Panic Disorder - Epidemiology, Pathogenesis, Clinical Manifestations, Course, Assessment, and Diagnosis PDF

Panic disorder: Epidemiology, pathogenesis, clinical manifestations, co...
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Panic disorder: Epidemiology, pathogenesis, clinical manifestations, course, assessment, and diagnosis Authors Wayne Katon, MD Paul Ciechanowski, MD Disclosures All topics are updated as new evidence becomes available and our peer review process is complete. Literature review current through: Oct 2013. | This topic last updated: Ago 28, 2013. INTRODUCTION Panic attacks and panic disorder are common problems in both primary care and psychiatric patients. With the revision of DSM-IV to DSM-5, agoraphobia is diagnosed independently of panic disorder [1]. A patient with panic attacks may present with classic, discrete episodes of intense fear that begin abruptly and last for several minutes to an hour. Patients also often present with autonomic symptoms of a panic attack such as chest pain or shortness of breath frequently precipitating an emergency room visit. In panic disorder, patients experience recurrent, unexpected panic attacks, and one month or more of either worry about future attacks/consequences, or a significant maladaptive change in behavior related to the attacks, such as avoidance of the precipitating circumstances. Panic attacks are not usually difficult to diagnose, given a sufficiently high level of awareness. Panic attacks can occur in other anxiety disorders. Recognition and treatment of common comorbidities, such as agoraphobia or depression, is also critical to achieving good clinical outcomes. Infrequent panic attacks can occur with other anxiety disorders, making an accurate differential diagnosis essential. This topic will address the epidemiology, pathogenesis, clinical manifestations, course, and diagnosis of panic disorder. The epidemiology, pathogenesis, clinical manifestations, course, and diagnosis of agoraphobia are discussed separately. The treatment of panic disorder is also discussed separately. (See "Agoraphobia in adults: Epidemiology, pathogenesis, clinical manifestations, course, and diagnosis" and "Pharmacotherapy for panic disorder" and "Psychotherapy for panic disorder".) EPIDEMIOLOGY The 12-month and lifetime prevalence of panic disorder in the United States (US) population (age 15 to 54 years) was 2.7 percent and 4.7 percent, respectively, in a 2005 nationally representative study [2]. A systematic review of 13 European studies reported a 12-month prevalence rate of panic disorder of 1.8 percent [3]. The prevalence of panic disorder among primary care patients is approximately twice as high as in the general population with rates of 4 to 8 percent [4-6]. Panic attacks (which can occur in disorders other than panic disorder) are much more common than panic disorder, occurring in up to one-third of individuals at some point in their lifetime [7-9]. The disorder is approximately twice as common in women as among men, with a 5 percent lifetime prevalence among women versus 2 percent among men [10]. There appears to be a bimodal distribution in the prevalence of panic disorder by age, with one peak in late adolescence (15 to 19 years old) and a second peak at later ages (35 to 50 years old). Patients who develop panic disorder in adolescence frequently develop depressive disorders or co-existing depression and anxiety during their early adult years [11]. Panic disorder is frequently accompanied by comorbid psychiatric disorders. One third to one half of individuals with panic disorder meet DSM-IV-TR criteria for major depression at initial presentation, while over 60 percent will have had one or more lifetime episodes of major depression [12-16]. The National Comorbidity Study found that other anxiety disorders, including social phobia, generalized anxiety disorder, and posttraumatic stress disorder also frequently co-occur with panic disorder [2]. Patients with bipolar disorder and alcohol abuse have been shown to have relatively high panic disorder prevalence rates [17]. (See "Generalized anxiety disorder: Epidemiology, pathogenesis, clinical manifestations, course, assessment, and diagnosis" and "Posttraumatic stress disorder: Section Editor Murray B Stein, MD, MPH Deputy Editor Richard Hermann, MD
