinics, and child development services. OT's use support groups, individual counseling sessions, and activity-based approaches to address psychiatric symptoms and maximize functioning in life activities. In chronic pain management, occupational therapists use the common cognitive behavioral therapy approach, often incorporating cognitive behavioral therapy techniques and helping
Clinical psychology clients generalize or integrate their pain management strategies into their lives. In this way, occupational therapists both support and extend the work that clinical psychologists carry out in a clinical setting.[80]
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Cover of The Psychological Clinic, the first journal of clinical psychology, published in 1907 by Lightner Witmer
Journal of Clinical Psychology in Medical Settings Journal of Clinical Psychopharmacology Journal of Consulting and Clinical Psychology Journal of Contemporary Psychotherapy Journal of Family Psychotherapy
Clinical psychology Journal of Psychotherapy Integration Journal of Psychotherapy Praxis & Research Journal of Rational-Emotive and Cognitive Behaviour Therapy Journal of Social and Clinical Psychology Psychopathology Psychotherapy & Psychosomatics Psychotherapy Research
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Major influences
Aaron Beck Abraham Maslow Albert Bandura Albert Ellis Alfred Adler Anna Freud Carl Gustav Jung Carl Rogers David Shakow Donald Woods Winnicott Erich Fromm Erik H. Erikson Fritz Perls George Kelly Gordon Allport Hans Eysenck Harry Stack Sullivan Heinz Kohut Irvin Yalom James Bugental John Bowlby John Gottman Joseph Wolpe Karen Horney Lightner Witmer Milton H. Erickson Otto F. Kernberg Otto Rank Rebecca Hill Robert Yerkes Rollo May Ronald David Laing Sigmund Freud Stanislav Grof
Clinical psychology Melanie Klein Morita Shoma Viktor Frankl Wilhelm Reich
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References
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External links
American Academy of Clinical Psychology (http://www.aacpsy.org/) American Association for Marriage and Family Therapy (http://www.aamft.org/) American Board of Professional Psychology (http://www.abpp.org/) Annual Review of Clinical Psychology (http://arjournals.annualreviews.org/loi/clinpsy/) APA Society of Clinical Psychology (Division 12) (http://www.apa.org/divisions/div12/homepage.html) Psychology Careers Blog (http://psycholocareersblog.com) Articles and other great content on Careers in Psychology Association of State and Provincial Psychology Boards (ASPPB) (http://www.asppb.org/) Info on the field of psychology form the U.S. Department of Labor, Bureau of Labor Statistics (http://www.bls. gov/oco/ocos056.htm) International Society of Clinical Psychology (http://www.iscp.org/) Journal of Clinical Psychiatry (http://www.psychiatrist.com/) NAMI: National Alliance on Mental Illness (http://www.nami.org/) National Institute of Mental Health (http://www.nimh.nih.gov/)
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Electroconvulsive therapy
Electroconvulsive therapy
Intervention ICD-10-PCS ICD-9-CM MeSH GZB 94.27 [1] [2] [3]
D004565
Electroconvulsive therapy (ECT), formerly known as electroshock, is a psychiatric treatment in which seizures are electrically induced in anesthetized patients for therapeutic effect. Its mode of action is unknown.[5] Today, ECT is most often recommended for use as a treatment for severe depression that has not responded to other treatment, and is also used in the treatment of mania and catatonia.[6] It was first introduced in 1938 by Italian neuropsychiatrists Ugo Cerletti and Lucio Bini, and gained widespread use as a form of treatment in the 1940s and 1950s.[7] [8] Electroconvulsive therapy can differ in its application in three ways: electrode placement, frequency of treatments, and the electrical waveform of the stimulus. These three forms of application have significant differences in both adverse side effects and positive outcomes. After treatment, drug therapy is usually continued, and some patients receive continuation/maintenance ECT. In the United Kingdom and Ireland, drug therapy is continued during ECT.[6] Informed consent is a standard of modern electroconvulsive therapy.[9] According to the Surgeon General, involuntary treatment is uncommon in the United States and is typically used only in cases of great extremity, and only when all other treatment options have been exhausted. The use of ECT is believed to be a potentially life-saving treatment.[10] However, caution must be exercised in interpreting this assertion as, in an American context, there does not appear to have been any attempt to survey at national level the usage of ECT as either an elective or involuntary procedure in almost twenty years.[11] In one of the few jurisdictions where recent statistics on ECT usage are available, a national audit of ECT by the Scottish ECT Accreditation Network indicated that 77% of patients who received the treatment in 2008 were capable of giving informed consent.[12] Despite the fact that the majority of psychiatric clinicians regard ECT as a safe and effective procedure, surveys of public opinion, the testimony of former patients, legal restrictions on its use and disputes as to the efficacy, ethics and adverse effects of ECT within the psychiatric and wider medical community indicate that the use of ECT remains controversial.[13] [14] [15] [16] [17] [18] This is reflected in the recent decision by the FDA's Neurological Devices Advisory Panel to maintain ECT devices in the Class III device category for high risk devices except for patients suffering from catatonia. This will result in the manufacturers of such devices having to do controlled trials on their safety and efficacy for the first time.[19] In justifying their position, panelists referred to the memory loss associated with ECT and the lack of long-term data.[20]
Electroconvulsive therapy
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History
As early as the 16th century, agents to produce seizures were used to treat psychiatric conditions. In 1785, the therapeutic use of seizure induction was documented in the London Medical Journal.[5] Convulsive therapy was introduced in 1934 by Hungarian neuropsychiatrist Ladislas J. Meduna who, believing mistakenly that schizophrenia and epilepsy were antagonistic disorders, induced seizures with first camphor and then metrazol (cardiazol).[21] [22] In 1937, the first international meeting on convulsive therapy was held in Switzerland by the Swiss psychiatrist Muller. The proceedings were published in the American Journal of Psychiatry and, within three years, cardiazol convulsive therapy was being used worldwide.[22] Italian Professor of neuropsychiatry Ugo Cerletti, who had been using electric shocks to produce seizures in animal experiments, and his colleague Lucio Bini developed the idea of using electricity as a substitute for metrazol A psychotron, apparatus for administering electroshocks in convulsive therapy and, in 1937, experimented for the first time on a person. Sherwin B. Nuland, having discussed the matter with a first-hand observer in the 1970s, gave the following description of the results of the first use of ECT on a person: "They thought, 'Well, we'll try 55 volts, two-tenths of a second. That's not going to do anything terrible to him.' So they did that. [...] This fellow remember, he wasn't even put to sleep after this major grand-mal convulsion, sat right up, looked at these three fellows and said, 'What the fuck are you assholes trying to do?' Well, they were happy as could be, because he hadn't said a rational word in the weeks of observation."[23] ECT soon replaced metrazol therapy all over the world because it was cheaper, less frightening and more convenient.[24] Cerletti and Bini were nominated for a Nobel Prize but did not receive one. By 1940, the procedure was introduced to both England and the US. In Germany and Austria it was promoted by Friedrich Meggendorfer. Through the 1940s and 1950s, the use of ECT became widespread. ECT is the only form of shock treatment still performed by modern medicine. In the early 1940s, in an attempt to reduce the memory disturbance and confusion associated with treatment, two modifications were introduced: the use of unilateral electrode placement and the replacement of sinusoidal current with brief pulse. It took many years for brief-pulse equipment to be widely adopted[25] Unilateral ECT has never been popular with psychiatrists and is still given to only a minority of ECT patients.[5] In the 1940s and early 1950s ECT was usually given in "unmodified" form, without muscle relaxants, and the seizure resulted in a full-scale convulsion. A rare but serious complication of unmodified ECT was fracture or dislocation of the long bones. In the 1940s psychiatrists began to experiment with curare, the muscle-paralysing South American poison, in order to modify the convulsions. The introduction of suxamethonium (succinylcholine), a safer synthetic alternative to curare, in 1951 led to the more widespread use of "modified" ECT. A short-acting anesthetic was usually given in addition to the muscle relaxant in order to spare patients the terrifying feeling of suffocation that can be experienced with muscle relaxants.[25] The steady growth of antidepressant use along with negative depictions of ECT in the mass media led to a marked decline in the use of ECT during the 1950s to the 1970s. The Surgeon General stated there were problems with electroshock therapy in the initial years before anesthesia was routinely given, and that "these now-antiquated
Electroconvulsive therapy practices contributed to the negative portrayal of ECT in the popular media."[26] The New York Times described the public's negative perception of ECT as being caused mainly by one movie. "For Big Nurse in One Flew Over the Cuckoo's Nest, it was a tool of terror, and, in the public mind, shock therapy has retained the tarnished image given it by Ken Kesey's novel: dangerous, inhumane and overused".[27] In 1976, Dr. Blatchley demonstrated the effectiveness of his constant current, brief pulse device ECT. This device eventually largely replaced earlier devices because of the reduction in cognitive side effects, although some ECT clinics in the US still use sine-wave devices.[28] The 1970s saw the publication of the first American Psychiatric Association task force report on electroconvulsive therapy (to be followed by further reports in 1990 and 2001). The report endorsed the use of ECT in the treatment of depression. The decade also saw criticism of ECT.[29] Specifically critics pointed to shortcomings such as noted side effects, the procedure being used as a form of abuse, and uneven application of ECT. The use of ECT declined until the 1980s, "when use began to increase amid growing awareness of its benefits and cost-effectiveness for treating severe depression".[26] In 1985 the National Institute of Mental Health and National Institutes of Health convened a consensus development conference on ECT and concluded that, whilst ECT was the most controversial treatment in psychiatry and had significant side-effects, it had been shown to be effective for a narrow range of severe psychiatric disorders.[30] Due to the backlash noted previously, national institutions reviewed past practices and set new standards. In 1978, The American Psychiatric Association released its first task force report in which new standards for consent were introduced and the use of unilateral electrode placement was recommended. The 1985 NIMH Consensus Conference confirmed the therapeutic role of ECT in certain circumstances. The American Psychiatric Association released its second task force report in 1990 where specific details on the delivery, education, and training of ECT were documented. Finally in 2001 the American Psychiatric Association released its latest task force report. This report emphasizes the importance of informed consent, and the expanded role that the procedure has in modern medicine.
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Mechanism of action
The aim of ECT is to induce a therapeutic clonic seizure (a seizure where the person loses consciousness and has convulsions) lasting for at least 15 seconds. Although a large amount of research has been carried out, the exact mechanism of action of ECT remains elusive. ECT doctors claim it may "jumpstart the brain", helping boost neurotransmission, while others like Dr. Peter Breggin [31], claim it causes the "euphoric" effects similar to the effects found in "closed head injury" or people with fresh traumatic brain injury. The main reasons for this are that the human brain can not be studied directly before and after ECT and therefore scientists rely on animal models of depression and ECT, with major limitations. While animal models are acknowledged to model merely aspects of depressive illness, human and animal brains are very similar at a molecular level, enabling detailed study of the molecular mechanisms involved in ECT.[5] There is a vast literature on the effects of Electroconvulsive Shock (ECS) in animals. In animal models of depression, particularly "Learned helplessness" and "Social defeat", there is evidence of pruning of normally dense synaptic connections in the hippocampus, a richly connected area deep in the temporal lobe which is vital in controlling both mood and memory.[32] ECS has been shown to increase levels of Brain-derived neurotrophic factor (BDNF) and Vascular Endothelial Growth Factor (VEGF) in the rodent hippocampus.[33] This reverses the toxic effects of depression on this area of the brain, increasing both new synapse formation and the formation of new brain cells (hippocampal neurogenesis). Both these effects have been noted to be present in antidepressant-treated animals, however they are neither necessary nor sufficient for antidepressant response is a more robust inducer of these neuroplastic effects than antidepressants.[34] Electroconvulsive Therapy (ECT) has also been shown to increase serum brain-derived neurotrophic factor (BDNF) in drug resistant depressed patients.[35] This suggests a common molecular mechanism of action, albeit in need of much further study.
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Efficacy
Duration of effect
ECT on its own does not usually have a sustained benefit. Half those who remit then relapse within six months. This is similar to the rate of relapse after discontinuing antidepressant medication, and is a function of the usual severity and chronicity of pre-existing illness rather than ECT itself.[43] The relapse rate in the first six months is reduced by the use of psychiatric medications or further ECT, but remains high.[44] [45]
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Probability of remission
The 1999 U.S. Surgeon General's Report on Mental Health summarized psychiatric opinion at the time about the effectiveness of ECT. It stated that both clinical experience and published studies had determined ECT to be effective (with an average 60 to 70 percent remission rate) in the treatment of severe depression, some acute psychotic states, and mania. Its effectiveness had not been demonstrated in dysthymia, substance abuse, anxiety, or personality disorder. The report stated that ECT does not have a long-term protective effect against suicide and should be regarded as a short-term treatment for an acute episode of illness, to be followed by continuation therapy in the form of drug treatment or further ECT at weekly to monthly intervals.[46] A 2004 large multicentre clinical follow-up study of ECT patients in New York describing itself as the first systematic documentation of the effectiveness of ECT in community practice in the 65 years of its use found remission rates of only 30 to 47 percent, with 64 percent of those relapsing within six months.[47] However, when patients with co-morbid personality disorders or who were suffering from schizoaffective disorder were removed from the analysis, the remission rates climbed to 60-70%.[47]
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Adverse effects
Aside from effects in the brain, the general physical risks of ECT are similar to those of brief general anesthesia; the United States' Surgeon General's report says that there are "no absolute health contraindications" to its use.[46] Immediately following treatment, the most common adverse effects are confusion and memory loss. The state of confusion usually disappears after a few hours. It can be tolerated by pregnant women who are not suffering major complications. It can be used with diabetic or obese patients, and with caution in those whose cancers are in remission or under control. It can be used in some immunocompromised patients. It must be used very cautiously in people with epilepsy or other neurological disorders because by its nature it provokes small tonic-clonic seizures, and so would likely not be given to a person whose epilepsy is not well-controlled.[50] [51] Some patients experience muscle soreness after ECT. This is due to the muscle relaxants given during the procedure and rarely due to muscle activity. The death rate due to ECT is around 4 per 100,000 procedures.[52]
Effects on memory
It is the purported effects of ECT on long-term memory that give rise to much of the concern surrounding its use.[53] The acute effects of ECT can include amnesia, both retrograde (for events occurring before the treatment) and anterograde (for events occurring after the treatment).[54] However, the vast majority of these effects are short lived. Memory loss and confusion are more pronounced with bilateral electrode placement rather than unilateral, and with outdated sine-wave rather than brief-pulse currents. The vast majority of modern treatment uses brief pulse currents.[54] Research by Harold Sackeim has shown that excessive current causes more risk for memory loss, and using right-sided electrode placement may reduce verbal memory disturbance.[27] Retrograde amnesia is most marked for events occurring in the weeks or months before treatment, with one study showing that although some people lose memories from years prior to treatment, recovery of such memories was "virtually complete" by seven months post-treatment, with the only enduring loss being memories in the weeks and months prior to the treatment.[55] [56] Anterograde memory loss is usually limited to the time of treatment itself or shortly afterwards. In the weeks and months following ECT these memory problems gradually improve, but some people have persistent losses, especially with bilateral ECT.[5] [54] One published review summarizing the results of questionnaires about subjective memory loss found that between 29% and 55% of respondents believed they experienced long-lasting or permanent memory changes.[57] In 2000, American psychiatrist Sarah Lisanby and colleagues found that bilateral ECT left patients with more persistently impaired memory of public events as compared to RUL ECT.[53] Some studies have found that patients are often unaware of cognitive deficits induced by ECT.[58] [59] For example, in June 2008, a Duke University study[58] was published assessing the neuropsychological effects and attitudes in patients after ECT. Forty-six patients participated in the study, which involved neuropsychological and psychological testing before and after ECT. The study documented substantial cognitive impairment after ECT on a variety of memory tests, including "verbal memory for word lists and prose passages and visual memory of geometric designs." The study further found that a significant number of patients believed that their memory had improved after ECT despite the fact that neuropsychological testing clearly showed the opposite. As stated by the researchers, "Indeed, there was a slight trend towards [patients reporting] improved memory functioning, despite the objective neuropsychological data indicating significantly lower recognition and delayed recall." Based on their findings, the authors issued the following recommendation:
Electroconvulsive therapy "When ECT is provided to adolescents, the potential impact of such cognitive changes should be discussed with the patients and their parents or guardians in terms of implications for not only the patients emotional functioning but cognitive functioning as well, particularly upon his or her academic performance. In summary, we argue that an individual cost-benefit analysis should be made in light of the implications of the potential benefits versus costs of ECT upon improving emotional functioning and the impact that potential memory changes may have on real-world functioning and quality of life."[58] Severe memory loss from ECT is described in an autobiographical book, Doctors of Deception: What They Don't Want You to Know about Shock Treatment.[60]
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Electroconvulsive therapy of ECT in an article entitled, Electroconvulsive Therapy: Myths and Evidences.[68] In their review, the researchers conclude that ECT is an "efficient, safe and even life saving treatment for several psychiatric disorders." In 2008, Yale researchers published a review on the safety and efficacy of ECT in elderly patients.[75] According to the authors, "ECT is well established as a safe and effective treatment for several psychiatric disorders." And in a June 2009 article published in the Journal of ECT, Iranian researchers observe that, "Despite the wide consensus over the safety and efficacy of electroconvulsive therapy (ECT), it still faces negative publicity and unfavorable attitudes of patients and families."[74] Psychiatrist Peter Breggin, chief editor of the journal Ethical Human Psychology and Psychiatry, is a leading critic of ECT who believes the procedure is neither safe nor effective. In a published article reviewing the findings of Harold Sackeim's 2007 study[61] on the cognitive effects of ECT, Breggin accuses Max Fink and other pro-ECT researchers of having a history of "systematically covering up damage done to millions of [ECT] patients throughout the world."[62] He disagrees with the position that findings of chronic, global cognitive deficits should have no bearing on the risk-benefit ratio of ECT, and he believes it's important to address the "actual impact of these losses on the lives of individual patients." In a section of his paper entitled Destroying Lives, Dr. Breggin writes, "Even when these injured people can continue to function on a superficial social basis, they nonetheless suffer devastation of their identities due to the obliteration of key aspects of their personal lives. The loss of the ability to retain and learn new material is not only humiliating and depressing but also disabling. Even when relatively subtle, these activities can disrupt routine activities of living."[62] A study published in 2004 in the Journal of Mental Health reported that 35 to 42% of patients responding to a questionnaire reported ECT resulted in loss of intelligence.[76] The study also reported, "There is no overlap between clinical and consumer studies on the question of benefit." Doctors of Deception: What They Don't Want You to Know About Shock Treatment reports before-and-after IQ testing of persons receiving ECT, including the author, that show 30 to 40 point losses.[60] A recent opinion article by a neuropsychologist and a psychiatrist in Dublin suggests that ECT patients who experience cognitive problems following ECT should be offered some form of cognitive rehabilitation. The authors say that the failure to attempt to rehabilitate patients may be partly responsible for the negative public image of ECT. The article speculates on what aspects of such rehabilitation might be useful, without reviewing the literature on its presence or absence.[77]
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Electroconvulsive therapy examination showed that it was possible to distinguish the 8 shocked animals from the 8 non-shocked animals with remarkable accuracy based on statistically significant structural changes to the brain, including vessel wall changes, gliosis, and nerve cell changes. Based on the detection of shadow cells and neuronophagia, Hartelius determined that there was irreversible damage to neurons associated with electroshock.[80] Proponents argue that the addition of hyperoxygenation and refinement in technique in the last thirty years has made ECT safe, and a majority of published reviews in recent decades have reflected this position.[82] In a 2004 study designed to evaluate whether modern ECT techniques lead to identifiable brain damage, twelve monkeys underwent daily electroshock for six weeks under conditions meant to simulate human ECT; the animals were then sacrificed and their brains were compared to monkeys undergoing anesthesia alone. According to the researchers, "None of the ECT-treated monkeys showed pathological findings."[83] There are recent animal studies that have documented significant brain damage after an electroshock series. For example, in 2005, Russian researchers published a study entitled, Electroconvulsive Shock Induces Neuron Death in the Mouse Hippocampus: Correlation of Neurodegeneration with Convulsive Activity. In this study, the researchers found that after an electroshock series, there was a significant loss of neurons in parts of the brain and particularly in defined parts of the hippocampus where up to 10% of neurons were killed. The researchers conclude that "the main cause of neuron death is convulsions evoked by electric shocks."[84] In 2008, Portuguese researchers conducted a rat study aimed at answering the question of whether an electroshock series causes structural changes in vulnerable parts of the brain.[85] According to the authors, "This study answers positively the question of whether repeated administration of ECS seizures can cause brain lesions. Our data are consistent with findings from other animal models and from human studies in showing that neurons located in the entorhinal cortex and in the hilus of the dentate gyrus are particularly vulnerable to repeated seizures." However, they question the applicability of their own research with respect to Electroconvulsive therapy in humans: "An important caveat of our results is that it is unclear to what extent they are relevant to the use of electroconvulsive therapy in psychiatry, because the protocol employed in this study is different from that used clinically. Evidence from previous studies (Gombos et al., [1999]; Vaidya et al., [1999]) and from our pilot experiments indicates that treating rats either with five to ten widely spaced ECS (at 24- or 48-hr schedules) or with two stimulations only 2 hr apart does not lead to loss of hippocampal neurons".[85] Many expert proponents of ECT maintain that the procedure is safe and does not cause brain damage. Dr. Charles Kellner, a prominent ECT researcher and former chief editor of the Journal of ECT, states in a recent published interview that, "There are a number of well-designed studies that show ECT does not cause brain damage and numerous reports of patients who have received a large number of treatments over their lifetime and have suffered no significant problems due to ECT."[86] Dr. Kellner cites specifically to a study purporting to show an absence of cognitive impairment in eight subjects after more than 100 lifetime ECT treatments.[87] One of the authors of the cited study, Harold Sackeim, published a large-scale study less than a month after this interview concluding that the type of ECT used in the eight patients receiving the 100 lifetime treatments, bilateral sine wave, routinely leads to persistent, global cognitive deficits[61] (discussed above). Dr. Kellner states that, "Rather than cause brain damage, there is evidence that ECT may reverse some of the damaging effects of serious psychiatric illness."[86]
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Effects in pregnancy
If steps are taken to decrease potential risks, ECT is generally accepted to be relatively safe during all trimesters of pregnancy, particularly when compared to pharmacological treatments.[88] [89] [90] Suggested preparation for ECT during pregnancy includes a pelvic examination, discontinuation of nonessential anticholinergic medication, uterine tocodynamometry, intravenous hydration, and administration of a nonparticulate antacid. During ECT, elevation of the pregnant woman's right hip, external fetal cardiac monitoring, intubation, and avoidance of excessive hyperventilation are recommended.[88] Much of the medical literature in this area is composed of case studies of single or twin pregnancies, and although some have reported serious complications,[91] [92] the majority have found ECT to be safe.[93] ECT is not performed on the fetus.
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Administration
Informed consent is sought before treatment. Patients are informed about the risks and benefits of the procedure. Patients are also made aware of risks and benefits of other treatments and of not having the procedure done at all. Depending on the jurisdiction, the need for further inputs from other medical professionals or legal professionals may be required. ECT is usually given on an in-patient basis. Prior to treatment, a patient is given a short-acting anesthetic such as methohexital, etomidate, or thiopental,[5] a muscle relaxant such as suxamethonium (succinylcholine), and occasionally atropine to inhibit salivation. Both electrodes can be placed on the same side of the patient's head. This is known as unilateral ECT. Unilateral ECT is used first to minimize side effects (memory loss). When electrodes are placed on both sides of the head, this is known as bilateral ECT. In bifrontal ECT, an uncommon variation, the electrode position is somewhere between bilateral and unilateral. Unilateral is thought to cause fewer cognitive effects than bilateral but is considered less effective.[5] In the USA most patients receive bilateral ECT.[28] In the UK almost all patients receive bilateral ECT.[94] The electrodes deliver an electrical stimulus. The stimulus levels recommended for ECT are in excess of an individual's seizure threshold: about one and a half times seizure threshold for bilateral ECT and up to 12 times for unilateral ECT.[5] Below these levels treatment may not be effective in spite of a seizure, while doses massively above threshold level, especially with bilateral ECT, expose patients to the risk of more severe cognitive impairment without additional therapeutic gains.[95] Seizure threshold is determined by trial and error ("dose titration"). Some psychiatrists use dose titration, some still use "fixed dose" (that is, all patients are given the same dose) and others compromise by roughly estimating a patient's threshold according to age and sex.[28] Older men tend to have higher thresholds than younger women, but it is not a hard and fast rule, and other factors, for example drugs, affect seizure threshold.
ECT machines
Most modern ECT machines deliver a brief-pulse current, which is thought to cause fewer cognitive effects than the sine-wave currents which were originally used in ECT.[5] A small minority of psychiatrists in the USA still use sine-wave stimuli.[28] Sine-wave is no longer used in the UK or Ireland.[94] Typically, the electrical stimulus used in ECT is about 800 milliamps and has up to several hundred watts, and the current flows for between one and 6 seconds.[95] In the USA, ECT machines are manufactured by two companies, Somatics, which is owned by psychiatrists Richard Abrams and Conrad Swartz, and Mecta. The Food and Drug Administration has classified the devices used to administer ECT as Class III medical devices.[96] Class III is the highest-risk class of medical devices. In the UK, the market for ECT machines was long monopolized by Ectron Ltd, although in recent years some hospitals have started using American machines. Ectron Ltd was set up by psychiatrist Robert Russell, who together with a colleague from the Three Counties Asylum, Bedfordshire, invented the PageRussell technique of intensive ECT.
