COGNITIVE DISORDERS

OVERVIEW:-

The term cognition refers to the broad range of mental abilities that enable us to know about
the world around abilities that enable us to know about the world around us. These
abilities include memory, language, attention, us. These abilities include memory, language,
attention, perception, and reasoning. perception, and reasoning.

Cognition is the ability of your brain to think, to process and store information, to solve
problems. Cognition is and store information, to solve problems. Cognition is a high level
of behaviour unique to humans. This high level of behaviour unique to humans. This
behaviour is disrupted by an illness.

Cognitive disorders are necessarily brain disorders, and these are increasingly common after
middle age. These are increasingly common after middle age. Perhaps the most important of
these illnesses is Perhaps the most important of these illnesses is Alzheimer's disease, one
cause of severe cognitive loss Alzheimer's disease, one cause of severe cognitive loss
(dementia) in old age (dementia) in old age.

ORGANIC MENTAL DISORDER

Organic mental disorder is a psychological or behavioral abnormality associated with
transient or permanent dysfunction of brain.
Types of organic brain disorder-

 Acute organic psychosis

 Chronic organic psychosis

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1) Acute organic psychosis- It is caused by variety of condition such as drug intoxication,
nutritional deficiencies, mild head injury.
2) Chronic organic psychosis- In this permanent brain tissue destruction as a result of brain
injury, degenerative disease of CNS e.g. senile dementia

DEFINITION :-
Cognitive disorders (CDs), also known as neurocognitive disorders (NCDs), are a
category of mental health disorders that primarily affect cognitive abilities including learning,
memory, perception, and problem solving. Neurocognitive disorders include delirium and
mild and major neurocognitive disorder (previously known as dementia). They are defined by
deficits in cognitive ability that are acquired (as opposed to developmental), typically
represent decline, and may have an underlying brain pathology. The DSM-5 defines six key
domains of cognitive function: executive function, learning and memory, perceptual-motor
function, language, complex attention, and social cognition.
According to DSM:- ‘A pattern of organic psychological and behaviour symptoms
associated with permanent or transient brain dysfunction but without reference to etiology’.

CAUSES:

 Vascular disease- cerebral arteriosclerosis, intracranial hemorrhage, circulatory

collapse

 Infection- encephlitis, meningitis,

 Neoplastic causes- space occupying lesion such as gliomas , meningiomas, abscess

 Degenerative causes- senile or presenile dementia such as Alzheimer’s disease

 Intoxication- chronic intoxication & withdrawal effect of sedatives, anticonvulsants

drugs.

 Congenital causes – epilepsy, post ictal state

 Traumatic causes- subdural, epidural hematoma, contusion

 Intraventricular- normal pressure hydrocephalus

 Vitamin- deficiency of thiamine, niacin & B12

 Endocrine & metabolic disorder- diabetic coma, shock, uremia, hyperthyroidism,

hepatic failure acidosis& alklosis.

 Metal- heavy metal ( lead , mercury , magnese),Carbon monoxide, toxins

 Anoxia- sec. to respiratory syndrome, anemia

CLASSIFICATION ACCORDING TO ICD 10

F00-F09
Organic, including symptomatic, mental disorders

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F00 Dementia in Alzheimer's disease
F00.0Dementia in Alzheimer's disease with early onset
F00.1Dementia in Alzheimer's disease with late onset
F00.2Dementia in Alzheimer's disease, atypical or mixed type
F00.9Dementia in Alzheimer's disease, unspecified

F01Vascular dementia
F01.0Vascular dementia of acute onset
F01.1Multi-infarct dementia
F01.2Subcortical vascular dementia
F01.3Mixed cortical and subcortical vascular dementia
F01.8Other vascular dementia
F01.9Vascular dementia, unspecified

F02Dementia in other diseases classified elsewhere

F02.0Dementia in Pick's disease
F02.1Dementia in Creutzfeldt-Jakob disease
F02.2Dementia in Huntington's disease
F02.3Dementia in Parkinson's disease
F02.4Dementia in human immunodeficiency virus [HIV] disease
F02.8Dementia in other specified diseases classified elsewhere

F03Unspecified dementia
A fifth character may be added to specify dementia in F00-F03, as follows:
.x0 Without additional symptoms
.x1 Other symptoms, predominantly delusional
.x2 Other symptoms, predominantly hallucinatory
.x3 Other symptoms, predominantly depressive
.x4 Other mixed symptoms

F04Organic amnesic syndrome, not induced by alcohol and other substances

F05Delirium, not induced by alcohol and other psychoactive substances
F05.0Delirium, not superimposed on dementia, so described

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F05.1Delirium, superimposed on dementia
F05.8Other delirium
F05.9Delirium, unspecified
F06Other mental disorders due to brain damage and dysfunction and to physical
disease
F06.0Organic hallucinosis
F06.1Organic catatonic disorder
F06.2Organic delusional [schizophrenia-like] disorder
F06.3Organic mood [affective] disorders
.30 Organic manic disorder
.31 Organic bipolar affective disorder
.32 Organic depressive disorder
.33 Organic mixed affective disorder
F06.4Organic anxiety disorder
F06.5Organic dissociative disorder
F06.6Organic emotionally labile [asthenic] disorder
F06.7Mild cognitive disorder
F06.8Other specified mental disorders due to brain damage and dysfunction and to physical
disease
F06.9Unspecified mental disorder due to brain damage and dysfunction and to physical
disease

F07Personality and behavioral disorder due to brain disease, damage and dysfunction
F07.0Organic personality disorder
F07.1Postencephalitic syndrome
F07.2Postconcussional syndrome
F07.8Other organic personality and behavioral disorder due to brain disease, damage and
dysfunction

F09Unspecified organic or symptomatic mental disorder

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 DEMENTIA

(Chronic Brain Syndrome)

INTRODUCTION

The word ‘dementia’ is derived from two latin words ‘de’means ‘apart’or ‘away’ and
‘mens’or ‘mentis’ means ‘mind’. In Latin ‘dementia’ means ‘irrationality’.

Dementia is classified under organic brain disorders. The term ‘organic’means that the
syndrome can be attributed to cerebral or systemic disease or disorder. Organic mental
disorder(organic brain syndrome or OBS)is a psychological or behavioural abnormality
associated with transient or permanent dysfunction of brain disorders

It may be acute or chronic.

 Acute e.g. Delirium

 Chronic e.g Dementia

Dementia is not a disease by itself, but rather a group of symptoms that are caused by various
disease conditions. If it is severe, it will interfere with a person’s daily functioning. It is a late
life disease ,as it tends to develop mostly in elderly people.

DEFINITION:

Acc.to Wikipedia Encyclopedia;

‘The progressive decline in cognitive functions (particularly affected areas like thinking,
reasoning, memory, attention, language, and problem solving) due to damage or disease in
the brain beyond, what might be expected from normal aging’.

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Acc.to ICD-10;

A chronic progressive disease of the brain affecting cortical functions in multiple ways and
resulting into disturbances or decline in intellectual functioning. For e.g., memory, thinking,
orientation, comprehension, learning capacity, calculation, language and judgement but not
affecting consciousness commonly associated with deterioration in emotional control and
social behaviour.

INCIDENCE AND PREVALENCE:

 Dementia occur more commonly in elderly than in middle aged.

 In western countries and Australia(1.03% of total population)are commonly affected.

 The prevalence of dementia is rising as the global life expectancy is rising.5-8% of

all people over the age of 65 have one or other form of dementia and this no. doubles
every five years above that age

 It is a disease which is strongly associated with age(1% of 60-65 yrs.of age;2% of 65-
69 yrs.of age;6% of 75-79 yrs.of age;20% of 85-89 yrs. Of age;45% of 95 yrs.of age
and older suffer with the disease).

CAUSES:

 Degenerative diseases like Alzheimer’s disease.

 Vascular causes,e.g.Multiple infarct dementia,Binswanger’s stroke ,hypertensive

encephalopathy,arteriosclerosis

 Toxic reactions,e.g.alcohol induced persisting dementia or drug abuse induced.

 Fronto-Temporal lobar degeneration ,e.g.Pick’s disease(degenerative disorder).

 Fronto-Temporal dementia.

 Semantic dementia.

 Progressive non fluent aphasia.

 General paresis

 Senile dementia

Consequences of ;

 Huntington’s disease(degenerative disease)

 Parkinson’s disease

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  HIV infection (AIDS dementia complex)

 Head trauma –dementia,subdural ,epidural hematoma, contusion

 Down syndrome may develop Alzheimer’s type

 Infections that affect brain and spinal cord-meningitis, carbon monoxide)

 Anoxia,e.g.secondary to respiratory syndrome,anaemia.

POTENTIALLY TREATABLE CAUSES;

 Endocrinal disorder,e.g. hypothyroidism, myxoedema,Addison’s disease.

 Vitamin deficiencies (B1,B12)and Vit-A deficiencies.

 Illnesses other than in the brain ,e.g complications of kidney, liver, lung diseases.

 Depression –depressive pseudo dementia, hysteria, catatonia.

 Normal pressure hydrocephalous.

 Brain tumours.

 Syphilis.

 Hypoglycemia.

 Neoplastic lesions –space occupying lesions,abscesses.

 Post anaesthesia.

 Chronic respiratory failure.

ETIOLOGICAL IMPLICATIONS AS PER DSM IV:

The disorders of dementia are differentiated by their etiology, although they share a common
symptom presentation. Categories of dementia include the following:

● Dementia of the Alzheimer’s type

● Vascular dementia

● Dementia due to HIV disease

● Dementia due to head trauma

● Dementia due to Lewy body disease

● Dementia due to Parkinson’s disease

● Dementia due to Huntington’s disease

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● Dementia due to Pick’s disease

● Dementia due to Creutzfeldt-Jakob disease

● Dementia due to other general medical conditions

● Substance-induced persisting dementia

● Dementia due to multiple etiologies

Dementia of the Alzheimer’s Type- This disorder is characterized by the syndrome of

symptoms identified as dementia in the DSM-IV-TR and in the seven stages described
previously. The onset of symptoms is slow and insidious, and the course of the disorder is
generally progressive and deteriorating. The DSM-IV-TR further categorizes this disorderas
early onset (fi rst symptoms occurring at age 65 or younger) or late onset (fi rst symptoms
occurring after age 65) and by the clinical presentation of behavioral disturbance (such as
wandering or agitation) superimposed on the dementia. Refi nement of diagnostic criteria
now enables clinicians to use specifi c clinical features to identify the disease with
considerable accuracy. Examination by computerized tomography (CT) scan or magnetic
resonance imaging (MRI) reveals a degenerative pathology of the brain that includes atrophy,
widened cortical sulci, and enlarged cerebral ventricles (Figs. 12–1 and 12–2). Microscopic
examinations reveal numerous neurofi brillary tangles and senile plaques in the brains of
clients with Alzheimer’s disease. These changes apparently occur as a part of the normal
aging process. However, in clients with DAT, they are found in dramatically increased
numbers, and their profusion is concentrated in the hippocampus and certain parts of the
cerebral cortex.

Etiology

The exact cause of Alzheimer’s disease is unknown. Several hypotheses have been supported
by varying amounts and quality of data. These hypotheses include the following:

1. Acetylcholine alterations: Research has indicated that in the brains of AD clients,

the enzyme required to produce acetylcholine is dramatically reduced. The reduction
seems to be greatest in the nucleus basalis of the inferior medial forebrain area
(Cummings & Mega, 2003). This decrease in production of acetylcholine reduces the
amount of the neurotransmitter that is released to cells in the cortex and hippocampus,
resulting in a disruption of the cognitive processes. Other neurotransmitters
implicated in the pathology and clinical symptoms of AD include norepinephrine,
serotonin, dopamine, and the amino acid glutamate. It has been proposed that in
dementia, excess glutamate leads to overstimulation of the N-methyl-d-aspartate
(NMDA) receptors, leading to increased intracellular calcium and subsequent
neuronal degeneration and cell death.
2. Plaques and tangles: As mentioned previously, an overabundance of structures
called plaques and tangles appear in the brains of individuals with AD. The plaques
are made of a protein called amyloid beta (A ), a fragment of a larger protein called
amyloid precursor protein (APP) (NIA, 2008). Plaques are formed when these
fragments clump together and mix with molecules and other cellular matter. Tangles
are formed from a special kind of cellular protein called tau protein, whose function it

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 is to provide stability to the neuron. In AD, the tau protein is chemically altered (NIA,
2008). Strands of the protein become tangled together, interfering with the neuronal
transport system. It is not known whether the plaques and tangles cause AD or are a
consequence of the AD process. It is thought that the plaques and tangles contribute to
the destruction and death of neurons, leading to memory failure, personality changes,
inability to carry out ADLs, and other features of the disease.
3. Head trauma: The etiology of AD has been associated with serious head trauma
(Tesco et al, 2007). Studies have shown that some individuals who had experienced
head trauma had subsequently (after years) developed AD. This hypothesis is being
investigated as a possible cause. Munoz and Feldman (2000) report an increased risk
for AD in individuals who are both genetically predisposed and who experience
traumatic head injury.
4. Genetic factors:
There is clearly a familial pattern with some forms of Alzheimer’s disease.
Some families exhibit a pattern of inheritance that suggests possible
autosomal-dominant gene transmission (Sadock & Sadock, 2007).

Some studies indicate that early-onset cases are more likely to be familial than
late-onset cases and that from one third to one half of all cases may be of the
genetic form. Some research indicates that there is a link between early-onset
Alzheimer’s disease and gene mutations found on chromosomes 21, 14, and 1
(Alzheimer’s Disease Education & Referral [ADEAR], 2008).

Mutations on chromosome 21 cause the formation of abnormal APP.