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Epidemiology, pathophysiology, clinical manifestations, course, and diagnosis" and "Clinical manifestations and diagnosis of depression" and "Bipolar disorder in adults: Epidemiology and pathogenesis" and "Alcohol use disorder: Epidemiology, pathogenesis, clinical manifestations, adverse consequences, and diagnosis" and "Social anxiety disorder: Epidemiology, clinical manifestations, and diagnosis".) Most studies have shown a higher likelihood of suicide attempts among people with panic disorder than in the general population [18-20]. A 2006 analysis of data from the National Comorbidity Survey, which studied a representative sample of US adults ages 15 to 54, found that panic disorder was associated with suicide attempts in the prior 12 months, controlling for sociodemographic and clinical factors [18]. The Netherlands Mental Health Survey found that a diagnosis of one or more anxiety disorders, including panic disorder, was associated with a higher rate of subsequent suicidal ideation and suicide attempts after controlling for sociodemographic factors and psychiatric comorbidity [19]. The study also found that individuals with co-occurring anxiety and mood disorders had a higher likelihood of suicide attempts compared to those with a mood disorder alone [19]. Another study found the association between panic disorder and suicidality to be explained by their association with comorbid major depression, personality disorders, or alcohol abuse [20]. (See "Suicidal ideation and behavior in adults".) PATHOGENESIS The pathogenesis of panic disorder fits a stress-diathesis model (ie, the combination of an underlying predisposition and life stress). Vulnerability factors include specific genetic factors, childhood adversity, and several personality traits, including anxiety sensitivity and neuroticism. Current stressful life events in association with one or more of these vulnerability factors often precipitate development of panic attacks [21-23]. Genetics Several lines of research indicate a genetic component to the disorder. First degree relatives of patients with panic disorder have been shown to meet criteria for the disorder in 18 to 41 percent of cases [24-26]. Twin studies have shown higher concordance for monozygotic compared to dizygotic twins (31 percent and 0 percent, respectively, in one study) [27]. Twin studies have suggested a heritability of approximately 40 percent with contributions of 10 percent from common familial environment and greater than 50 percent from individual-specific environmental effects [28]. Linkage studies in families that have panic disorder have been hindered by non-replication and small numbers [29]. Genetic linkage studies have suggested that chromosomal regions 13q, 14q, 22q, 4q31-34, and probably 9q31 are associated with panic disorder [30]. A meta-analysis has implicated the Val158Met polymorphism of the catechol-0-methyltransferase gene in susceptibility to panic disorder [31]. The specific role of this genetic variation in patients with panic disorder needs further study [31]. Temperament Anxious temperaments as measured by high neuroticism scores [32] and anxiety sensitivity [33] have also been shown to be risk factors for development of panic disorder. Neuroticism is a personality trait that is associated with poor stress resilience and often manifests in greater reactivity to life stressors [32]. Anxiety sensitivity is a measure of fear of anxiety symptoms and catastrophic cognitions regarding bodily sensations (eg, rapid heartbeat may be misinterpreted as a heart attack). Anxiety sensitivity has been shown to be associated with both genetic and environmental factors [34-36]. Subjects high in anxiety sensitivity have been shown to be more likely to develop panic disorder after experiencing stressful life experiences [36]. Research data suggest that a behavior trait, behavioral inhibition, which is likely a precursor to development of social phobia, may also explain how agoraphobia can develop in response to a fearful temperament [37]. Childhood adversity Studies have shown that childhood adversity such as a history of physical or sexual abuse increases the risk of panic disorder in adult years [38]. Both asthma in childhood [39,40] and smoking [41,42] have been shown to increase the risk for onset of panic disorder in adulthood. Life stress Panic attacks often occur at times of significant life stress. Controlled studies have found that individuals experiencing panic attacks have a higher frequency of stressful life events than controls, including: Events connoting danger and threat [21] Uncontrollable or undesirable events causing severely reduced self-esteem [22]