Electroconvulsive therapy developing countries in eliminating unmodified ECT is a lack of trained anesthesiologists available to administer the procedure.[102] A small minority of countries never seek consent before administering ECT. This significantly uneven application of ECT around the world continues to make ECT a controversial procedure. Sarah Hall reports, "ECT has been dogged by conflict between psychiatrists who swear by it, and some patients and families of patients who say that their lives have been ruined by it. It is controversial in some European countries such as the Netherlands and Italy, where its use is severely restricted".[103] United States In the United States, a survey of psychiatric practice in the late 1980s found that an estimated 100,000 people received ECT annually, with wide variation between metropolitan statistical areas.[104] Accurate statistics about the frequency, context and circumstances of ECT in the United States are difficult to obtain because only a few states have reporting laws that require the treating facility to supply state authorities with this information.[105] One state which does report such data is Texas, where in the mid-1990s ECT was used in about one third of psychiatric facilities and given to about 1,650 people annually.[41] Usage of ECT has since declined slightly; in 200001 ECT was given to about 1,500 people aged from 16 to 97 (in Texas it is illegal to give ECT to anyone under sixteen).[106] ECT is more commonly used in private psychiatric hospitals than in public hospitals, and minority patients are underrepresented in the ECT statistics.[5] In the United States, ECT is usually given three times a week; in the UK, it is usually given twice a week.[5] Occasionally it is given on a daily basis.[5] A course usually consists of 612 treatments, but may be more or fewer. Following a course of ECT some patients may be given continuation or maintenance ECT with further treatments at weekly, fortnightly or monthly intervals.[5] A few psychiatrists in the USA use multiple-monitored ECT (MMECT) where patients receive more than one treatment per anesthetic.[5] Electroconvulsive therapy is not a required subject in US medical schools and not a required skill in psychiatric residency training. Privileging for ECT practice at institutions is a local option, no national certification standards are established, and no ECT-specific continuing training experiences are required of ECT practitioners.[107] United Kingdom In the United Kingdom in 1980, an estimated 50,000 people received ECT annually, with use declining steadily since then[108] [109] to about 12,000 per annum. It is still used in nearly all psychiatric hospitals, with a survey of ECT use from 2002 finding that 71 percent of patients were women and 46 percent were over 65 years of age. Eighty-one percent had a diagnosis of mood disorder; schizophrenia was the next most common diagnosis. Sixteen percent were treated without their consent.[110] In 2003, the National Institute for Clinical Excellence, a government body which was set up to standardize treatment throughout the National Health Service in England and Wales, issued guidance on the use of ECT. Its use was recommended "only to achieve rapid and short-term improvement of severe symptoms after an adequate trial of treatment options has proven ineffective and/or when the condition is considered to be potentially life-threatening in individuals with severe depressive illness, catatonia or a prolonged manic episode".[111] The guidance received a mixed reception. It was welcomed by an editorial in the British Medical Journal[112] but the Royal College of Psychiatrists launched an unsuccessful appeal.[113] The NICE guidance, as the British Medical Journal editorial points out, is only a policy statement and psychiatrists may deviate from it if they see fit. Adherence to standards has not been universal in the past. A survey of ECT use in 1980 found that more than half of ECT clinics failed to meet minimum standards set by the Royal College of Psychiatrists, with a later survey in 1998 finding that minimum standards were largely adhered to, but that two-thirds of clinics still fell short of current guidelines, particularly in the training and supervision of junior doctors involved in the procedure.[114] A voluntary accreditation scheme, ECTAS, was set up in 2004 by the Royal College, but as of 2006 only a minority of ECT clinics in England, Wales, Northern Ireland and the Republic of Ireland have signed up.[115]
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Electroconvulsive therapy India The Union Health Ministry of India has decided in the Mental Health Care Bill of 2010 that they will no longer use direct ECT. The Health Ministry recommended a ban on the whole procedure.[116]
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Legal status
Informed consent
It is widely acknowledged internationally that obtaining the written, informed consent of the patient is important before ECT is administered. The World Health Organization, in its 2005 publication "Human Rights and Legislation WHO Resource Book on Mental Health," specifically states, "ECT should be administered only after obtaining informed consent."[117] In the US, this doctrine places a legal obligation on a doctor to make a patient aware of: the reason for treatment, the risks and benefits of a proposed treatment, the risks and benefits of alternative treatment, and the risks and benefits of receiving no treatment. The patient is then given the opportunity to accept or reject the treatment. The form states how many treatments are recommended and also makes the patient aware that the treatment may be revoked at anytime during a course of ECT.[46] The Surgeon General's Report on Mental Health states that patients should be warned that the benefits of ECT are short-lived without active continuation treatment in the form of drugs or further ECT, and that there may be some risk of permanent, severe memory loss after ECT.[46] The report advises psychiatrists to involve patients in discussion, possibly with the aid of leaflets or videos, both before and during a course of ECT. To demonstrate what he believes should be required to fully satisfy the legal obligation for informed consent, one psychiatrist, working for an anti-psychiatry organisation, has formulated his own consent form[118] using the consent form developed and enacted by the Texas Legislature as a model.[119] In the UK, in order for consent to be valid it requires an explanation in "broad terms" of the nature of the procedure and its likely effects.[120] One review from 2005 found that only about half of patients felt they were given sufficient information about ECT and its adverse effects[121] and another survey found that about fifty percent of psychiatrists and nurses agreed with them.[122] A 2005 study published in the British Journal of Psychiatry described patients' perspectives on the adequacy of informed consent before ECT.[121] The study found that, "About half (4555%) of patients reported they were given an adequate explanation of ECT, implying a similar percentage felt they were not." The authors also stated: "Approximately a third did not feel they had freely consented to ECT even when they had signed a consent form. The proportion who feel they did not freely choose the treatment has actually increased over time. The same themes arise whether the patient had received treatment a year ago or 30 years ago. Neither current nor proposed safeguards for patients are sufficient to ensure informed consent with respect to ECT, at least in England and Wales."[121]
Involuntary ECT
Procedures for involuntary ECT vary from country to country depending on local mental health laws. Legal proceedings are required in some countries, while in others ECT is seen as another form of treatment that may be given involuntarily as long as legal conditions are observed. Involuntary electroshock contravenes the principle of autonomy in medical ethics. The maxim of autonomy is "Voluntas aegroti suprema lex." This rule states that the will of the patient is supreme. It implies that a patient has the right to consent to, or to refuse a medical treatment, such as ECT. Persons considered not to be of sound mind are in many jurisdictions considered incapable of giving true consent. In such a case, the patient's "assent" may be sought; opinions are divided as to whether this should be routinely done, or whether a patient who is not competent to consent to therapy should retain the right to refuse it.
Electroconvulsive therapy Citizens in western societies often undergo emergency medical procedures when they have lost the capacity to consent (such as neurosurgery after head injury). Under these circumstances, the principles of benificence and non-maleficence must be adhered to. United States In most states in the USA, a judicial order following a formal hearing is needed before a patient can be forced to undergo involuntary ECT. Patients may be represented by legal counsel at the hearing. According to the Surgeon General's Report on Mental Health, "As a rule, the law requires that such petitions are granted only where the prompt institution of ECT is regarded as potentially lifesaving, as in the case of a person in grave danger because of lack of food or fluid intake caused by catatonia."[46] However, there are legal loopholes that thwart strict adherence to this principle. For example, an American citizen was being forced to undergo ECT against his will in 2009, even though his life was not in danger.[123] [124] In this March 17, 2009 video [125], the man, his mother, and advocates, speak out against his forced ECT. The description of the video states that "Though Sandford, 54, is not charged with any crime, he has received over 40 such rounds of shocks on an outpatient basis so far even after his original mental problems have long since subsided and he has repeatedly asked for the shocks to stop. Over the objections of Sandford, his mother and friends, his legal conservator at Lutheran Social Service of MN (LSSMN) has gone to court and succeeded in mandating a continuation of the procedure." Twin Cities Indymedia asserts "Like all other USA states, Minnesota has [legal] loopholes allowing [its] citizens to receive electroshock over their expressed wishes."[126] Great Britain Until 2009 in England and Wales, the Mental Health Act 1983 allowed the use of ECT on detained patients whether or not they had capacity to consent to it, so long as the treatment was likely to alleviate or prevent deterioration in a condition and was authorized by a psychiatrist from the Mental Health Act Commission's panel. However, following amendments which took effect in 2009, ECT may not be given to a patient who has capacity to refuse to consent to it, irrespective of his or her detention under the Act, although treatment may still be given to capacious patients in an emergency under Section 62 of the Act.[127] If the treating psychiatrist thinks the need for treatment is urgent they may start a course of ECT before authorization.[128] About 2,000 people a year in England and Wales are treated without their consent under the Mental Health Act.[129] In Scotland the Mental Health (Care and Treatment) (Scotland) Act 2003 also gives patients with capacity the right to refuse ECT.[130]
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Patient experience
The APA ECT taskforce guidelines report findings that most patients find ECT no worse than going to the dentist, and many found it less stressful than the dentist. They report that other research finds that most patients would voluntarily receive ECT again if needed. NICE ECT guidelines report that some individuals consider ECT to have been a beneficial and lifesaving treatment, while others reported feelings of terror, shame and distress, and found it positively harmful and an abusive invasion of personal autonomy, especially when administered without their consent.
Electroconvulsive therapy my kids, asking what my niece Betsy's phone number is, what we did yesterday and what we are planning to do tomorrow. I apologize prior to asking. I wonder when they are going to run out of patience with "Kitty being Kitty." I hate losing memories, which means losing control over my past and my mind, but the control ECT gives me over my disabling depression is worth this relatively minor cost. It just is.[131] American psychotherapist Martha Manning's autobiographical Undercurrents[132] acknowledges the downside of treatment: "I felt like I'd been hit by a truck for a while, but that was, comparatively speaking, not so bad," as well as the upside: "Afterwards, I thought, do regular people feel this way all the time? It's like you've not been in on a great joke for the whole of your life." In his autobiographical book Electroboy, American writer Andy Behrman describes undergoing ECT as a treatment for bipolar disorder while under house-arrest: "I wake up thirty minutes later and think I am in a hotel in Acapulco. My head feels as if I have just downed a frozen margarita too quickly. My jaws and limbs ache. But I am elated."[133] Curtis Hartmann, a lawyer in western Massachusetts, stated: "ECT, a treatment of last resort for severe, debilitating depression, is all that has ever worked for me. I awaken about 20 minutes later, and although I am still groggy with anesthesia, much of the hellish depression is gone. It is a disease that for me, literally steals me from myselfa disease that executes me and then forces me to stand and look down at my corpse. Thankfully, ECT has kept my monster at bay, my hope intact".[134] Beverley Callard is a British actress, best known for her role as Liz McDonald in Coronation Street. In her recently published autobiography titled "Unbroken", she describes her experience with ECT for severe depression, stating that the treatment was responsible, in part for her recovery.[135]
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Electroconvulsive therapy Despite former patients having reported devastating, permanent amnesia and cognitive impairment since ECT was first invented, the first lawsuit for ECT amnesia, Marilyn Rice v. John Nardini, was not brought until 1975; dozens of suits followed. While there have been a few settlements, including one for half a million dollars, no former patient had won a case until 2005. In a 2005 South Carolina court proceeding, Peggy S. Salters became the first ECT survivor to win a jury verdict and compensation. Ms. Salters sued Palmetto Baptist Medical Center in Columbia, as well as the three doctors responsible for her care, for an intensive course of outpatient ECT that she received in 2000, at age 55 years old, that caused her to lose all memories of the past 30 years of her life, including all memories of her husband of three decades, then deceased, and the births of her three children. She held a Masters of Science in nursing and, prior to the ECT, had a long career as a psychiatric nurse; but, as a result of the ECT, lost her knowledge of nursing skills and was unable to return to work. The jury awarded Salters $635,177 in compensation for her inability to work.[139] The judgement was upheld upon appeal in an unpublished opinion.[140] Accounts of severe cognitive diminishment Liz Spikol, the senior contributing editor of Philadelphia Weekly, wrote of her ECT in 1996, "Not only was the ECT ineffective, it was incredibly damaging to my cognitive functioning and memory. But sometimes it's hard to be sure of yourself when everyone 'credible' scientists, ECT docs, researchers are telling you that your reality isn't real. How many times have I been told my memory loss wasn't due to ECT but to depression? How many times have I been told that, like a lot of other consumers, I must be perceiving this incorrectly? How many times have people told me that my feelings of trauma related to the ECT are misplaced and unusual? It's as if I was raped and people kept telling me not to be upsetthat it wasn't that bad."[141] Involuntary or other problems in administrating ECT In 2007, a judge canceled a two-year-old court order that allowed the involuntary electroshock of Simone D., a psychiatric patient at Creedmoor Psychiatric Center in the state of New York.[142] Although Simone spoke only Spanish, she rarely received access to staff fluent in her language.[142] [143] Simone previously had 200 electroshocks.[142] [143] However, she communicated that she did not want more electroshock.[142] [143] Simone stated, "Electroshock causes more pain. I suffer more from shock treatment![142] " In 2008, David Tarloff, a psychiatric patient who had received electroshock, assaulted two therapists in the city of New York. Tarloff injured one therapist and killed the other. One of the therapists was Kent Shinbach, a psychiatrist who had an interest in electroconvulsive therapy. "It is not clear whether Dr. Shinbach played any role in Mr. Tarloff's shock therapy".[144] However, Tarloff told investigators that Shinbach had given Tarloff psychiatric treatment at a psychiatric facility initially in 1991.[145] Other descriptions In an interview with Houston Chronicle in 1996, Melissa Holliday, a former extra on Baywatch and model for Playboy stated the ECT she received in 1995, "ruined her life." She went on to state, "I've been through a rape, and electroshock therapy is worse. If you haven't gone through it, I can't explain it."[146]
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Fictional examples
Electroconvulsive therapy has been depicted in fiction and works based on true experiences. These include A Clockwork Orange, The Snake Pit, Quantum Leap (TV series), Frances, Requiem for a Dream, the novel One Flew Over the Cuckoo's Nest by Ken Kesey as well as the movie adaptation, Melrose Place, A Beautiful Mind, The Caretaker, The Best of Youth, House; The Bell Jar by Sylvia Plath, Shine, the film version of Girl, Interrupted, Insanitarium, Changeling, Ciao! Manhattan, Next to Normal, Return to Oz, Private Practice, Ghost Whisperer, From Beyond, the novel Zen and the Art of Motorcycle Maintenance, Helen, Oz, Six Feet Under, House on Haunted Hill, Royal Pains, and "The Wolfman (2010 film)."
External links
Psychiatry's Electroconvulsive Shock Treatment - A Crime Against Humanity [147] by Lawrence Stevens, J.D. American Psychiatric Association on ECT [148] brief article from the American Psychiatric Association. MIND on ECT [149] information on ECT from MIND (leading mental health charity in England and Wales). MindFreedom International [150] - information critical of electroshock. About to have ECT? ... [151] Psychiatric Times article on the portrayal of ECT by Hollywood ECT [152] - information from mental health charity The Royal College of Psychiatrists
Electroconvulsive Therapy (ECT) [153] ECT products and devices from MECTA Corporation TED talk on ECT [154] 30-year-practicing surgeon and successful writer Sherwin B. Nuland on the history of ECT and his personal experience with it. Pare-chocs, Pour l'abolition des lectrochocs [155] - A group in Montral, Qubec, Canada, for the abolition of electroshock.
References
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(March 2004). "Absence of histological lesions in primate models of ECT and magnetic seizure therapy". The American Journal of Psychiatry 161 (3): 57678. doi:10.1176/appi.ajp.161.3.576. PMID14992989. [84] Zarubenko II, et al. (september 2005). "Electroconvulsive shock induces neuron death in the mouse hippocampus: correlation of neurodegeneration with convulsive activity". Neuroscience and Behavioral Physiology 35 (7): 715721. doi:10.1007/s11055-005-0115-0. PMID16433067. [85] Cardoso A, et al. (January 2008). "Loss of synapses in the entorhinal-dentate gyrus pathway following repeated induction of electroshock seizures in the rat". Journal of Neuroscience Research 86 (1): 7183. doi:10.1002/jnr.21474. PMID17705293. [86] Sussman, M.D., Norman (December, 2006). "In Session with Charles H. Kellner, MD: Current Developments in Electroconvulsive Therapy" (http:/ / www. primarypsychiatry. com/ aspx/ articledetail. aspx?articleid=1028). Primary Psychiatry 2007;14(3):34-37. . Retrieved 2009-10-17. [87] Devanand DP, Sackeim HA, et al. (july 1991). "Absence of cognitive impairment after more than 100 lifetime ECT treatments". The American Journal of Psychiatry 148 (7): 92932. PMID2053635. [88] Miller LJ (May 1994). "Use of electroconvulsive therapy during pregnancy" (http:/ / ps. psychiatryonline. org/ cgi/ pmidlookup?view=long& pmid=8045538). Hosp Community Psychiatry 45 (5): 44450. PMID8045538. . [89] Walker R, Swartz CM (September 1994). "Electroconvulsive therapy during high-risk pregnancy". Gen Hosp Psychiatry 16 (5): 34853. doi:10.1016/0163-8343(94)90022-1. PMID7995506. [90] Ferrill MJ, Kehoe WA, Jacisin JJ (1992). "ECT During Pregnancy: Physiologic and Pharmacologic Considerations". Convuls Ther 8 (3): 186200. PMID11941169. [91] Echevarra Moreno M, Martin Muoz J, Sanchez Valderrabanos J, Vzquez Gutierrez T (December 1998). "Electroconvulsive therapy in the first trimester of pregnancy". The journal of ECT 14 (4): 2514. PMID9871846. [92] Pinette MG, Santarpio C, Wax JR, Blackstone J (August 2007). "Electroconvulsive therapy in pregnancy". Obstet Gynecol 110 (2 Pt 2): 4656. doi:10.1097/01.AOG.0000265588.79929.98. PMID17666629. [93] Yellowlees PM, Page T (1990). "Safe use of electroconvulsive therapy in pregnancy". The Medical journal of Australia 153 (1112): 67980. PMID2246991. [94] Duffett R, Lelliott P (1998). "Auditing electroconvulsive therapy. The third cycle". Br J Psychiatry 172 (5): 4015. doi:10.1192/bjp.172.5.401. PMID9747401. [95] Lock, T (1995). "Stimulus dosing". In C Freeman (ed.) The ECT Handbook. London: Royal College of Psychiatrists, 7287. [96] Federal Register (1979), p. 51776 [97] See the Slovenian government website (http:/ / e-uprava. gov. si/ e-uprava/ en/ faqKategorijaVprasanje. euprava?faq. id=74& faq. vprasanje. id=328) for information about ECT in Slovenia. [98] Motohashi N, Awata S, Higuchi T (2004). "A questionnaire survey of ECT practice in university hospitals and national hospitals in Japan". J ECT 20 (1): 213. doi:10.1097/00124509-200403000-00005. PMID15087992.