Mutations on chromosome 14 cause abnormal presenilin 1 (PS-1) to be made,
and mutations on chromosome 1 leads to the formation of abnormal presenilin
2 (PS-2). Each of these mutations results in an increased amount of the A
protein that is a major component of the plaques associated with AD.

Individuals with Down syndrome (who carry an extra copy of chromosome

21) have been found to be unusually susceptible to AD (Blazer, 2008). Two
genetic variants have been identifi ed as risk factors for late-onset AD. The
apolipoprotein E epsilon 4 (ApoE 4) gene, found on chromosome 19, was
identified in 1993. Its exact role in the development of AD is not yet clear
(ADEAR, 2008).

A second genetic variant, the SORL1 gene, was identifi ed in 2007 (Rogaeva
et al, 2007). The researchers believe that the altered gene function results in
increasing production of the toxic A protein and subsequently the plaques
associated with AD.

Vascular Dementia

In this disorder, the clinical syndrome of dementia is due to significant

cerebrovascular disease. The blood vessels of the brain are affected, and progressive
intellectual deterioration occurs. Vascular dementia is the second most common form
of dementia, ranking after Alzheimer’s disease (Bourgeois et al, 2008).
Vascular dementia differs from Alzheimer’s disease in that it has a more abrupt onset
and runs a highly variable course. Progression of the symptoms occurs in “steps”

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 rather than as a gradual deterioration; that is, at times the dementia seems to clear up
and the individual exhibits fairly lucid thinking.
Memory may seem better, and the client may become optimistic that improvement is
occurring, only to experience further decline of functioning in a fluctuating pattern of
progression. This irregular pattern of decline appears to be an intense source of
anxiety for the client with this disorder.
In vascular dementia, clients suffer the equivalent of small strokes that destroy many
areas of the brain. The pattern of deficits is variable, depending on which regions of
the brain have been affected (APA, 2000). Certain focal neurological signs are
commonly seen with vascular dementia, including weaknesses of the limbs, small-
stepped gait, and diffi culty with speech.
The disorder is more common in men than in women (APA, 2000). Arvanitakis
(2000) states: Prognosis for patients with vascular dementia is worse than that for
Alzheimer’s patients. The three-year mortality rate in cases over the age of 85 years
old is quoted at 67 percent as compared to 42 percent in Alzheimer’s disease, and 23
percent in non-demented individuals. However, outcome is ultimately dependent on
the underlying risk factors and mechanism of disease, and further studies taking these
distinctions into account are warranted. The diagnosis can be subtyped when the
dementia is superimposed with symptoms of delirium, delusions, or depressed mood.

Etiology

 The cause of vascular dementia is directly related to an interruption of blood flow to

the brain.
 Symptoms result from death of nerve cells in regions nourished by diseased vessels.
Various diseases and conditions that interfere with blood circulation have been
implicated.
 High blood pressure is thought to be one of the most significant factors in the etiology
of multiple small strokes or cerebral infarcts.
 Hypertension leads to damage to the lining of blood vessels. This can result in rupture
of the blood vessel, with subsequent haemorrhage , or an accumulation of fibrin in the
vessel, with intravascular clotting and inhibited blood flow (De Martinis, 2005).
 Dementia also can result from infarcts related to occlusion of blood vessels by
particulate matter that travels through the bloodstream to the brain. These emboli may
be solid (e.g., clots, cellular debris, platelet aggregates), gaseous (e.g., air, nitrogen),
or liquid (e.g., fat, following soft tissue trauma or fracture of long bones). Cognitive
impairment can occur with multiple small infarcts (sometimes called “silent strokes”)
over time or with a single cerebrovascular insult that occurs in a strategic area of the
brain.
 An individual may have both vascular dementia and AD simultaneously. This is
referred to as mixed dementia, the prevalence of which is likely to increase as the
population ages (Langa, Foster, & Larson, 2004).

Dementia Due to HIV

Infection with the HIV-1 produces a dementing illness called HIV-1-associated

cognitive/motor complex. A less severe form, known as HIV-1-associated minor cognitive/
motor disorder, also occurs. The severity of symptoms is correlated to the extent of brain

10
pathology. The immune dysfunction associated with HIV disease can lead to brain infections
by other organisms, and the HIV-1 also appears to cause dementia directly. In the early
stages, neuropsychiatric symptoms may be manifested by barely perceptible changes in a
person’s normal psychological presentation. Severe cognitive changes, particularly
confusion, changes in behavior, and sometimes psychoses, are not uncommon in the later
stages. With the advent of the highly active antiretroviral therapies (HAART), incidence rates
of dementia associated with HIV disease have been on the decline. However, it is possible
that the prolonged life span of HIV-infected patients taking medications may actually
increase the numbers of individuals living with HIV associated dementia.

Dementia Due to Head Trauma

Serious head trauma can result in symptoms associated with the syndrome of dementia.
Amnesia is the most common neurobehavioral symptom following head trauma, and a degree
of permanent disturbance may persist (Bourgeois et al, 2008). Repeated head trauma, such as
the type experienced by boxers, can result in dementia pugilistica, a syndrome characterized
by emotional lability, dysarthria, ataxia, and impulsivity (Sadock & Sadock, 2007).

Dementia Due to Lewy Body Disease

Clinically, Lewy body disease is fairly similar to AD; however, it tends to progress more
rapidly, and there is an earlier appearance of visual hallucinations and parkinsonian features
(Rabins, 2006). This disorder is distinctive by the presence of Lewy bodies— eosinophilic
inclusion bodies—seen in the cerebral cortex and brainstem (Andreasen & Black, 2006).
These patients are highly sensitive to extrapyramidal effects of antipsychotic medications.
The disease is progressive and irreversible and may account for as many as 25 percent of all
dementia cases.

Dementia Due to Parkinson’s Disease

Dementia is observed in as many as 60 percent of clients with Parkinson’s disease (Bourgeois

et al, 2008). In this disease, there is a loss of nerve cells located in the substantia nigra, and
dopamine activity is diminished, resulting in involuntary muscle movements, slowness, and
rigidity. Tremor in the upper extremities is characteristic. In some instances, the cerebral
changes that occur in dementia of Parkinson’s disease closely resemble those of AD.

Dementia Due to Huntington’s Disease

Huntington’s disease is transmitted as a Mendelian dominant gene. Damage is seen in the

areas of the basal ganglia and the cerebral cortex. The onset of symptoms (i.e., involuntary
twitching of the limbs or facial muscles, mild cognitive changes, depression and apathy)
usually occurs between age 30 and 50 years. The client usually declines into a profound state
of dementia and ataxia. The average duration of the disease is based on age at onset. One
study concluded that juvenile-onset and late-onset clients have the shortest duration (Foroud
et al, 1999). In this study, the median duration of the disease was 21.4 years.

Dementia Due to Pick’s Disease

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The cause of Pick’s disease is unknown, but a genetic factor appears to be involved. The
clinical picture is strikingly similar to that of AD. One major difference is that the initial
symptom in Pick’s disease is usually personality change, whereas the initial symptom in AD
is memory impairment. Studies reveal that pathology of Pick’s disease results from atrophy in
the frontal and temporal lobes of the brain, in contrast to AD, which is more widely
distributed.

Dementia Due to Creutzfeldt-Jakob Disease

Creutzfeldt-Jakob disease is an uncommon neurodegenerative disease caused by a

transmissible agent known as a “slow virus” or prion (APA, 2000). Five to 15 percent of
cases have a genetic component. The clinical presentation is typical of the syndrome of
dementia, along with involuntary movements, muscle rigidity, and ataxia. Symptoms may
develop at any age in adults, but typically occur between ages 40 and 60 years. The clinical
course is extremely rapid, with the progression from diagnosis to death in less than 2 years
(Rentz, 2008).

Dementia Due to Other General Medical Conditions

A number of other general medical conditions can cause dementia. Some of these include
endocrine conditions (e.g., hypoglycemia, hypothyroidism), pulmonary disease, hepatic or
renal failure, cardiopulmonary insufficiency, fl uid and electrolyte imbalances, nutritional
deficiencies, frontal or temporal lobe lesions, central nervous system (CNS) or systemic
infections, uncontrolled epilepsy, and other neurological conditions such as multiple sclerosis
(APA, 2000).

Substance-Induced Persisting Dementia

The features associated with this type of dementia are those associated with dementias in
general; however, evidence must exist from the history, physical examination, or laboratory fi
ndings to show that the deficits are etiologically related to the persisting effects of substance
use (APA, 2000). The term persisting is used to indicate that the dementia persists long after
the effects of substance intoxication or substance withdrawal have subsided. The DSM-IV-TR
identifi es the following types of substances with which persisting dementia is associated:

1. Alcohol

2. Inhalants

3. Sedatives, hypnotics, and anxiolytics

4. Medications

a. Anticonvulsants

b. Intrathecal methotrexate

5. Toxins

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 a. Lead

b. Mercury

c. Carbon monoxide

d. Organophosphate insecticides

e. Industrial solvents

The diagnosis is made according to the specific etiological substance involved. For example,
if the substance known to cause the dementia is alcohol, the diagnosis is Alcohol-Induced
Persisting Dementia. If the exact substance presumed to be causing the dementia is unknown,
the diagnosis would be Unknown Substance-Induced Persisting Dementia.

Dementia Due to Multiple Etiologies

This diagnosis is used when the symptoms of dementia are attributed to more than one cause.
For example, the dementia may be related to more than one medical condition or to the
combined effects of a general medical condition and the long-term use of a substance (APA
2000).

SIGN AND SYMPTOMS-

Stage 1. No apparent symptoms: In the first stage of the illness, there is no apparent decline
in memory.

Stage 2. Forgetfulness: The individual begins to lose things or forget names of people.
Losses in short term memory are common. The individual is aware of the intellectual decline
and may feel ashamed, becoming anxious and depressed, which in turn may worsen the
symptoms. Maintaining organization with lists and a structured routine provide some
compensation. These symptoms often are not observed by others.

Stage 3. Mild cognitive decline: In this stage, there is interference with work performance,
which becomes noticeable to coworkers. The individual may get lost when driving his or her
car. Concentration may be interrupted. There is difficulty recalling names or words, which
becomes noticeable to family and close associates. A decline occurs in the ability to plan or
organize.

Stage 4. Mild-to-moderate cognitive decline; confusion: At this stage, the individual may
forget major events in personal history, such as his or her own child’s birthday; experience
declining ability to perform tasks, such as shopping and managing personal finances; or be
unable to understand current news events. He or she may deny that a problem exists by
covering up memory loss with confabulation (creating imaginary events to fi ll in memory
gaps). Depression and social withdrawal are common.

Stage 5. Moderate cognitive decline; early dementia: In the early stages of dementia, the
individual loses the ability to perform some activities of daily living (ADLs) independently,

13
such as hygiene, dressing, and grooming, and requires some assistance to manage these on an
ongoing basis. They may forget addresses, phone numbers, and names of close relatives.
They may become disoriented about place and time, but they maintain knowledge about
themselves. Frustration, withdrawal, and self-absorption are common.

Stage 6. Moderate-to-severe cognitive decline; middle dementia: At this stage, the

individual may be unable to recall recent major life events or even the name of his or her
spouse. Disorientation to surroundings is common, and the person may be unable to recall the
day, season, or year. The person is unable to manage ADLs without assistance. Urinary and
fecal incontinence are common. Sleeping becomes a problem. Psychomotor symptoms
include wandering, obsessiveness, agitation, and aggression. Symptoms seem to worsen in
the late afternoon and evening—a phenomenon termed sundowning. Communication
becomes more diffi cult, with increasing loss of language skills. Institutional care is usually
required at this stage.

Stage 7. Severe cognitive decline; late dementia: In the end stages of DAT, the individual
is unable to recognize family members. He or she most commonly is bedfast and aphasic.
Problems of immobility, such as decubiti and contractures, may occur. Stanley and associates
(2005) describe the late stages of dementia in the following manner: During late-stage
dementia, the person becomes more chairbound or bedbound. Muscles are rigid, contractures
may develop, and primitive reflexes may be present.

TYPES OF DEMENTIA

Based on etiology of disease:-

 Reversible dementia.

 Irreversible dementia.

PATHOPHYSIOLOGY

The pathophysiology varies depending on the basic cause of dementia.

(1)In Alzheimer’s Disease:

Causes

There are characteristic changes in the brain.

Marked reduction in the population of neurons particularly in the hippocampus,substantia

innominata , locus cerulus , and temporoparietal and frontal cortex

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 ↓

Appearance of neurofibrillary tangles made of paired helical filaments

Neurotic plaques, which consist largely of amyloid and show a definite progression in their
development

Development of granulovacuolar bodies.

Neurochemical changes (reduction in enzyme choline acetyltransferase,in acetyl itself,and in

other neurotransmitters and neuromodulators.

Development of clinical features.

2.In Vascular Dementia:- Infarction of the brain due to vascular diseases , including
hypertensive cerebrovascular disease.

3.In Pick’s disease:- The neuropathological picture is suggestive of the frontal and temporal
lobes ,but without the occurrence of neuritic plaques and neuro fibrilliary tangles in excess of
that seen in normal aging.

4.In Huntington’s disease: There is a wide spread degeneration of the brain.

5.In Parkinson’s disease: There is a manifestation of a occurence of either Alzheimer’s or

vascular dementia.

CLINICAL MANIFESTATIONS:

 Affected persons may be disoriented in time,in place and in person.

15
 Forgetfulness with effects at work ;they may forget names or appointments as
memory function is declined.

 Difficulties with familiar activities ,e.g.absent mindedness like keeping vessel on the
stove and forgetting.

 Language difficulties,e.g.difficulty in finding right words,inappropriate filling –up of

words,which others cannot be able to understand it.(aphasia).

 Problem with spatial and temporary orientation ,e.g.forgets the day of the week or
they may lost in unfamiliar surroundings.