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An accident, trauma, rape, assault, or physical illness (including endocrinologic changes, eg, hyperthyroidism). Severe illness or death in a friend or relative [23]. Neurobiology Research into underlying possible causative biologic factors is gradually emerging and is described below. Several neuroanatomic areas as well as a number of neurotransmitters (serotonin, norepinephrine, and gamma-aminobutyric acid [GABA]) have become the focus of research into the pathophysiology of panic attacks and panic disorder. The figure describes the proposed neural circuitry of panic (figure 1) [43]. Researchers have focused on specific areas in the amygdala or hypothalamus as the potential site of neural triggers for panic attacks, suggesting that patients may inherit specific brain areas that are hyperexcitable and make the patient susceptible to unprovoked panic symptoms when exposed to mild interoceptive stressors such as an increased heart or respiratory rate; affected individuals may have a sensitivity to a wide range of agents such as carbon dioxide, lactate, caffeine, yohimbine, cholecystokinin, and isoproterenol, in provoking anxiety attacks in experimental situations [43,44]. Alternatively, cognitive researchers have suggested that catastrophic thoughts associated with minor somatic symptoms provoked by the above challenge agents cause panic disorder [45]. The amygdala, a structure in the temporal lobe, has been posited to be an anxiety way station that integrates: Sensory information from the environment via the thalamus and sensory cortex Stored memory of prior experience via the frontal cortex and hippocampus Efferent pathways to a variety of brain regions involved in a panic or anxiety response including the locus ceruleus, hypothalamus, periaqueductal grey (PAG) and parabrachial nucleus [43,46]. Studies have also hypothesized that the dorsomedial hypothalamus/perifornical (DMH/PeF) region coordinates rapid mobilization of behavioral, autonomic, respiratory, and endocrinologic responses to stress [44]. Rats with disrupted GABA inhibition in the DMH/PeF exhibit panic-like responses to lactate infusion similar to patients with panic disorder [44]. Decreased inhibitory signaling associated with abnormalities in the GABA system has also been posited as causing panic disorder [29]. Patients with panic disorder have been found to have increased benzodiazepine binding in the right lateral frontal gyrus and temporal cortex [47], but decreased binding in the left hippocampus [48]. Based on magnetic resonance scans, decreased GABA concentrations have been found in the occipital cortex [49], basal ganglia and anterior cingulate cortex [50] in patients with panic disorder compared to controls. Other biologic studies have implicated key differences in the brain neurobiologic fear system in patients with panic disorder compared with controls. Patients with panic disorder who were administered a respiratory stimulant, doxapram, were shown to have a larger increase in amygdala and cingulate gyrus activity and a greater decrease in prefrontal cortex activity than control subjects [51]. Magnetic resonance imaging studies have found reductions in volume of the amygdala [52] and left temporal lobe in patients with panic disorder compared to controls [53]. Studies have shown elevated glucose uptake in the amygdala, hippocampus, midbrain, thalamus, caudal pons, medulla, and cerebrum as measured by positron emission tomography (PET) scan in patients with panic disorder [29]. Magnetic resonance imaging (MRI) data have shown an increasing grey matter volume in the insula and upper brain stem and a decrease in the anterior cingulate gyrus (ACC) in patients with panic disorder versus healthy controls [46]. A study using quantitative PET image analysis found a marked reduction in the density of the serotonin type
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1a receptor in the anterior and posterior cingulate areas in the midbrain raphe in patients with panic disorder compared to controls [54]. The insula and ACC are thought to translate bodily signals into emotional feelings and patients with panic often overestimate and catastrophize bodily signals. These two areas are hypothesized to be a possible neural substrate of hypersensitivity to bodily signals often seen in patients with panic disorder and a possible site for pharmacologic intervention as well as cognitive behavioral therapy [54]. Antidepressants may prevent panic attacks by enhancing 5-HT inhibition of the PAG [54]. CLINICAL MANIFESTATIONS Panic disorder Panic attacks are characterized by the sudden onset of intense apprehension, fear or terror, and by the abrupt development of specific somatic, cognitive, and affective symptoms. In panic disorder, panic attacks lead to persistent concern or anxiety about possible recurrence and resulting changes in behavior, such as agoraphobia, hypochondriacal concerns, and high medical utilization. Somatic features Somatic symptoms of panic disorder often predominate in patients clinical presentations. In a study of 55 primary care patients with panic disorder, presenting complaints included the following [55]: Cardiac 39 percent (chest pain in 22 percent, tachycardia in 25 percent) Neurologic 44 percent (headaches in 20 percent, dizziness in 18 percent, faintness and pseudoseizures in 9 percent) Gastrointestinal - 33 percent (epigastric pain in 15 percent) Among patients with a presenting symptom of chest pain, panic disorder is a common diagnosis, but