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[99] Chanpattana W, Kunigiri G, Kramer BA, Gangadhar BN (2005). "Survey of the practice of electroconvulsive therapy in teaching hospitals in India". J ECT 21 (2): 1004. doi:10.1097/01.yct.0000166634.73555.e6. PMID15905751. [100] Ikeji OC, Ohaeri JU, Osahon RO, Agidee RO (1999). "Naturalistic comparative study of outcome and cognitive effects of unmodified electro-convulsive therapy in schizophrenia, mania and severe depression in Nigeria" (http:/ / www. ncbi. nlm. nih. gov/ sites/ entrez?db=pubmed& uid=10734527& cmd=showdetailview& indexed=google). East Afr Med J 76 (11): 64450. PMID10734527. . [101] "Abusive practice of "unmodified" electroshock treatment abolished at main psychiatric facility of Turkey" (http:/ / v1. dpi. org/ lang-en/ resources/ topics_detail?page=557). Disabled Peoples' International. . Retrieved 2008-03-25. [102] Dutta, Rita (2003). "Psychiatrists plead against ban of direct electro convulsive therapy" (http:/ / www. expresshealthcaremgmt. com/ 20030531/ medethics. shtml). Indian Express Group of Newspapers. . Retrieved 2007-12-31. [103] Rise In Electric Shock Therapy In County. (http:/ / mindfreedomireland. com/ new/ index. php?view=article& catid=1:administrator& id=196:rise-in-electric-shock-therapy-in-county& format=pdf& option=com_content& Itemid=19) Sarah Hall, Norwich Evening News 24, June 4, 2008. Accessed: June 4, 2008. [104] Hermann R, Dorwart R, Hoover C, Brody J (1995). "Variation in ECT use in the United States". Am J Psychiatry 152 (6): 86975. PMID7755116. [105] Cauchon, Dennis (1995-12-06). "Patients often aren't informed of full danger" (http:/ / www. harborside. com/ ~equinox/ ect1. htm). USA Today. . [106] Texas Department of State (2002) Electroconvulsive therapy reports (http:/ / www. dshs. state. tx. us/ mhquality/ ECT_Complete_Report_FY01. pdf). [107] Fink, M. & Taylor, A.M. (2007) Electroconvulsive therapy: Evidence and Challenges (http:/ / jama. ama-assn. org/ cgi/ content/ full/ 298/ 3/ 330) JAMA Vol. 298 No. 3, p330332. [108] Pippard, J and Ellam, L (1981). Electroconvulsive treatment in Great Britain, 1980. London: Gaskell. [109] Pippard J, Ellam L (1981). "Electroconvulsion treatment in Great Britain 1980". Lancet 2 (8256): 11601. PMID6118592. [110] Electro convulsive therapy: survey covering the period from January 2002 to March 2002 (http:/ / www. dh. gov. uk/ en/ Publicationsandstatistics/ Publications/ PublicationsStatistics/ DH_4083142), Statistical Bulletin 2003/08 (http:/ / www. dh. gov. uk/ en/ Publicationsandstatistics/ Statistics/ StatisticalWorkAreas/ Statisticalhealthcare/ DH_4000216). Department of Health. [111] NICE 2003. Electroconvulsive therapy (ECT) (http:/ / www. nice. org. uk/ guidance/ index. jsp?action=byID& o=11494). Retrieved on 2007-12-29. [112] Carney, S; Geddes, J (2003). "Electroconvulsive therapy: recent recommendations are likely to improve standards and uniformity of use". British Medical Journal 326 (7403): 13434. doi:10.1136/bmj.326.7403.1343. PMC1126234. PMID12816798. [113] NICE (2003). Appraisal of electroconvulsive therapy: decision of the appeal panel (http:/ / www. nice. org. uk/ page. aspx?o=62452). London: NICE. [114] Duffett, R; Lelliot, P (1998). "Auditing electroconvulsive therapy: the third cycle" (http:/ / bjp. rcpsych. org/ cgi/ content/ abstract/ 172/ 5/ 401). British Journal of Psychiatry 172 (5): 401405. doi:10.1192/bjp.172.5.401. PMID9747401. . [115] Royal College of Psychiatrists (2006). ECTAS newsletter (http:/ / www. rcpsych. ac. uk/ crtu/ centreforqualityimprovement/ electroconvulsivetherapy. aspx) issue 5. [116] Electroshocks for mentally ill patients to be banned (2011). (http:/ / www. indianexpress. com/ news/ Electroshocks-for-mentally-ill-patients-to-be-banned/ 766051/ ) Teena Thacker [117] World Health Organisation (2005). WHO Resource Book on Mental Health, Human Rights and Legislation (http:/ / www. who. int/ mental_health/ policy/ resource_book_MHLeg. pdf). Geneva, 64. [118] Johnson, R. "An informed consent form for electroconvulsive therapy, draft 1." (http:/ / www. psychrights. org/ Research/ Digest/ InformedConsent/ DrJohnsonECTInformedConsent. pdf) (PDF). PsychRights. . [119] Texas Legislature (2004). Health & Safety Code Chapter 578, Electroconvulsive And Other Therapies Sec.578.001 (http:/ / www. statutes. legis. state. tx. us/ Docs/ HS/ htm/ HS. 578. htm#578. 001). [120] Jones, R (1996) Mental Health Act Manual, 5th edition. London: Sweet and Maxwell, page 225. [121] Rose D, Wykes T, Bindman J, Fleischmann P (2005) "Information, consent and perceived coercion: patients' perspectives on electroconvulsive therapy" (http:/ / bjp. rcpsych. org/ cgi/ content/ abstract/ 186/ 1/ 54). British Journal of Psychiatry 186:5459. [122] Lutchman, RD et al. (2001). "Mental health professionals' attitudes towards and knowledge of electroconvulsive therapy" (http:/ / informahealthcare. com/ doi/ abs/ 10. 1080/ 09638230124779). Journal of Mental Health 10 (20): 141150. doi:10.1080/09638230124779. . [123] Benson, Lorna (December 15, 2008). "Man Fights Order To Undergo Electroshock Therapy" (http:/ / www. npr. org/ templates/ story/ story. php?storyId=98273451). Day to Day. National Public Radio. . [124] "Ray Gateway: Campaign to End Forced Outpatient Electroshock of Ray Sandford" (http:/ / www. mindfreedom. org/ ray). Mindfreedom.org. . [125] http:/ / www. youtube. com/ watch?v=2fJpvNHqXm0 [126] "haloka" (2009-03-17). "In Their Own Words: ECT Survivor, Advocates Speak Out Against Continued Forced Electroshocks" (http:/ / www. tc. indymedia. org/ 2009/ mar/ their-own-words-ect-survivor-advocates-speak-out-against-continued-forced-electroshocks). Twin Cities Indymedia. . [127] The Mental Health Act 1983 (http:/ / www. cqc. org. uk/ _db/ _documents/ Mental_Health_Act_1983_201001202031. pdf) Part 4, Section 58. Care Quality Commission
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[128] The Mental Health Act 1983 (http:/ / www. cqc. org. uk/ _db/ _documents/ Mental_Health_Act_1983_201001202031. pdf) Part 4, Section 62. Care Quality Commission [129] The Mental Health Act Commission (2005) In Place of Fear? eleventh biennial report, 20032005, 236. The Stationery Office. [130] The Mental Health (Care and Treatment) (Scotland) Act 2003, Part 16, sections 237239. [131] Dukakis, K; Tye, L (2006). September 18: 6263. [132] Manning, Martha (March 1996). Undercurrents: A Therapist's Reckoning with Her Own Depression. Harper San Francisco. ISBN978-0062511843. [133] Behrman, Andy (February 2003). Electroboy: A Memoir of Mania. Random House. ISBN978-0812967081. [134] Personal Accounts: Life as Death: Hope Regained With ECT Hartmann '''53'''(4): 413 Psychiatr Serv (http:/ / psychservices. psychiatryonline. org/ cgi/ content/ full/ 53/ 4/ 413). Psychservices.psychiatryonline.org. doi:10.1176/appi.ps.53.4.413. . Retrieved 2009-10-17. [135] Callard, Beverley (February 2010). Unbroken. Hodder. ISBN9781444705270. [136] A. E. Hotchner, Papa Hemingway: A Personal Memoir, ISBN 0786705922; pg 280 [137] Cody, Barbara (Approximately 19952006). "Letters in response to "Shock Therapy: It's Back (Wash. Post, 1996-09-28)"" (http:/ / web. archive. org/ web/ 20001201231500/ http:/ / www. healthyplace. com/ Communities/ Depression/ ect/ media/ postltrs. html). Washington Post (at HealthyPlace.com. Archived from the original (http:/ / www. healthyplace. com/ Communities/ Depression/ ect/ media/ postltrs. html) on 2000-12-01. . Retrieved 2006-09-23. [138] Johnanton Cott, On the Sea of Memory: A Journey from Forgetting to Remembering Random House, October 4, 2005, ISBN 1400060583, ISBN 978-1400060580 [139] "ECT verdict awards dollar judgment" (http:/ / www. peoplewho. org/ documents/ ctip. ectverdict. htm). Peoplewho.org. June 17, 2005. . Retrieved 2009-10-17. [140] "2007-UP-187 - Salters v. Palmetto Health Alliance" (http:/ / www. judicial. state. sc. us/ opinions/ displayUnPubOpinion. cfm?caseNo=2007-UP-187). Supreme Court, South Carolina Court of Appeals. 2007. . [141] Spikol, Liz (2006-12-22). "Funday: ECT study shocks. Ha ha." (http:/ / trouble. philadelphiaweekly. com/ archives/ 2006/ 12/ funday_ect_stud. html). The Trouble With Spikol. Philadelphia Weekly. . Retrieved 2009-10-17. [142] MindFreedom International. Another victory against forced electroshock. Simone D. wins! (http:/ / www. mindfreedom. org/ campaign/ kb/ mental-health-abuse/ electroshock/ simone-d) August 28, 2007. Accessed: April 18, 2008. [143] Lauren Tenney. Testimony from Lauren Tenney, Member of FUTURE Views and the Mental Patients Liberation Alliance. (http:/ / www. omh. state. ny. us/ omhweb/ statewideplan/ 2006/ testimony/ 507/ nyc/ tenney. html) New York State Office of Mental Health, October 5, 2007. Accessed: April 18, 2008. [144] "Shock Therapy Emerges As Detail in Therapist's Killing" (http:/ / www. nysun. com/ new-york/ shock-therapy-emerges-as-detail-in-therapists/ 71616/ ). The New York Sun. February 21, 2008. . Retrieved 2009-10-17. [145] Christopher Faherty (2008-04-02). "Suspected Killer 'Didn't Mean To Hurt Anyone'" (http:/ / www. nysun. com/ news/ new-york/ suspected-killer-didnt-mean-hurt-anyone). The New York Sun. . Retrieved 2008-04-13. [146] Makeig, John (1996-06-26). "Woman Says Electric Shock Treatment Destroyed Her Life" (http:/ / www. healthyplace. com/ Communities/ Depression/ ect/ news/ woman. asp). Houston Chronicle(at Healthyplace.com). . Retrieved 2009-10-17. [147] http:/ / www. antipsychiatry. org/ ect. htm [148] http:/ / www. psych. org/ research/ apire/ training_fund/ clin_res/ index. cfm [149] http:/ / www. mind. org. uk/ help/ medical_and_alternative_care/ making_sense_of_ect [150] http:/ / www. mindfreedom. org/ kb/ mental-health-abuse/ electroshock/ [151] http:/ / www. psychiatrictimes. com/ display/ article/ 10168/ 48111 [152] http:/ / www. rcpsych. ac. uk/ mentalhealthinfo/ treatments/ ect. aspx [153] http:/ / www. mectacorp. com/ home. html [154] http:/ / www. ted. com/ index. php/ talks/ view/ id/ 189 [155] http:/ / www. actionautonomie. qc. ca/ parechocs/ parec. html
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Involuntary commitment
Involuntary commitment or civil commitment is a legal process through which an individual with symptoms of severe mental illness is court-ordered into treatment in a hospital (inpatient) or in the community (outpatient). Criteria for civil commitment are established by law, which varies between nations and, in the U.S., from state to state. Commitment proceedings often follow a period of emergency hospitalization during which an individual with acute psychiatric symptoms is confined for a relatively short duration (e.g. 72 hours) in a treatment facility for evaluation and stabilization by mental health professionals - who may then determine whether further civil commitment is appropriate or necessary. If civil commitment proceedings follow, the evaluation is presented in a formal court hearing where testimony and other evidence may also be submitted. The subject of the hearing typically is entitled to legal counsel and may challenge a commitment order through habeas corpus rules. Historically, until the first third of the twentieth century or later in most jurisdictions, all committals to public psychiatric facilities and most committals to private ones were involuntary. Since then, there have been alternating trends towards the abolition or substantial reduction of involuntary commitment,[1] a trend known as "deinstitutionalization."
Purpose
In most jurisdictions, involuntary commitment is specifically applied to individuals found to be suffering from a mental illness that impairs their reasoning ability to such an extent that the laws, state or courts find that decisions must or should be made for them under a legal framework. (In some jurisdictions this is a distinct proceeding from being "found incompetent.") Involuntary commitment is used to some degree for each of the following headings although different jurisdictions have different criteria. Some jurisdictions limit court-ordered treatment to individuals who meet statutory criteria for presenting a danger "to self or others." Other jurisdictions have criteria that are broader.
First aid
Training is gradually becoming available in mental health first aid to equip community members such as teachers, school administrators, police officers, and medical workers in recognizing and managing situations where evaluations of behavior might be appropriate.[2] The extension of first aid training to cover mental health problems and crises is a quite recent development.[3] [4] A mental health first aid training course was developed in Australia in 2001 and has been found to improve assistance provided to persons with a mental illness or in a mental health crisis. This form of training has now spread to a number of other countries (Canada, Finland, Hong Kong, Ireland, Singapore, Scotland, England, Wales, United States).[5] Mental health triage may be used in an emergency room to evaluate the degree of risk and prioritize treatment.
Observation
Observation is sometimes used to determine if a person warrants involuntary commitment. It is not always clear on a relatively brief examination whether a person is psychotic or otherwise warrants commitment.
Containment of danger
A common reason given for involuntary commitment is to prevent danger to the individual or society. People with suicidal thoughts may act on these thoughts and harm or kill themselves. People with psychoses are occasionally driven by their delusions or hallucinations to harm themselves or others. People with certain types of personality disorders can occasionally present a danger to themselves or others.
Involuntary commitment This concern has found expression in the standards for involuntary commitment in every U.S. state and in other countries as the "danger to self or others" standard, sometimes supplemented by the requirement that the danger be "imminent." In some jurisdictions, "danger to self or others" standard has been broadened in recent years to include need-for-treatment criteria such as "gravely disabled." In Arizona, the government can mandate in-patient treatment for anyone determined to be "persistently or acutely disabled." Virtually anyone who suspects that someone has mental problems and needs help could file an application to a state-licensed healthcare agency for a court-ordered evaluation. In Connecticut, someone can be committed only if he or she has "psychiatric disabilities and is dangerous to himself or herself or others or gravely disabled". "Gravely disabled" has usually been interpreted to mean that the person is unable on his own to obtain adequate food, shelter and clothing. In Iowa, any "interested person" may begin commitment proceedings by submitting a written statement to the court. If the court finds that the respondent is "seriously mentally impaired," he or she will be placed in a psychiatric hospital for further evaluation and possibly treatment. Further hearings are required at specific intervals for as long as the person is being involuntarily held. The Michigan Mental Health Code provides that a person "whose judgment is so impaired that he or she is unable to understand his or her need for treatment and whose continued behavior as the result of this mental illness can reasonably be expected, on the basis of competent clinical opinion, to result in significant physical harm to himself or herself or others" may be subjected to involuntary commitment, a provision paralleled in the laws of many other jurisdictions. These types of provisions have been criticized as a sort of "heads I win, tails you lose". Understanding one's "need for treatment" would cause one to agree to voluntary commitment, but the Bazelon Center has said that this "lack of insight" is "often no more than disagreement with the treating professional"[6] and this disagreement might form part of the evidence to support one's involuntary commitment. In Nevada, prior to confining someone, the state must demonstrate that the person "is mentally ill and, because of that illness, is likely to harm himself or others if allowed his liberty." In Oregon, the standard that the allegedly mentally ill person "Peter [h]as been committed and hospitalized twice in the last three years, is showing symptoms or behavior similar to those that preceded and led to a prior hospitalization and, unless treated, will continue, to a reasonable medical probability, to deteriorate to become a danger to self or others or unable to provide for basic needs" may be substituted for the danger to self or others standard. In Utah, the standard is that "the proposed patient has a mental illness which poses a substantial danger".[7] "Substantial danger" means the person, by his or her behavior, due to mental illness: (a) is at serious risk to: (i) commit suicide, (ii) inflict serious bodily injury on himself or herself; or (iii) because of his or her actions or inaction, suffer serious bodily injury because he or she is incapable of providing the basic necessities of life, such as food, clothing, and shelter; (b) is at serious risk to cause or attempt to cause serious bodily injury; or (c) has inflicted or attempted to inflict serious bodily injury on another.[8]
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Deinstitutionalization
Starting in the 1960s, there has been a worldwide trend toward moving psychiatric patients from hospital settings to less restricting settings in the community, a shift known as "deinstitutionalization." Because the shift typically was not accompanied by a commensurate development of community-based services, critics say that deinstitutionalization has led to large numbers of people who would once have been inpatients being incarcerated in jails and prisons or becoming homeless when outpatient services are not available or they choose not adhere to treatment outside the hospital. In some jurisdictions, laws authorizing court-ordered outpatient treatment have been passed in an effort to compel individuals with chronic, untreated severe mental illness to accept treatment while living outside the hospital.
Involuntary commitment
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Australia
In Australia, court hearings are not required for involuntary commitment. Mental health law is constitutionally under the state powers. Each state thus has different laws, many of which have been updated in recent years. Referral for service The usual requirement is that a police officer or a physician determine that a person requires a psychiatric examination, usually through a psychiatric hospital. If the person is detained in the hospital, they usually must be seen by an authorized psychiatrist within a set period of time. In some states, after a further set period or at the request of the person or their representative, a tribunal hearing is held to determine whether the person should continue to be detained. In states where tribunals are not instituted, there is another form of appeal. Some Australian states require that the person is a danger to the society or themselves; other states only require that the person be suffering from a mental illness that requires treatment. The Victorian Mental Health Act (1986) specifies in part that: "(1) A person may be admitted to and detained in an approved mental health service as an involuntary patient in accordance with the procedures specified in this Act only if (a) the person appears to be mentally ill; and (b) the person's mental illness requires immediate treatment and that treatment can be obtained by admission to and detention in an approved mental health service; and (c) because of the person's mental illness, the person should be admitted and detained for treatment as an involuntary patient for his or her health or safety (whether to prevent a deterioration in the person's physical or mental condition or otherwise) or for the protection of members of the public; and (d) the person has refused or is unable to consent to the necessary treatment for the mental illness; and (e) the person cannot receive adequate treatment for the mental illness in a manner less restrictive of that person's freedom of decision and action. There are additional qualifications and restrictions but the effect of these provisions is that people who are assessed by doctors as being in need of treatment may be admitted involuntarily without the need of demonstrating a risk of danger. This then overcomes the pressure described above to exaggerate issues of violence to obtain an admission.
Involuntary commitment Treatment In general, once the person is under involuntary commitment, treatment may be instituted without further requirements. Some treatments such as electroconvulsive therapy (ECT) often require further procedures to comply with the law before they may be administered involuntarily. Community treatment orders can be used in the first instance or after a period of admission to hospital as a voluntary or involuntary patient. With the trend towards deinstitutionalization this is becoming increasingly frequent and hospital admission is restricted to people with severe mental illnesses.
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Europe
Germany In Germany there is a growing tendency to use the law on legal guardianship, instead of mental health law, to justify involuntary commitment or treatment. The ward's legal guardian decides that he/she must go into mental hospital for treatment, and the police will act on this decision. This is simpler for the government and family members than the formal process for commitment under mental health laws. In German criminal law a person that was convicted of certain crimes can also be sentenced to be kept in preventive detention; see article on preventive detention. Netherlands In Dutch criminal law a convict can be sentenced to involuntary psychiatric treatment in a special institute called a TBS-clinic. TBS is an abbreviation for "Ter Beschikkingstelling," literally meaning "being placed at disposal." Legally, such a sentence is not regarded as punishment like a prison sentence, but as a special measure. In the Netherlands, it is common practice to sentence criminals to a combination of a normal prison term and TBS. The convict will then be placed in a TBS-clinic after serving time in prison (usually two-thirds of the original prison sentence, although this practice is under discussion). According to Dutch law, meeting three conditions is required for a convict to be sentenced to TBS. These conditions are: the crime committed must have been directly related to a psychiatric disorder, recidivism must be likely, and the convict can not, or only partially, be held accountable for the crime. To determine if these conditions are met, the suspect is observed in a forensic psychiatric detention center, the Pieter Baan Centre.[9] Neither the prosecution or the defense can effectively challenge the Pieter Baan Centre's report, since it is the only institution that can conduct such investigations. Fatal mistakes have occurred, for instance, when a child molester regarded by the Pieter Baan Center as "not dangerous" killed a child upon release. The conclusions in the centre's report are not binding, the judge can decide to ignore, or only partially accept them. Every convict detained in a TBS-clinic may get temporary leave, after serving a certain time or after some progress in treatment. This is regarded as an essential part of treatment, as the convict will be gradually re-entering society this way. At first the convict will be escorted by a therapist, and will be allowed outside the clinic for only a few hours. After evaluation, time and freedom of movement will be expanded until the convict can move freely outside the clinic without escort (usually for one day at a time). At that time, the convict will find work or follow an education. Generally, the convict is released after being in this situation for one or two years without incident. The time to be served in TBS can be indefinite, and it may be used as a form of preventive detention. Evaluation by the court will occur every one or two years. During these evaluations the court determines if any progress is made in treatment of the convict, and if it will be safe to release the convict into society. In general, the court will follow conclusions made by the TBS-clinic. Average time served in a TBS-clinic by a convict is slightly over eight years.
Involuntary commitment Dutch TBS-clinics In the Netherlands there are currently 12 institutions regarded as TBS-clinics: AMC de Meren/Arkin, Amsterdam Dr. Henri van der Hoevenstichting, Utrecht Dr. S. van Mesdagkliniek, Groningen Hoeve Boschoord, Boschoord FPC Veldzicht, Balkbrug Pompestichting, Nijmegen Oostvaarderskliniek, Almere De Kijvelanden/FPC Tweelanden, Poortugaal FPC Oldenkotte, Rekken FPC De Rooyse Wissel, Venray GGz Drenthe, Assen GGz Eindhoven/De Woenselse Poort, Eindhoven
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These institutions combined currently are holding about 1840 convicts. By the end of the 20th century, it was concluded that some convicts could not be treated and therefore could not be safely released into society. For these convicts, TBS-clinics formed special wards, called "long-stay wards". Transfer to such a ward means that the convict will no longer be actively treated, but merely detained. This is regarded as more cost-effective. In general, the convicts in these wards will be incarcerated for the rest of their lives, although their detention is eligible for regular review by the court. Controversy Since the latter half of the 1990s considerable controversy has grown among Dutch society, about the TBS-system. This controversy has two main reasons. The first reason is the media increasingly reported cases of convicts committing crimes while still in, or after, treatment in a TBS-clinic. Some examples of these cases are: During 1992, a truck driver was convicted for raping and murdering three young children. Eight years earlier he was released from a TBS-clinic after being treated for child molestation. A convict, about to be released from a TBS-clinic, murdered the owner of a garage in 1996 while under the influence of drugs. An ex-convict, treated in a TBS-clinic, murdered two women in 1994 and 1997. A convict, still treated by a TBS-clinic, randomly killed a man in the city of Groningen in 1999. Between 2000 and 2004, an ex-convict tortured several animals and killed a homeless man. He had been treated in a TBS-clinic. In 2002 an ex-convict was sentenced for triple murder. He also was released earlier. In 2005 a convict escaped his escort during leave. He was arrested several days later after killing a man. Political and social commotion increased, and debate started about the effectiveness of the TBS-system and if convicts should be granted leave from TBS-clinics. Especially right-wing politicians pleaded the TBS-system should be discarded altogether. Numerous articles in newspapers, magazines, television and radio programs and a revealing book written by an ex-convict (which for the first time openly questioned the effectiveness of the TBS-system) boosted discussion. Prior to that, any problems had been mostly denied by TBS-clinics themselves. The center of attention became a highly renowned TBS-clinic, Dr. S. Van Mesdagkliniek in the city of Groningen. Events that took place there, by the end of the 1990s and the first years of the 21st century, initiated the second reason for controversy. Concern rose about signs of unprofessional behavior by staff working in TBS-clinics, and the Dr. S. Van Mesdagkliniek proved to be among the most infamous for these problems. This TBS-clinic has been plagued with unprofessional and even criminal acts by its staff since 1999. During that year, the Dr. S. Van
Involuntary commitment Mesdagkliniek came under investigation by Dutch police after rumors about female staffmembers committing sexual offenses against convicts.[10] Five such cases were discovered during the investigation, and also numerous cases of drug-abuse, smuggling and trading of contraband such as: alcohol, mobile phones, pornographic material and hard drugs.[11] It became apparent that staff members did not have the required education, had not been informed about rules and regulations, disregarded legal procedures, gave false testimonies, tampered with evidence, uttered false accusations against convicts, and intimidated colleagues.[10] At least one psychiatrist, employed as such by the Dr. S. Van Mesdagkliniek, proved to be not qualified,[12] and treatment of convicts was in many cases simply non-existent.[13] These problems had been known for long by the management, but were always kept hidden. After public outcry about this situation, management was replaced[14] and all of the nine (at the time) TBS-clinics in the Netherlands were subjected to investigation. Six of them proved to be below the required legal standards.[15] However, problems for the expensive Dutch TBS-system did not end there. In spite of many measures taken by the government, convicts still were released without proper treatment. As a consequence, numerous crimes were committed by convicts that were regarded as treated by TBS-clinics. Also, sexual offenses against convicts by staff members and smuggling of contraband did not cease in several TBS-clinics.[16] In 2006, the Dutch government formed a committee to investigate the TBS-system. Some, however not the worst, problems were recognized and measures were proclaimed. One of the known actual results is that fewer convicts escape during temporary release. Controversy regarding the, often praised, Dutch TBS-system does not cease to exist. In 2005, a staff member working in the Dr. S. Van Mesdagkliniek was caught while smuggling liquor to convicts suffering from alcohol-related problems.[17] In 2007, a female staff member committed sexual offenses against a convict, and had smuggled contraband.[18] She was sentenced to three months in prison in 2009. That same year, investigation proved convicts still had ample access to illicit drugs[19] and four inmates from the Dr. S. Van Mesdagkliniek were arrested for possession of child pornography.[20] Many crimes committed by released convicts treated in TBS-clinics, escape statistics because they occurred in other countries, or because they differ from the crime the convict was originally convicted for (many convicts released from TBS-clinics find their way in illegal drug trade and related crimes). Because there seems to be no acceptable alternative available, political support for the much plagued TBS-system remains, in spite of controversy. United Kingdom In the United Kingdom, the process known in the United States as involuntary commitment is informally known as "sectioning", after the various sections of the Mental Health Act 1983 (covering England and Wales), the Mental Health (Northern Ireland) Order 1986 and the Mental Health (Care and Treatment) (Scotland) Act 2003 that provide its legal basis. In England and Wales, Approved Mental Health Professionals have a lead role in coordinating Mental Health Act assessments, which they conduct in cooperation with usually two medical practitioners. Under the Mental Health Act, detention is determined by utility and purpose. Mentally ill individuals may be detained under Section 2 for a period of assessment lasting up to 28 days or Section 3 for a period of treatment lasting up to 6 months. Patients already on a ward may be detained under section 5(2) for up to 72 hours for the purposes of allowing an assessment to take place for section 2 or 3. Separate sections deal with mentally ill criminal offenders. In all cases detention needs to be justified on the basis that the person has a mental disorder and poses a risk of harm to their own health, safety, or the safety of others.[21] Under the amended Mental Health Act 2007, which came into force in November 2008, to be detained under Section 3 for treatment, appropriate treatment must be available in the place of detention. Supervised Community Treatment orders means people can be discharged to the community on a conditional basis, remaining liable to recall to hospital if they break the conditions of the community treatment order.
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United States
Involuntary commitment is governed by state law and procedures vary from state to state. In some jurisdictions, laws regarding the commitment of juveniles may vary, with what is the de facto involuntary commitment of a juvenile perhaps de jure defined as "voluntary" if his parents agree, though he may still have a right to protest and attempt to get released. However, there is a body of case law governing the civil commitment of individuals under the Fourteenth Amendment through U.S. Supreme Court rulings beginning with Addington v. Texas in 1979 which set the bar for involuntary commitment for treatment by raising the burden of proof required to commit persons from the usual civil burden of proof of "preponderance of the evidence" to the higher standard of "clear and convincing" evidence.[22] In 1975, the U.S. Supreme Court ruled that involuntary hospitalization and/or treatment violates an individual's civil rights in O'Connor v. Donaldson. This ruling forced individual states to change their statutes. For example, the individual must be exhibiting behavior that is a danger to himself or others in order to be held, the hold must be for evaluation only and a court order must be received for more than very short term treatment or hospitalization (typically no longer than 72 hours). This ruling has severely limited involuntary treatment and hospitalization in the U.S.[23] In the U.S. the specifics of the relevant statutes vary from state to state.[24] This was the case in a famous United States Supreme Court decision in 1975, O'Connor v. Donaldson, when Kenneth Donaldson, a patient committed to Florida State Hospital, sued the hospital and staff for confining him for 15 years against his will. The decision means that it is unconstitutional to commit for treatment a person who is not imminently a danger to himself or others and is capable to a minimal degree of surviving on his own.[25] An example of involuntary commitment procedures is the Baker Act used in Florida. Under this law, a person may be committed only if they present a danger to themselves or others. A police officer, doctor, nurse or licensed mental health professional may initiate an involuntary examination that lasts for up to 72 hours. Within this time, two psychiatrists may ask a judge to extend the commitment and order involuntary treatment. The Baker Act also requires that all commitment orders be reviewed every six months in addition to ensuring certain rights to the committed including the right to contact outsiders. Also, a person under an involuntary commitment order has a right to counsel and a right to have the state provide a public defender if they cannot afford a lawyer. While the Florida law allows police to initiate the examination, it is the recommendations of two psychiatrists that guide the decisions of the court. In the 1990s, involuntary commitment laws were extended under various state laws commonly recognized under the umbrella term SVP laws to hold some convicted sex offenders in psychiatric facilities after their prison terms were completed.[26] (This is generally referred to as "civil commitment," not "involuntary commitment," since involuntary commitment can be criminal or civil). This matter has been the subject of a number of cases before the Supreme Court, most notably Kansas v. Hendricks and United States v. Comstock[27] in regard to the Adam Walsh Child Protection and Safety Act, which does not require a conviction on sex offences, but only that the person be in federal custody and be deemed a "sexually dangerous person".[28] Controversy about liberty The impact of involuntary commitment on the right of self-determination has been a cause of concern.[29] Critics of involuntary commitment have advocated that "the due process protections... provided to criminal defendants" be extended to them.[30] The Libertarian Party opposes the practice in its platform. Thomas Szasz and the anti-psychiatry movement has also been prominent in challenging involuntary commitment. A small number of individuals in the U.S. have opposed involuntary commitment in those cases in which the diagnosis forming the justification for the involuntary commitment rests, or the individuals say it rests, on the speech or writings of the person committed, saying that to deprive him of liberty based in whole or part on such speech and writings violates the First Amendment. Other individuals have opposed involuntary commitment on the bases that they claim (despite the amendment generally being held to apply only to criminal cases) it violates the Fifth
Involuntary commitment Amendment in a number of ways, particularly its privilege against self-incrimination, as the psychiatrically examined individual may not be free to remain silent, and such silence may actually be used as "proof" of his "mental illness".[31] Although patients involuntarily committed theoretically have a legal right to refuse treatment, refusal to take medications or participate in other treatments is noted by hospital staff. Court reviews usually are heavily weighted toward the hospital staff, with the patient input during such hearings minimal. In Kansas v. Hendricks, the US Supreme Court found that civil commitment is constitutional regardless of whether any treatment is provided.[32] Alternatives Accompanying deinstitutionalization was the development of laws expanding the power of courts to order people to take psychiatric medication on an outpatient basis. Though the practice had occasionally occurred earlier, outpatient commitment was used for many people who would otherwise have been involuntarily committed. The court orders often specified that a person who violated the court order and refused to take the medication would be subject to involuntary commitment. Involuntary commitment is distinguished from conservatorship and guardianship. The intent of conservatorship or guardianship is to protect those not mentally able to handle their affairs from the effects of their bad decisions, particularly with respect to financial dealings.[33] For example, a conservatorship might be used to take control of the finances of a person with dementia, so that the person's assets and income are used to meet his basic needs, e.g., by paying rent and utility bills. Advance psychiatric directives may have a bearing on involuntary commitment.[34] [35] Individual state policies and procedures US military The service member can be held under the so-called Boxer law. California 5150 (Involuntary psychiatric hold) District of Columbia In the District of Columbia any police officer, physician, or mental health professional can request to have you evaluated at St. Elizabeths Hospital, where the physician on duty can hold the patient for up to 48 hours. A family member or concerned citizen can also petition the Department of Mental Health, but the claim will be evaluated prior to the police acting upon it. In order to be held further, a request must be filed with the Department of Mental Health. However, this only can keep the patient involuntary admitted for up to seven days. For further commitment, the patient is evaluated by a mental health court, part of family court, for which the public defender assists the patient. This can result in the patient being held up to one year at which point the patient returns to mental health court. This is different for someone first admitted to St. Elizabeths Hospital due to criminal charges. If found to not ever become competent for trial, they will be evaluated via a Jackson hearing for possible continued commitment to protect the public. If they have been found not guilty by reason of insanity, their dangerousness is evaluated at a Bolton Hearing.