 Impaired capacity of judgement,i.e.people with dementia can not be able to judge the
things by themselves like wearing inappropriate clothes based on seasonwise.

 Problems related to abstract thinking ,e.g. the client’s cannot be able to do simple
calculations.

 Leaving things behind ,e.g. client’s will forget where they left their belongings like
purse ,umbrella .

 Client’s may have sudden mood swing ,depressed.

 Pronounced personality changes suddenly or over a longer period of time,e.g. a

person who is friendly in nature , with dementia suddenly becomes aggressive without
any reason, mentally fatigue.

 Looses interest in their work and hobbies , manifests lack of interest or zeal in
cultivation of new activities.

 Possesses stereotyped behaviour.

 Neurological syndrome:drowsiness,confusion, ataxia.

 Catastrophic reactions ,e.g.agitation.

 Impairment in thinking and reasoning capacity, reduction in flow of

ideas.(Alzheimer’s type)

 Not able to attend more than one stimuli at a time.

 Usable to follow social norm.

 Isolation , withdrawal.

 Inappropriate,indecent behaviour ,e.g. lack of interest in hygiene.

 Lack of emotional control.

 Development of functional reactions , e.g. anxiety ,depression,paranoid delusions.

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DIAGNOSTIC CRITERIA AS PER ICD-10:

F00 Dementia in Alzheimer's disease

 Alzheimer's disease is a primary degenerative cerebral disease of unknown etiology,

with characteristic neuropathological and neurochemical features. It is usually
insidious in onset and develops slowly but steadily over a period of years. This period
can be as short as 2 or 3 years, but can occasionally be considerably longer.
 The onset can be in middle adult life or even earlier (Alzheimer's disease with early
onset), but the incidence is higher in later life (Alzheimer's disease with late onset).
 In cases with onset before the age of 65-70, there is the likelihood of a family history
of a similar dementia, a more rapid course, and prominence of features of temporal
and parietal lobe damage, including dysphasia or dyspraxia.
 In cases with a later onset, the course tends to be slower and to be characterized by
more general impairment of higher cortical functions. Patients with Down's syndrome
are at high risk of developing Alzheimer's disease.
There are characteristic changes in the brain:

 A marked reduction in the population of neurons, particularly in the hippocampus,

substantia innominata, locus ceruleus, and temporoparietal and frontal cortex;
appearance of neurofibrillary tangles made of paired helical filaments; neuritic
(argentophil) plaques, which consist largely of amyloid and show a definite
progression in their development (although plaques without amyloid are also known
to exist); and granulovacuolar bodies.
 Neurochemical changes have also been found, including a marked reduction in the
enzyme choline acetyltransferase, in acetylcholine itself, and in other
neurotransmitters and neuromodulators.
 As originally described, the clinical features are accompanied by the above brain
changes. However. it now appears that the two do not always progress in parallel: one
may be indisputably present with only minimal evidence of the other.
 Nevertheless, the clinical features of Alzheimer's disease are such that it is often
possible to make a presumptive diagnosis on clinical grounds alone. Dementia in
Alzheimer's disease is at present irreversible.

Diagnostic guidelines

The following features are essential for a definite diagnosis:

(a) Presence of a dementia as described above.

(b)Insidious onset with slow deterioration. While the onset usually seems difficult to pinpoint
in time, realization by others that the defects exist may come suddenly. An apparent plateau
may occur in the progression.

(c)Absence of clinical evidence, or findings from special investigations, to suggest that the
mental state may be due to other systemic or brain disease which can induce a dementia (e.g.

17
hypothyroidism, hypercalcaemia, vitamin B12 deficiency, niacin deficiency, neurosyphilis,
normal pressure hydrocephalus, or subdural haematoma).

(d)Absence of a sudden, apoplectic onset, or of neurological signs of focal damage such as

hemiparesis, sensory loss, visual field defects, and incoordination occurring early in the
illness (although these phenomena may be superimposedlater). In a certain proportion of
cases, the features of Alzheimer's disease and vascular dementia may both be present. In such
cases, double diagnosis (and coding) should be made. When the vascular dementia precedes
the Alzheimer's disease, it may be impossible to diagnose the latter on clinical grounds.

Includes: primary degenerative dementia of the Alzheimer's type

Differential diagnosis. Consider: a depressive disorder (F30-F39); delirium (F05.-); organic

amnesic syndrome (F04); other primary dementias, such as in Pick's, Creutzfeldt-Jakob or
Huntington's disease (F02.-); secondary dementias associated with a variety of physical
diseases, toxic states, etc. (F02.8); mild, moderate or severe mental retardation (F70-F72).
Dementia in Alzheimer's disease may coexist with vascular dementia (to be coded F00.2), as
when cerebrovascular episodes (multi-infarct phenomena) are superimposed on a clinical
picture and history suggesting Alzheimer's disease. Such episodes may result in sudden
exacerbations of the manifestations of dementia. According to postmortem findings, both
types may coexist in as many as 10-15% of all dementia cases.

F00.0 Dementia in Alzheimer's disease with early onset

Dementia in Alzheimer's disease beginning before the age of 65. There is relatively rapid
deterioration, with marked multiple disorders of the higher cortical functions. Aphasia,
agraphia, alexia, and apraxia occur relatively early in the course of the dementia in most
cases.

Diagnostic guidelines

As for dementia, described above, with onset before the age of 65 years, and usually with
rapid progression of symptoms. Family history of Alzheimer's disease is a contributory but
not necessary factor for the diagnosis, as is a family history of Down's syndrome or of
lymphoma.

Includes: Alzheimer's disease, type 2 presenile dementia, Alzheimer's type

F00.1 Dementia in Alzheimer's disease with late onset

Dementia in Alzheimer's disease where the clinically observable onset is after the age of 65
years and usually in the late 70s or thereafter, with a slow progression, and usually with
memory impairment as the principal feature.

Diagnostic guidelines

18
As for dementia, described above, with attention to the presence or absence of features
differentiating the disorder from the early-onset subtype (F00.0).

Includes: Alzheimer's disease, type 1 senile dementia, Alzheimer's type

F00.2 Dementia in Alzheimer's disease, atypical or mixed type

Dementias that do not fit the descriptions and guidelines for either F00.0 or F00.1 should be
classified here; mixed Alzheimer's and vascular dementias are also included here.

F00.9 Dementia in Alzheimer's disease, unspecified

F01 Vascular dementia

Vascular (formerly arteriosclerotic) dementia, which includes multi-infarct dementia, is

distinguished from dementia in Alzheimer's disease by its history of onset, clinical features,
and subsequent course. Typically, there is a history of transient ischaemic attacks with brief
impairment of consciousness, fleeting pareses, or visual loss. The dementia may also follow a
succession of acute cerebrovascular accidents or, less commonly, a single major stroke. Some
impairment of memory and thinking then becomes apparent. Onset, which is usually in later
life, can be abrupt, following one particular ischaemic episode, or there may be more gradual
emergence. The dementia is usually the result of infarction of the brain due to vascular
diseases, including hypertensive cerebrovascular disease. The infarcts are usually small but
cumulative in their effect.

Diagnostic guidelines

The diagnosis presupposes the presence of a dementia as described above. Impairment

of cognitive function is commonly uneven, so that there may be memory loss,
intellectual impairment, and focal neurological signs. Insight and judgement may be
relatively well preserved. An abrupt onset or a stepwise deterioration, as well as the
presence of focal neurological signs and symptoms, increases the probability of the
diagnosis; in some cases, confirmation can be provided only by computerized axial
tomography or, ultimately, neuropathological examination.
Associated features are: hypertension, carotid bruit, emotional lability with transient
depressive mood, weeping or explosive laughter, and transient episodes of clouded
consciousness or delirium, often provoked by further infarction. Personality is
believed to be relatively well preserved, but personality changes may be evident in a
proportion of cases with apathy, disinhibition, or accentuation of previous traits such
as egocentricity, paranoid attitudes, or irritability.

Includes: arteriosclerotic dementia

Differential diagnosis. Consider: delirium (F05.-); other dementia, particularly in Alzheimer's

disease (F00.-); mood [affective] disorders (F30-F39); mild or moderate mental retardation
(F70-F71); subdural haemorrhage (traumatic (S06.5), nontraumatic(162.0)). Vascular
dementia may coexist with dementia in Alzheimer's disease (to be coded F00.2), as when

19
evidence of a vascular episode is superimposed on a clinical picture and history suggesting
Alzheimer's disease.

F01.0 Vascular dementia of acute onset

Usually develops rapidly after a succession of strokes from cerebrovascular thrombosis,

embolism, or haemorrhage, In rare cases, a single large infarction may be the cause.

F01.1 Multi-infarct dementia

This is more gradual in onset than the acute form, following a number of minor ischaemic
episodes which produce an accumulation of infarcts in the cerebral parenchyma.

Includes: predominantly cortical dementia

F01.2 Subcortical vascular dementia

There may be a history of hypertension and foci of ischaemic destruction in the deep white
matter of the cerebral hemispheres, which can be suspected on clinical grounds and
demonstrated on computerized axial tomography scans. The cerebral cortex is usually
preserved and this contrasts with the clinical picture, which may closely resemble that of
dementia in Alzheimer's disease. (Where diffuse demyelination of white matter can be
demonstrated, the term "'Binswanger's encephalopathy" may be used.)

F01.3 Mixed cortical and subcortical vascular dementia

Mixed cortical and subcortical components of the vascular dementia may be suspected from
the clinical features, the results of investigations (including autopsy), or both.

F01.8 Other vascular dementia

F01.9 Vascular dementia, unspecified

F02Dementia in other diseases classified elsewhere :Cases of dementia due, or presumed

to be due, to causes other than Alzheimer's disease or cerebrovascular disease. Onset may be
at any time in life, though rarely in old age.

Diagnostic guidelines

Presence of a dementia as described above; presence of features characteristic of one of the

specified syndromes, as set out in the following categories.

F02.0 Dementia in Pick's disease

A progressive dementia, commencing in middle life (usually between 50 and 60 years),

characterized by slowly progressing changes of character and social deterioration, followed
by impairment of intellect, memory, and language functions, with apathy, euphoria, and
(occasionally) extrapyramidal phenomena. The neuropathological picture is one of selective
atrophy of the frontal and temporal lobes, but without the occurrence of neuritic plaques and
neurofibrillary tangles in excess of that seen in normal aging. Cases with early onset tend to
20
exhibit a more malignant course. The social and behavioural manifestations often precede
frank memory impairment.

Diagnostic guidelines

The following features are required for a definite diagnosis:

(a) A progressive dementia;

(b) A predominance of frontal lobe features with euphoria, emotional blunting, and
coarsening of social behaviour, disinhibition, and either apathy or restlessness;

(c) Behavioural manifestations, which commonly precede frank memory impairment. Frontal
lobe features are more marked than temporal and parietal, unlike Alzheimer's disease.

Differential diagnosis. Consider: dementia in Alzheimer's disease (F00); vascular dementia

(F01); dementia secondary to other disorders such as neurosyphilis (F02.8); normal pressure
hydrocephalus (characterized by extreme psychomotor slowing, and gait and sphincter
disturbances) (G91.2); other neurological or metabolic disorders.

F02.1 Dementia in Creutzfeldt-Jakob disease

A progressive dementia with extensive neurological signs, due to specific neuropathological

changes (subacute spongiform encephalopathy) that are presumed to be caused by a
transmissible agent. Onset is usually in middle or later life, typically in the fifth decade, but
may be at any adult age. The course is subacute, leading to death within 1-2 years.

Diagnostic guidelines

Creutzfeldt-Jakob disease should be suspected in all cases of a dementia that progresses fairly
rapidly over months to 1 or 2 years and that is accompanied or followed by multiple
neurological symptoms. In some cases, such as the so-called amyotrophic form, the
neurological signs may precede the onset of the dementia. There is usually a progressive
spastic paralysis of the limbs, accompanied by extrapyramidal signs with tremor, rigidity, and
choreoathetoid movements. Other variants may include ataxia, visual failure, or muscle
fibrillation and atrophy of the upper motor neuron type. The triad consisting of

- Rapidly progressing, devastating dementia,

- Pyramidal and extrapyramidal disease with myoclonus, and

- A characteristic (triphasic) electroencephalogramis thought to be highly suggestive of this

disease.

Differential diagnosis. Consider: Alzheimer's disease (F00.-) or Pick's disease (F02.0);

Parkinson's disease (F02.3); postencephalitic parkinsonism (G21.3). The rapid course and
early motor involvement should suggest Creutzfeldt-Jakob disease.

21
F02.2 Dementia in Huntington's disease

A dementia occurring as part of a widespread degeneration of the brain. Huntington's disease

is transmitted by a single autosomal dominant gene. Symptoms typically emerge in the third
and fourth decade, and the sex incidence is probably equal. In a proportion of cases, the
earliest symptoms may be depression, anxiety, or frank paranoid illness, accompanied by a
personality change. Progression is slow, leadi leading to death usually within 10 to 15 year.

Diagnostic guidelines

The association of choreiform movement disorder, dementia, and family history of

Huntington's disease is highly suggestive of the diagnosis, though sporadic cases undoubtedly
occur. Involuntary choreiform movements, typically of the face, hands, and shoulders, or in
the gait, are early manifestations. They usually precede the dementia and only rarely remain
absent until the dementia is very advanced. Other motor phenomena may predominate when
the onset is at an unusually young age (e.g. striatal rigidity) or at a late age (e.g. intention
tremor). The dementia is characterized by the predominant involvement of frontal lobe
functions in the early stage, with relative preservation of memory until later.

Includes: dementia in Huntington's chorea

Differential diagnosis. Consider: other cases of choreic movements; Alzheimer's, Pick's or

Creutzfeldt-Jakob disease (F00.-, F02.0, F02.1).