the relationship between the disorder and general medical illnesses can be complex. A review of 38 studies found panic disorder to be present in 30 percent of patients presenting with chest pain and minimal or no coronary disease. However, panic disorder can also coexist with coronary disease [56]. (See "Differential diagnosis of chest pain in adults", section on 'Psychogenic/psychosomatic causes of chest pain'.) Agoraphobia Patients with panic attacks can develop agoraphobia ie, anxiety about and avoidance of situations where help may not be available or where it may be difficult to leave the situation in the event of developing panic-like symptoms or other incapacitating or embarrassing symptoms [1]. With revision of the DSM from the fourth to fifth edition, agoraphobia is diagnosed independently of panic disorder. The epidemiology, clinical manifestations, course, and diagnosis of agoraphobia are discussed separately. (See "Agoraphobia in adults: Epidemiology, pathogenesis, clinical manifestations, course, and diagnosis".) Utilization of medical services With somatic symptoms often prominent in the presentation of a panic attack, most patients seek health care from a general medical rather than mental health clinician. In one study of 97 patients with panic disorder, 35 percent initially presented to their primary care clinician, 32 percent to a hospital emergency department, and only 26 percent to a mental health clinician [57]. Many patients who present to primary care physicians with unexplained medical symptoms meet diagnostic criteria for panic disorder. Patients with panic disorder are often unsatisfied with a negative general medical work-up and repeatedly seek care for continuing frightening symptoms. In one study, 40 of 57 patients (70 percent) saw an average of 10 clinicians before finally receiving a diagnosis of panic disorder [58]. Other studies have shown that patients with panic disorder have significantly higher utilization of medical services (eg, consultation rates, specialty clinician referrals, emergency department visits, hospital admissions, medication prescription, and laboratory tests) compared to age- and gender-matched controls; their extensive use of resources often precedes the diagnosis of panic disorder by as long as ten years [59]. These data are consistent with several analyses from the Epidemiological Catchment Area data, which found that respondents with panic disorder had the highest likelihood among those with psychiatric or substance use disorders of high utilization of medical services when compared with controls without psychiatric illness (8.2 for men and 5.2 for women) [60,61]. Utilization of primary care services among patients with panic disorder is roughly three times that of the typical patient receiving health care in the US [62].
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Substance use Panic disorder has been shown to have a relatively high prevalence among patients with bipolar disorder and alcohol abuse [63]. Patients may use alcohol or sedative hypnotics in desperation to control symptoms of panic disorder. These agents have a short-lived anxiolytic action, but are subsequently associated with rebound exacerbation of anxiety and panic attacks when blood levels decline. In addition, coexisting alcohol abuse with recurrent withdrawal can lead to a kindling effect on central controls of the sympathetic nervous system, resulting in more frequent and severe panic attacks [64]. (See "Bipolar disorder in adults: Epidemiology and pathogenesis" and "Alcohol use disorder: Epidemiology, pathogenesis, clinical manifestations, adverse consequences, and diagnosis".) Medical comorbidity Both community-based and clinic-based studies have shown that respondents with panic disorder may have a higher prevalence of other medical disorders compared to controls including: Asthma [39,40] Hypertension [65] Irritable bowel syndrome [66] Interstitial cystitis [67] Migraine headaches [68] The previously reported association between mitral valve prolapse and panic disorder [69] has been questioned because of inconsistent results and methodologic limitations in the supporting research, including flawed diagnostic criteria for mitral valve prolapse, which resulted in over-diagnosis of this condition [70]. (See "Mitral valve prolapse syndrome".) Mitral valve prolapse may be encountered in patients with panic disorder, but is unlikely to be the cause of the panic symptoms; in such instances, the panic disorder should be treated. (See "Pharmacotherapy for panic disorder" and "Psychotherapy for panic disorder".) Data suggest that a history of panic attacks is associated with an increased risk of mortality due to vascular causes [71]. In the observational Women's Health Initiative study, the occurrence of at least one full-blown panic attack over a six-month period was associated