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Involuntary commitment Maryland In Maryland any person may request, via a Emergency Evaluation form, that another individual be evaluated against their will by an emergency room physician for involuntary admission. If the judge concurs, he will direct the police to escort the individual to the hospital. A licensed physician, psychologist, social worker, or nurse practitioner who has examined the patient or a police officer may bring a potential patient to the emergency room for forced evaluation without approval from a judge. The patient may be kept in the hospital for up to thirty hours. If by then two physicians, or one physician and one psychologist then decide that the patient meets the Maryland criteria for an involuntary psychiatric admission, then he or she may be kept inpatient involuntarily for up to ten days. During this time an administrative law judge determines if criteria for longer civil commitment are met: a person has a mental illness; a person needs inpatient care or treatment; a person presents a danger to themselves or to others; a person are unable or unwilling to be admitted voluntarily; there is no available, less restrictive form of care or treatment to meet the person's needs.
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Virginia As of 2008 Virginia was one of only five states requiring imminent danger in order to involuntarily commit someone. But after the Virginia Tech Massacre, there was significant political consensus to strengthen the protections for society and allow more leniency in determining that an individual needed to be committed against their will. the person has a mental illness and there is a substantial likelihood that, as a result of mental illness, the person will, in the near future, (1) cause serious physical harm to himself or others as evidenced by recent behavior causing, attempting, or threatening harm and other relevant information, if any the person has a mental illness and there is a substantial likelihood that, as a result of mental illness, the person will, in the near future, (2) suffer serious harm due to his lack of capacity to protect himself from harm or to provide for his basic human needs "Imminent danger" was found to have too much variability throughout Virginia due to vagueness. The new standard is more specific in that substantial likelihood is more clear. However, in order to not limit potential detainee's freedoms too much it is characterized by the time limit of near future. "Recent acts" is legally established to require more than a mere recitation of past events.
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Notes
[1] Hendin, Herbert (1996). Suicide in America. W. W. Norton & Company. p.214. ISBN0393313689. [2] Mental Health First Aid USA (http:/ / www. mentalhealthfirstaid. org/ cs/ background) [3] Kitchener BA, Jorm AF. Mental health first aid training for the public: evaluation of effects on knowledge, attitudes and helping behaviour. BMC Psychiatry 2002; 2: 10. [4] Kitchener BA, Jorm AF. Mental Health First Aid Manual, Melbourne: ORYGEN Research Centre, 2002. [5] Kitchener BA, Jorm AF. (2008). Mental health first aid: an international program for early intervention. Early Intervention in Psychiatry, 2, 55-61. [6] Bazelon Center Involuntary Commitment Issues Page (http:/ / www. bazelon. org/ issues/ commitment/ positionstatement. html) [7] Utah Code Annotated 62A-15-631(3) (2003) [8] Utah Code Annotated 62A-15-602(13) (2003) [9] Onder Dwang, H. Ludwig and R. Blom 2001, ISBN 9020405233 [10] Nieuwe Revu Magazine, 1999 [11] Onder Dwang, H. Ludwig & R. Blom, 2001, ISBN 9020405233 [12] Trouw, August 8, 2000 [13] Algemeen Dagblad, October 27, 1999 [14] Algemeen Dagblad, December 22, 1999 [15] NRC Handelsblad, March 3, 2001 [16] Metro,february 8,2006 [17] Algemeen Dagblad, September 22, 2005 [18] RTV Noord, February 9, 2009 [19] RTV Noord, September 3, 2009 [20] RTV Noord, January 29, 2009 [21] Mental Health Act, 1983 (amended 2007) [22] Hays, Jr. (December 1989). "The role of Addington v Texas on involuntary civil commitment". Psychological reports 65 (3 Pt 2): 12115. PMID2623112. [23] "O'Connor v. Donaldson, 422 U.S. 563 (1975)" (http:/ / www. treatmentadvocacycenter. org/ LegalResources/ CaseLaws/ Case1. htm). . Retrieved 2007-10-02. [24] "Legal standard/requirements for assisted treatment, by state" (http:/ / www. psychlaws. org/ LegalResources/ index. htm#statutes). . Retrieved 2007-10-02. [25] "O'Connor v. Donaldson, 422 U.S. 563 (1975)" (http:/ / www. treatmentadvocacycenter. org/ LegalResources/ CaseLaws/ Case1. htm). . Retrieved 2007-10-03. [26] http:/ / www. jaapl. org/ cgi/ reprint/ 36/ 4/ 443. pdf [27] Breyer, Stephen (May 2010). "UNITED STATES v. COMSTOCK ET AL." (http:/ / www. supremecourt. gov/ opinions/ 09pdf/ 08-1224. pdf). . Retrieved 2010-05-17. [28] Barker, The Adam Walsh Act: Un-civil Commitment, available at http:/ / papers. ssrn. com/ sol3/ papers. cfm?abstract_id=1496934# [29] Veatch, Robert M. (1997). Medical Ethics (2nd ed.). Jones & Bartlett Publishers. p.305. ISBN0867209747. [30] Hendin, p.214 [31] Kevin Wadzuk. [? "Violations of the Rights of the "Mentally Ill" in the District of Columbia"]. ?. [32] "Psychological Evaluation for the Courts, Second Edition - A Handbook for Mental Health Professionals and Lawyers - 9.04 Special Sentencing Provisions (b) Sexual Offender Statutes" (http:/ / www. guilford. com/ cgi-bin/ cartscript. cgi?page=etc/ courts_updates. html& cart_id=#part_two). Guilford.com. . Retrieved 2007-10-19. [33] Kapp, Martin (2008). Sajatovic, Martha; Loue, Sana; Koroukian, Siran M.. ed. Encyclopedia of Aging and Public Health. Berlin: Springer. pp.230232. ISBN0-387-33753-9. [34] About.com: http:/ / www. bazelon. org/ advdir. html (http:/ / bipolar. about. com/ gi/ dynamic/ offsite. htm?site=http:/ / www. bazelon. org/ advdir. html) [35] National Resource Center on Psychiatric Advance Directives (http:/ / www. nrc-pad. org) [36] Moshik, Temkin (2009). The Sacco-Vanzetti Affair. Yale University Press Publishers. p.316. ISBN9780300124842.
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References
Atkinson, J. (2006) Private and Public Protection: Civil Mental Health Legislation, Edinburgh, Dunedin Academic Press 1 Rosenhan, D.L. (1973). On being sane in insane places. Science, 179, 250-258. 2 Spitzer, R.L. (1975). On pseudoscience in science, logic in remission, and psychiatric diagnosis: A critique of Rosenhan's "On being sane in insane places." Journal of Abnormal Psychology, 84, 442-452. 3 Perlin, M.L. (1993/1994). The ADA and Persons with Mental Disabilities: Can Sanist Attitudes Be Undone? Journal of Law and Health,, 8 JLHEALTH 15, 33-34. 4 Torrey, E. Fuller. (1997). Out of the Shadows: Confronting America's Mental Illness Crisis. New York: John Wiley and Sons. Black Hands of Beijing: Lives of Defiance in China's Democracy Movement, by George Black and Robin Munro, New York: John Wiley & Sons, Inc., 1993. Tsesis, Alexander, Protecting Children Against Unnecessary Institutionalization, South Texas Law Review, vol. 39, p.995 (1998) papers.ssrn.com (http://papers.ssrn.com/sol3/papers.cfm?abstract_id=1031713)
External links
National Mental Health Consumers' Self-Help Clearinghouse (http://www.mhselfhelp.org/) Victorian legislation and parliamentary documents (Australia) (http://www.dms.dpc.vic.gov.au/Domino/ Web_Notes/LDMS/PubLawToday.nsf?OpenDatabase) - search using "mental health act" for the latest version of the act Mental health review board site (Victoria, Australia) (http://www.mhrb.vic.gov.au/) - the official site of the MHRB Keys to Commitment (A Guide for Family Members) by Robert J. Kaplan, J.D. (http://www.psychlaws.org/ GeneralResources/article218.htm) State-by-state chart of U.S. commitment laws (http://www.psychlaws.org/LegalResources/statechart.htm) Psychiatric Imprisonment in Oregon (http://www.progress.org/fold265.htm) Rogers Law (http://www.psychlaws.org/LegalResources/CaseLaws/Case3.htm), concerning involuntary treatment/commitment in Massachusetts Comprehensive Journal Article Discussing Civil Commitment Law and Reform Regarding Sex Offenders (http:// www.freewebs.com/adamshajnfeld) National Resource Center on Psychiatric Advance Directives (http://www.nrc-pad.org) "AlterNet: Movie Mix: Must-See Indy Film Exposes Cruel Teen Correction Programs" (http://www.alternet. org/movies/56241/). Retrieved 2007-07-08. Baker Act Reporting Center (related to Florida's Civil Commitment Statute) (http://bakeract.fmhi.usf.edu/) National Alliance on Mental Illness (http://www.nami.org) Unjustified Psychiatric Commitment in the USA (http://www.antipsychiatry.org/unjustif.htm) "Getting Someone to Psychiatric Treatment Can Be Difficult and Inconclusive" (http://www.nytimes.com/ 2011/01/19/us/19mental.html) New York Times January 18, 2011
Light therapy
285
Light therapy
Light therapy
Intervention
Bright light therapy is a common treatment for seasonal affective disorder and for circadian rhythm disorders. ICD-10-PCS ICD-9: MeSH 6A6 [1] , GZJ [2] [4]
99.83
[3]
, 99.88 [5]
D010789
Light therapy or phototherapy (classically referred to as heliotherapy) consists of exposure to daylight or to specific wavelengths of light using lasers, light-emitting diodes, fluorescent lamps, dichroic lamps or very bright, full-spectrum light, usually controlled with various devices. The light is administered for a prescribed amount of time and, in some cases, at a specific time of day. Common use of the term is associated with the treatment of skin disorders (chiefly psoriasis), sleep disorder and some psychiatric disorders. Light therapy directed at the skin is also used to treat acne vulgaris, eczema and neonatal jaundice. Light therapy which strikes the retina of the eyes is used to treat circadian rhythm disorders such as delayed sleep phase syndrome and can also be used to treat seasonal affective disorder, with some support for its use also with non-seasonal psychiatric disorders. Other medical applications of light therapy also include pain management, accelerated wound healing, hair growth, improvement in blood properties and blood circulation, and sinus-related diseases and disorders. Many of these use low level laser therapy and red light therapy in the 620660nm range.
History
Many ancient cultures practiced various forms of heliotherapy, including people of the Ancient Greece, ancient egypt, and ancient Rome.[6] The Inca, Assyrian and early German settlers also worshipped the sun as a health bringing deity. Indian medical literature dating to 1500 BC describes a treatment combining herbs with natural sunlight to treat non-pigmented skin areas. Buddhist literature from about 200 AD and 10th-century Chinese documents made similar references. Faroese physician Niels Finsen is believed to be the father of modern phototherapy. He developed the first artificial light source for this purpose, and used his invention to treat lupus vulgaris. He received the Nobel Prize in Physiology or Medicine in 1903. Since then a large array of treatments have been developed from the use of controlled light. Though the popular consumer understanding of "light therapy" is associated with treating seasonal affective disorder and skin conditions
Light therapy like psoriasis, other applications include the application of low level laser, red light, near-infrared and ultraviolet lights for pain management, hair growth, skin treatments, accelerated wound healing.
286
Skin related
Psoriasis
Three percent of the population suffer from psoriasis, and UVB phototherapy has been shown to effectively treat the disease.[7] A feature of psoriasis is localized inflammation mediated by the immune system. Ultraviolet radiation is known to suppress the immune system and reduce inflammatory responses. Light therapy for skin conditions like psoriasis use UV-A (315400nm wavelength) or UV-B (280315nm wavelength) light waves. UV-A, combined with a drug taken orally, is known as PUVA treatment.
Acne vulgaris
Sunlight was long known to improve acne, and this was thought to be due to antibacterial and other effects of the ultraviolet spectrum which cannot be used as a long-term treatment due to the likelihood of skin damage.[8] It was found that some of the visible violet light present in sunlight (in the range 415430nm) activates a porphyrin (Coproporphyrin III) in Propionibacterium acnes which damages and ultimately kills the bacteria by releasing singlet oxygen. A total of 320J/cm2 of light within this range renders the bacteria non-viable.[9] Since there are few porphyrins naturally found in the skin, the treatment is believed safe except in patients with porphyria;[10] although eye protection is used due to light-sensitive chemicals in the retina. The light is usually created by superluminous LEDs. This form of treatment has been approved by the FDA for some lightwave systems . Overall improvements of on average 76% for 80% of patients occurs over three months; most studies show that it performs better than benzoyl peroxide and the treatment is far better tolerated. However, approximately 10% of users see no improvement.[9]
Tanning
Tanning is caused by the effects of two different spectrums of ultraviolet radiation: UV-A and UV-B.
Wound healing
Some case studies[11] have found low-level laser light to be possibly helpful as an adjuctive treatment in wound healing, although a review of the overall scientific literature[12] does not support the use of low-level laser therapy for this purpose.
Light therapy
287
Photodynamic therapy
This treatment is based on a photo-sensitive liquid that is injected to the body. this liquid is attached to the unhealthy cells of the body. When it is exposed from outside to strong light it become solid, and thus it kills the unhealthy cells. One of the treatments is using blue light with aminolevulinic acid for the treatment of actinic keratosis. This is not a U.S. FDA-approved treatment for acne vulgaris.[13]
Light therapy
288
Non-seasonal depression
Light therapy has also been suggested in the treatment of non-seasonal depression and other psychiatric disturbances, including major depressive disorder, bipolar disorder[26] and postpartum depression.[27] [28] A meta-analysis by the Cochrane Collaboration concluded that "For patients suffering from non-seasonal depression, light therapy offers modest though promising antidepressive efficacy."[29]
Neonatal jaundice
Light therapy is used to treat cases of neonatal jaundice[35] through the isomerization of the bilirubin and consequently transformation into compounds that the newborn can excrete via urine and stools. A common treatment of neonatal jaundice is the Bili light.
Parkinson's disease
Bright light therapy may ease Parkinson's disease by reducing patients' tremors.[36] [37]
A newborn infant undergoing white-light phototherapy to treat neonatal jaundice.
Light therapy
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Safety
Ultraviolet light causes progressive damage to human skin. This is mediated by genetic damage, collagen damage, as well as destruction of vitamin A and vitamin C in the skin and free radical generation. Ultraviolet light is also known to be a factor in formation of cataracts. Researchers have questioned whether limiting blue light exposure could reduce the risk of age-related macular degeneration.[38] Modern phototherapy lamps used in the treatment of seasonal affective disorder and sleep disorders either filter out or do not emit ultraviolet light and are considered safe and effective for the intended purpose, as long as photosensitizing drugs are not being taken at the same time and in the absence of any existing eye conditions. Light therapy is a mood altering treatment, and just as with drug treatments, there is a possibility of triggering a manic state from a depressive state, causing anxiety and other side effects. While these side effects are usually controllable, it is recommended that patients undertake light therapy under the supervision of an experienced clinician, rather than attempting to self-medicate.[39] It is reported that bright light therapy may activate the production of reproductive hormones, such as testosterone, luteinizing hormone, follicle-stimulating hormone, and estradiol.[40] [41] There are few absolute contraindications to light therapy, although there are some circumstances in which caution is required. These include when a patient has a condition that might render his or her eyes more vulnerable to phototoxicity, has a tendency toward mania, has a photosensitive skin condition, or is taking a photosensitizing herb (such as St. John's wort) or medication.[42] Patients with porphyria should avoid most forms of light therapy. Patients on certain drugs like methotrexate or chloroquine should use caution with light therapy as there is a chance that these drugs could cause porphyria.
Side effects
Side effects of light therapy for sleep phase disorders include jumpiness or jitteriness, headache, and nausea. Some nondepressive physical complaints (such as poor vision and skin rash or irritation) may improve with light therapy.[43]
References
[1] [2] [3] [4] [5] [6] [7] http:/ / www. icd10data. com/ ICD10PCS/ Codes/ 6/ A/ 6 http:/ / www. icd10data. com/ ICD10PCS/ Codes/ G/ Z/ J http:/ / icd9cm. chrisendres. com/ index. php?srchtype=procs& srchtext=99. 83& Submit=Search& action=search http:/ / icd9cm. chrisendres. com/ index. php?srchtype=procs& srchtext=99. 88& Submit=Search& action=search http:/ / www. nlm. nih. gov/ cgi/ mesh/ 2011/ MB_cgi?field=uid& term=D010789 F. Ellinger Medical Radiation Biology Springfield 1957 Diffey BL (1980). "Ultraviolet radiation physics and the skin". Phys. Med. Biol. 25 (3): 405426. doi:10.1088/0031-9155/25/3/001. PMID6996006. [8] "Health effects of UV radiation" (http:/ / www. who. int/ uv/ health/ en/ ). Ultraviolet radiation and the INTERSUN Programme. World Health Organization. . Retrieved 2010-02-23. [9] Papageorgiou P, Katsambas A, Chu A (May 2000). "Phototherapy with blue (415 nm) and red (660 nm) light in the treatment of acne vulgaris". Br. J. Dermatol. 142 (5): 9738. doi:10.1046/j.1365-2133.2000.03481.x. PMID10809858. [10] Hebel, JL; Poh-Fitzpatrick, MB (2009-01-12). "Congenital Erythropoietic Porphyria" (http:/ / www. emedicine. com/ DERM/ topic145. htm). eMedicine. . Retrieved 2009-06-09. [11] Sutterfield R (2008 Jan-Feb). "Light therapy and advanced wound care for a neuropathic plantar ulcer on a Charcot foot". J Wound Ostomy Continence Nurs 35 (1): 113115. doi:10.1097/01.WON.0000308628.60958.d9. PMID18199948. (http:/ / www. nursingcenter. com/ Library/ JournalArticle. asp?Article_ID=767846) [12] Posten W, Wrone DA, Dover JS, Arndt KA, Silapunt S, Alam M (March 2005). "Low-level laser therapy for wound healing: mechanism and efficacy". Dermatol Surg 31 (3): 33440. doi:10.1111/j.1524-4725.2005.31086. PMID15841638. [13] Aetna policy bulletin re: Phototherapy for Acne (http:/ / www. aetna. com/ cpb/ medical/ data/ 600_699/ 0656. html) [14] Wright HR, Lack LC, Kennaway DJ. (March 2004). "Differential effects of light wavelength in phase advancing the melatonin rhythm". J. Pineal Res. 36 (2): 1404. doi:10.1046/j.1600-079X.2003.00108.x. PMID14962066. [15] Litebook LED SAD Light (http:/ / www. litebook. co. uk/ litebook-elite. html)
Light therapy
[16] Saeeduddin Ahmed, Neil L Cutter, Alfred J. Lewy, Vance K. Bauer, Robert L Sack and Mary S. Cardoza (1995). "Phase Response Curve of Low-Intensity Green Light in Winter Depressives". Sleep Research 24: 508. ""The magnitude of the phase shifts [using low-level green light therapy] are comparable to those obtained using high-intensity white light in winter-depressives."" [17] Michel A. Paul, James C. Miller, Gary Gray, Fred Buick, Sofi Blazeski and Josephine Arendt (July 2007). "Circadian Phase Delay Induced by Phototherapeutic Devices" (http:/ / www. ingentaconnect. com/ content/ asma/ asem/ 2007/ 00000078/ 00000007/ art00001). Sleep Research 78 (7): 645652. . [18] J.J. Gooley, S.M.W. Rajaratnam, G.C. Brainard, R.E. Kronauer, C.A. Czeisler, S.W. Lockley (May 2010). "Spectral Responses of the Human Circadian System Depend on the Irradiance and Duration of Exposure to Light" (http:/ / stm. sciencemag. org/ content/ 2/ 31. cover-expansion). Science Translational Medicine 2 (31): 3133. doi:10.1126/scitranslmed.3000741. PMID20463367. . [19] "Light Box Selection" (http:/ / www. cet. org/ eng/ Therapy_LightboxSelection_ENG. html). Center for Environmental Therapeutics. CET. . Retrieved 25 May 2011. [20] "Seasonal affective disorder treatment Choosing a light box" (http:/ / www. mayoclinic. com/ health/ seasonal-affective-disorder-treatment/ DN00013/ NSECTIONGROUP=2). Mayo Clinic. 2010-10-01. . Retrieved 2011-01-07. [21] "Light therapy why it's done" (http:/ / www. mayoclinic. com/ health/ light-therapy/ MY00195/ DSECTION=why-its-done). Mayo Clinic. 2008-10-07. . Retrieved 2009-06-09. [22] McGinniss Paul (2007-09-24). "Seasonal affective disorder (SAD) Treatment and drugs" (http:/ / www. mayoclinic. com/ health/ seasonal-affective-disorder/ DS00195/ DSECTION=treatments-and-drugs). Mayo Clinic. . Retrieved 2009-06-09. [23] "Applications: Health" (http:/ / www. practicalsolar. com/ applications. html). Practical Solar. . Retrieved 2009-06-09. [24] "Grab the Sun With Heliostats" (http:/ / www. newyorkhousemagazine. com/ pages/ full_story?page_label=home_main_top& id=2631630& widget=push& instance=home_green_future& article-Grab the Sun With Heliostats =& open=& ). New York House. 2009-06-01. . Retrieved 2009-12-08. [25] Thompson C, Stinson D, Smith A (September 1990). "Seasonal affective disorder and season-dependent abnormalities of melatonin suppression by light". Lancet 336 (8717): 7036. doi:10.1016/0140-6736(90)92202-S. PMID1975891. [26] Benedetti F, Colombo C, Pontiggia A, Bernasconi A, Florita M, Smeraldi E, (2003) Morning light treatment hastens the antidepressant effect of citalopram: a placebo-controlled trial, J Clin Psychiatry. Jun; 64(6):648-53. [27] Prasko J (November 2008). "Bright light therapy". Neuro Endocrinol. Lett. 29 Suppl 1: 3364. PMID19029878. [28] Terman M (December 2007). "Evolving applications of light therapy" (http:/ / www. chronobiology. ch/ chronobiology. data/ Dokumente/ PDF/ PDF_Chrono_Psychiatry/ Terman_07. pdf) (pdf). Sleep Med Rev 11 (6): 497507. doi:10.1016/j.smrv.2007.06.003. PMID17964200. . [29] Tuunainen A, Kripke DF, Endo T (2004). Tuunainen, Arja. ed. "Light therapy for non-seasonal depression" (http:/ / mrw. interscience. wiley. com/ cochrane/ clsysrev/ articles/ CD004050/ frame. html). Cochrane Database of Systematic Reviews 2004, Issue 2. Art. No.: CD004050 (2): CD004050. doi:10.1002/14651858.CD004050.pub2. PMID15106233. . Retrieved 2010-02-02. [30] Light therapy for DSPS treatment (http:/ / www. litebook. co. uk/ clinical/ delayed-sleep-phase-syndrome. html). Retrieved 01/11/2010 [31] Smith MR, Eastman CI (December 2008). "Night shift performance is improved by a compromise circadian phase position: study 3. Circadian phase after 7 night shifts with an intervening weekend off". Sleep 31 (12): 163945. PMC2603486. PMID19090319. [32] How an SAD light box can help shift workers (http:/ / www. litebook. co. uk/ personal/ light-therapy-and-shift-work. html). Retrieved 01/11/2010 [33] Brown GM, Pandi-Perumal SR, Trakht I, Cardinali DP (March 2009). "Melatonin and its relevance to jet lag". Travel Med Infect Dis 7 (2): 6981. doi:10.1016/j.tmaid.2008.09.004. PMID19237140. [34] How to use a light box to prevent a cure jet lag (http:/ / www. litebook. co. uk/ personal/ jet-lag-personal. html). Retrieved 01/11/2010 [35] Newman TB, Kuzniewicz MW, Liljestrand P, Wi S, McCulloch C, Escobar GJ (May 2009). "Numbers needed to treat with phototherapy according to American Academy of Pediatrics guidelines". Pediatrics 123 (5): 13529. doi:10.1542/peds.2008-1635. PMC2843697. PMID19403502. [36] Paus S, Schmitz-Hbsch T, Wllner U, Vogel A, Klockgether T, Abele M (July 2007). "Bright light therapy in Parkinson's disease: a pilot study". Mov. Disord. 22 (10): 14958. doi:10.1002/mds.21542. PMID17516492. [37] Willis GL, Turner EJ (2007). "Primary and secondary features of Parkinson's disease improve with strategic exposure to bright light: a case series study". Chronobiol. Int. 24 (3): 52137. doi:10.1080/07420520701420717. PMID17612949. [38] Glazer-Hockstein C, Dunaief JL (January 2006). "Could blue light-blocking lenses decrease the risk of age-related macular degeneration?". Retina (Philadelphia, Pa.) 26 (1): 14. doi:10.1097/00006982-200601000-00001. PMID16395131. [39] Terman M, Terman JS (August 2005). "Light therapy for seasonal and nonseasonal depression: efficacy, protocol, safety, and side effects". CNS Spectr 10 (8): 64763; quiz 672. PMID16041296. [40] "Bright Light May Boost Testosterone" (http:/ / www. webmd. com/ erectile-dysfunction/ news/ 20030422/ bright-light-may-boost-testosterone). WebMD. . Retrieved 2008-12-15. [41] Danilenko KV, Samoilova EA (2007). "Stimulatory effect of morning bright light on reproductive hormones and ovulation: results of a controlled crossover trial". PLoS Clin Trials 2 (2): e7. doi:10.1371/journal.pctr.0020007. PMC1851732. PMID17290302. [42] Gagarina, AK (2007-12-08). "Light Therapy Diagnostic Indications and Contraindications" (http:/ / www. health. am/ psy/ more/ light_therapy1/ ). American Medical Network. . Retrieved 2009-06-09. [43] Roger DR (2007-12-04). "Practical aspects of light therapy" (http:/ / www. health. am/ psy/ more/ light_therapy4/ ). American Medical Network. . Retrieved 2009-06-09.