F02.3 Dementia in Parkinson's disease

A dementia developing in the course of established Parkinson's disease (especially its severe
forms). No particular distinguishing clinical features have yet been demonstrated. The
dementia may be different from that in either Alzheimer's disease or vascular dementia;
however, there is also evidence that it may be the manifestation of a co-occurrence of one of
these conditions with Parkinson's disease. This justifies the identification of cases of
Parkinson's disease with dementia for research until the issue is resolved.

Diagnostic guidelines

Dementia developing in an individual with advanced, usually severe, Parkinson's disease.

Includes: dementia in paralysis agitans dementia in parkinsonism

Differential diagnosis. Consider: other secondary dementias (F02.8); multi-infarct dementia

(F01.1) associated with hypertensive or diabetic vascular disease; brain tumor (C70-C72);
normal pressure hydrocephalus (G91.2).

F02.4 Dementia in human immunodeficiency virus [HIV] disease

A disorder characterized by cognitive deficits meeting the clinical diagnostic criteria for
dementia, in the absence of a concurrent illness or condition other than HIV infection that
could explain the findings. HIV dementia typically presents with complaints of forgetfulness,

22
slowness, poor concentration, and difficulties with problem-solving and reading. Apathy,
reduced spontaneity, and social withdrawal are common, and in a significant minority of
affected individuals the illness may present atypically as an affective disorder, psychosis, or
seizures. Physical examination often reveals tremor, impaired rapid repetitive movements,
imbalance, ataxia, hypertonia, generalized hyperreflexia, positive frontal release signs, and
impaired pursuit and saccadic eye movements. Children also develop an HIV-associated
neurodevelopmental disorder characterized by developmental delay, hypertonia,
microcephaly, and basal ganglia calcification. The neurological involvement most often
occurs in the absence of opportunistic infections and neoplasms, which is not the case for
adults. HIV dementia generally, but not invariably, progresses quickly (over weeks or
months) to severe global dementia, mutism, and death.

Includes: AIDS-dementia complex HIV encephalopathy or subacute encephalitis

F02.8 Dementia in other specified diseases classified elsewhere

Dementia can occur as a manifestation or consequence of a variety of cerebral and somatic

conditions. To specify the etiology, the ICD-10 code for the underlying condition should be
added. Parkinsonism-dementia complex of Guam should also be coded here (identified by a
fifth character, if necessary). It is a rapidly progressing dementia followed by extrapyramidal
dysfunction and, in some cases, amyotrophic lateral sclerosis. The disease was originally
described on the island of Guam where it occurs with high frequency in the indigenous
population, affecting twice as many males as females; it is now known to occur also in Papua
New Guinea and Japan.

Includes:

Dementia in: carbon monoxide poisoning (T58) cerebral lipidosis (E75.-) epilepsy (G40.-)
general paralysis of the insane (A52.1) hepatolenticular degeneration (Wilson's disease)
(E83.0) hypercalcaemia (E83.5) hypothyroidism, acquired (E00.-, E02) intoxications (T36-
T65) multiple sclerosis (G35) neurosyphilis (A52.1) niacin deficiency [pellagra] (E52)
polyarteritis nodosa (M30.0) systemic lupus erythematosus (M32.-) trypanosomiasis (African
B56.-, American B57.-) vitamin B12 deficiency (E53.8)

F03 Unspecified dementia

This category should be used when the general criteria for the diagnosis of dementia are
satisfied, but when it is not possible to identify one of the specific types (F00.0- F02.9).

Includes: presenile or senile dementia NOS presenile or senile psychosis NOS primary
degenerative dementia NOS

F04 Organic amnesic syndrome, not induced by alcohol and other psychoactive
substances

23
A syndrome of prominent impairment of recent and remote memory. While immediate recall
is preserved, the ability to learn new material is markedly reduced and this results in
anterograde amnesia and disorientation in time. Retrograde amnesia of varying intensity is
also present but its extent may lessen over time if the underlying lesion or pathological
process has a tendency to recover.

Confabulation may be a marked feature but is not invariably present. Perception and other
cognitive functions, including the intellect, are usually intact and provide a background
against which the memory disturbance appears as particularly striking. The prognosis
depends on the course of the underlying lesion (which typically affects the hypothalamic-
diencephalic system or the hippocampal region); almost complete recovery is, in principle,
possible.

Diagnostic guidelines

For a definitive diagnosis it is necessary to establish:

(a)Presence of a memory impairment manifest in a defect of recent memory (impaired

learning of new material); anterograde and retrograde amnesia, and a reduced ability to recall
past experiences in reverse order of their occurrence;

(b)History or objective evidence of an insult to, or a disease of, the brain (especially with
bilateral involvement of the diencephalic and medial temporal structures);

(c)Absence of a defect in immediate recall (as tested, for example, by the digit span), of
disturbances of attention and consciousness, and of global intellectual impairment.
Confabulations, lack of insight and emotional changes (apathy, lack of initiative) are
additional, though not in every case necessary, pointers to the diagnosis.

Includes: Korsakov's syndrome or psychosis, nonalcoholic

Differential diagnosis. This disorder should be distinguished from other organic syndromes
in which memory impairment is prominent (e.g. dementia or delirium), from dissociative
amnesia (F44.0), from impaired memory function in depressive disorders (F30-F39), and
from malingering presenting with a complaint of memory loss (Z76.5). Korsakov's syndrome
induced by alcohol or drugs should not be coded here but in the appropriate section (F1x.6).

F05 Delirium, not induced by alcohol and other psychoactive substances

An etiologically nonspecific syndrome characterized by concurrent disturbances of

consciousness and attention, perception, thinking, memory, psychomotor behaviour emotion,
and the sleep-wake cycle. It may occur at any age but is most common after the age of 60
years. The delirious state is transient and of fluctuating intensity; most cases recover within 4
weeks or less. However, delirium lasting, with fluctuations, for up to 6 months is not
uncommon.

Diagnostic guidelines

24
For a definite diagnosis, symptoms, mild or severe, should be present in each one of the
following areas:

(a)Impairment of consciousness and attention (on a continuum from clouding to coma;

reduced ability to direct, focus, sustain, and shift attention);

(b)Global disturbance of cognition (perceptual distortions, illusions and hallucinations most

often visual; impairment of abstract thinking and comprehension, with or without transient
delusions, but typically with some degree of incoherence; impairment of immediate recall
and of recent memory but with relatively intact remote memory; disorientation for time as
well as, in more severe cases, for place and person);

(c)Psychomotor disturbances (hypo- or hyperactivity and unpredictable shifts from one to the
other; increased reaction time; increased or decreased flow of speech; enhanced startle
reaction);

(d)Disturbance of the sleep-wake cycle (insomnia or, in severe cases, total sleep loss or
reversal of the sleep-wake cycle; daytime drowsiness; nocturnal worsening of symptoms;
disturbing dreams or nightmares, which may continue as hallucinations after awakening);

(e)Emotional disturbances, e.g. depression, anxiety or fear, irritability, euphoria, apathy,or

wondering perplexity. The onset is usually rapid, the course diurnally fluctuating, and the
total duration of the condition less than 6 months. The above clinical picture is so
characteristic that a fairly confident diagnosis of delirium can be made even if the underlying
cause is not clearly established. In addition to a history of an underlying physical or brain
disease, evidence of cerebral dysfunction (e.g. an abnormal electroencephalogram, usually
but not invariably showing a slowing of the background activity) may be required if the
diagnosis is in doubt.

Includes: -acute brain syndrome

-acute confusional state (nonalcoholic)

-acute infective psychosis

-acute organic reaction

-acute psycho-organic syndrome

Differential diagnosis. Delirium should be distinguished from other organic syndromes,

especially dementia (F00-F03), from acute and transient psychotic disorders (F23.-), and
from acute states in schizophrenia (F20.-) or mood [affective] disorders (F30-F39) in which
confusional features may be present. Delirium, induced by alcohol and other psychoactive
substances, should be coded in the appropriate section (F1x.4).

F05.0 Delirium, not superimposed on dementia, so described

This code should be used for delirium that is not superimposed upon pre-existing dementia.

25
F05.1 Delirium, superimposed on dementia

This code should be used for conditions meeting the above criteria but developing in the
course of a dementia (F00-F03).

F05.8 Other delirium

Includes: delirium of mixed origin subacute confusional state or delirium

F05.9 Delirium, unspecified

F06 Other mental disorders due to brain damage and dysfunction and to physical
disease

This category includes miscellaneous conditions causally related to brain dysfunction due to
primary cerebral disease, to systemic disease affecting the brain secondarily, to endocrine
disorders such as Cushing's syndrome or other somatic illnesses, and to some exogenous
toxic substances (but excluding alcohol and drugs classified under F10-F19) or hormones.
These conditions have in common clinical features that do not by themselves allow a
presumptive diagnosis of an organic mental disorder, such as dementia or delirium. Rather,
the clinical manifestations resemble, or are identical with, those of disorders not regarded as
"organic" in the specific sense restricted to this block of the classification. Their inclusion
here is based on the hypothesis that they are directly caused by cerebral disease or
dysfunction rather than resulting from either a fortuitous association with such disease or
dysfunction, or a psychological reaction to its symptoms, such as schizophrenia-like disorders
associated with longstanding epilepsy. The decision to classify a clinical syndrome here is
supported by the following:

(a)Evidence of cerebral disease, damage or dysfunction or of systemic physical disease,

known to be associated with one of the listed syndromes;

(b)A temporal relationship (weeks or a few months) between the development of the
underlying disease and the onset of the mental syndrome;

(c)Recovery from the mental disorder following removal or improvement of the underlying
presumed cause.

(d)Absence of evidence to suggest an alternative cause of the mental syndrome (such as a

strong family history or precipitating stress).

Conditions (a) and (b) justify a provisional diagnosis; if all four are present, the certainty of
diagnostic classification is significantly increased.

The following are among the conditions known to increase the relative risk for the syndromes
classified here: epilepsy; limbic encephalitis; Huntington's disease; head trauma; brain
neoplasms; extracranial neoplasms with remote CNS effects (especially carcinoma of the
pancreas); vascular cerebral disease, lesions, or malformations; lupus erythematosus and
other collagen diseases; endocrine disease (especially hypoand hyperthyroidism, Cushing's

26
disease); metabolic disorders (e.g., hypoglycaemia, porphyria, hypoxia); tropical infectious
and parasitic diseases (e.g. trypanosomiasis); toxic effects of nonpsychotropic drugs
(propranolol, levodopa, methyldopa, steroids, antihypertensives, antimalarials).

Excludes: mental disorders associated with delirium (F05.-) mental disorders associated with
dementia as classified in F00-F03

F06.0 Organic hallucinosis

A disorder of persistent or recurrent hallucinations, usually visual or auditory, that occur in

clear consciousness and may or may not be recognized by the subject as such. Delusional
elaboration of the hallucinations may occur, but insight is not infrequently preserved.

Diagnostic guidelines

In addition to the general criteria in the introduction to F06 above, there should be evidence
of persistent or recurrent hallucinations in any modality; no clouding of consciousness; no
significant intellectual decline; no predominant disturbance of mood; and no predominance of
delusions.

Includes: Dermatozoenwahn organic hallucinatory state (nonalcoholic)

Excludes: alcoholic hallucinosis (F10.52) schizophrenia (F20.-)

F06.1 Organic catatonic disorder

A disorder of diminished (stupor) or increased (excitement) psychomotor activity associated

with catatonic symptoms. The extremes of psychomotor disturbance may alternate. It is not
known whether the full range of catatonic disturbances described in schizophrenia occurs in
such organic states, nor has it been conclusively determined whether an organic catatonic
state may occur in clear consciousness or whether it is always a manifestation of delirium,
with subsequent partial or total amnesia. This calls for caution in making this diagnosis and
for a careful delimitation of the condition from delirium. Encephalitis and carbon monoxide
poisoning are presumed to be associated with this syndrome more often than other organic
causes.

Diagnostic guidelines

The general criteria for assuming organic etiology, laid down in the introduction to F06, must
be met. In addition, there should be one of the following:

(a)Stupor (diminution or complete absence of spontaneous movement with partial or

complete mutism, negativism, and rigid posturing);

(b)Excitement (gross hypermotility with or without a tendency to assaultiveness);

(c)Both (shifting rapidly and unpredictably from hypo- to hyperactivity). Other catatonic
phenomena that increase confidence in the diagnosis are: stereotypies, waxy flexibility, and
impulsive acts.

27
Excludes: catatonic schizophrenia (20.2) dissociative stupor (F44.2) stupor NOS (R40.1)

F06.2 Organic delusional [schizophrenia-like] disorder

A disorder in which persistent or recurrent delusions dominate the clinical picture. The
delusions may be accompanied by hallucinations but are not confined to their content.
Features suggestive of schizophrenia, such as bizarre delusions, hallucinations, or thought
disorder, may also be present.

Diagnostic guidelines

The general criteria for assuming an organic etiology, laid down in the introduction to F06,
must be met. In addition, there should be delusions (persecutory, of bodily change, jealousy,
disease, or death of the subject or another person). Hallucinations, thought disorder, or
isolated catatonic phenomena may be present. Consciousness and memory must not be
affected. This diagnosis should not be made if the presumed evidence of organic causation is
nonspecific or limited to findings such as enlarged cerebral ventricles (visualized on
computerized axial tomography) or "soft" neurological signs.