with an increased incidence of coronary heart disease over a five year follow-up period (hazard ratio [HR] 4.2, 95% CI 1.8-10) among 3400 postmenopausal women. All-cause mortality was also increased (HR 1.75) and there was a trend toward an increased risk for stroke. The risk for coronary heart disease was intermediate for women reporting limited symptom panic episodes. COURSE Panic disorder is a recurrent or chronic disease in the majority of cases. A review of 16 studies of panic disorder diagnosed with modern psychiatric criteria found that most patients had improvement in panic symptoms over a period of 15 to 60 months, but few experienced complete resolution of the disorder [72]. A large community-based study of panic disorder followed over a two-year course found that remission occurred in 64 percent of subjects with time to remission of 5.7 months [73]. However, remission had not occurred in one year in 43 percent of those with panic disorder. Panic attacks recurred in 21 percent of those who had achieved remission [73]. Predictors of remission in the community-based trial were female gender, absence of ongoing life stressors, low initial frequency of attacks, and sub-threshold panic [73]. Other studies have found comorbid major depression, agoraphobia, and personality disorders to predict a poorer outcome in patients with panic disorder [72]. Panic disorder reduces the quality of life and function in affected patients and their families. Decrements in familial, social, and vocational functioning occur to a degree comparable to that seen with major depression [74,75]. In one study, the number of disability days taken by patients with anxiety disorders was significantly greater than in those with diabetes, cardiac disease, or renal disease [76]. Both infrequent panic attacks and panic disorder are associated with higher medical utilization, in large part resulting from frightening physical symptoms such as chest pain, palpitations or dizziness, and increased functional impairment [60,61,74]. ASSESSMENT AND DIAGNOSIS 5 de 10 02/12/2013 05:06
History and physical examination A complete psychiatric examination, including a medical history and thorough physical and neurologic examination to rule out organic causes of symptoms, will lead to an accurate diagnosis of panic disorder in most cases. The history taking process should begin in an open-ended manner and be unhurried. Interviewing family members can provide valuable information about current symptoms and precipitating events. Information should be elicited about current life stress, separations, recent deaths, patient concerns and fears, interpersonal problems, recent substance abuse, and use of medications. The patient should be asked about avoidance patterns that have developed since the onset of panic attacks. Testing Limited laboratory testing, such as thyroid function tests, complete blood count, and a chemistry panel are sufficient in most uncomplicated cases. Other laboratory and radiological tests may be needed based on findings from the patients history and physical exam. An electrocardiogram (and, at times, ambulatory Holter monitoring) is required for anyone with significant cardiovascular symptoms. Diagnostic criteria DSM-5 criteria for panic attacks and panic disorder are described as follows [1]. Panic attack A panic attack is not a mental disorder. Panic attacks occur in the context of panic disorder, with any anxiety disorder, and with other mental disorders (eg, depressive disorders, posttraumatic stress disorder, substance use disorders) and some medical conditions. When the presence of a panic attack is identified in conjunction with a mental disorder other than panic disorder, it should be noted as a specifier (eg, "posttraumatic stress disorder with panic attacks"). DSM-5 diagnostic criteria for a panic attack are described below [1]. An abrupt surge* of intense fear or intense discomfort that reaches a peak within minutes, and during which time four or more of the following 13 symptoms occur: Palpitations, pounding heart, or accelerated heart rate Sweating Trembling or shaking Sensations of shortness of breath or smothering Feelings of choking Chest pain or discomfort Nausea or abdominal distress Feeling dizzy, unsteady, light-headed, or faint Chills or heat sensations Paresthesias (numbness or tingling sensations) Derealization (feelings of unreality) or depersonalization (being detached from oneself). Fear of losing control or "going crazy" Fear of dying * The abrupt surge can occur from a calm state or an anxious state. Note: Culture-specific symptoms (eg, tinnitus, neck soreness, headache, uncontrollable screaming or crying) may be seen. Such symptoms should not count as one of the four required symptoms. The diagnosis of agoraphobia is discussed separately. (See "Agoraphobia in adults: Epidemiology, pathogenesis, clinical manifestations, course, and diagnosis".) Panic disorder DSM-5 diagnostic criteria for panic disorder are described below [1]. A. Recurrent unexpected panic attacks (See 'Panic attack' above.) B. At least one of the attacks has been followed by a month or more of one or both of the following: 1. Persistent concern or worry about additional panic attacks or their consequences (eg, losing control, having a heart attack, "going crazy"). 2. A significant maladaptive change in behavior related to the attacks (eg, behaviors designed to avoid