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Psychotherapy
Psychotherapy is a general term referring to any form of therapeutic interaction or treatment contracted between a trained professional and a client or patient; family, couple or group. The problems addressed are psychological in nature and of no specific kind or degree, but rather depend on the specialty of the practitioner. Psychotherapy aims to increase the individual's sense of his own well-being. Psychotherapists employ a range of techniques based on experiential relationship building, dialogue, communication and behavior change that are designed to improve the mental health of a client or patient, or to improve group relationships (such as in a family). Psychotherapy may also be performed by practitioners with a number of different qualifications, including psychiatry, clinical psychology, counseling psychology, clinical or psychiatric social work, mental health counseling, marriage and family therapy, rehabilitation counseling, school counseling, play therapy, music therapy, art therapy, drama therapy, dance/movement therapy, occupational therapy, psychiatric nursing, psychoanalysis and those from other psychotherapies. It may be legally regulated, voluntarily regulated or unregulated, depending on the jurisdiction. Requirements of these professions vary, but often require graduate school and supervised clinical experience. Psychotherapy in Europe is increasingly being seen as an independent profession, rather than being restricted to being practiced only by psychologists and psychiatrists as is stipulated in some countries.
Regulation
Continental Europe
In Germany, the Psychotherapy Act (PsychThG, 1998) restricts the practice of psychotherapy to the professions of psychology and psychiatry.[1] In Italy, the Ossicini Act (no. 56/1989, art. 3) restricts the practice of psychotherapy to graduates in psychology or medicine who have completed a four-year postgraduate course in psychotherapy at a training school recognised by the state;[2] French legislation restricts use of the title "psychotherapist" to professionals on the National Register of Psychotherapists;.[3] The inscription on this register requires a training in clinical psychopathology and a period of internship which is only open to physicians or titulars of a master's degree in psychology or psychoanalysis. Austria and Switzerland (2011) have laws that recognize multidifunctional-disciplinary approaches; other European countries have not yet regulated psychotherapy.
United Kingdom
In the United Kingdom, psychotherapy is voluntarily regulated. National registers for psychotherapists and counsellors are maintained by three main umbrella bodies:[4] 1. the United Kingdom Council for Psychotherapy (UKCP) 2. the British Association for Counselling and Psychotherapy (BACP) 3. the British Psychoanalytic Council (BPC - formerly the British Confederation of Psychotherapists). There are many smaller professional bodies and associations such as the Association of Child Psychotherapists (ACP)[5] and the British Association of Psychotherapists (BAP).[6] The United Kingdom Health Professions Council (HPC) have recently consulted on potential statutory regulation of psychotherapists and counsellors. The HPC [7] is an official state regulator that regulates some 15 professions at present.
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Etymology
Psychotherapy is an English word of Greek origin, deriving from Ancient Greek psyche ( meaning "breath; spirit; soul") and therapia ( "healing; medical treatment"). According to the Oxford English Dictionary, psychotherapy first meant "hypnotherapy" instead of "psychotherapy". The original meaning, "the treatment of disease by psychic [i.e., hypnotic] methods", was first recorded in 1853 as "Psychotherapeia, or the remedial influence of mind". The modern meaning, "the treatment of disorders of the mind or personality by psychological or psychophysiological methods", was first used in 1892 by Frederik van Eeden translating "Suggestive Psycho-therapy" for his French "Psychothrapie Suggestive". Van Eeden credited borrowing this term from Daniel Hack Tuke and noted, "Psycho-therapy ... had the misfortune to be taken in tow by hypnotism."[8] The psychiatrist Jerome Frank defined psychotherapy as the relief of distress or disability in one person by another, using an approach based on a particular theory or paradigm, and a requirement that the agent performing the therapy has had some form of training in delivering this. It is these latter two points which distinguish psychotherapy from other forms of counseling or caregiving.[9]
Forms
Most forms of psychotherapy use spoken conversation. Some also use various other forms of communication such as the written word, artwork, drama, narrative story or music. Psychotherapy with children and their parents often involves play, dramatization (i.e. role-play), and drawing, with a co-constructed narrative from these non-verbal and displaced modes of interacting.[10] Psychotherapy occurs within a structured encounter between a trained therapist and client(s). Purposeful, theoretically based psychotherapy began in the 19th century with psychoanalysis; since then, scores of other approaches have been developed and continue to be created. Therapy is generally used in response to a variety of specific or non-specific manifestations of clinically diagnosable and/or existential crises. Treatment of everyday problems is more often referred to as counseling (a distinction originally adopted by Carl Rogers). However, the term counseling is sometimes used interchangeably with "psychotherapy". While some psychotherapeutic interventions are designed to treat the patient using the medical model, many psychotherapeutic approaches do not adhere to the symptom-based model of "illness/cure". Some practitioners, such as humanistic therapists, see themselves more in a facilitative/helper role. As sensitive and deeply personal topics are often discussed during psychotherapy, therapists are expected, and usually legally bound, to respect client or patient confidentiality. The critical importance of confidentiality is enshrined in the regulatory psychotherapeutic organizations' codes of ethical practice.
Systems
There are several main broad systems of psychotherapy: Psychoanalytic - it was the first practice to be called a psychotherapy. It encourages the verbalization of all the patient's thoughts, including free associations, fantasies, and dreams, from which the analyst formulates the nature of the unconscious conflicts which are causing the patient's symptoms and character problems. Behavior Therapy/applied behavior analysis focuses on changing maladaptive patterns of behavior to improve emotional responses, cognitions, and interactions with others. Cognitive behavioral - generally seeks to identify maladaptive cognition, appraisal, beliefs and reactions with the aim of influencing destructive negative emotions and problematic dysfunctional behaviors. Psychodynamic - is a form of depth psychology, whose primary focus is to reveal the unconscious content of a client's psyche in an effort to alleviate psychic tension. Although its roots are in psychoanalysis, psychodynamic therapy tends to be briefer and less intensive than traditional psychoanalysis.
Psychotherapy Existential - is based on the existential belief that human beings are alone in the world. This isolation leads to feelings of meaninglessness, which can be overcome only by creating one's own values and meanings. Existential therapy is philosophically associated with phenomenology. Humanistic - emerged in reaction to both behaviorism and psychoanalysis and is therefore known as the Third Force in the development of psychology. It is explicitly concerned with the human context of the development of the individual with an emphasis on subjective meaning, a rejection of determinism, and a concern for positive growth rather than pathology. It posits an inherent human capacity to maximize potential, 'the self-actualizing tendency'. The task of Humanistic therapy is to create a relational environment where this tendency might flourish. Humanistic psychology is philosophically rooted in existentialism. Brief - "Brief therapy" is an umbrella term for a variety of approaches to psychotherapy. It differs from other schools of therapy in that it emphasizes (1) a focus on a specific problem and (2) direct intervention. It is solution-based rather than problem-oriented. It is less concerned with how a problem arose than with the current factors sustaining it and preventing change. Systemic - seeks to address people not at an individual level, as is often the focus of other forms of therapy, but as people in relationship, dealing with the interactions of groups, their patterns and dynamics (includes family therapy & marriage counseling). Community psychology is a type of systemic psychology. Transpersonal - Addresses the client in the context of a spiritual understanding of consciousness. Body Psychotherapy - Addresses problems of the mind as being closely correlated with bodily phenomena, including a person's sexuality, musculature, breathing habits, physiology etc. This therapy may involve massage and other body exercises as well as talking. There are hundreds of psychotherapeutic approaches or schools of thought. By 1980 there were more than 250;[11] by 1996 there were more than 450.[12] The development of new and hybrid approaches continues around the wide variety of theoretical backgrounds. Many practitioners use several approaches in their work and alter their approach based on client need.
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History
In an informal sense, psychotherapy can be said to have been practiced through the ages, as individuals received psychological counsel and reassurance from others. According to Colin Feltham, "The Stoics were one of the main Hellenistic schools of philosophy and therapy, along with the Sceptics and Epicureans (Nussbaum, 1994). Philosophers and physicians from these schools practised psychotherapy among the Greeks and Romans from about the late 4th century BC to the 4th century AD."[13] Psychoanalysis was perhaps the first specific school of psychotherapy, developed by Sigmund Freud and others through the early 20th century. Trained as a neurologist, Freud began focusing on problems that appeared to have no discernible organic basis, and theorized that they had psychological causes originating in childhood experiences and the unconscious mind. Techniques such as dream interpretation, free association, transference and analysis of the id, ego and superego were developed. Many theorists, including Anna Freud, Alfred Adler, Carl Jung, Karen Horney, Otto Rank, Erik Erikson, Melanie Klein, and Heinz Kohut, built upon Freud's fundamental ideas and often formed their own differentiating systems of psychotherapy. These were all later categorized as psychodynamic, meaning anything that involved the psyche's conscious/unconscious influence on external relationships and the self. Sessions tended to number into the hundreds over several years. Behaviorism developed in the 1920s, and behavior modification as a therapy became popularized in the 1950s and 1960s. Notable contributors were Joseph Wolpe in South Africa, M.B. Shipiro and Hans Eysenck in Britain, and John B. Watson and B.F. Skinner in the United States. Behavioral therapy approaches relied on principles of operant conditioning, classical conditioning and social learning theory to bring about therapeutic change in observable symptoms. The approach became commonly used for phobias, as well as other disorders.
Psychotherapy Some therapeutic approaches developed out of the European school of existential philosophy. Concerned mainly with the individual's ability to develop and preserve a sense of meaning and purpose throughout life, major contributors to the field in the US (e.g., Irvin Yalom, Rollo May) and Europe (Viktor Frankl, Ludwig Binswanger, Medard Boss, R.D.Laing, Emmy van Deurzen) and later in the 1960s and 1970s both in the United Kingdom and in Canada, Eugene Heimler [14] [15] attempted to create therapies sensitive to common 'life crises' springing from the essential bleakness of human self-awareness, previously accessible only through the complex writings of existential philosophers (e.g., Sren Kierkegaard, Jean-Paul Sartre, Gabriel Marcel, Martin Heidegger, Friedrich Nietzsche). The uniqueness of the patient-therapist relationship thus also forms a vehicle for therapeutic inquiry. A related body of thought in psychotherapy started in the 1950s with Carl Rogers. Based on existentialism and the works of Abraham Maslow and his hierarchy of human needs, Rogers brought person-centered psychotherapy into mainstream focus. The primary requirement of Rogers is that the client should be in receipt of three core 'conditions' from his counsellor or therapist: unconditional positive regard, also sometimes described as 'prizing' the person or valuing the humanity of an individual, congruence [authenticity/genuineness/transparency], and empathic understanding. The aim in using the 'core conditions' is to facilitate therapeutic change within a non-directive relationship conducive to enhancing the client's psychological well being. This type of interaction enables the client to fully experience and express himself. Others developed the approach, like Fritz and Laura Perls in the creation of Gestalt therapy, as well as Marshall Rosenberg, founder of Nonviolent Communication, and Eric Berne, founder of Transactional Analysis. Later these fields of psychotherapy would become what is known as humanistic psychotherapy today. Self-help groups and books became widespread. During the 1950s, Albert Ellis originated Rational Emotive Behavior Therapy (REBT). A few years later, psychiatrist Aaron T. Beck developed a form of psychotherapy known as cognitive therapy. Both of these generally included relatively short, structured and present-focused therapy aimed at identifying and changing a person's beliefs, appraisals and reaction-patterns, by contrast with the more long-lasting insight-based approach of psychodynamic or humanistic therapies. Cognitive and behavioral therapy approaches were combined and grouped under the heading and umbrella-term Cognitive behavioral therapy (CBT) in the 1970s. Many approaches within CBT are oriented towards active/directive collaborative empiricism and mapping, assessing and modifying clients core beliefs and dysfunctional schemas. These approaches gained widespread acceptance as a primary treatment for numerous disorders. A "third wave" of cognitive and behavioral therapies developed, including Acceptance and Commitment Therapy and Dialectical behavior therapy, which expanded the concepts to other disorders and/or added novel components and mindfulness exercises. Counseling methods developed, including solution-focused therapy and systemic coaching. During the 1960s and 1970s Eugene Heimler, after training in the new discipline of psychiatric social work, developed Heimler method of Human Social Functioning, a methodology based on the principle that frustration is the potential to human flourishing.[14] [15] Postmodern psychotherapies such as Narrative Therapy and Coherence Therapy did not impose definitions of mental health and illness, but rather saw the goal of therapy as something constructed by the client and therapist in a social context. Systems Therapy also developed, which focuses on family and group dynamicsand Transpersonal psychology, which focuses on the spiritual facet of human experience. Other important orientations developed in the last three decades include Feminist therapy, Brief therapy, Somatic Psychology, Expressive therapy, applied Positive psychology and the Human Givens approach which is building on the best of what has gone before.[16] A survey of over 2,500 US therapists in 2006 revealed the most utilized models of therapy and the ten most influential therapists of the previous quarter-century.[17]
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General description
Psychotherapy can be seen as an interpersonal invitation offered by (often trained and regulated) psychotherapists to aid clients in reaching their full potential or to cope better with problems of life. Psychotherapists usually receive remuneration in some form in return for their time and skills. This is one way in which the relationship can be distinguished from an altruistic offer of assistance. Psychotherapists and counselors often require to create a therapeutic environment referred to as the frame, which is characterized by a free yet secure climate that enables the client to open up. The degree to which client feels related to the therapist may well depend on the methods and approaches used by the therapist or counselor. Psychotherapy often includes techniques to increase awareness and the capacity for self observation, change behavior and cognition, and develop insight and empathy. A desired result enable other choices of thought, feeling or action; to increase the sense of well-being and to better manage subjective discomfort or distress. Perception of reality is hopefully improved. Grieving might be enhanced producing less long term depression. Psychotherapy can improve medication response where such medication is also needed. Psychotherapy can be provided on a one-to-one basis, in group therapy, conjointly with couples and with entire families. It can occur face to face (individual), over the telephone, or, much less commonly, the Internet. Its time frame may be a matter of weeks or many years. Therapy may address specific forms of diagnosable mental illness, or everyday problems in managing or maintaining interpersonal relationships or meeting personal goals. Treatment in families with children can favorably influence a childs development, lasting for life and into future generations. Better parenting may be an indirect result of therapy or purposefully learned as parenting techniques. Divorces can be prevented, or made far less traumatic. Treatment of everyday problems is more often referred to as counseling (a distinction originally adopted by Carl Rogers) but the term is sometimes used interchangeably with "psychotherapy". Therapeutic skills can be used in mental health consultation to business and public agencies to improve efficiency and assist with coworkers or clients. Psychotherapists use a range of techniques to influence or persuade the client to adapt or change in the direction the client has chosen. These can be based on clear thinking about their options; experiential relationship building; dialogue, communication and adoption of behavior change strategies. Each is designed to improve the mental health of a client or patient, or to improve group relationships (as in a family). Most forms of psychotherapy use only spoken conversation, though some also use other forms of communication such as the written word, artwork, drama, narrative story, or therapeutic touch. Psychotherapy occurs within a structured encounter between a trained therapist and client(s). Because sensitive topics are often discussed during psychotherapy, therapists are expected, and usually legally bound, to respect client or patient confidentiality. Psychotherapists are often trained, certified, and licensed, with a range of different certifications and licensing requirements depending on the jurisdiction. Psychotherapy may be undertaken by clinical psychologists,counseling psychologists, social workers, marriage-family therapists, adult and child psychiatrists and expressive therapists, trained nurses, psychiatrists, psychoanalysts, mental health counselors, school counselors, or professionals of other mental health disciplines. Psychiatrists have medical qualifications and may also administer prescription medication. The primary training of a psychiatrist uses the ' Bio-Psycho-Social' model, medical training in practical psychology and applied psychotherapy. Psychiatric training begins in medical school, first in the doctor patient relationship with ill people, and later in psychiatric residency for specialists. The focus is usually eclectic but includes biological, cultural, and social aspects. They are advanced in understanding patients from the inception of medical training. Today there are two doctoral degrees in psychology, the PsyD and PhD. Training for these degrees overlap, but the PsyD is more clinical and the Phd stresses research. Both degrees have clinical education components. Clinical Social Workers have specialized training in clinical casework. They hold a masters in social work which entails two years of clinical internships, and a period of at least three years in the US of post-masters experience in psychotherapy. Marriage-family therapists have specific training and experience working with relationships and family issues. A licensed professional counselor (LPC) generally has special training in career, mental health, school, or rehabilitation
Psychotherapy counseling to include evaluation and assessments as well as psychotherapy. Many of the wide variety of training programs are multiprofessional, that is, psychiatrists, psychologists, mental health nurses, and social workers may be found in the same training group. All these degrees commonly work together as a team, especially in institutional settings. All those doing specialized psychotherapeutic work, in most countries, require a program of continuing education after the basic degree, or involve multiple certifications attached to one specific degree, and 'board certification' in psychiatry. Specialty exams are used to confirm competence or board exams with psychiatrists .
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Psychoanalysis
Psychoanalysis was developed in the late 19th century by Sigmund Freud. His therapy explores the dynamic workings of a mind understood to consist of three parts: the hedonistic id (German: das Es, "the it"), the rational ego (das Ich, "the I"), and the moral superego (das berich, "the above-I"). Because the majority of these dynamics are said to occur outside people's awareness, Freudian psychoanalysis seeks to probe the unconscious by way of various techniques, including dream interpretation and free association. Freud maintained that the condition of the unconscious mind is profoundly influenced by childhood experiences. So, in addition to dealing with the defense mechanisms used by an overburdened ego, his therapy addresses fixations and other issues by probing deeply into clients' youth.
Freud , seated left of picture with Jung seated at right of picture. 1909
Other psychodynamic theories and techniques have been developed and used by psychotherapists, psychologists, psychiatrists, personal growth facilitators, occupational therapists and social workers. Techniques for group therapy have also been developed. While behaviour is often a target of the work, many approaches value working with feelings and thoughts. This is especially true of the psychodynamic schools of psychotherapy, which today include Jungian therapy and Psychodrama as well as the psychoanalytic schools.
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Gestalt therapy
Gestalt Therapy is a major overhaul of psychoanalysis. In its early development it was called "concentration therapy" by its founders, Frederick and Laura Perls. However, its mix of theoretical influences became most organized around the work of the gestalt psychologists; thus, by the time 'Gestalt Therapy, Excitement and Growth in the Human Personality' (Perls, Hefferline, and Goodman) was written, the approach became known as "Gestalt Therapy." Gestalt Therapy stands on top of essentially four load bearing theoretical walls: phenomenological method, dialogical relationship, field-theoretical strategies, and experimental freedom. Some have considered it an existential phenomenology while others have described it as a phenomenological behaviorism. Gestalt therapy is a humanistic, holistic, and experiential approach that does not rely on talking alone, but facilitates awareness in the various contexts of life by moving from talking about situations relatively remote to action and direct, current experience.
Group psychotherapy
The therapeutic use of groups in modern clinical practice can be traced to the early 20th century, when the American chest physician Pratt, working in Boston, described forming 'classes' of 15 to 20 patients with tuberculosis who had been rejected for sanatorium treatment. The term group therapy, however, was first used around 1920 by Jacob L. Moreno, whose main contribution was the development of psychodrama, in which groups were used as both cast and audience for the exploration of individual problems by reenactment under the direction of the leader. The more analytic and exploratory use of groups in both hospital and out-patient settings was pioneered by a few European psychoanalysts who emigrated to the USA, such as Paul Schilder, who treated severely neurotic and mildly psychotic out-patients in small groups at Bellevue Hospital, New York. The power of groups was most influentially demonstrated in Britain during the Second World War, when several psychoanalysts and psychiatrists proved the value of group methods for officer selection in the War Office Selection Boards. A chance to run an Army psychiatric unit on group lines was then given to several of these pioneers, notably Wilfred Bion and Rickman, followed by S. H. Foulkes, Main, and Bridger. The Northfield Hospital in Birmingham gave its name to what came to be called the two 'Northfield Experiments', which provided the impetus for the development since the war of both social therapy, that is, the therapeutic community movement, and the use of small groups for the treatment of neurotic and personality disorders. Today group therapy is used in clinical settings and in private practice settings. It has been shown to be as or more effective than individual therapy.[20]
Behavior therapy
Behavior therapy focuses on modifying overt behavior and helping clients to achieve goals. This approach is built on the principles of learning theory including operant and respondent conditioning, which makes up the area of applied behavior analysis or behavior modification. This approach includes acceptance and commitment therapy, functional analytic psychotherapy, and dialectical behavior therapy. Sometimes it is integrated with cognitive therapy to make cognitive behavior therapy. By nature, behavioral therapies are empirical (data-driven), contextual (focused on the environment and context), functional (interested in the effect or consequence a behavior ultimately has), probabilistic (viewing behavior as statistically predictable), monistic (rejecting mind-body dualism and treating the person as a unit), and relational (analyzing bidirectional interactions).[21]
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Body-oriented psychotherapy
Body-oriented psychotherapy or Body Psychotherapy is also known as Somatic Psychology, especially in the USA. There are many very different psychotherapeutic approaches. They generally focus on the link between the mind and the body and try to access deeper levels of the psyche through greater awareness of the physical body and the emotions which gave rise to the various body-oriented based psychotherapeutic approaches, such as Reichian (Wilhelm Reich) Character-Analytic Vegetotherapy and Orgonomy; neo-Reichian Alexander Lowen's Bioenergetic analysis; Peter Levine's Somatic Experiencing; Jack Rosenberg's Integrative body psychotherapy; Ron Kurtz's Hakomi psychotherapy; Pat Ogden's sensorimotor psychotherapy; David Boadella's Biosynthesis psychotherapy; Gerda Boyesen's Biodynamic psychotherapy; etc. These body-oriented psychotherapies are not to be confused with alternative medicine body-work or body-therapies that seek primarily to improve physical health through direct work (touch and manipulation) on the body because, despite the fact that bodywork techniques (for example Alexander Technique, Rolfing, and the Feldenkrais Method) can also affect the emotions, these techniques are not designed to work on psychological issues, neither are their practitioners so trained.
Expressive therapy
Expressive therapy is a form of therapy that utilizes artistic expression as its core means of treating clients. Expressive therapists use the different disciplines of the creative arts as therapeutic interventions. This includes the modalities dance therapy, drama therapy, art therapy, music therapy, writing therapy, among others. Expressive therapists believe that often the most effective way of treating a client is through the expression of imagination in a creative work and integrating and processing what issues are raised in the act.