Includes: paranoid and paranoid-hallucinatory organic states schizophrenia-like psychosis in

epilepsy

Excludes: acute and transient psychotic disorders (F23.-) drug-induced psychotic disorders
(F1x.5) persistent delusional disorder (F22.-) schizophrenia (F20.-)

F06.3 Organic mood [affective] disorders

Disorders characterized by a change in mood or affect, usually accompanied by a change in

the overall level of activity. The only criterion for inclusion of these disorders in this block is
their presumed direct causation by a cerebral or other physical disorder whose presence must
either be demonstrated independently (e.g. by means of appropriate physical and laboratory
investigations) or assumed on the basis of adequate history information. The affective
disorder must follow the presumed organic factor and be judged not to represent an emotional
response to the patient's knowledge of having, or having the symptoms of, a concurrent brain
disorder. Postinfective depression (e.g. following influenza) is a common example and should
be coded here. Persistent mild euphoria not amounting to hypomania (which is sometimes
seen, for instance, in association with steroid therapy or antidepressants) should not be coded
here but under F06.8.

Diagnostic guidelines

In addition to the general criteria for assuming organic etiology, laid down in the introduction
to F06, the condition must meet the requirements for a diagnosis of one of the disorders listed
under F30-F33.

Excludes: mood [affective] disorders, nonorganic or unspecified (F30-F39) right hemispheric

affective disorder (F07.8)

28
The following five-character codes might be used to specify the clinical disorder:

F06.30 Or Organic manic disorder

F06.31 Organic bipolar affective disorder

F06.32 Organic depressive disorder

F06.33 Organic mixed affective disorder

F06.4 Organic anxiety disorder

A disorder characterized by the essential descriptive features of a generalized anxiety

disorder (41.1), a panic disorder (F41.0), or a combination of both, but arising as a
consequence of an organic disorder capable of causing cerebral dysfunction (e.g. temporal
lobe epilepsy, thyrotoxicosis, or phaechromocytoma).

Excludes: anxiety disorders, nonorganic or unspecified (F41.-)

F06.5 Organic dissociative disorder

A disorder that meets the requirements for one of the disorders in F44.- (dissociative
[conversion] disorder) and for which the general criteria for organic etiology are also fulfilled
(as described in the introduction to this block).

Excludes: dissociative [conversion] disorders, nonorganic or unspecified (F44.-)

F06.6 Organic emotionally labile [asthenic] disorder

A disorder characterized by marked and persistent emotional incontinence or lability,

fatiguability, or a variety of unpleasant physical sensations (e.g. dizziness) and pains regarded
as being due to the presence of an organic disorder. This disorder is thought to occur in
association with cerebrovascular disease or hypertension more often than with other causes.

Excludes: somatoform disorders, nonorganic or unspecified (F45.-)

F06.7 Mild cognitive disorder

This disorder may precede, accompany, or follow a wide variety of infections and physical
disorders, both cerebral and systemic (including HIV infection). Direct neurological evidence
of cerebral involvement is not necessarily present, but there may nevertheless be distress and
interference with usual activities. The boundaries of this category are still to be firmly
established. When associated with a physical disorder from which the patient recovers, mild
cognitive disorder does not last for more than a few additional weeks. This diagnosis should
not be made if the condition is clearly attributable to a mental or behavioural disorder
classified in any of the remaining blocks in this book.

Diagnostic guidelines

29
The main feature is a decline in cognitive performance. This may include memory
impairment, learning or concentration difficulties. Objective tests usually indicate
abnormality. The symptoms are such that a diagnosis of dementia (F00-F03), organic
amnesic syndrome (F04) or delirium (F05.-) cannot be made.

Differential diagnosis. The disorder can be differentiated from postencephalitic syndrome

(F07.1) and postconcussional syndrome (F07.2) by its different etiology, more restricted
range of generally milder symptoms, and usually shorter duration.

F06.8 Other specified mental disorders due to brain damage and dysfunction and to
physical disease

Examples are abnormal mood states occurring during treatment with steroids or

antidepressants.

Includes: epileptic psychosis NOS

F06.9 Unspecified mental disorder due to brain damage and dysfunc- tion and to
physical disease

F07Personality and behavioural disorders due to brain disease, damage and dysfunction

Alteration of personality and behaviour can be a residual or concomitant disorder of brain

disease, damage, or dysfunction. In some instances, differences in the manifestation of such
residual or concomitant personality and behavioural syndromes may be suggestive of the type
and/or localization of the intracerebral problem, but the reliability of this kind of diagnostic
inference should not be overestimated. Thus the underlying etiology should always be sought
by independent means and, if known, recorded.

F07.0 Organic personality disorder

This disorder is characterized by a significant alteration of the habitual patterns of premorbid

behaviour. The expression of emotions, needs, and impulses is particularly affected.
Cognitive functions may be defective mainly or even exclusively in the areas of planning and
anticipating the likely personal and social consequences, as in the socalled frontal lobe
syndrome. However, it is now known that this syndrome occurs not only with frontal lobe
lesions but also with lesions to other circumscribed areas of the brain.

Diagnostic guidelines

In addition to an established history or other evidence of brain disease, damage, or

dysfunction, a definitive diagnosis requires the presence of two or more of the following
features:

(a)Consistently reduced ability to persevere with goal-directed activities, especially those

involving longer periods of time and postponed gratification;

30
(b)Altered emotional behaviour, characterized by emotional lability, shallow and
unwarranted cheerfulness (euphoria, inappropriate jocularity), and easy change to irritability
or short-lived outbursts of anger and aggression; in some instances apathy may be a more
prominent feature.

(c)Expression of needs and impulses without consideration of consequences or social

convention (the patient may engage in dissocial acts, such as stealing, inappropriate sexual
advances, or voracious eating, or may exhibit disregard for personal hygiene);

(d)Cognitive disturbances, in the form of suspiciousness or paranoid ideation, and/or

excessive preoccupation with a single, usually abstract, theme (e.g. religion, "right" and
"wrong");

(e)Marked alteration of the rate and flow of language production, with features such as
circumstantiality, over-inclusiveness, viscosity, and hypergraphia;

(f)Altered sexual behaviour (hyposexuality or change of sexual preference).

Includes: frontal lobe syndrome limbic epilepsy personality syndrome lobotomy syndrome
organic pseudopsychopathic personality organic pseudoretarded personality postleucotomy
syndrome

Excludes: enduring personality change after catastrophic experience (F62.0) enduring

personality change after psychiatric illness (F62.1) postconcussional syndrome (F07.2)
postencephalitic syndrome (F07.1) specific personality disorder (F60.-)

F07.1 Postencephalitic syndrome

The syndrome includes residual behavioural change following recovery from either viral or
bacterial encephalitis. Symptoms are nonspecific and vary from individual to individual, from
one infectious agent to another, and, most consistently, with the age of the individual at the
time of infection. The principal difference between this disorder and the organic personality
disorders is that it is often reversible.

Diagnostic guidelines

The manifestations may include general malaise, apathy or irritability, some lowering of
cognitive functioning (learning difficulties), altered sleep and eating patterns, and changes in
sexuality and in social judgement. There may be a variety of residual neurological
dysfunctions such as paralysis, deafness, aphasia, constructional apraxia, and acalculia.

Excludes: organic personality disorder (F07.0)

F07.2 Postconcussional syndrome

The syndrome occurs following head trauma (usually sufficiently severe to result in
loss of consciousness) and includes a number of disparate symptoms such as
headache, dizziness (usually lacking the features of true vertigo), fatigue, irritability,

31
 difficulty in concentrating and performing mental tasks, impairment of memory,
insomnia, and reduced tolerance to stress, emotional excitement, or alcohol.
These symptoms may be accompanied by feelings of depression or anxiety, resulting
from some loss of self-esteem and fear of permanent brain damage. Such feelings
enhance the original symptoms and a vicious circle results.
Some patients become hypochondriacal, embark on a search for diagnosis and cure,
and may adopt a permanent sick role. The etiology of these symptoms is not always
clear, and both organic and psychological factors have been proposed to account for
them.
The nosological status of this condition is thus somewhat uncertain. There is little
doubt, however, that this syndrome is common and distressing to the patient.

Diagnostic guidelines

At least three of the features described above should be present for a definite diagnosis.
Careful evaluation with laboratory techniques (electroencephalography, brain stem evoked
potentials, brain imaging, oculonystagmography) may yield objective evidence to
substantiate the symptoms but results are often negative. The complaints are not necessarily
associated with compensation motives.

Includes: postcontusional syndrome (encephalopathy) post-traumatic brain syndrome,

nonpsychotic

F07.8 Other organic personality and behavioural disorders due to brain disease,
damage and dysfunction

Brain disease, damage , or dysfunction may produce a variety of cognitive, emotional,

personality, and behavioural disorders, not all of which are classifiable under the preceding
rubrics. However, since the nosological status of the tentative syndromes in this area is
uncertain, they should be coded as "other". A fifth character may be added, if necessary, to
identify presumptive individual entities such as:

Right hemispheric organic affective disorder (changes in the ability to express or comprehend
emotion in individuals with right hemisphere disorder). Although the patient may
superficially appear to be depressed, depression is not usually present: it is the expression of
emotion that is restricted. Also coded here:

(a)Any other specified but presumptive syndromes of personality or behavioural change due
to brain disease, damage, or dysfunction other than those listed under F07.0-F07.2; and

(b)Conditions with mild degrees of cognitive impairment not yet amounting to dementia in
progressive mental disorders such as Alzheimer's disease, Parkinson's disease, etc. The
diagnosis should be changed when the criteria for dementia are fulfilled.

Excludes: delirium (F05.-)

F07.9 Unspecified organic personality and behavioural disorder due to brain disease,
damage and dysfunction

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Includes: organic psychosyndrome

F09Unspecified organic or symptomatic mental disorder

This category should only be used for recording mental disorders of known organic etiology.

Includes: organic psychosis NOS symptomatic psychosis NOS

Excludes: psychosis NOS (F29)

DIAGNOSIS

1.INVESTIGATIONS:-

-Blood –CBC ,ESR,Electrolytes –Serum calcium,potassium,sodium,glucose,cholesterol,Liver

enzymes,TFT ,(T3,T4 TSH)VDRL, Drug Screen ,Heavy metals ,ABG.

-Urine –urine analysis for albumin, sugar,catecholamines- steroids.

-Procedures – ECG,EEG,CSF analysis, Brain biopsy.

-Radiography – Skull X-Ray, CT Scans, MRI,pneumoencephalogram.

-Mini mental status examination.

-Neuropsychology testing.

-Hormonal assay.

DIAGNOSTIC GUIDELINES FOR DEMENTIA:-

The requirement for diagnosis is evidence of a decline in both memory and thinking
which is sufficient to impair personal activities of daily living.
The impairment of memory typically affects the registration, storage , and retrieval of
new information , but previously learned and familiar material may also be lost,
particularly in the later stages.
Dementia is more than dysmnesia: there is also impairment of thinking and reasoning
capacity, and a reduction in the flow of ideas.
The processing of information is impaired, in that the individual finds it increasingly
difficult to attend to more than one stimulus at a time, such as taking part in
conversation with several persons, and to shift the focus of attention from one topic to
another.
If dementia is soul diagnosis, evidence of clear consciousness is required.
The above symptoms & impairments should have been evident for at least 6 months
for a confident clinical diagnosis of dementia to be made.

TREATMENT:

 Training of thinking & memory functions are carried out carefully.

 Reality orientation training.

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  Improve brain function by using drugs, e.g. psychotropic drugs, antipsychotic drugs,
antidepressants, antianxiety drugs.

 Organization of environment.

 Cognitive & behavioral interventions may be appropriate.

 Educating & providing emotional support to the care givers is of importance.

Validation therapy-

When the client has degenerative, irreversible cognitive impairment, the clients’ sense of
being will be understood by nursing fraternity, in order to enhance quality of life , reduce the
incidence of agitation & catastrophic reaction, the nursing staff tries to enter to clients’ world
& render care-oriented activities, to meet the Clients’ needs.

Re motivation therapy:-

 To provide opportunity for the client to derive pleasure & sensory stimulation by
world to feel safe & comfortable.
 To interrupt self- absorption.
 To overcome isolation.

Briefly theme has to be explained .

 Clients are motivated to reminisce in relation to group’s objective or theme.

 If the client attends meeting &contributes, nurse will appreciate for his unique
contribution.

 Makes the client to touch some objects e.g. flowers to attain sensory stimulation.

Drug therapy:-

 Antipsychotics such as tab. Haloperidol and risperidone are given. olanzapine, a new
atypical antipsychotic , is currently being investigated for the treatment of agitation
and aggression associated with dementia.

 Anticholinestrase agent is given to improve memory and functioning, especially for

clients in the early stage of dementia.

 Tab. ‘Tacrine’ (tetra hydro amino acridine) long acting inhibitor of acetylcholine&
also delays the progression of illness.

 Antipsychotics such as Tab. Haloperidol

 M.O.A- Reduce & block the production of dopamine

 Relief from the behavioral symptoms e.g. agitation, aggression.

34
  Tb.donepezil can enhance mental abilities by improving memory ,reasoning,
orientation and language especially for clients in early stages of dementia.

 Short acting benzodiazepines such as lorazepam along with antipsychotics are

given for severe agitation and insomnia.

 Sedating antidepressants such as trazodone and nefazodone are given to clients

with concurrent depression.

ACTIVITIES

 Involve the person in simple activities.

 Help the person get started on an activity. Break the activity down into small steps &
praise the person for each step he/she completes.

 Incorporate activities the person seems to enjoy into your daily routine &try to do
them at a similar time each day.

 Reminence therapy

 Dancing & music therapy

 Gardening

 Regular exercise - This promotes weight loss and increases stamina.

APPROACHING DEMENTIA PATIENT

 Provide firm & friendly .

 Calm approach

 Reorienting

 Reassurance

 Give information.

DIET

 High protein intake, high in fiber.

 Supplementation with vitamins, high caloric diet.

 Well balanced diet.

PREVENTION

 Lead an active life ,both mentally and physically.