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having panic attacks, such as avoidance of exercise or unfamiliar situations). C. The disturbance is not attributable to the physiological effects of a substance (eg, medication or illicit drug) or another medical condition (eg, hyperthyroidism, cardiopulmonary disorders). D. The disturbance is not better explained by another mental disorder. As examples, the panic attacks do not occur only in response to Feared social situations, as in social anxiety disorder Circumscribed phobic objects or situations, as in specific phobia; Obsessions, as in obsessive-compulsive disorder Reminders of traumatic events, as in posttraumatic stress disorder Separation from attachment figures, as in separation anxiety disorder Differential diagnosis The presentation of panic disorder can overlap with manifestations of other psychiatric disorders and mimic a number of general medical conditions. Somatic symptom disorder One of the most difficult psychiatric diagnoses to differentiate from panic disorder is somatic symptom disorder (formerly called somatization disorder in DSM-IV). Patients with both panic disorder and somatic symptom disorder present with multiple physical symptoms. Many patients with somatic symptom disorder also have comorbid panic attacks or disorder. In one study, for example, 32 of 78 women (41 percent) with somatic symptom disorder also met criteria for panic disorder [77]. (See "Somatization: Epidemiology, pathogenesis, clinical features, medical evaluation, and diagnosis".). Somatic symptom disorder occurs in patients with a high likelihood of developmental histories of physical, sexual, and emotional abuse, and emotional neglect. Patients with somatic symptom disorder also have a lifetime history of responding to stressors with multiple physical symptoms and high utilization of medical services. Patients experiencing somatic symptom disorder with a history of abuse and neglect may feel interpersonally powerless and as a result draw attention to their somatic symptoms. They may use these symptoms to avoid role responsibilities, avoid intimacy, to obtain disability coverage, or to obtain prescribed medications and use them to regulate emotions (eg, opiates and benzodiazepines) [78]. Identifying patients with concurrent somatic symptom disorder requires questions regarding the existence of chronic somatization symptoms since adolescence, family history of females with somatic symptom disorder, family history of males with antisocial personality disorder or substance abuse problems, chaotic family histories, childhood sexual or physical abuse or emotional neglect, abuse of prescription drugs, poor stress resilience and coping, and abuse of street drugs, or alcohol. Illness anxiety disorder Illness anxiety disorder is defined in DSM-5 as individuals with high health anxiety without somatic symptoms unless their health anxiety is better explained by a primary anxiety disorder such as panic disorder. Many patients with panic disorder develop anxiety and fears of having a serious medical illness such as HIV or cancer but can be differentiated from patients with illness anxiety by also having multiple somatic symptoms such as tachycardia, chest pain and shortness of breath. Treatment of panic disorder in patients with milder forms of somatization frequently leads to remission of both physical symptoms and the tendency to have illness anxiety. In contrast, treatment of panic disorder in those with somatic symptom disorder may only lead to a 30 to 40 percent reduction in somatic symptoms because of the development of chronic social stressors and maladaptive patterns of coping with stress. Other mental disorders To meet criteria for panic disorder, symptoms of panic attacks must be distinguished from panic-like symptoms that occur as part of other mental disorders. At least some of the panic attacks should be spontaneous and should not be limited to a specific situation, such as heights as in acrophobia, or to other specific circumstances as described in Criterion D above. (See 'Panic disorder' above.) Stimulant abuse Overuse of caffeine as well as abuse of stimulant drugs such as cocaine and amphetamines can precipitate panic attacks. (See "Benefits and risks of caffeine and caffeinated beverages", section on 'Psychiatric' and "Cocaine use disorder in adults: Epidemiology, pharmacology, clinical manifestations,