Interpersonal psychotherapy
Interpersonal psychotherapy (IPT) is a time-limited psychotherapy that focuses on the interpersonal context and on building interpersonal skills. IPT is based on the belief that interpersonal factors may contribute heavily to psychological problems. It is commonly distinguished from other forms of therapy in its emphasis on interpersonal processes rather than intrapsychic processes. IPT aims to change a person's interpersonal behavior by fostering adaptation to current interpersonal roles and situations.
Narrative therapy
Narrative therapy gives attention to each person's "dominant story" by means of therapeutic conversations, which also may involve exploring unhelpful ideas and how they came to prominence. Possible social and cultural influences may be explored if the client deems it helpful.
Integrative psychotherapy
Integrative psychotherapy is an attempt to combine ideas and strategies from more than one theoretical approach.[22] These approaches include mixing core beliefs and combining proven techniques. Forms of integrative psychotherapy include multimodal therapy, the transtheoretical model, cyclical psychodynamics, systematic treatment selection, cognitive analytic therapy, Internal Family Systems Model, multitheoretical psychotherapy and conceptual interaction. In practice, most experienced psychotherapists develop their own integrative approach over time.
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Hypnotherapy
Hypnotherapy is therapy that is undertaken with a subject in hypnosis. Hypnotherapy is often applied in order to modify a subject's behavior, emotional content, and attitudes, as well as a wide range of conditions including dysfunctional habits, anxiety, stress-related illness, pain management, and personal development.
===Confidentiality===
Further information: client confidentiality, and physician-patient privilege Confidentiality is an integral part of the therapeutic relationship and psychotherapy in general. It includes protecting specific groups of people, like children, while treating private information in a manner that is in line with the American Psychological Association (APA) ethics code.
Psychotherapy As early as 1952, in one of the earliest studies of psychotherapy treatment, Hans Eysenck reported that two thirds of therapy patients improved significantly or recovered on their own within two years, whether or not they received psychotherapy.[31] Many psychotherapists believe that the nuances of psychotherapy cannot be captured by questionnaire-style observation, and prefer to rely on their own clinical experiences and conceptual arguments to support the type of treatment they practice. In 2001, Bruce Wampold of the University of Wisconsin published the book The Great Psychotherapy Debate.[32] In it Wampold, a former statistician who went on to train as a counseling psychologist, reported that 1. psychotherapy is indeed effective, 2. the type of treatment is not a factor, 3. the theoretical bases of the techniques used, and the strictness of adherence to those techniques are both not factors, 4. the therapist's strength of belief in the efficacy of the technique is a factor, 5. the personality of the therapist is a significant factor, 6. the alliance between the patient(s) and the therapist (meaning affectionate and trusting feelings toward the therapist, motivation and collaboration of the client, and empathic response of the therapist) is a key factor. Wampold therefore concludes that "we do not know why psychotherapy works". Although the Great Psychotherapy Debate dealt primarily with data on depressed patients, subsequent articles have made similar findings for post-traumatic stress disorder[33] and youth disorders.[34] There have also been studies of Panic Disorder, where treatment effectiveness is measured in the abatement of panic attacks. Psychoanalytic psychotherapy has been found to be as effective as Cognitive Behavioral Therapy for immediate relief and more effective over the long term [35] [36] Some report that by attempting to program or manualize treatment, psychotherapists may be reducing efficacy, although the unstructured approach of many psychotherapists cannot appeal to patients motivated to solve their difficulties through the application of specific techniques different from their past "mistakes." Critics of psychotherapy are skeptical of the healing power of a psychotherapeutic relationship.[37] Because any intervention takes time, critics note that the passage of time alone, without therapeutic intervention, often results in psycho-social healing.[38] Social contact with others is universally seen as beneficial for all humans and regularly scheduled visits with anyone would be likely to diminish both mild and severe emotional difficulty. Many resources available to a person experiencing emotional distressthe friendly support of friends, peers, family members, clergy contacts, personal reading, healthy exercise, research, and independent copingall present considerable value. Critics note that humans have been dealing with crises, navigating severe social problems and finding solutions to life problems long before the advent of psychotherapy.[39] Of course, it may well be something in the patient that does not develop these "natural" supports that requires therapy. Further critiques have emerged from feminist, constructionist and discursive sources. Key to these is the issue of power. In this regard there is a concern that clients are persuadedboth inside and outside the consulting roomto understand themselves and their difficulties in ways that are consistent with therapeutic ideas. This means that alternative ideas (e.g., feminist, economic, spiritual) are sometimes implicitly undermined. Critics suggest that we idealise the situation when we think of therapy only as a helping relation. It is also fundamentally a political practice, in that some cultural ideas and practices are supported while others are undermined or disqualified. So, while it is seldom intended, the therapist-client relationship always participates in society's power relations and political dynamics.[40]
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References
[1] "Gesetz ber die Berufe des Psychologischen Psychotherapeuten und des Kinder- und Jugendlichenpsychotherapeuten" (http:/ / bundesrecht. juris. de/ psychthg/ index. html). . Retrieved 21 July 2010. "The title "psychotherapist" may not be used by persons other than physicians, psychological psychotherapists or child and adolescent psychotherapists." [2] "Ordinamento della professione di psicologo: Esercizio dell'attivit psicoterapeutica" (http:/ / www. psico. unifi. it/ upload/ sub/ Tirocinio/ L56-1989. pdf). . Retrieved 22 July 2010. "The practice of psychotherapy is subject to specific professional training, to be acquired after graduation in psychology or in medicine and surgery, through specialized courses of at least four years duration providing adequate training in psychotherapy, at specialized schools or university institutes approved for that purpose by procedures under Article 3 of Presidential Decree no 162 of March 10, 1982." [3] "Arrt du 9 juin 2010 relatif aux demandes d'inscription au registre national des psychothrapeutes" (http:/ / www. legifrance. gouv. fr/ affichTexte. do?cidTexte=JORFTEXT000022336754& dateTexte=& categorieLien=id). . Retrieved 21 July 2010. "Permission to use the title of psychotherapist is reserved for professionals on the national register of psychotherapists, in accordance with the provisions of Article 7 of the Decree of May 20, 2010 ... The provisions of this Order shall come into force from 1 July 2010" [4] Priebe, Stefan; Wright, Donna (2006). "The provision of psychotherapy an international comparison" (http:/ / webspace. qmul. ac. uk/ spriebe/ / publications/ 2006/ 2006_The_provision_of_psychotherapy-an_international_comparison. pdf). Journal of Public Mental Health 3: 16. . Retrieved 15 July 2010. "The three national registers for psychotherapists and counsellors are maintained by three main umbrella bodies in the fields of psychotherapy and counselling: the United Kingdom Council for Psychotherapy (UKCP), the British Association for Counselling and Psychotherapy (BACP), and the British Psychoanalytic Council (BPC) for psychoanalytic psychotherapists." [5] "Entry requirements and training as a psychotherapist" (http:/ / www. nhscareers. nhs. uk/ details/ Default. aspx?Id=461). UK National Health Service. . Retrieved 15 July 2010. [6] "Psychotherapist Job Profile" (http:/ / careersadvice. direct. gov. uk/ LSCGOVUK/ Templates/ CareersAdviceService/ JobProfiles/ JobProfile. aspx?NRMODE=Published& NRNODEGUID={364AB16C-F07E-4284-96DC-5CEC464365CC}& NRORIGINALURL=/ helpwithyourcareer/ jobprofiles/ JobProfile?jobprofileid=1390& jobprofilename=Psychotherapist& code=355874219& NRCACHEHINT=Guest& jobprofilename=Psychotherapist& jobprofileid=1390& code=355874219). UK Government Careers Advice Service. . Retrieved 15 July 2010. [7] http:/ / www. hpc-uk. org [8] Oxford English Dictionary, online edition, 2004, s.v. "psychotherapy". [9] Frank, Jerome (1988) [1979]. "What is Psychotherapy?". In Bloch, Sidney (ed.). An Introduction to the Psychotherapies. Oxford: Oxford University Press. pp.12. ISBN0-19-261469-X. [10] Schechter DS, Coates SW (2006). Relationally and Developmentally Focused Interventions with Young Children and Their Caregivers Affected by the Events of 9/11. In Y. Neria, R. Gross, R. Marshall, E. Susser (Eds.) September 11, 2001: Treatment, Research and Public Mental Health in the Wake of a Terrorist Attack, New York: Cambridge University Press. pp. 402-427. [11] Henrick 1980 [12] Maclennan 1996 [13] " Which psychotherapy?: leading exponents explain their differences (http:/ / books. google. com/ books?id=ryqW330yYCUC& pg=PA80& dq& hl=en#v=onepage& q=& f=false)". Colin Feltham (1997). p.80. ISBN 0-8039-7479-5 [14] Heimler, E. (1975), Survival in Society, London, Weidenfeld and Nicolson [15] http:/ / www. heimler-international. org [16] Corp, N.; Tsaroucha, A.; Kingston, P. (2008). "Human Givens Therapy: The Evidence Base" (http:/ / pavilionjournals. metapress. com/ index/ P83X3Q14J6J5187J. pdf). Mental Health Review Journal 13 (4): 4452. doi:10.1108/13619322200800027. . Retrieved 2009-06-03 [17] The Top 10: The Most Influential Therapists of the Past Quarter-Century. (http:/ / www. psychotherapynetworker. org/ magazine/ populartopics/ 219-the-top-10) Psychotherapy Networker.: 2007, March/April (retrieved 7 Oct 2010) [18] Hans Strupp and Jeffrey Binder, Psychotherapy in a New Key. New York, Basic Books, 1984, ISBN 978-0-465-06747-3 [19] Anthony Roth and Peter Fonagy, What Works for Whom? A Critical Review of Psychotherapy Research, Guilford Press, 2005, ISBN 572306505 [20] Dr. Cara Gardenswartz 2009, Los Angeles, CA [21] Sundberg, Norman (2001). Clinical Psychology: Evolving Theory, Practice, and Research. Englewood Cliffs: Prentice Hall. ISBN0130871192. [22] Handbook of Psychotherapy, (Norcross&Goldried, 2005) [23] Schechter DS, Willheim E (2009). When parenting becomes unthinkable: Intervening with traumatized parents and their toddlers. Journal of the American Academy of Child & Adolescent Psychiatry, 48(3), 249-254. [24] Lieberman, A.F., Van Horn, P., Ippen, C.G. (2005). Towards evidence-based treatment: Child-parent psychotherapy with preschoolers exposed to marital violence. Journal of the American Academy of Child and Adolescent Psychiatry, 44, 1241-1248. [25] Donner, M.B., VanderCreek, L., Gonsiorek, J.C. (2008). Balancing Confidentiality: Protecting Privacy and Protecting the Public. Professional Psychology: Research and Practice, 39(3), 369-376. [26] Silverman, DK (2005). "What Works in Psychotherapy and How Do We Know?: What Evidence-Based Practice Has to Offer". Psychoanalytic Psychology 22 (2): 306312. doi:10.1037/0736-9735.22.2.306
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[27] Hrknen, T; Knekt, P; Virtala, E; Lindfors, O; the Helsinki Psychotherapy Study Group (2005). "A case study in comparing therapies involving informative drop-out, non-ignorable non-compliance and repeated measurements". Statistics in medicine 24 (24): 37733787. doi:10.1002/sim.2409. PMID16320283 [28] Helsinki Psychotherapy Study (http:/ / www. ktl. fi/ tto/ hps/ index. en. html) [29] For Psychotherapy's Claims, Skeptics Demand Proof (http:/ / www. nytimes. com/ 2004/ 08/ 10/ health/ psychology/ 10ther. html?pagewanted=1& ei=5090& en=e6560227dc7526f7& ex=1249876800& partner=rssuserland) Benedict Carey, The New York Times, August 10, 2004. Retrieved December 2006. [30] Wierzbicki, M; Pekarik, G (May 1993). "A Meta-Analysis of Psychotherapy Dropout" (http:/ / psycnet. apa. org/ index. cfm?fa=search. displayRecord& uid=1993-30339-001). Professional Psychology: Research and Practice 24 (2): 190195. doi:10.1037/0735-7028.24.2.190. [31] Eysenck, Hans (1952). The Effects of Psychotherapy: An Evaluation. Journal of Consulting Psychology. pp.16: 319324. [32] The Great Psychotherapy Debate (http:/ / www. education. wisc. edu/ cp/ faculty/ book. asp) Bruce E. Wampold, Ph.D. University of Wisconsin-Madison . Retrieved December 2006. [33] Benish, S. G., Imel, Z. E., \& Wampold, B. E. (in press). The Relative Efficacy of Bona Fide Psychotherapies for Treating Posttraumatic Stress Disorder: A Meta-Analysis of Direct Comparisons Clinical Psychology Review. [34] Miller, S. D., Wampold, B. E., & Varhely, K. (In press). Direct comparisons of treatment modalities for youth disorders: A meta-analysis. Psychotherapy Research [35] Milrod, B., Leon, A., Busch, F., Rudden, M., Schwalberg, M., Clarkin, J., Aronson, A., Singer, M. Turchin, W, Klass, E., Graf, E., Teres, J., Shear, M. (2007), A randomized controlled clinical trial of psychoanalytic psychotherapy for panic disorder. American Journal of Psychiatry, 164:265-272. [36] Blechner, M. (2007) Approaches to panic attacks. Neuro-Psychoanalysis, 9:93-102. [37] 1988. Against Therapy: Emotional Tyranny and the Myth of Psychological Healing. ISBN 0-689-11929-1, Jeffrey Moussaieff Masson [38] Therapy's Delusions, The Myth of the Unconscious and the Exploitation of Today's Walking Worried (http:/ / www. antipsychiatry. org/ br-thdel. htm) by Ethan Watters & Richard Ofshe published by Scribner, New York, 1999 [39] Fredi, F. (2003) Therapy Culture: Cultivating Vulnerability in an Uncertain Age (http:/ / books. google. com/ books?id=gGkHK7Y9-dwC& pg=PA137& dq=isbn:041532159X& sig=fXiDQ1Zayaf4EQvuFFgo1YhzwIM#PPP1,M1): Routledge, (ISBN 0-415-32159-X) [40] Guilfoyle, M. (2005). From therapeutic power to resistance: Therapy and cultural hegemony. Theory & Psychology, 15(1), 101-124:
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Henrik, R. (ed) The Psychotherapy Handbook. The A-Z handbook to more than 250 psychotherapies as used today (1980) New American Library. Maclennan, Nigel. Counselling For Managers (1996) Gower. ISBN 0-566-08092-3 Asay, Ted P., and Michael J. Lambert (1999). The Empirical Case for the Common Factors in Therapy: Quantitative Findings. In Hubble, Duncan, Miller (Eds), The Heart and Soul of Change (pp.2355)
Psychodynamic schools
Aziz, Robert (1990). C.G. Jung's Psychology of Religion and Synchronicity (10 ed.). The State University of New York Press. ISBN0-7914-0166-9. Aziz, Robert (1999). "Synchronicity and the Transformation of the Ethical in Jungian Psychology". In Becker, Carl. Asian and Jungian Views of Ethics. Greenwood. ISBN0-313-30452-1. Aziz, Robert (2007). The Syndetic Paradigm: The Untrodden Path Beyond Freud and Jung. The State University of New York Press. ISBN978-0-7914-6982-8. Aziz, Robert (2008). "Foreword". In Storm, Lance. Synchronicity: Multiple Perspectives on Meaningful Coincidence. Pari Publishing. ISBN978-88-95604-02-2. Bateman, Anthony; Brown, Dennis and Pedder, Jonathan (2000). Introduction to Psychotherapy: An Outline of Psychodynamic Principles and Practice. Routledge. ISBN0-415-20569-7. Bateman, A.; and Holmes, J. (1995). Introduction to Psychoanalysis: Contemporary Theory and Practice. Routledge. ISBN0-415-10739-3. Oberst, U. E. and Stewart, A. E. (2003). Adlerian Psychotherapy: An Advanced Approach to Individual Psychology. New York: Brunner-Routledge. ISBN 1-58391-122-7 Ellenberger, Henri F. (1970). The Discovery of the Unconscious: The History and Evolution of Dynamic Psychiatry. Basic Books. ISBN0465016723.
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Humanistic schools
Schneider (et al.), Kirk (2001). The Handbook of Humanistic Psychology. SAGE Publications. ISBN0-7619-2121-4. Rowan, John (2001). Ordinary Ecstasy. Brunner-Routledge. ISBN0-415-23632-0. Ansel Woldt, Sarah Toman (eds) (2005). Gestalt Therapy History, Theory, and Practice. Gestalt Press. ISBN0-7619-2791-3 (pbk.). Crocker, Sylvia (1999). A Well-Lived Life, Essays in Gestalt Therapy. SAGE Publications. ISBN0-88163-287-2 (pbk.). Russon, John (2003). Human Experience: Philosophy, Neurosis, and the Elements of Everyday Life. State University of New York Press. ISBN9780791457542 (pbk.). Yontef, Gary (1993). Awareness, Dialogue, and Process. The Gestalt Journal Press, Inc.. ISBN0-939266-20-2 (pbk.).
External links
National Council of Psychotherapists UK (http://www.ncphq.co.uk/) Royal College of Psychiatrists UK (http://www.rcpsych.ac.uk/) United Kingdom Council for Psychotherapy UK (http://www.psychotherapy.org.uk/) What is Psychotherapy? (http://chandospractice.org/page1/page1.html)
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Transcranial magnetic stimulation (TMS) is a noninvasive method to cause depolarization or hyperpolarization in the neurons of the brain. TMS uses electromagnetic induction to induce weak electric currents using a rapidly changing magnetic field; this can cause activity in specific or general parts of the brain with minimal discomfort, allowing the functioning and interconnections of the brain to be studied. A variant of TMS, repetitive transcranial magnetic stimulation (rTMS), has been tested as a treatment tool for various neurological and psychiatric disorders including migraines, strokes, Parkinson's disease, dystonia, tinnitus, depression and auditory hallucinations.
Background
The principle of inductive brain stimulation with eddy currents has been noted since the 20th century. The first successful TMS study was performed in 1985 by Anthony Barker and his colleagues in Sheffield, England.[2] Its earliest application demonstrated conduction of nerve impulses from the motor cortex to the spinal cord, stimulating muscle contractions. The use of magnets rather than a direct electric current to the brain reduced the discomfort of the procedure and research and allowed mapping of the cerebral cortex and its connections.
Transcranial magnetic stimulation Repetitive TMS produces longer-lasting effects which persist past the initial period of stimulation. rTMS can increase or decrease the excitability of the corticospinal tract depending on the intensity of stimulation, coil orientation and frequency. The mechanism of these effects is not clear although it is widely believed to reflect changes in synaptic efficacy akin to long-term potentiation (LTP) and long-term depression (LTD).[4]
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Risks
Although TMS is often regarded as safe, the greatest acute risk of TMS is the rare occurrence of induced seizures and syncope.[5] More than 16 cases of TMS-related seizure have been reported in the literature, with at least seven reported before the publication of safety guidelines in 1998,[6] and more than nine reported afterwards. The seizures have been associated with single-pulse and rTMS. Reports have stated that in at least some cases, predisposing factors (medication, brain lesions or genetic susceptibility) may have contributed to the seizure. A review of nine seizures associated with rTMS that had been reported after 1998 stated that four seizures were within the safety parameters, four were outside of those parameters, and one had occurred in a healthy volunteer with no predisposing factors. A 2009 international consensus statement on TMS that contained this review concluded that based on the number of studies, subjects and patients involved with TMS research, the risk of seizure with rTMS is considered very low.[5] Besides seizures, other risks include fainting, minor pains such as headache or local discomfort, minor cognitive changes and psychiatric symptoms (particularly a low risk of mania in depressed patients).[5] Though other side effects are thought to be possibly associated with TMS (alterations to the endocrine system, altered neurotransmitter and immune system activity) they are considered investigational and lacking substantive proof.[5] Other adverse effects of TMS are: Discomfort or pain from the stimulation of the scalp and associated nerves and muscles on the overlying skin;[7] this is more common with rTMS than single pulse TMS,[6] Rapid deformation of the TMS coil produces a loud clicking sound which increases with the stimulator intensity that can affect hearing with sufficient exposure, particularly relevant for rTMS (hearing protection may be used to prevent this),[6] rTMS in the presence of incompatible EEG electrodes can result in electrode heating and, in severe cases, skin burns.[8] Non-metallic electrodes are used if concurrent EEG data is required.
Clinical uses
The uses of TMS and rTMS can be divided into diagnostic and therapeutic uses.
Diagnosis
TMS can be used clinically to measure activity and function of specific brain circuits in humans. The most robust and widely-accepted use is in measuring the connection between the primary motor cortex and a muscle to evaluate damage from strokes, spinal cord injuries, multiple sclerosis and motor neuron disease.[9] [10] [11] TMS has been suggested as a means of assessing short-interval intracortical inhibition (SICI) which measures the internal pathways of the motor cortex but this use has not yet been validated.[12]
Therapy
Studies of the use of TMS and rTMS to treat neurological and psychiatric conditions have shown only modest effects with little confirmation of results.[13] However, publications reporting the results of reviews and statistical meta-analyses of earlier investigations have stated that rTMS appeared to be effective in the treatment of certain types of major depression under certain specific conditions.[13] [14] [15] [16] [17] [18] [19] rTMS devices are marketed for the treatment of such disorders in Canada, Australia, New Zealand, the European Union, Israel and the United
Transcranial magnetic stimulation States.[15] [20] A recent meta-analysis of 34 studies comparing rTMS to sham treatment showed an effect size of 0.55 (p<.001).[13] This is comparable to commonly reported effect sizes of pharmacotherapeutic strategies for treatment of depression in the range of 0.17-0.46.[13] However, that same meta-analysis found that rTMS was significantly worse than electroconvulsive therapy (effect size -0.47), although side effects were significantly better with rTMS. An analysis of one of the studies included in the meta-analysis showed that one extra remission from depression occurs for every 3 patients given electroconvulsive therapy rather than rTMS (number needed to treat 2.36).[21] There is evidence that rTMS can temporarily reduce chronic pain and change pain-related brain and nerve activity, and TMS has been used to predict the success of surgically implanted electrical brain stimulation for the treatment of pain.[22] Other areas of research include the rehabilitation of aphasia and motor disability after stroke,[5] [10] [11] [23] tinnitus,[24] Parkinson's disease[25] [26] and the negative symptoms of schizophrenia.[27] TMS has failed to show effectiveness for the treatment of brain death, coma, and other persistent vegetative states.[28] It is difficult to establish a convincing form of "sham" TMS to test for placebo effects during controlled trials in conscious individuals, due to the neck pain, headache and twitching in the scalp or upper face associated with the intervention.[5] "Sham" TMS manipulations can affect cerebral glucose metabolism and MEPs, which may confound results.[15] This problem is exacerbated when using subjective measures of improvement. Depending on the research question asked and the experimental design, matching this discomfort to distinguish true effects from placebo can be an important and challenging issue.[5] A recent multicenter trial of rTMS in depression used a "sham" placebo treatment that appeared to mimic the sound and scalp stimulation associated with active TMS treatment. The investigators concluded: "Although the treatment effect was statistically significant on a clinically meaningful variable (remission), the overall number of remitters and responders was less than one would like with a treatment that requires daily intervention for 3 weeks or more, even with a benign adverse effect profile".[29] However, a review of the trial's report has questioned the adequacy of the placebo, noting that treaters were able to guess whether patients were receiving treatment with active or sham TMS, better than chance.[30]
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Transcranial magnetic stimulation effectiveness of these devices". The rule identified the rTMS system as "an external device that delivers transcranial pulsed magnetic fields of sufficient magnitude to induce neural action potentials in the prefrontal cortex to treat the symptoms of major depressive disorder without inducing seizure in patients who have failed at least one antidepressant medication and are currently not on any antidepressant therapy".[33] An FDA guidance document issued in conjunction with the final rule describes the special controls that support the classification of the rTMS system into Class II.[34]
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Technical information
TMS uses electromagnetic induction to generate an electric current across the scalp and skull without physical contact. A plastic-enclosed coil of wire is held next to the skull and when activated, produces a magnetic field oriented orthogonally to the plane of the coil. The magnetic field passes unimpeded through the skin and skull, inducing an oppositely directed current in the brain that activates nearby nerve cells in much the same way as currents applied directly to the cortical surface.[36] The path of this current is difficult to model because the brain is irregularly shaped and electricity and magnetism are not conducted uniformly throughout its tissues. The magnetic field is about the same strength as an MRI, and the pulse generally reaches no more than 5 centimeters into the brain.[37]
Coil types
The design of transcranial magnetic stimulation coils used in either treatment or diagnostic/experimental studies may differ in a variety of ways. These differences should be considered in the interpretation of any study result, and the type of coil used should be specified in the study methods for any published reports. The most important considerations include: the type of material used to construct the core of the coil the geometry of the coil configuration the biophysical characteristics of the pulse produced by the coil.