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  Proper screening and treatment of underlying disease is essential.

 Provision of situational support, mutual concern is of much importance.

NURSING MANAGEMENT:

ASSESSMENT:

Assessment of clients’ with dementia is difficult and must rely ,to a great degree, on
information from sources other than the clients’(usually the caregivers).

Assessment of the environment

 When interviewing the client or administering an assessment test, a positive physical

and emotional environment is critical.

 The rooms should be free from distractions, quiet and away from the noise of any
activity.

 Visual and auditory defects may be present in client, and the evaluator must establish
eye contact , speak directly to the client in a low frequency range and enunciate
clearly.

 Hearing aids or glasses, if usually worn by the client, should be in clean , working
conditions.

 Any printed material from which a client response is expected should be presented in
large , heavy type that is easily read.

 In general , the attitude of the evaluator must be friendly , non –threatening and non-
judgemental.

Cognitive assessment tools:-

 A variety of tools can lend insight into a person’s cognitive status .Among the most
common are:-

 Mini mental status examination.

 NIMH dementia mood assessment scale.

 Blessed dementia rating scale.

NEUROLOGICAL DEFICITS

 Determining the status of client with dementia must involve assessment of

neurological deficits such as following :-

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  Perception and organization

 Attention span

 Language

 Memory

 Emotional control

 Listening and judgement.

EMOTIONAL STATUS

 Mood and state of mind

 Depression

 Functional ability

 Behaviour

PHYSICAL MANIFESTATIONS

 Weight changes

 Choking

 Dehydration

 Changes in gait

 Incontinence

 Feeling cold

NURSING DIAGNOSIS

1.Impaired communication related to cerebral impairment as evidenced by altered

memory judgement and word finding.

Expected outcome-Demonstrate congruent verbal and nonverbal communication.

Interventions- Speak slowly and use short, simple words and phrases.

 Consistently identify yourself, and address the person by name at each meeting.
 Focus on one piece of information at a time. Review what has been discussed with
patient.
 If patient has vision or hearing disturbances, have him wear prescription eyeglasses
and/or a hearing device.

37
  Keep environment well lit.
 Use clocks, calendars, and familiar personal effects in the patient’s view.
 If patient becomes verbally aggressive, identify and acknowledge feelings.
 If patient becomes aggressive, shift the topic to a safer, more familiar one.
 If patient becomes delusional, acknowledge feelings and reinforce reality. Do not
attempt to challenge the content of the delusion.

Evaluation-Demonstrates decreased anxiety and increased feelings of security in supportive

environment.

2.Self care deficit related to cognitive impairment as evidenced by inattention and

inability to complete ADL’s.

Expected outcome-Independence in Self-Care

Interventions

 Assess and monitor patient’s ability to perform ADLs.

 Encourage decision making regarding ADLs as much as possible.
 Label clothes with patient’s name, address, and telephone number.
 Use clothing with elastic and Velcro for fastenings rather than buttons or zippers,
which may be too difficult for patient to manipulate.
 Monitor food and fluid intake.
 Weigh patient weekly.
 Provide food that patient can eat while moving.
 Sit with patient during meals and assist by cueing.
 Initiate a bowel and bladder program early in the disease process to maintain
continence and prevent constipation or urine retention.

Evaluation-Maintains maximum degree of orientation and self-care within level of ability

3.Risk for injury related to cognitive impairment and wandering behaviour as

evidenced by complaints of other patients.

Expected outcome-Risk of injury will reduce.

Interventions

 Discuss restriction of driving when recommended.

 Assess patient’s home for safety: remove throw rugs, label rooms, and keep the house
well lit.
 Assess community for safety.
 Alert neighbors about the patient’s wandering behavior.
 Alert police and have current pictures taken.
 Provide patient with a Medic Alert bracelet.

38
  Install complex safety locks on doors to outside or basement.
 Install safety bars in bathroom.
 Closely observe patient while he is smoking.
 Encourage physical activity during the daytime.
 Give patient a card with simple instructions (address and phone number) should the
patient get lost.
 Use night-lights.
 Install alarm

Evaluation-Safety precautions and close surveillance maintained; no injury

4.Impaired social interaction related to cognitive impairment as evidenced by no or very

less friends.

Expected outcome-Patient will socialize with others.

Interventions

 Provide magazines with pictures as reading and language abilities diminish.

 Encourage participation in simple, familiar group activities, such as singing,
reminiscing, doing puzzles, and painting.
 Encourage participation in simple activities that promote the exercise of large muscle
groups.

Evaluation-Attends group activities; sings, exercises with group

5.Risk for violence –self directed or others directed related to suspicion as evidenced by
inability to recognize people and places.

Expected outcome-Risk of violence will reduce.

Interventions-

 Respond calmly and do not raise your voice.

 Remove objects that might be used to harm self or others.
 Identify stressors that increase agitation.
 Distract patient when an upsetting situation develops.

Evaluation-Risk of violence is reduced.

PROGNOSIS

It carries poor prognosis.

Family history:

Family history of dementia carries poor prognosis.

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HEALTH EDUCATION

 Teach the family members to label all the rooms & drawers & other objects.

 To wear a medical alert bracelet (name, address, phone no.) to the client so he/ she
can be easily identified by the police, neighbors & other hospital personnel.

 Install safety bars in the bathroom to prevent falls.

 Orient the patient to reality to decrease confusion. E.g. clock with large faces help in
orientation to time.

 Orientation of place , person & time should be given before approaching the patient.

 Avoid stressful activities for client.

 Great care should be taken to avoid accidents , proper lightening should be there.

ORGANIC AMNESIA
The inability to retain or recall past experiences. The condition may be temporary or
permanent, depending on aetiology.

Amnesia also known as amnesic syndrome, is a deficit in memory caused by brain damage,
disease, or psychological trauma. Amnesia can also be caused temporarily by the use of
various sedatives and hypnotic drugs. Essentially, amnesia is loss of memory. The memory
can be either wholly or partially lost due to the extent of damage that was caused.

There are two main types of amnesia with two additional types:-

40
 a) Retrograde amnesia
b) Anterograde amnesia.
c) Transient global amnesia
d) Infantile amnesia
a) Retrograde amnesia- is the inability to retrieve information that was acquired
before a particular date, usually the date of an accident or operation. In some cases
the memory loss can extend back decades, while in others the person may lose
only a few months of memory.
b) Anterograde amnesia- is the inability to transfer new information from the short-
term store into the long-term store. People with this type of amnesia cannot reme
mber things for long periods of time.

Causes-

There are three generalized categories in which amnesia could be acquired by a person. The
three categories are head trauma (example: head injuries), traumatic events (example: seeing
something devastating to the mind), or physical deficiencies (example: atrophy of the
hippocampus). The majority of amnesia and related memory issues derive from the first two
categories as these are more common and the third could be considered a sub category of the
first.

 Head trauma is a very broad range as it deals with any kind of injury or active action
toward the brain which might cause amnesia. Retrograde and Anterograde amnesia are
more often seen from events like this, an exact example of a cause of the two would be
electroshock therapy, which would cause both briefly for the receiving patient.
 Traumatic events are more subjective. What is traumatic is dependent on what the person
finds to be traumatic. Regardless, a traumatic event is an event where something so
distressing occurs that the mind chooses to forget rather than deal with the stress. A
common example of amnesia that is caused by traumatic events is dissociative amnesia,
which occurs when the person forgets an event that has deeply disturbed them. An
example would be a person forgetting a fatal and graphic car accident involving their
loved ones.
 Physical deficiencies are different from head trauma as physical lean more toward
passive physical issues. The difference would be having surgery that removes part of the
brain, this would be active and thus head trauma, while the surgery caused the
surrounding areas to atrophy, which is passive. Henry Molaison is a great example of
physical deficiencies as parts of his brain began to atrophy after his surgery.
Amongst specific causes of amnesia are the following:

 Electroconvulsive therapy in which seizures are electrically induced in patients for

therapeutic effect can have acute effects including both retrograde and anterograde
amnesia.
41
 Alcohol can both cause blackouts and have deleterious effects on memory formation.
 Bilateral temporal lobectomy
 Hypoxia
 Herpes simplex encephalitis
 Stroke

Other Etiological Implications

Amnestic disorders share a common symptom presentation of memory impairment, but are
differentiated in the DSM-IV-TR (APA, 2000) according to the following etiology:

Amnestic disorder due to a general medical condition

Substance-induced persisting amnestic disorder

Amnestic Disorder Due to a General Medical Condition

In this type of amnestic disorder, evidence must exist from the history, physical examination,
or laboratory findings to show that the memory impairment is the direct physiological
consequence of a general medical condition (APA, 2000). The diagnosis is specified further
by indicating whether the symptoms are transient (present for no more than 1 month) or
chronic (present for more than 1 month). General medical conditions that may be associated
with amnestic disorder include head trauma, cerebrovascular disease, cerebral neoplastic
disease, cerebral anoxia, herpes simplex encephalitis, poorly controlled insulin-dependent
diabetes, and surgical intervention to the brain (Andreasen & Black, 2006; APA, 2000).
Transient amnestic syndromes can occur from cerebrovascular disease, cardiac arrhythmias,
migraine, thyroid disorders, and epilepsy (Bourgeois et al, 2008).

Substance-Induced Persisting Amnestic Disorder

In this disorder, evidence must exist from the history, physical examination, or laboratory fi
ndings that the memory impairment is related to the persisting effects of substance use (e.g., a
drug of abuse, a medication, or toxin exposure) (APA, 2000). The term persisting is used to
indicate that the symptoms exist long after the effects of substance intoxication or
withdrawalhave subsided. The DSM-IV-TR identifi es the following substances with which
amnestic disorder can be associated:

1. Alcohol

2. Sedatives, hypnotics, and anxiolytics

3. Medications

a. Anticonvulsants

b. Intrathecal methotrexate

4. Toxins

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 a. Lead

b. Mercury

c. Carbon monoxide

d. Organophosphate insecticides

e. Industrial solvents.

The diagnosis is made according to the specific etiological substance involved. For example,
if the substance known to be the cause of the amnestic disorder is alcohol, the diagnosis
would be Alcohol-Induced Persisting Amnestic Disorder.

Types-

 Anterograde amnesia- refers to the inability to create new memories due to brain
damage, while long-term memories from before the event remain intact. The brain
damage can be caused by the effects of long-term alcoholism, severe malnutrition, stroke,
head trauma, surgery, Wernicke-Korsakoff Syndrome, cerebrovascular events, anoxia or
other trauma. The two brain regions related with this condition are medial temporal lobe
and medial diencephalon. Anterograde amnesia cannot be treated with pharmacological
methods due to neuronal loss. However, treatment exists in educating patients to define
their daily routines and after several steps they begin to benefit from their procedural
memory. Likewise, social and emotional support is critical to improving quality of life
for anterograde amnesia sufferers.
 Retrograde amnesia- refers to inability to recall memories before onset of amnesia. One
may be able to encode new memories after the incident. Retrograde is usually caused by
head trauma or brain damage to parts of the brain besides the hippocampus. The
hippocampus is responsible for encoding new memory. Episodic memory is more likely
to be affected than semantic memory. The damage is usually caused by head trauma,
cerebrovascular accident, stroke, tumor, hypoxia, encephalitis, or chronic alcoholism.
People suffering from retrograde amnesia are more likely to remember general
knowledge rather than specifics. Recent memories are less likely to be recovered, but
older memories will be easier to recall due to strengthening over time.[ Retrograde
amnesia is usually temporary and can be treated by exposing them to memories from the
loss.Another type of consolidation (process by which memories become stable in the
brain) occurs over much longer periods of time/days, weeks, months and years and likely
involves transfer of information from the hippocampus to more permanent storage site in
the cortex. The operation of this longer-term consolidation process is seen in the
retrograde amnesia of patients with hippocampal damage who can recall memories from
childhood relatively normally, but are impaired when recalling experiences that occurred
just a few years prior to the time they became amnesic.