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medical consequences, and diagnosis" and "Prescription drug abuse and addiction: Clinical features, epidemiology, and contributing factors", section on 'Types of drugs abused'.) General medical conditions The possibility of organic etiologies should be considered prior to making the diagnosis of panic disorder. A number of conditions can mimic symptoms of panic attacks including: Angina (See "Differential diagnosis of chest pain in adults", section on 'Cardiovascular causes of chest pain'.) Arrhythmias (See "Differential diagnosis of chest pain in adults", section on 'Cardiovascular causes of chest pain'.) Chronic obstructive pulmonary disease (See "Approach to the adult with interstitial lung disease: Diagnostic testing".) Temporal lobe epilepsy (See "Localization-related (partial) epilepsy: Causes and clinical features".) Pulmonary embolus (See "Diagnosis of acute pulmonary embolism".) Asthma (See "Diagnosis of asthma in adolescents and adults".) Hyperthyroidism (See "Diagnosis of hyperthyroidism".) Pheochromocytoma (See "Clinical presentation and diagnosis of pheochromocytoma".) Treatment side effects, eg, hypoglycemia in patients with diabetes, toxic serum aminophylline concentrations in patients with asthma. (See "Hypoglycemia in adults without diabetes mellitus: Diagnostic approach" and "Theophylline use in asthma".) INFORMATION FOR PATIENTS UpToDate offers two types of patient education materials, The Basics and Beyond the Basics. The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon. Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on patient info and the keyword(s) of interest.) Basics topics (see "Patient information: Panic disorder (The Basics)") SUMMARY AND RECOMMENDATIONS Panic attacks are characterized by an abrupt surge of intense fear or intense discomfort that reaches a peak within minutes, and the abrupt development of specific somatic, cognitive, and affective symptoms. In panic disorder, panic attacks lead to persistent concern or anxiety about possible recurrence and/or resulting changes in behavior, such as agoraphobia, hypochondriacal concerns, and high medical utilization. (See 'Clinical manifestations' above and "Agoraphobia in adults: Epidemiology, pathogenesis, clinical manifestations, course, and diagnosis", section on 'Clinical manifestations'.) The biological basis of panic disorder is not yet known, but functional imaging and other translational studies strongly suggest the involvement of fear circuitry (including the amygdala) in its pathogenesis. (See 'Pathogenesis' above.) Somatic symptoms of panic disorder often predominate in patients clinical presentations. Cardiac symptoms, (eg, chest pain and tachycardia) are common, as are neurologic (eg, headaches and dizziness) and gastrointestinal (eg, epigastric pain) symptoms. (See 'Somatic features' above.)
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Patients with panic attacks can develop agoraphobia ie, anxiety about and avoidance of situations where help may not be available or where it may be difficult to leave the situation in the event of developing panic-like symptoms or other incapacitating or embarrassing symptoms [1]. With revision of the DSM from the fourth to fifth edition, agoraphobia is diagnosed independently of panic disorder. Agoraphobia and its co-occurrence with panic disorder are discussed separately. (See "Agoraphobia in adults: Epidemiology, pathogenesis, clinical manifestations, course, and diagnosis".) Panic disorder is a recurrent or chronic disease in the majority of cases. Predictors of remission include female gender, absence of ongoing life stressors, low initial frequency of attacks, and sub-threshold panic. (See 'Course' above.) Prior to making a diagnosis of panic disorder, organic etiologies for symptoms of panic should be considered. Medical conditions that can mimic panic attacks include angina, arrhythmias, asthma, chronic obstructive pulmonary disease, pulmonary embolus, thyroid disease and, very rarely, temporal lobe epilepsy or pheochromocytoma. Substances that may trigger or worsen panic disorder include excessive caffeine use or the use of other stimulants, including certain drugs of abuse. (See 'Differential diagnosis' above.) Use of UpToDate is subject to the Subscription and License Agreement. Topic 14628 Version 11.0
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GRAPHICS Neural circuitry of panic attacks
Original figure modified for this publication. Roy-Byrne, P, Craske, MG, Stein, MB. Panic disorder. Lancet 2006; 368:1023. Illustration used with the permission of Elsevier Inc. All rights reserved.
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Official reprint from UpToDate www.uptodate.com 2013 UpToDate