With regard to coil composition, the core material may be either a magnetically inert substrate (i.e., the so-called air-corecoil design), or possess a solid, ferromagnetically active material (ie, the so-called solid-core design). Solid core coil design result in a more efficient transfer of electrical energy into a magnetic field, with a substantially reduced amount of energy dissipated as heat, and so can be operated under more aggressive duty cycles often mandated in therapeutic protocols, without treatment interruption
Transcranial magnetic stimulation due to heat accumulation, or the use of an accessory method of cooling the coil during operation. Varying the geometric shape of the coil itself may also result in variations in the focality, shape, and depth of cortical penetration of the magnetic field. Differences in the coil substance as well as the electronic operation of the power supply to the coil may also result in variations in the biophysical characteristics of the resulting magnetic pulse (e.g., width or duration of the magnetic field pulse). All of these features should be considered when comparing results obtained from different studies, with respect to both safety and efficacy.[38] A number of different types of coils exist, each of which produce different magnetic field patterns. Some examples: round coil: the original type of TMS coil figure-eight coil (i.e. butterfly coil): results in a more focal pattern of activation double-cone coil: conforms to shape of head, useful for deeper stimulation four-leaf coil: for focal stimulation of peripheral nerves[39]
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Design variations in the shape of the TMS coils allow much deeper penetration of the brain than the standard depth of 1.5cm. Circular, H-shaped, double cone coils and other experimental variations can induce excitation or inhibition of neurons deeper in the brain including activation of motor neurons for the cerebellum, legs and pelvic floor. Though able to penetrate deeper in the brain, they are less able to produced a focused, localized response and are relatively non-focal.[5]
References
[1] http:/ / www. nlm. nih. gov/ cgi/ mesh/ 2011/ MB_cgi?field=uid& term=D050781 [2] Barker AT, Jalinous R, Freeston IL. (May 1985). "Non-invasive magnetic stimulation of human motor cortex". The Lancet 1 (8437): 11061107. doi:10.1016/S0140-6736(85)92413-4. PMID2860322. [3] Pascual-Leone A; Davey N; Rothwell J; Wassermann EM; Puri BK (2002). Handbook of Transcranial Magnetic Stimulation. Hodder Arnold. ISBN0340720093. [4] Fitzgerald PB; Fountain S; Daskalakis J (December 2006). "A comprehensive review of the effects of rTMS on motor cortical excitability and inhibition". Clinical Neurophysiology 117 (12): 258496. doi:10.1016/j.clinph.2006.06.712. PMID16890483. [5] This citation will be automatically completed in the next few minutes. You can jump the queue or expand by hand (http:/ / en. wikipedia. org/ wiki/ Template:cite_doi/ _10. 1016. 2fj. clinph. 2009. 08. 016?preload=Template:Cite_doi/ preload& editintro=Template:Cite_doi/ editintro& action=edit) [6] Wassermann EM (1998). "Risk and safety of repetitive transcranial magnetic stimulation: report and suggested guidelines from the International Workshop on the Safety of Repetitive Transcranial Magnetic Stimulation, June 57, 1996" (http:/ / www. icts. uci. edu/ neuroimaging/ Wassermann_rTMS_Safety1998. pdf) (pdf). Electroencephalography and clinical Neurophysiology 108 (1): 116. doi:10.1016/S0168-5597(97)00096-8. PMID9474057. . [7] "Transcranial Magnetic Stimulation (TMS)" (http:/ / www. nami. org/ Content/ ContentGroups/ Helpline1/ Transcranial_Magnetic_Stimulation_(rTMS). htm). National Alliance on Mental Illness. . Retrieved 2008-12-15. [8] Roth BJ; Pascual-Leone A; Cohen LG; Hallett M (1992). "The heating of metal electrodes during rapid-rate magnetic stimulation: A possible safety hazard". Electroenceph. Clin. Neurophysiol. 85 (2): 116123. doi:10.1016/0168-5597(92)90077-O. PMID1373364. [9] Rossini, P; Rossi, S (2007). "Transcranial magnetic stimulation: diagnostic, therapeutic, and research potential". Neurology 68 (7): 484488. doi:10.1212/01.wnl.0000250268.13789.b2. PMID17296913. [10] Dimyan, MA; Cohen, L (2010). "Contribution of transcranial magnetic stimulation to the understanding of mechanisms of functional recovery after stroke". Neurorehabilitation and Neural Repair 24 (2): 125135. doi:10.1177/1545968309345270. PMC2945387. PMID19767591. [11] Nowak, D; Bsl, K; Podubeck, J; Carey, J (2010). "Noninvasive brain stimulation and motor recovery after stroke". Restorative Neurology and Neuroscience 28 (4): 531544. doi:10.3233/RNN-2010-0552. PMID20714076. [12] Kujirai T, Caramia MD, Rothwell JC, et al. (November 1993). "Corticocortical inhibition in human motor cortex" (http:/ / www. jphysiol. org/ cgi/ pmidlookup?view=long& pmid=8120818). J. Physiol. (Lond.) 471: 50119. PMC1143973. PMID8120818. . [13] Slotema, CW; Blom, JD; Hoek, HW; Sommer, IEC (2010). "Should We Expand the Toolbox of Psychiatric Treatment Methods to Include Repetitive Transcranial Magnetic Stimulation (rTMS)?". The Journal of Clinical Psychiatry 71 (7): 873884. doi:10.4088/JCP.08m04872gre. PMID20361902. [14] RTI International-University of North Carolina (RTI-UNC) Evidence-based Practice Center, Research Triangle Park, North Carolina (September 2011). "Nonpharmacologic Interventions for Treatment-Resistant Depression in Adults" (http:/ / www. effectivehealthcare. ahrq. gov/ ehc/ products/ 76/ 792/ TRD_CER33_20111110. pdf). Effective Health Care Program: Comparative Effectiveness Review: Number 33. Rockville, Maryland: Agency for Healthcare Research and Quality, United States Department of Health and Human Services. . Retrieved
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Further reading
Wassermann, E.M; Epstein, C.M.; Ziemann, U.; Walsh, V.; Paus, T.; Lisanby, S.H. (2008). Oxford Handbook of Transcranial Stimulation (Oxford Handbooks) (http://books.google.com/?id=YeKleGrKwC4C& printsec=frontcover#v=onepage&q). Oxford University Press, USA. ISBN0-19-856892-4.
External links
Stuttering Triggered by Transcranial Magnetic Stimulation (video) (http://www.overstream.net/view. php?oid=n7aomgtia5ul)
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Related subjects
Affective spectrum
The affective spectrum is a grouping of related psychiatric and medical disorders which may accompany bipolar, unipolar, and schizoaffective disorders at statistically higher rates than would normally be expected. These disorders are identified by a common positive response to the same types of pharmacologic treatments. They also aggregate strongly in families and may therefore share common heritable underlying physiologic anomalies. Affective spectrum disorders include: Attention-deficit hyperactivity disorder[1] [2] Bipolar disorder Body dysmorphic disorder Bulimia nervosa[1] [2] and other eating disorders Cataplexy[1] [2] Dysthymia[2] Fibromyalgia[2] General anxiety disorder[2] Hypersexuality Irritable Bowel Syndrome[1] [2] Impulse-control disorders Kleptomania Migraine[1] [2] Major Depressive Disorder[1] [2] Narcolepsy Obsessive-compulsive disorder[1] [2] Panic disorder[1] [2] Posttraumatic stress disorder[2] Premenstrual dysphoric disorder[2] Social phobia[2]
The following may also be part of the spectrum accompanying affective disorders. Chronic pain Intermittent explosive disorder Pathological gambling Personality disorder Pyromania Substance abuse and addiction (includes alcoholism) Trichotillomania
Also, there are now studies linking heart disease. Please note that many of the terms above overlap. The generally accepted definition of these terms can be found in the Diagnostic and Statistical Manual of Mental Disorders (DSM).
Affective spectrum
312
Footnotes
[1] Hudson JI, Pope HG Jr. (1990). "Affective spectrum disorder: does antidepressant response identify a family of disorders with a common pathophysiology?". Am J Psychiatry 147 (5): 55264. PMID11859906. [2] Hudson JI, Mangweth B, Pope HG Jr, De Col C, Hausmann A, Gutweniger S, Laird NM, Biebl W, Tsuang MT (1990). "Family study of affective spectrum disorder". Arch Gen Psychiatry 60 (2): 1707. doi:10.1001/archpsyc.60.2.170. PMID12578434.
List
: Top 09 A B C D E F G H I J K L M N O P Q R S T U V W X Y Z
A
Rigoberto Alpizar, shooting victim.[1] Sophie Anderton, model.[2] Adam Ant, musician.[3] Emilie Autumn, musician.[4]
B
Andy Behrman, author of the book Electroboy: A Memoir of Mania.[5] [6] Max Bemis, frontman of the band Say Anything, spoke about his diagnosis in an interview with Spin magazine in 2006.[7] Maurice Benard, actor. He has discussed his diagnosis with Oprah Winfrey, and has since become active in promoting bipolar awareness.[8] Ludwig Boltzmann, physicist and mathematician. He "suffered from an alternation of depressed moods with elevated, expansive or irritable moods." [9] Adrian Borland, British musician.[10] Russell Brand, comedian and actor. "In a low-key admission at the end of the book, he says he was finally diagnosed with bipolar disorder manic depression after he kicked the drugs for good in 2002 which goes some way to explaining his almost superhuman indifference to the chaos and catastrophe that almost lead him to obscurity."[11] Andrea Breth, German stage-director.[12] Jeremy Brett, actor.[13] Frank Bruno, boxer; was hospitalized for a short period and is currently on lithium.[14] [15] [16] Barney Bubbles, graphic designer.[17] [18]
313
C
Robert Calvert, former Hawkwind frontman.[19] [20] Alastair Campbell, press advisor.[21] [22] Georg Cantor, mathematician. Cantor's recurring bouts of depression from 1884 to the end of his life were once blamed on the hostile attitude of many of his contemporaries,[23] but these bouts can now be seen as probable manifestations of bipolar disorder.[24] Dick Cavett, television journalist. "CAVETT: Both in hypomanic, which I have had, and incidentally, one has to admit many patients say I am cured now, I am fine. But I must say I miss those hypomanic states. They are better off where they are."[25] Iris Chang, historian and journalist for the San Francisco Chronicle.[26] John Clare, poet.[27] [28] Kurt Cobain, musician. His cousin, Beverly Cobain, a "registered nurse () [with] experience as a mental health professional" and author of a book, When Nothing Matters Anymore: A Survival Guide for Depressed Teens ISBN 1-57542-036-8, stated in an interview: "Kurt was diagnosed at a young age with Attention Deficit Disorder [ADD], then later with bipolar disorder; () As Kurt undoubtedly knew, bipolar illness can be very difficult to manage, and the correct diagnosis is crucial. Unfortunately for Kurt, compliance with the appropriate treatment is also a critical factor."[29] Neil Cole, former Australian Labor party politician. "Associate Professor Cole was the first politician in Australia or overseas to admit to having a mental illness, namely bipolar mood disorder."[30] Rosemary Clooney, singer and actress.[31] Patricia Cornwell, American crime writer.[32] [33] Robert S. Corrington, theologist. In his book Riding the Windhorse: Manic-Depressive Disorder and the Quest for Wholeness[34] he gives a personal account of his own struggles with the condition. Michael Costa, former Australian Labor party politician and Treasurer of NSW. "Mr Costa said a number of state parliamentary colleagues approached him about their mental health problems after he publicly revealed his battle with bipolar disorder in 2001."[35] Vincent Crane, keyboard player of Atomic Rooster.[36]
D
Ray Davies, musician: is openly bipolar; also see his autobiography, X-Ray. Disco D, record producer and composer. On returning to the United States from his 2005 Australian trek, Shayman went public about his struggle with bipolar disorder.[37] DMX (rapper), has spoken openly about his manic depression.[38] Mike Doughty, musician. First described himself diagnosed as bipolar in 2007 on his blog.[39] Charmaine Dragun, former Australian journalist/newsreader. Misdiagnosed with depression. Inquest concluded she had bipolar II disorder.[40] Richard Dreyfuss, actor, BBC Documentary.[41] Patty Duke, actress.[42]
314
F
Carrie Fisher, actress and writer. "'I ended up being diagnosed as a bipolar II,' says Fisher."[41] [43] Connie Francis, singer.[44] Stephen Fry, actor, comedian and writer. "As a sufferer of the disorder, Stephen Fry is speaking to other sufferers to find out about their experiences and visiting leading experts in the UK and US to examine the current state of understanding and research." Stephen has recorded a documentary about the life of the manic depressive which aired on the BBC.[41] Justin Furstenfeld, Lead singer of the band, "Blue October".[45]
G
Alan Garner, novelist. According to the Guardian, "In The Voice that Thunders (Harvill), a collection of critical and autobiographical essays, Garner casts light on his writing and thinking, and the role that manic depression plays in his creativity".[46] [47] Paul Gascoigne, English footballer. "His second book, released this year, centres on his therapy - for alcoholism, eating disorders, OCD, and bipolar disorder, among others."[48] Mel Gibson, actor and director.[49] Matthew Good, Canadian musician. He first disclosed his illness in a personal blog. It was during the writing and recording of Hospital Music that he suffered one of his worst episodes.[50] Philip Graham, publisher and businessman. "It had finally penetrated to me that Phil's diagnosis was manic-depression" Katherine Graham (1997), Personal History, p.328; Knopf, 1997, ISBN 0-394-58585-2 (book has numerous other references). Macy Gray, musician and actor. As documented in an interview with Saul Williams.[51] Graham Greene, English novelist.[52] Extract from Graham Greene: A Life in Letters: "Greene was managing the impulses of bipolar illness, involving mood swings from elation, expansiveness or irritability to despair and would quickly be guilty of repeated infidelities." Ivor Gurney, English composer and poet.[53]
H
Terry Hall, lead singer of The Specials.[54] Linda Hamilton, actress. Star of the Terminator movies. Was diagnosed at the age of 40.[55] Robert Hansen, serial killer.[56] Mariette Hartley, American actress, has publicly spoken about her bipolar disorder.[57] Jonathan Hay, Australian rules footballer[58] Ernest Hemingway, writer [59] [60] Kristin Hersh, musician, formerly of rock band Throwing Muses, has spoken about her bipolar disorder.[61] Abbie Hoffman, political activist: "Abbie was diagnosed in 1980 as having bipolar disorder, more commonly known as manic depression." [62] Marya Hornbacher, writer. Hornbacher wrote Madness, a memoir of her struggle with bipolar disorder, after writing Wasted, which detailed her eating disorder.
315
I
Jack Irons, drummer, formerly of Red Hot Chili Peppers and Pearl Jam.[63]
J
Kay Redfield Jamison, clinical psychologist and Professor of Psychiatry at the Johns Hopkins University School of Medicine, who profiled her own bipolar disorder in her 1995 memoir An Unquiet Mind and argued for a connection between bipolar disorder and artistic creativity in her 1993 book, Touched with Fire. Daniel Johnston, musician: "Johnston's output in his late teens and early 20s proved to be a symptom of his worsening manic depression." The Guardian Unlimited, Saturday August 20, 2005: "Personal demons", review of film, The Devil and Daniel Johnston:[64] Andrew Johns, Australian rugby league player. Publicly announced his condition following retirement.[65] Lee Joon, Korean actor and musician [66]
K
Chris Kanyon American professional wrestler.[67] Kerry Katona, English television presenter, writer, magazine columnist and former pop singer with girl band Atomic Kitten. BBC.[68] Rep. Patrick J. Kennedy has been open about mental health issues, including being diagnosed with bipolar disorder.[69] Otto Klemperer, conductor.[70] Margot Kidder, actress self-described.[71] Patrick Kroupa, writer and hacker, has been very open about his drug use and mental health issues, after his last heroin detox in 1999. He mentions bipolar disorder openly in several interviews.[72] [73] [74]
L
Vivien Leigh, actress[75] Jenifer Lewis, American actress, spoke about her diagnosis on Oprah in September 2007.[76] Bill Lichtenstein, print and broadcast journalist and documentary filmmaker, profiled in Time magazine, October 10, 1994.[77] Jack London, American author [78] Demi Lovato, American actress, singer, Disney star, revealed her illness in April 2011 in an interview with People magazine.[79]
M
Arthur McIntyre, Australian artist.[80] Kristy McNichol, actress. The former child star and teen idol left the show Empty Nest due to her battle with the depression. McNichol later returned to the show for a few episodes during the series' last season.[81] [82] [83] [84] Burgess Meredith, actor; with cyclothymia (milder bipolar disorder).[85] Eric Millegan, actor, played Zack Addy on Bones. In 2009, Millegan released a YouTube video of how being bipolar affects his life. He has rapid-cycling bipolar disorder. Kate Millett, author, The Loony-Bin Trip (1990) discusses her diagnosis of bipolar disorder, describing experiences with hospitalization and her decision to discontinue lithium therapy. Spike Milligan, comedian.[86] Ben Moody, musician. The former guitarist from Evanescence.[87] Seaneen Molloy, Northern Irish blogger.[88]
List of people with bipolar disorder John A. Mulheren, American financier, stock and option trader and philanthropist.[89] Edvard Munch, artist.[90] Robert Munsch, author.[91]
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N
Florence Nightingale, nurse and health campaigner. BPW "Florence heard voices and experienced a number of severe depressive episodes in her teens and early 20s - symptoms consistent with the onset of bipolar disorder", Dr. Kathy Wisner, a professor of psychiatry at the University of Pittsburgh Medical Center.[92]
O
Sinad O'Connor, musician. She discussed her diagnosis in a Guardian interview in 2010.[93] Graeme Obree, Scottish racing cyclist. World hour record 1993. Individual pursuit world champion in 1993 and 1995. Cited in 2003 autobiography, Flying Scotsman: Cycling to Triumph Through My Darkest Hours and 2006 film. Phil Ochs, musician.[94] Bill Oddie, naturalist, comedian and television presenter.[95] [96] Ozzy Osbourne, singer. Lead singer of Black Sabbath and his self-titled band. Cited in VH1's "Heavy: The History of Metal" in 2006. Cheri Oteri, actress. Saturday Night Live Cast Member. Cited in Shales T.& Miller A. (2002) Live From New York, A Uncensored History of Saturday Night Live. Craig Owens, singer for American band Destroy Rebuild Until God Shows.[97]
P
Nicola Pagett, actor. Wrote about her bipolar disorder in her autobiography Diamonds Behind My Eyes ISBN 0575602678 Emma Parker Bowles, model.[98] Jaco Pastorius, jazz musician. "Jaco was diagnosed with this clinical bipolar condition in the fall of 1982. The events which led up to it were considered "uncontrolled and reckless" incidences."[99] Jane Pauley, TV presenter and journalist. The former Today and Dateline host describes being diagnosed with bipolar disorder in her autobiography "Skywriting: A Life Out of the Blue", which she wrote in 2004, as well as on her short-lived talk show.[100] [101] [102] [103] [104] [105] Edgar Allan Poe, poet and writer, may have experienced bipolar disorder.[106] [107] [108] Jackson Pollock, American artist.[90] Odean Pope, American jazz musician.[109] Gail Porter, British TV presenter.[110] Emil Post, mathematician.[111] Charley Pride, country music artist. (autobiography) Pride: The Charley Pride Story. Publisher: Quill (May 1995). "Pride discusses business ventures that succeeded and those that failed, as well as his bouts with manic depression. He tells his story with no bitterness but lots of homespun advice and humor."
317
R
Rene Rivkin, entrepreneur.[112] Barret Robbins, former NFL Pro Bowler.[113] Axl Rose, lead singer and frontman best known for Guns N' Roses.[114] "I went to a clinic, thinking it would help my moods. The only thing I did was take one 500-question test - ya know, filling in the little black dots. All of sudden I'm diagnosed manic-depressive." Richard Rossi, filmmaker, musician, and maverick minister, revealed for the first time in a live interview on the Lynn Cullen show on June 5, 2008 the link between his artistic productivity and his depression to bipolar disorder, stating that "my father was bi-polar one, and I'm bi-polar two." He spoke of the relationship between creativity and the illness.
S
Robert Schumann, German composer[115] [116] [117] Nina Simone, American singer. Interview with her daughter Simone, The Sunday Times June 24, 2007[118] Michael Slater, International Australian cricketer, forced to retire because of related symptoms.[119] [120] Tony Slattery, actor and comedian.[41] "I rented a huge warehouse by the river Thames. I just stayed in there on my own, didn't open the mail or answer the phone for months and months and months. I was just in a pool of despair and mania." BBC Documentary[41] Sidney Sheldon, producer, writer; wrote about being a victim of bipolar disorder in his autobiography The Other Side of Me. Tim Smith, rugby league player whose career with NRL side Parramatta Eels was ended due to his bipolar condition, and pressure from the media.[121] Peter Steele, frontman, Type O Negative.[122] [123] David Strickland, Actor, Suddenly Susan.[124] [125] Poly Styrene (real name Marion Elliot-Said), singer.[126] Stuart Sutherland, British psychologist and writer[127]
T
Mackenzie Taylor, British comedian.[128] Michael Thalbourne, Australian psychologist and parapsychologist.[129] Steven Thomas, American entrepreneur.[130] [131] Gene Tierney, Academy Award nominated actress, Best Actress (1945).[132] Devin Townsend, musician, Strapping Young Lad, The Devin Townsend Band. He took himself off of his medication to write lyrics for Strapping Young Lad's album Alien.[133] Nick Traina, singer,[134] "in the last year of his life, he began telling people he was manic-depressive." Timothy Treadwell, American environmentalist and bear enthusiast, featured in the 2005 documentary film by Werner Herzog titled Grizzly Man.[135] [136] Margaret Trudeau, Canadian celebrity and ex-wife of former Canadian Prime Minister Pierre Elliot Trudeau (deceased). She now travels Canada and other countries speaking out against the stigmas on mental illness.[137]
318
V
Jean-Claude Van Damme, actor.[138] [139] Vincent Van Gogh, artist.[140] [141] [142] (among numerous other hypotheses) Townes Van Zandt, singer-songwriter.[143] Mark Vonnegut, author.[144]
W
David Walliams, actor/comedian/author/charity fundraiser.[145] [146] Ruby Wax, comedian.[147] [148] Scott Weiland, musician. (Stone Temple Pilots, Velvet Revolver)[149] Pete Wentz, musician. Fall Out Boy[150] Delonte West, American basketball player[151] Mark Whitacre, business executive described in the true story movie, The Informant.[152] Brian Wilson, musician, founding member of The Beach Boys.[153] Amy Winehouse, musician[154] Virginia Woolf, writer.[155]
Z
Catherine Zeta-Jones, actress [156]
References
Resources
Jamison, Kay Redfield (1993): Touched with Fire: Manic-Depressive Illness and the Artistic Temperament, New York, The Free Press. ISBN 0-02-916030-8
Notes
[1] "Probe after Miami airport killing" (http:/ / news. bbc. co. uk/ 2/ hi/ americas/ 4509516. stm). BBC News. 2005-12-08. . Retrieved 2006-10-05. [2] "Sophie Why Im always moody" (http:/ / www. thesun. co. uk/ article/ 0,,2-2006420086,00. html). The Sun (London). 2007-05-17. . [3] channel4.com | Adam Ant | Interview | 4music interview from 4music on Channel4.com (http:/ / www. channel4. com/ music/ features/ interview. jsp?featureId=195) [4] Liz Ohanesian (October 23, 2009). "Interview: Neo-Victorian Violinist, Singer Emilie Autumn" (http:/ / blogs. laweekly. com/ westcoastsound/ synthful/ emilie-autumn/ ). LA Weekly. . Retrieved March 20, 2010. [5] Andy Behrman - Electroboy - A look at Manic Depression (http:/ / www. electroboy. com/ meetelectroboy. htm) [6] Andy Behrman: Author of Electroboy answers some questions from Matt Borondy (http:/ / www. identitytheory. com/ interviews/ behrman_interview. php) [7] Q&A: Say Anything's Max Bemis | Spin Magazine Online (http:/ / www. spin. com/ features/ magazine/ 2006/ 03/ 0604_sayanything/ ) [8] Actor Maurice Benard Update (http:/ / www2. oprah. com/ tows/ slide/ 200709/ 20070924/ slide_20070924_284_108. jhtml) [9] John J. O'Connor, Edmund F. Robertson (September 1998). "Ludwig Boltzmann" (http:/ / www-groups. dcs. st-and. ac. uk/ ~history/ Biographies/ Boltzmann. html). . Retrieved 2010-09-15. "He suffered from an alternation of depressed moods with elevated, expansive or irritable moods." [10] Brittle Heaven - The official ADRIAN BORLAND website (http:/ / www. brittleheaven. com/ index. php?section=2& category=& page=4& id=286) [11] Camden New Journal - Books: My booky wook by Russell Brand (http:/ / www. thecnj. com/ review/ 2007/ 122007/ books122007_02. html?headline=Won_over_by_an_idiot_whos_interesting) [12] http:/ / www. profil. at/ articles/ 0726/ 560/ 177193/ dieser-selbstverwirklichungsirrsinn [13] TBE: Jeremy Brett FAQ - Frequently Asked Questions (http:/ / www. brettish. com/ tbe-faq. html) [14] "Q: Did you feel suicidal before you were sectioned? A: Nah, I'm not that brave or clever. I wouldn't know how to tie a rope, know what I mean?" (http:/ / www. guardian. co. uk/ print/ 0,3858,5316803-110418,00. html). The Guardian (London). 2005-10-24. . Retrieved
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Diagnosis
The diagnosis of childhood BD is controversial,[8] although it is not under discussion that BD typical symptoms are dysfunctional and have negative consequences for minors suffering them.[9] Main discussion is centered on whether what is called BD in children refers to the same disorder than when diagnosing adults,[9] and the related question on whether adults criteria for diagnosis are useful and accurate when applied to children.[8] More specifically main discussion over diagnosis in children circles around mania symptomatology and its differences between children and adults.[8] For the diagnosis of mania the American Psychiatric Association's Diagnostic and Statistical Manual (DSM-IV-TR) requires a "distinct period of abnormally and persistently elevated, expansive or irritable mood" during at least four days, and a number of extra behavioral and cognitive symptoms such as grandiosity, reduced sleep need and risk seeking behaviors.[8] Regarding diagnosis of children some experts recommend to follow the same DSM criteria than for adults, although taking into account the age of the individual and the normal behavior of those of his age.[8] Others believe that these criteria do not separate correctly children with BD from other problems such as ADHD, and emphasize fast mood cycles.[8] Still others argue that what accurately differentiates children with BD is the distinct irritability with which it courses.[8] The practice parameters of the American Academy of Child and Adolescent Psychiatry encourage the first strategy.[8] [9]
Increase
Number of American children and adolescents diagnosed of BD in community hospitals increased 4-fold reaching rates of up to 40% in 10 years around the beginning of the current century, while in outpatient clinics it doubled reaching the 6%.[8] Outpatient office visits for children and adolescents with bipolar disorder in the United States increased from 20,000 in 199495 to 800,000 in 200203.[10] The data suggest that doctors had been more aggressively applying the diagnosis to children, rather than that the incidence of the disorder has increased. The reasons for this increase in diagnosis are unclear. On the one hand, the recent consensus from the scientific community (see above) will have educated clinicians about the nature of the disorder and the methods for diagnosis and treatment in children. That, in turn, should increase the rate of diagnosis. On the other hand, assumptions regarding behavior, particularly in regard to the differential diagnosis of bipolar disorder, ADHD, and conduct disorder in children and adolescents, may also play a role. In addition, some argue that the rise in diagnosis of pediatric bipolar disorder is the result of the influence of the pharmaceutical industry on psychiatry, especially with regard to big pharma's recent push to expand the market of atypical antipsychotics to children and the elderly.[11]
National differences
Another factor is that the "consensus" regarding the diagnosis in the pediatric age group seems to apply only to the USA. The British National Institute on Health and Clinical Excellence (NICE) guidelines on bipolar disorder in 2006 [12] specifically described the broadened criteria used in the USA to diagnose bipolar disorder in children as suitable "only for research" and "were not convinced that evidence currently exists to support the everyday clinical use of (pediatric bipolar phenotype) diagnoses" which increase the "risk that medicines may be used to inappropriately treat a bipolar diathesis that does not exist."(p526). A 2002 German survey [13] of 251 child and adolescent psychiatrists (average 15 years clinical experience) found only 8% had ever diagnosed a pre-pubertal case of bipolar disorder in their careers. A similar survey of 199 child & adolescent psychiatrists (av 15 years clinical experience) in Australia and New Zealand [14] also found much lower rates of diagnosis than in the USA and a consensus that bipolar disorder was overdiagnosed in children and youth in the USA. Concerns about overdiagnosis in the USA have also been expressed by American child & adolescent psychiatrists [15] [16] [17] [18] and a series of essays in the book "Bipolar children: Cutting-edge controversy, insights and research" [19] highlight several controversies and suggest the science still lacks consensus with regard to bipolar disorder diagnosis in the pediatric age group.