43
 Post-traumatic amnesia- is generally due to a head injury (example: a fall, a knock on
the head). Traumatic amnesia is often transient, but may be permanent or either
anterograde, retrograde, or mixed type. The extent of the period covered by the amnesia
is related to the degree of injury and may give an indication of the prognosis for recovery
of other functions. Mild trauma, such as a car accident that results in no more than mild
whiplash, might cause the occupant of a car to have no memory of the moments just
before the accident due to a brief interruption in the short/long-term memory transfer
mechanism. The sufferer may also lose knowledge of who people are. Having longer
periods of amnesia or consciousness after an injury may be an indication that recovery
from remaining concussion symptoms will take much longer.
 Dissociative amnesia- results from a psychological cause as opposed to direct damage to
the brain caused by head injury, physical trauma or disease, which is known as organic
amnesia.
 Repressed memory- refers to the inability to recall information, usually about stressful
or traumatic events in persons' lives, such as a violent attack or disaster. The memory is
stored in long-term memory, but access to it is impaired because of psychological defense
mechanisms. Persons retain the capacity to learn new information and there may be some
later partial or complete recovery of memory. Formerly known as "Psychogenic
Amnesia".
 Dissociative fugue- (formerly psychogenic fugue) is also known as fugue state. It is
caused by psychological trauma and is usually temporary, unresolved and therefore may
return. An individual with dissociative fugue disorder is unaware or confused about his or
her identity and will travel in journeys away from familiar surroundings to discover or
create new identities. The Merck Manual defines it as " one or more episodes of amnesia
in which patients cannot recall some or all of their past and either lose their identity or
form a new identity. The episodes, called fugues, result from trauma or stress.
Dissociative fugue often manifests as sudden, unexpected, purposeful travel away from
home." While popular in fiction, it is extremely rare.
 Posthypnotic amnesia- occurs when events during hypnosis are forgotten, or where past
memories are unable to be recalled. The failure to remember those events is induced by
suggestions made during the hypnosis.
 Lacunar amnesia- is the loss of memory about one specific event.
 Childhood amnesia- (also known as infantile amnesia) is the common inability to
remember events from one's own childhood. Sigmund Freud notoriously attributed this to
sexual repression, while modern scientific approaches generally attribute it to aspects
of brain development or developmental psychology, including language development,
which may be why people do not easily remember pre-language events. Researchers have
found that implicit memories cannot be recalled or described. Remembering how to play
the piano is a common example of implicit memory, as is walking, speaking and other
everyday activities that would be difficult to focus on if they had to be relearned every
time one got up in the morning. Explicit memories, on the other hand, can be recalled and

44
 described in words. Remembering the first time meeting a teacher is an example of
explicit memories.
 Transient global amnesia- is a well-described medical and clinical phenomenon. This
form of amnesia is distinct in that abnormalities in the hippocampus can sometimes be
visualized using a special form of magnetic resonance imaging of the brain known
as diffusion-weighted imaging (DWI). Symptoms typically last for less than a day and
there is often no clear precipitating factor or any other neurological deficits. The cause of
this syndrome is not clear. The hypothesis of the syndrome includes transient reduced
blood flow, possible seizure or an atypical type of migraine. Patients are typically
amnestic of events more than a few minutes in the past, though immediate recall is
usually preserved.
 Source amnesia- is the inability to remember where, when or how previously learned
information has been acquired, while retaining the factual knowledge. Source amnesia is
both part of ordinary forgetting and can be a memory disorder caused by different
factors. People suffering from source amnesia can also get confused about the content of
what is remembered. This confusion has been loosely termed memory distrust syndrome.
Individuals who suffer from this syndrome distrust their memory and may be motivated
to rely on external (non-self) sources.
 Korsakoff's syndrome -can result from long-term alcoholism or malnutrition. It is
caused by brain damage due to a vitamin B1 deficiency and will be progressive if alcohol
intake and nutrition pattern are not modified. Other neurological problems are likely to be
present in combination with this type of Amnesia. Korsakoff's syndrome is also known to
be connected with confabulation. It should be noted that the person's short-term memory
may appear to be normal, but the person may have a difficult time attempting to recall a
past story, or with unrelated words, as well as complicated patterns.
 Drug-induced amnesia- is intentionally caused by injection of an amnesiac drug to help
a patient forget surgery or medical procedures, particularly those not performed under
full anesthesia, or likely to be particularly traumatic. Such drugs are also referred to as
"premedicants."Most commonly a 2'-halogenated benzodiazepine such as
midazolam or flunitrazepam is the drug of choice, although other strongly amnestic
drugs such as propofol or scopolamine may also be used for this application. Memories
of the short time-frame in which the procedure was performed are permanently lost or at
least substantially reduced, but once the drug wears off, memory is no longer affected.
 Situation-Specific amnesia -can arise in a variety of circumstances (e.g., committing an
offence, child sexual abuse) resulting in PTSD. It has been claimed that it involves a
narrowing of consciousness with attention focused on central perceptual details and/or
that the emotional or traumatic events are processed differently from ordinary memories.
 Transient epileptic amnesia- is a rare and unrecognized form of temporal lobe epilepsy,
which is typically an episodic isolated memory loss. It has been recognized as a
treatment-responsive syndrome congenial to anti-epileptic drugs.

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 Transient global amnesia (TGA) is a poorly understood condition. If you develop it,
you will experience confusion or agitation that comes and goes repeatedly over the
course of several hours. You may experience memory loss in the hours before the attack,
and you will probably have no lasting memory of the experience. Scientists think that
TGA occurs as the result of seizure-like activity or a brief blockage of the blood vessels
supplying your brain. It occurs more frequently in middle-aged and older adults
 Infantile amnesia :- Most people can’t remember the first three to five years of life. This
common phenomenon is called infantile or childhood amnesia.

Treatment-

Cognitive therapy- One of these ways is cognitive or occupational therapy. In therapy,

amnesiacs will develop the memory skills they have and try to regain some they have lost by
finding which techniques help retrieve memories or create new retrieval paths.
Coping mechanism- Another coping mechanism is taking advantage of technological
assistance, such as a personal digital device to keep track of day-to-day tasks. Reminders can
be set up for appointments, when to take medications, birthdays and other important events.
Many pictures can also be stored to help amnesiacs remember names of friends, family and
co-workers. Notebooks, wall calendars, pill reminders and photographs of people and places
are low-tech memory aids that can help as well.
While there are no medications available to treat amnesia, underlying medical conditions can
be treated to improve memory. Although improvements occur when patients receive certain
treatments, there is still no actual cure remedy for amnesia so far.

Nursing Diagnoses
 Anxiety
 Ineffective coping
 Disturbed thought processes
 Disturbed personal identity
 Chronic low self-esteem
 Situational low self-esteem

Nursing Interventions
-Establish accepting, supportive relationship
-Encourage self-awareness
-Identify stressors and strengths/resources
-Help client explore feelings, thoughts, and beliefs about stressors
-Validate feelings and strengths
-Assist client to assume responsibility and set realistic goals

-Confront irrational thoughts and unrealistic goals/expectations

-Explore alternatives and consequences
-Support client in trying and evaluating new behaviours

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-Teach stress management techniques and coping strategies
-Encourage social interaction

DELIRIUM

INTRODUCTION

Delirium is derived from the Latin deliro—to be crazy, from de- + lira, a furrow (i.e., to go
out of the furrow), according to Stedman's 24th edition, 1982.

Delirium, often called acute confusional state, begins with confusion and progresses to
disorientation. The patient may experience an altered level of consciousness ranging from
stupor to excessive activity.

Thinking is disorganized, and the attention span is characteristically short. Hallucinations,

delusions, fear, anxiety, and paranoia may also be evident. Because of the acute and
unexpected onset of symptoms and the unknown underlying cause, delirium is a medical
emergency. Delirium occurs secondary to a number of causes, including physical illness,
medication or alcohol toxicity, dehydration, faecal impaction, malnutrition, infection, head
trauma, lack of environmental cues, and sensory deprivation or overload.

Older adults are particularly vulnerable to acute confusion because of their decreased biologic
reserve and the large number of medications that many take. The nurse must recognize the
grave implications of the acute symptoms and report them immediately. If the delirium goes
unrecognized and the underlying cause is not treated, permanent, irreversible brain damage or
death can follow.

DEFINITION

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It is a neuropsychiatric syndrome also called acute confusional state or acute brain failure that
is common among the medically ill and often is misdiagnosed as a psychiatric illness which
can result in delay of appropriate medical intervention.

Delirium is an acute organic mental disorder characterized by impairment of consciousness

disorientation and disturbances in perception and restlessness”.

“Delirium is a disturbance in consciousness and a change in cognition that develops over a

short time”.

INCIDENCE :-

Delirium has the highest incidence among organic mental disorders. About 10 to 25% of
medical-surgical inpatients, and about 20 to 40% of geriatric patients meet the criteria for
delirium during hospitalization.

• Although delirium may occur in any age group, it is most common among the elderly

• Estimated prevalence rates range from 10% to 30% of patients

• 60% of those older than the age of 75 years.

CLASSIFICATION OF DELIRIUM AS PER ICD-10

F05 Delirium, not induced by alcohol and other psychoactive substances

F05.0 Delirium, not superimposed on dementia, so described

F05.1 Delirium, superimposed on dementia

F05.8 Other delirium

F05.9 Delirium, unspecified

F05 Delirium, not induced by alcohol and other psychoactive substances

An etiologically nonspecific syndrome characterized by concurrent disturbances of

consciousness and attention, perception, thinking, memory, psychomotor behaviour,
emotion, and the sleep-wake cycle.
It may occur at any age but is most common after the age of 60 years. The delirious
state is transient and of fluctuating intensity; most cases recover within 4 weeks or
less. However, delirium lasting, with fluctuations, for up to 6 months is not
uncommon.
when arising in the course of chronic liver disease, carcinoma, or sub acute bacterial
endocarditis. The distinction that is sometimes made between acute and subacute
delirium is of little clinical relevance; the condition should be seen as a unitary
syndrome of variable duration and severity ranging from mild to very severe.
A delirious state may be superimposed on, or progress into, dementia. This category
should not be used for states of delirium associated with the use of psychoactive drugs
specified in F10-F19.

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 Delirious states due to prescribed medication (such as acute confusional states in
elderly patients due to antidepressants) should be coded here. In such cases, the
medication concerned should also be recorded by means of an additional T code from
Chapter XIX of ICD-10.

Diagnostic guidelines

For a definite diagnosis, symptoms, mild or severe, should be present in each one of the
following areas:

(a)Impairment of consciousness and attention (on a continuum from clouding to coma;

reduced ability to direct, focus, sustain, and shift attention);

(b)Global disturbance of cognition (perceptual distortions, illusions and hallucinations most

often visual; impairment of abstract thinking and comprehension, with or without transient
delusions, but typically with some degree of incoherence; impairment of immediate recall
and of recent memory but with relatively intact remote memory; disorientation for time as
well as, in more severe cases, for place and person);

(c)Psychomotor disturbances (hypo- or hyperactivity and unpredictable shifts from one to the
other; increased reaction time; increased or decreased flow of speech; enhanced startle
reaction);

(d)Disturbance of the sleep-wake cycle (insomnia or, in severe cases, total sleep loss or
reversal of the sleep-wake cycle; daytime drowsiness; nocturnal worsening of symptoms;
disturbing dreams or nightmares, which may continue as hallucinations after awakening);

(e)Emotional disturbances, e.g. depression, anxiety or fear, irritability, euphoria, apathy,or

wondering perplexity. The onset is usually rapid, the course diurnally fluctuating, and the
total duration of the condition less than 6 months. The above clinical picture is so
characteristic that a fairly confident diagnosis of delirium can be made even if the underlying
cause is not clearly established. In addition to a history of an underlying physical or brain
disease, evidence of cerebral dysfunction (e.g. an abnormal electroencephalogram, usually
but not invariably showing a slowing of the background activity) may be required if the
diagnosis is in doubt.

Includes: acute brain syndrome

-acute confusional state (nonalcoholic)

-acute infective psychosis

-acute organic reaction

-acute psycho-organic syndrome

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Differential diagnosis. Delirium should be distinguished from other organic syndromes,
especially dementia (F00-F03), from acute and transient psychotic disorders (F23.-), and
from acute states in schizophrenia (F20.-) or mood [affective] disorders (F30-F39) in which
confusional features may be present. Delirium, induced by alcohol and other psychoactive
substances, should be coded in the appropriate section (F1x.4).

F05.0 Delirium, not superimposed on dementia, so described

This code should be used for delirium that is not superimposed upon pre-existing dementia.

F05.1 Delirium, superimposed on dementia

This code should be used for conditions meeting the above criteria but developing in the
course of a dementia (F00-F03).

F05.8 Other delirium

Includes: delirium of mixed origin subacute confusional state or delirium

F05.9 Delirium, unspecified

TYPES

Hyperactive or hyper alert

 The patient is hyperactive, combative and uncooperative.

 May appear to be responding to internal stimuli
 Frequently these patients come to our attention because they are difficult to care for.

Hypoactive or hypo alert

 Pt appears to be napping on and off throughout the day

 Unable to sustain attention when awakened, quickly falling back asleep
 Misses meals, medications, appointments
 Does not ask for care or attention
 This type is easy to miss because caring for these patients is not problematic to staff

Mixed

 A combination of both types just described

The most common types are hypoactive and mixed accounting for approximately 80% of
delirium cases.

DIAGNOSTIC CRITERIA-

DSM-IV-TR Diagnostic Criteria for Delirium Due to a General Medical Condition

A. Disturbance of consciousness (i.e., reduced clarity of awareness of the environment) with

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reduced ability to focus, to sustain, or to shift attention.

B. A change in cognition (such as memory deficit, disorientation, or language disturbance) or

the development of a perceptual disturbance that is not better accounted for by a preexisting,
established, or evolving dementia.

C. The disturbance develops over a short period of time (usually hours to days) and tends to
fluctuate during the course of the day.

D. There is evidence from the history, physical examination, or laboratory findings that the
disturbance is caused by the direct physiological consequences of a general medical
condition.

DSM-IV-TR Diagnostic Criteria for Substance Intoxication Delirium

A. Disturbance of consciousness (i.e., reduced clarity of awareness of the environment) with

reduced ability to focus, to sustain, or to shift attention.

B. A change in cognition (such as memory deficit, disorientation, or language disturbance) or

the development of a perceptual disturbance that is not better accounted for by a preexisting,
established, or evolving dementia.

C. The disturbance develops over a short period of time (usually hours to days) and tends to
fluctuate during the course of the day.

D. There is evidence from the history, physical examination, or laboratory findings of the
following:

(1) The symptoms in Criteria A and B developed during substance intoxication.

(2) Medication use is etiologically related to the disturbance

DSM-IV-TR Diagnostic Criteria for Substance Withdrawal Delirium

A. Disturbance of consciousness (i.e., reduced clarity of awareness of the environment) with

reduced ability to focus, to sustain, or to shift attention.

B. A change in cognition (such as memory deficit, disorientation, or language disturbance) or

the development of a perceptual disturbance that is not better accounted for by a preexisting,
established, or evolving dementia.

C. The disturbance develops over a short period of time (usually hours to days) and tends to
fluctuate during the course of the day.

D. There is evidence from the history, physical examination, or laboratory findings that the

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symptoms in Criteria A and B developed during, or shortly after, a withdrawal syndrome.

DSM-IV-TR Diagnostic Criteria for Delirium Due to Multiple aetiologies

A. Disturbance of consciousness (i.e., reduced clarity of awareness of the environment) with

reduced ability to focus, to sustain, or to shift attention.

B. A change in cognition (such as memory deficit, disorientation, or language disturbance) or

the development of a perceptual disturbance that is not better accounted for by a pre existing,
established, or evolving dementia.

C. The disturbance develops over a short period of time (usually hours to days) and tends to
fluctuate during the course of the day.

D. There is evidence from the history, physical examination, or laboratory findings that the
delirium has more than one etiology (e.g., more than one etiological general medical
condition, a general medical condition plus substance intoxication, or medication side effect).

ETIOLOGY

It is usually multifactorial

 Systemic illness
 Medications- any psychoactive medication can cause delirium
 Presence of risk factors

SYSTEMATIC ILLNESS

 Infections
 Electrolyte abnormalities
 Endocrine dysfunctions (hypo or hyper)
 Liver failure- hepatic encephalopathy
 Renal failure- uremic encephalopathy
 Pulmonary disease with hypoxemia
 Cardiovascular disease/events: CHF, arrhythmias, MI
 CNS pathology: tumors, strokes, seizures
 Deficiency states: Thiamine, nicotinic or folic acid, B12

MEDICATIONS- THAT CAUSE DELIRIUM

 Anticholinergics (Frusemide, digoxin, theophylline, cimetidine, prednisolone)

 Analgesics (morphine, codeine)
 Steroids
 Antiparkinson (anticholinergic and dopaminergic)
 Sedatives (benzodiazepines, barbiturates)
 Anticonvulsants
 Antihistamines

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  Antiarrhythmics (digitalis)
 Antihypertensives
 Antidepressants
 Antimicrobials (penicillin, cephalosporins, quinolones)
 Sympathomimetics

PRESENCE OF RISK FACTORS

 >60 years of age

 Male sex
 Visual impairment
 Underlying brain pathology such as stroke, tumor, vasculitis, trauma, dementia
 Major medical illness
 Recent major surgery
 Depression
 Functional dependence
 Dehydration

ETIOLOGICAL IMPLICATIONS ACC TO DSM:

The DSM-IV-TR (APA, 2000) differentiates between the disorders of delirium by their
etiology, although they share a common symptom presentation. Categories of delirium
include the following:

● Delirium due to a general medical condition

● Substance-induced delirium

● Substance-intoxication delirium

● Substance-withdrawal delirium

● Delirium due to multiple etiologies

Delirium Due to a General Medical Condition

In delirium due to a general medical condition, evidence must exist (from history, physical
examination, or laboratory fi ndings) to show that the symptoms of delirium are a direct result
of the physiological consequences of a general medical condition (APA, 2000). Such
conditions include systemic infections, metabolic disorders (e.g., hypoxia, hypercarbia,
hypoglycemia), Fluid or electrolyte imbalances, hepatic or renal disease, thiamine defi
ciency, postoperative states, hypertensive encephalopathy, postictal states, sequelae of head
trauma, and others (APA, 2000).

Substance-Induced Delirium

This disorder is characterized by the symptoms of delirium that are attributed to medication
side effects or exposure to a toxin. The DSM-IV-TR (APA, 2000) lists the following examples

53
of medications that have been reported to result in substance-induced delirium: anesthetics,
analgesics, antiasthmatic agents, anticonvulsants, antihistamines, antihypertensive and
cardiovascular medications, antimicrobials, antiparkinsonian drugs, corticosteroids,
gastrointestinal medications, histamine H2-receptor antagonists (e.g., cimetidine),
immunosuppressive agents, lithium, muscle relaxants, and psychotropic medications with
anticholinergic side effects. Toxins reported to cause delirium include organophosphate
(anticholinesterase), insecticides, carbon monoxide, and volatile substances such as fuel or
organic solvents.

Substance-Intoxication Delirium

With this disorder, the symptoms of delirium may arise within minutes to hours after taking
relatively high doses of certain drugs such as cannabis, cocaine, and hallucinogens. It may
take longer periods of sustained intoxication to produce delirium symptoms with alcohol,
anxiolytics, or narcotics (APA, 2000).

Substance-Withdrawal Delirium

Withdrawal delirium symptoms develop after reduction or termination of sustained, usually

high-dose use of certain substances, such as alcohol, sedatives, hypnotics, or anxiolytics
(APA, 2000). The duration of the delirium is directly related to the half-life of the substance
involved and may last from a few hours to 2 to 4 weeks.

Delirium Due to Multiple Etiologies

This diagnosis is used when the symptoms of delirium are brought on by more than one
cause. For example, the delirium may be related to more than one general medical condition
or it may be a result of the combined effects of a general medical condition and substance use
(APA, 2000).

PATHOPHYSIOLOGY OF DELIRIUM

Decreased oxidative metabolism

Reduced cholinergic function

Dopamine excess

Norepinephrine excess
Glutamate excess
Serotonin imbalance

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 γ-Aminobutyric acid imbalance

Decreased beta endorphin

Abnormal signal transduction

CLINICAL MANIFESTATIONS:

 Fluctuating levels of awareness

 Clouding of consciousness (confused and disoriented)
 Perceptual disturbances (illusions and hallucinations)
 Memory, especially recent memory, is disturbed
 Alternations in sleep-wake cycle
 EEG changes
 Reversible when underlying cause has been treated
 A relative acute onset
 Disorientation
 Mental confusion
 Impulsive, irrational and violent behavior
 Lack of insight
 Psychomotor disturbances
 Emotional disturbances

DIAGNOSTIC FINDINGS:

 Basic laboratory examination, including CBC with differential, chemistry panel

(including blood urea nitrogen, creatinine, and ammonia), arterial blood gas values,
chest x-ray, toxicology screen, thyroid function tests and serologic tests for syphilis.
 Additional tests may include CT scan, MRI, additional blood chemistries, lumber
puncture, PET/ single-photon emission computed tomography scans.
 Complete mental status examination.
 Comprehensive physical examination.

DIFFERENCE BETWEEN DELIRIUM AND PSYCHIATRIC DISORDERS:

 Clouded consciousness or decreased level of alertness

 Disorientation
 Acuity of onset and course- serial mental status exams can help demonstrate this
 Age >40 without prior psych history
 Presence of risk factors for delirium, recent medical illness or treatment

SCHIZOPHRENIA VS DELIRIUM

 Onset of schizophrenia is rarely after 50.

 Auditory hallucinations are much more common than visual hallucinations
 Memory is grossly intact and disorientation is rare

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  Speech is not dysarthric
 No wide fluctuations over the course of a day

MOOD DISORDER VS DELIRIUM

 Mood disorders manifest persistent rather than labile mood with more gradual onset
 In mania the patient can be very agitated however cognitive performance is not
usually as impaired
 Flight of ideas usually have some thread of coherence unlike simple distractibility
 Disorientation is unusual in mania.

DELERIUM DEMENTIA

 Onset- Accute & rapid.  Slow & sudden.

 Duration- days to weeks.  Months to years.

 Causes- reversible but may  Irreversible.

progressed to dementia.

Clinical features-
Clinical features
 Level of consciousness-
 Level of consciousness is not
 Fluctuating/ clouded disturbed
 Usually normal.
 Orientation- impaired.
 Normal( except in late stage)

 Attention & conconcentration

impaired.  Good (except in late stage).

 Comprehension- poor
 Immediate, retention & recall is
disturbed.
 Memory- immediate, retention,  Hallucination may occur.
recall& recent memory is
disturbed.

 Perception- delusion&  Delusion are rare.

hallucination( visual hallucination
& very much frightening)

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  Thinking- unsystematised rapidly  Usually normal.
changing frightening delusion .

 Sleep- grossly disturbed.

 Not characteristics
 Anatomy dysfunction-  Inc. sensitivity to CO2, forced
hyperventilation, apnea
 Common postural hypotension,  Flexion posture, paratonic
flushing of face, high B.P. , rigidity in limbs
respiratory dysfunction & nausea

 Others- unstable/ coma

 Degenerative arteriosclerosis
Etiology- physical illness,
infections, trauma , endocrine&
metabolic disorder.

 Treatment- is given to primary

cause.
 Supportive treatment is given.

MEDICAL MANAGEMENT:

 Treatment generally occurs in acute hospital based settings where the goal is
diagnosis to identify specific reversible causes of the delirium so that treatment is
focused on ameliorating the causative factors.
 Pharmacologic therapy is dependent on underlying causes; additional drugs may be
used that are directed toward the reduction of the acute symptoms of delirium. These
include;
a. Benzodiazepines, such as lorazepam, for substance withdrawl states.
b. Neurolepticus, such as risperidone and haloperidol, for agitation.
c. Combined administration of haloperidol and lorazepam for agitated and psychotic
symptomatology.
 Environmental management:
a. Safe, structured environment.
b. Orientation facilitated by accurate clocks and calendars.
 Family teaching about the nature of the disorder.
 Family participation in the treatment plan in order to assist in the management of
behavior.

COMPLICATIONS:

 Falls with serious orthopedic or cerebral injuries.

 Self- inflicted injuries.
 Aggression or violence toward self, others or property.

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  Wandering events, in which the person can get lost and potentially suffer exposure,
hypothermia, injury and even death.
 Serious depression is demonstrated in caregivers who receive inadequate support.
 Caregiver stress and burden may result in patients neglect or abuse.

NURSING ASSESSMENT:

 Assess the onset and characteristics of symptoms.

 Establish cognitive status using standard measurement tools.
 Determine self care abilities.
 Assess threats to physical safety.
 Assess effect and emotional responsiveness.
 Assess ability and level of support available to caregivers.

NURSING DIAGNOSIS:

 Impaired verbal communication related to cerebral impairment as demonstrated by

altered memory, judgment, and word finding.
 Bathing and dressing self-care deficit related to cognitive impairment as demonstrated
by inattention and ability to complete ADLs.
 Risk for injury related to cognitive impairment and wandering behavior.
 Impaired social interaction related to cognitive impairment.
 Risk for violence: self directed or other directed related to suspicion and inability to
recognize people or places.

NURSING INTERVENTIONS:

IMPROVING COMMUNICATION

 Speak slowly and use short, simple words and phrases.

 Consistently identify yourself and address the person by name at each meeting.
 Focus on one piece of information at a time. Review what has been discussed with
patient.
 If patient has vision or hearing disturbances, have him or her wear prescription
eyeglasses or a hearing device.
 Keep environment well lit.
 Use clocks, calendars and familiar personal effects in patient’s view.
 If patient becomes verbally aggressive, identify and acknowledge feelings.
 If patient becomes aggressive, shift the topic to a safer, more familiar one.
 If patient becomes delusional, acknowledge feelings and reinforce reality. Do not
attempt to challenge the content of the delusion.

PROMOTING INDEPENDENCE IN SELF CARE

 Assess and monitor patients ability to perform ADLs.

 Encourage decision making regarding ADLs as much as possible.
 Label clothes with patient’s name, address, and telephone number.
 Use clothing with elastic and Velcro for fastenings rather than buttons or zippers,
which may be too difficult for patients to manipulate.

58
  Monitor food and fluid intake.
 Weigh patient weekly.
 Provide food that patient can eat while moving.
 Sit with patient during meals and assist by cueing.
 Initiate a bowel and bladder program early in the disease process to maintain
continence and prevent constipation or urine retention.

ENSURING SAFETY

 Discuss restriction of driving when recommended.

 Assess, patient’s home for safety: remove throw rugs, label rooms, and keep the house
well lit.
 Assess community for safety.
 Alert neighbors about patient’s wandering behavior.
 Alert police and have current pictures taken.
 Provide patients with a medic alert bracelet.
 Install complex safety locks on doors to outside or basement.
 Install safety bars in bathroom.
 Closely observe patient while he or she is smoking.
 Encourage physical activity during the daytime.
 Give patient a card with simple instructions in case he or she gets lost.
 Use nightlights.
 Install alarm and sensor devices on doors.

IMPROVING SOCIALIZATION

 Provide magazines with pictures as regarding and language abilities diminish.

 Encourage participation in simple, familiar group activities, such as singing,
reminiscing, doing puzzles, and painting.
 Encourage participation in simple activities that promote the exercise of large muscle
groups.

PREVENTING VIOLENCE AND AGGRESSION

 Respond calmly and do not raise your voice.

 Remove objects that might be used to harm self or others.
 Identify stressors that increase agitation.
 Distract patient when an upsetting situation develops.

HEALTH EDUCATION:

 Instruct family about the process of the disorder.

 Instruct family about safety measures, environment supports, and effective
interventions for common symptoms in order to provide care in the home.
 Instruct about and refer family members to community based groups.
 For additional information and support refer to health associations.

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BIBLIOGRAPHY

 Dr.Lalita K, “Mental health and psychiatric nursing”, edition 3rd, published by

Ananda.
 Neerja KP, “Essentials of mental health and psychiatric nursing”, edition 1st,
published by jaypee brothers.
 Sreevani R, “A guide to mental health and psychiatric nursing”, edition 3rd, published
by jaypee brothers.
 Lippincott; "Manual of nursing practice", published by Wolterskluwer, 10th edition,
Pp 1831-1835

 Victor's and Adams; "Principles of Neurology", published by Ropper H. Allan and

Brown H. Robert, 8th edition, Pg no- 114-123.

 Townsend Mary C, “Psychiatric Mental Health Nursing”, edition 4th, Philadelphia

publishers, page no-383-410.

 Sartorius Norman, “The ICD-10 Classification of Mental and Behavioural

Disorders”, Clinical descriptions and diagnostic guidelines, pg no-48-66.
 Sadock's & Kaplan, “Comprehensive Textbook of Psychiatry”, 8th Edition
Copyright ©2005 Lippincott Williams & Wilkins, pg no-1054-1058.
 www.google.com
 www.wikipedia.com

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