326
Epidemiology
Studies using DSM criteria show that up to 2% of youth may have bipolar disorder.[2] [9] Studies in clinics using these criteria show that up to 20% of youth referred to psychiatric clinics have bipolar disorder.[20] [21]
Treatment
Usual treatment involves medication and psychotherapy.[8] Nevertheless studies on the treatment of BD in children are scarce and of low quality, and many times approaches are directly derived from studies and practice with adults.[8] Drug prescription is commonly used as the initial treatment.[8] It aims to reduce symptomatology and maximize the positive effect of psychotherapeutic interventions that may come afterwards.[8] It usually consists in mood stabilizers, atypical antipsychotics, or a combination of both.[8] Among the formers lithium is the only compound approved Lithium carbonate. Lithium is the only drug by the Food and Drug Administration for children with BD (above 12 approved for children with BD by the FDA years old).[9] Combined therapy has been recommended for cases with partial or no response to a single medication and for individuals with psychosis.[8] Medications can produce important side effects so interventions have been recommended to be closely monitored and families of patients be informed of the different possible problems that can arise.[9] Atypical antipsychotics may produce weight gains as well as other metabolic problems, including diabetes mellitus type 2 and hyperlipidemia.[9] Extrapyramidal secondary effects may appear with these medications. These include tardive dyskinesia, a difficult-to-treat movement disorder (dyskinesia) that can appear after long-term use of antipsychotics.[9] Liver and kidney damage are a possibility with mood stabilizers.[9] Psychological treatment usually includes some combination of education on the disease, group therapy and cognitive behavioral therapy.[8] Children with BD and their families are informed, in ways accordingly to their age and family role, about the different aspects of BD and its management including causes, signs and symptoms and treatments.[8] Group therapy aims to improve social skills and manage group conflicts, with role-playing as a critical tool.[8] Finally cognitive-behavioral training is directed towards the participants having a better understanding and control over their emotions and behaviors.[8] Family therapy has strong support for treatment of pediatric bipolar disorder. Family Therapy is a branch of psychotherapy that works with families. It tends to view change in terms of the systems of interactions between family members. Families are seen as an interconnected force where the actions of the family members affect the health or dysfunction of each individual and the family as a whole. Family therapists focus on relationship patterns and are generally more interested in what goes on between family members rather than within one or more individuals. One family member may have a problem and the family relationships may be contributing to or maintaining that problem. For example, when a child has a behavior problem, family therapists may see the child as a 'scapegoat' and view the problem as actually residing within the family system. Family therapists avoid blaming any family member for the problem, and instead help the family interact in different ways that may solve the problem. There are both general, historical models of Family therapy (i.e., Structural, Strategic, Bowenian) and more specific, evidence-based approaches that are based on the earlier models. Strong research evidence suggests that both general and specific family therapy approaches are effective with a wide variety of clinical problems, including the treatment of bipolar spectrum disorders.[22]
Bipolar disorder in children Cognitive behavioral therapy (CBT) is also effective in treating bipolar disorder in young people. CBT is the term used for a group of psychological treatments that are based on scientific evidence. These treatments have been proven to be effective in treating many psychological disorders among children and adolescents, as well as adults.[23] When all treatment options are ineffective clozapine and electroconvulsive therapy have been proposed as last choice possibilities.[8]
327
Prognosis
Chronic medication is often needed, with relapses of individuals reaching rates over 90% in those not following medication indications and almost to 40% in those complying with medication regimens in some studies.[8] Compared to adults, a juvenile onset has in general a similar or worse course, although age of onset predicts the duration of the episodes more than the prognosis.[9] A risk factor for a worse outcome is the existence of additional (comorbid) pathologies.[9]
History
Emil Kraepelin in the 1920s noted that mania episodes were rare before puberty.[9] In general BD in children was not recognized in the first half of the XX century with first reviews of cases being published in the 60s.[9] [24] True recognition came twenty years after, with epidemiological studies showing that in approximately 20% of adults with BD already had symptoms in childhood or adolescence.[9] Nevertheless onset before age 10 was thought to be rare, below 0.5% of the cases.[9] During the second half of the century misdiagnosis with schizophrenia was not rare in the non-adult population due to common co-occurrence of psychosis and mania, this issue diminishing with an increased following of the DSM criteria in the last part of the XXth century.[9]
Research directions
Current research directions for BD in children include optimizing treatments for this population through well designed clinical trials, Emil Kraepelin increasing the knowledge of the genetic and neurobiological basis of the pediatric disorder, finding out why so many pediatric cases are among boys whereas many adult cases are in women, and improving diagnostic criteria.[8] Regarding the latter the mental health professionals charged with forming the new Diagnostic and Statistical Manual for Mental Disorders (the DSM-V) have proposed a new diagnosis, Disruptive Mood Dysregulation Disorder, which (though it is still a biologically based mental illness requiring drug and psychotherapeutic treatment) is considered to cover some presentations involving behavioral outbursts in different settings and locations that is as of now currently thought of as simple childhood-onset bipolar disorder occurring before puberty.[25] [26]
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References
[1] cite url=http://www.abct.org/sccap/?m=sPublic&fa=pub_BipolarDisorder|Information about Bipolar Disorder [2] Van Meter, A., Moreira, A. L., & Youngstrom, E. (2011). Meta-analysis of Epidemiological Studies of Pediatric Bipolar Disorder. Journal of Clinical Psychiatry. [3] Scheffer RE, Tripathi A, Kirkpatrick FG, Schultz T (2010) Rapid Quetiapine Loading in Youths with Bipolar Disorder J. Child Adol. Psychop 20:441-445 [4] Mana S, Martinot MLP, Martinot JL (2010) Brain Imaging Findings in Children and Adolescents with Mental Disorders: A Cross-sectional Review J Eurpsy 25: 345-354 [5] Nandagopal JJ and DelBello MP (2010) Pharmacotherapy for Pediatric Bipolar Disorder Psychiatric Annals 4:221-230 [6] Wagner KD, Redden L, Kowatch RA, Willens T, Segal S, et al. (2009) A double-blind, randomized, placebo-controlled trial of divalproex extended-release in the treatment of bipolar disorder in children and adolescents J Am Acad Child Adolesc Psychiatry 48: 519-532 [7] McClellan J, Kowatch R, Findling R (2008) Practice Parameter for the Assessment and Treatment of Children and Adolescents With Bipolar Disorder J Am Acad Child Adolesc Psychiatry 1: 107-125 [8] Leibenluft E, Rich BA (2008). "Pediatric bipolar disorder". Annu Rev Clin Psychol 4: 16387. doi:10.1146/annurev.clinpsy.4.022007.141216. PMID17716034. [9] McClellan J, Kowatch R, Findling RL (January 2007). "Practice parameter for the assessment and treatment of children and adolescents with bipolar disorder". J Am Acad Child Adolesc Psychiatry 46 (1): 10725. doi:10.1097/01.chi.0000242240.69678.c4. PMID17195735. [10] Kaplan, Stuart L. (2011-06-19). "Mommy, Am I Really Bipolar?" (http:/ / www. newsweek. com/ 2011/ 06/ 19/ mommy-am-i-really-bipolar. html). Newsweek. . Retrieved 2011-06-19. [11] Robbins, Brent D.; Higgins, Meghan; Fisher, Maureen; Over, Katie (2011-01). "Conflicts of interest in research on antipsychotic treatment of pediatric bipolar disorder, temper dysregulation disorder, and attenuated psychotic symptoms syndrome: Exploring the unholy alliance between big pharma and psychiatry". Journal of Psychological Issues in Organizational Culture (Journal of Psychological Issues in Organizational Culture) 1 (4): 32. doi:10.1002/jpoc.20039. [12] National Institute of Health and Clinical Excellence (2006). National clinical practice guidelines number 38: Bipolar disorder: the management of bipolar disorder in adults, children and adolescents in primary and secondary care. London: National Collaborating Centre for Mental Health. [13] Meyer TD, Komann-Bhm S, Schlottke PF. Do child psychiatrists in Germany diagnose bipolar disorders in children and adolescents? Result from a survey. Bipolar Disorders, 2004; 6: 426 431 [14] Parry P, Furber G, Allison S. The paediatric bipolar hypothesis: the view from Australia and New Zealand. Child and Adolescent Mental Health. (in press) [15] Carlson, G; Meyer, S. (2006). "Phenomenology and diagnosis of bipolar disorder in children, adolescents, and adults: Complexities and developmental issues". Development and Psychopathology 18 (4): 939969. doi:10.1017/S0954579406060470. PMID17064424. [16] Harris J. Child & adolescent psychiatry: the increased diagnosis of juvenile bipolar disorder: what are we treating? Psychiatr Serv 2005; 56: 529 531 [17] McClellan, J. (2005). "Commentary: treatment guidelines for child and adolescent bipolar disorder". Journal of the American Academy of Child and Adolescent Psychiatry 44 (3): 236239. doi:10.1097/00004583-200503000-00007. PMID15725967. [18] Laurel Williams. Mental health and children: Too often the system conspires to treat behavioural problems with pills. Los Angeles Times 14 Dec 2008 available at: http:/ / www. latimes. com/ news/ opinion/ commentary/ la-oe-williams14-2008dec14,0,3774809. story [19] Bipolar Children: Cutting-edge controversy, insights and research. Childhood in America series. editor Sharna Olfman. 2007. Praeger press. Westport CT. http:/ / www. amazon. com/ dp/ 0275997308 [20] Weller, Weller; Tucker, EB; Fristad, SG; Fristad, MA (1986). "Mania in prepubertal children: Has it been underdiagnosed". Journal of Affective Disorders 11 (2): 151154. doi:10.1016/0165-0327(86)90022-4. PMID2948989. [21] Wozniak, Biederman; Kiely, Ablon; Faraone, Mundy; Mennin, JS; Faraone, SV; Mundy, E; Mennin, D (1995). "Mania-like symptoms suggestive of childhood onset bipolar disorder in clinically referred children". Journal of the American Academy of Child and Adolescent Psychiatry 34 (7): 867876. doi:10.1097/00004583-199507000-00010. PMID7649957. [22] http:/ / www. abct. org/ sccap/ ?m=sPublic& fa=pub_WhatIsFT| | What is Family Therapy? [23] http:/ / www. abct. org/ sccap/ ?m=sPublic& fa=pub_WhatIsCBT | What is Cognitive Behavioral Therapy? [24] Anthony, James; Scott, Peter (1960). "Manic-depressive psychosis in childhood". Journal of Child Psychology and Psychiatry 1: 5372. doi:10.1111/j.1469-7610.1960.tb01979.x. [25] http:/ / www. dsm5. org/ Proposed%20Revision%20Attachments/ Justification%20for%20Temper%20Dysregulation%20Disorder%20with%20Dysphoria. pdf [26] http:/ / www. dsm5. org/ Newsroom/ Documents/ Diag%20%20Criteria%20General%20FINAL%202. 05. pdf
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Further reading
Handbooks for researchers and clinicians
Bipolar Disorder in Childhood ad Early Adolescence. Gellar, B., & BelBello, M. (ed) (http:/ / books. google. com/ books?vid=ISBN1593852932& id=m2mSld3Oq0IC& pg=PP1& lpg=PP1& ots=vSJU2klrYo& dq=barbara+ geller+ bipolar&sig=28-yq7S2V5PZb6Lt3WhOujoQj58)
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Organisations
International Society for Bipolar Disorders
The International Society for Bipolar Disorders (ISBD) is a non-profit organization based in Pittsburgh, Pennsylvania, USA, where it was founded June 17, 1999 [1]. The society focuses on research and education in bipolar disorders.[2] The Society has a membership consisting of mental health professionals, patients and their family members representing 50 countries. The mission of the Society is to advance the treatment of all aspects of bipolar disorder, thereby improving patient outcomes and quality of life, through fostering international collaboration in education and research. The Society hosts biennial professional meetings and offers educational programs. The Society journal is Bipolar Disorders: An International Journal of Psychiatry and Neurosciences.
ISBD logo
History
ISBD was launched at the 3rd International Conference on Bipolar Disorder, in Pittsburgh, USA in June 1999 by David J. Kupfer and Thomas Detre of the University of Pittsburgh Medical Center.[3] In September 1999, the official peer reviewed Society journal, Bipolar Disorders: An International Journal of Psychiatry and Neurosciences, published its first issue. In 2000, Bipolar Disorders was first tracked by the Institute for Scientific Information (ISI), and in 2001 MEDLINE and Index medicus began indexing the journal's content. In 2005, the journal was rated 11th out of 94 peer-reviewed psychiatric journals with an impact factor of over 4.8.[4] The ISBD held its first meeting in Sydney, Australia in February 2004 with over 400 delegates in attendance. The Society held its second meeting in August 2006 in Edinburgh, Scotland with over 600 attendees. The Society has over 725 members in 50 countries with an elected board representing 10 countries.
Officers
President: Mauricio Tohen; Vice-President for Research: Sophia Frangou; Vice-Presidence for Governance: Aysegul Ozerdem; Vice-President for Global Outreach: Kyoosoeb Ha; Secretary and Treasurer: Ihsan Salloum
Educational programs
The Psychiatric Trainee Support program offers psychiatric trainees a free two-year membership in the Society in order to enhance knowledge of bipolar disorder among this group, narrow the gap between bipolar research and clinical practice, and ultimately to improve diagnosis, treatment and outcomes for patients with bipolar disorder. These supported memberships are open to psychiatric residents, postgraduate students and junior faculty up to the Assistant Professor or equivalent level with less than five years as faculty in their career trajectory. The programs seek to support 70% of trainees from developing countries. The Samuel Gershon Awards for Junior Investigators, named in honor of Dr. Samuel Gershon, past ISBD President and pioneer of early lithium research, offer four awards for original research submissions. Awards are based on the originality of the content, as well as the significance of the findings reported, and are evaluated by an international scientific panel under the auspices of the ISBD. These awards are open to psychiatric trainees,
International Society for Bipolar Disorders postgraduate students and junior faculty up to the Assistant Professor rank from around the world. The awards are presented in conjunction with the Societys biennial meeting where the winners present their research in a special session showcasing the work of junior people in the field. The ISBD Research Fellowship for Junior Investigators provides an opportunity for the recipient to travel to another facility to get training in a particular type of research methodology (i.e. brain imaging, genetics, clinical trials, etc.). The Fellowship is intended to cover up to 6 months support for salary, travel, or some combination of these costs as they are incurred in pursuit of additional training. This could take the form of summer programs, participation in smaller prospective studies, or through some other opportunity.
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Conferences
The third biennial Conference of the International Society for Bipolar Disorders was held in India in January 2008. Future conferences will be held in So Paulo, Brazil in 2010 and Istanbul, Turkey in 2012. The conference provides updates on topics such as epidemiology, pharmacotherapy, psychotherapies, genetics and neurobiology, imaging research, and bipolar disorder in special populations. The meeting serves as a forum for the ISBD membership meeting and a venue for the Societys awards presentations.
Bipolar Disorders: Understanding the Full Spectrum is an educational video released in 2003 by the ISBD. The piece includes interviews with patients, their families, and medical professionals. An updated version was released on DVD in late fall 2007. The Neurocognition task force of the ISBD has developed recommendations for a cognitive test battery (BANC) for use in Bipolar Research both for clinical and research purposes. The task force included Lakshmi N Yatham [6], Ivan J Torres, Gin S Malhi [7], Sophia Frangou, David C Glahn [8], Carrie E Bearden [9], Katherine E Burdick [10], Anabel Martnez-Arn, Sandra Dittmann, Joseph F Goldberg, Aysegul Ozerdem, Omer Aydemir, K N Roy Chengappa. The battery has been published in Bipolar Disorders (abstract [11])
References
[1] [2] [3] [4] http:/ / www. isbd. org/ edcenter/ aboutisbd. asp Internal Revenue Service of the Department of the United States Treasury (http:/ / apps. irs. gov/ charities/ charitable/ index. html) Official Website of the International Society for Bipolar Disorders (http:/ / www. isbd. org) Blackwell Publishing - Publisher of Bipolar Disorders: An International Journal of Psychiatry and Neurosciences (http:/ / www. blackwellpublishing. com/ society. asp?ref=1398-5647) [5] http:/ / www. wiley. com/ bw/ journal. asp?ref=1398-5647 [6] http:/ / www. crestbd. ca/ researchers/ yatham-lakshmi. php [7] http:/ / sydney. edu. au/ medicine/ people/ academics/ profiles/ gmalhi. php [8] http:/ / www. glahngroup. org/ [9] http:/ / www. semel. ucla. edu/ profile/ carrie-bearden [10] http:/ / www. einstein. yu. edu/ home/ faculty/ profile. asp?id=10278 [11] http:/ / onlinelibrary. wiley. com/ doi/ 10. 1111/ j. 1399-5618. 2010. 00830. x/ abstract
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External links
International Society for Bipolar Disorders website (http://www.isbd.org) Guidestar.org (http://www.guidestar.org/pqShowFastResults. do;jsessionid=25869ABD567F57419AED8A4E9DBADF37.web04Worker.web04Worker?partner=guidestar& source=homepage) Idealist.org (http://www.idealist.org/en/org/154871-321)
Icarus Project
. The Icarus Project http:/ / theicarusproject. net is a mental health movement characterized by the view that many phenomena commonly labeled as mental illness should actually be regarded as "dangerous gifts". The name is derived from the Icarus mythology and is metaphorically used to convey that these experiences can lead to "potential[ly] flying dangerously close to the sun." [1]
History
In 2002, Sascha Altman DuBrul wrote an article published by the San Francisco Bay Guardian entitled Bipolar World, relating to his personal experiences being diagnosed with bipolar disorder. Among the dozens of e-mails and other correspondence that he received after this publication was a letter from Ashley McNamara, an artist and writer who identified strongly with his experiences.[1] The two founders, DuBrul and McNamara, corresponded for a few weeks before finally meeting in person and deciding to start The Icarus Project. The first step, they decided, was creating a website where people who identified with "bipolar and other 'mental illness' [could] find real community and contribute to it."[2]
Mission
The Icarus Project's stated aims are to provide a viable alternative to current methods of approaching and treating mental illnesses. The national Icarus Collective staff is set up to support local groups instead of creating the smaller organizations themselves. The responsibilities of the local group are to gather people locally for support, education, activism, and access to alternatives.[3] The Project advocates self-determination and caution when approaching psychiatric care. It encourages harm reduction, alternatives to the medical model, and self-determination in treatment and diagnosis.
Structure/Funding
The Icarus Project is currently under the fiscal sponsorship of FJC, a non-profit 501(c)3 umbrella organization arm of an investment firm, based in New York City. The Icarus Project currently gets the bulk of its money from foundation grants, but also has many individual donors. There has been considerable talk for many years of alternate funding structures, and efforts are currently underway to explore 501c3 and cooperative structures. The Icarus Project maintains a financial transparency page. [4] The Icarus Project does not accept funding from pharmaceutical companies.[3]
Icarus Project
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Publications
Navigating the Space Between Brilliance and Madness; A Reader and Roadmap of Bipolar Worlds, was self-published by the Icarus Project in March 2004. The book is currently in its 6th printing.[6] In July, 2006, The Icarus Project released the first draft of Friends Make the Best Medicine: A Guide to Creating Community Mental Health Support Networks.[7] In 2008 The Icarus Project released Through the Labyrinth; A Harm Reduction Guide to Coming Off Psychiatric Drugs, and in 2009 this publication was translated into Spanish and German and made available for free download on the The Icarus Project website.[8]
Media Mentions
The Icarus Project has been mentioned in the New York Times,[9] by Frontline 20/20, and many local media outlets.[10] [11]
References
[1] [2] [3] [4] [5] (http:/ / www. theicarusproject. net/ icarus-organizational/ origins-and-purpose) (http:/ / www. eastbayexpress. com/ issues/ 2005-08-03/ news/ feature. html) (http:/ / www. theicarusproject. net/ about-us/ icarus-project-mission-statement) "TIP: Financial Reports" (http:/ / theicarusproject. net/ financialtransparency). The Icarus Project. . Retrieved 2010-08-11. "View Forum - Local Meetups and Community Organizing" (http:/ / theicarusproject. net/ forums/ viewforum. php?f=84). Icarus Project. . Retrieved 2010-08-11. [6] (http:/ / www. theicarusproject. net/ publications/ navigating-the-space-between-brilliance-and-madness-reader) [7] (http:/ / www. theicarusproject. net/ icarus-downloads/ friends-make-the-best-medicine-icarus-support-manual-draft) [8] "Harm Reduction Guide To Coming Off Psychiatric Drugs & Withdrawal" (http:/ / theicarusproject. net/ alternative-treatments/ harm-reduction-guide-to-coming-off-psychiatric-drugs). The Icarus Project. 2008-04-23. . Retrieved 2010-08-11. [9] Heffernan, Virginia (2010-04-16). "Psycho-Babble - An Online Support Group" (http:/ / www. nytimes. com/ 2010/ 04/ 18/ magazine/ 18fob-Medium-t. html). The New York Times. . [10] Jill Carlson on Friday 07/17/2009, (1) Comment (2009-07-17). "Saying no to drugs with Mad Pride - Isthmus | The Daily Page" (http:/ / isthmus. com/ isthmus/ article. php?article=26420). Isthmus. . Retrieved 2010-08-11. [11] Jansen, Steve (2010-07-30). "Mental Health Collective Inaugural Meeting - Phoenix Art - Jackalope Ranch" (http:/ / blogs. phoenixnewtimes. com/ jackalope/ 2010/ 07/ mental_health_collective_inaug. php). Blogs.phoenixnewtimes.com. . Retrieved 2010-08-11.
Icarus Project
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External links
Eas6t Bay Express, August 3, 2005 - Off Their Meds - Modern psychiatrists prescribe pills for hundreds of "biological" disorders. The radical mental health movement isn't so sure - By Stefanie Kalem (http://www. eastbayexpress.com/2005-08-03/news/off-their-meds/) Columbia News Service, Nov 1, 2005 - A new movement views bipolar disorder as a dangerous gift - By Jennifer Itzenson (http://jscms.jrn.columbia.edu/cns/2005-11-01/itzenson-bipolardisorder) MindFreedom Radio - Sascha DuBrul of Icarus Project Next Guest on MF Radio (http://www.mindfreedom. org/campaign/media/mfradio/show/sascha-debrul-guest)
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License
Creative Commons Attribution-Share Alike 3.0 Unported //creativecommons.org/licenses/by-sa/3.0/