ORGANIC MENTAL DISORDERS

ORGANIC MENTAL DISORDERS

Introduction

Organic mental disorders refer to psychological disturbances arising out of brain dysfunction. The three terms delirium, dementia, and amnesic syndrome appear together in the classification manuals because they share a common, but not exclusive, organic etiology. However, these conditions have little in common from a historical, clinical, and psychopathological perspective. Because the notion of ‘organicity' is imprecise, it would perhaps be preferable to use Schneider's term ‘corporeally based manifestations’.

History

Hippocratus introduced the term ‘phrenitis and referred to its association between physical and febrile diseases. Celsus elaborated up on the concept of delirium and dementias in book ‘ De Medicana’. Aretaeus categorized the organic mental disorders in to acute and chronic types. Acute type included phrenitis/ delirium and lethargy, while dementia comes under chronic type.

Von Bonhoeffer introduced the term clouding of consciousness. He considered it as the core feature of acute organic mental disorders and he said its mainly due to systemic diseases like uremia, hepatic failure etc. he called them as acute exogenous reactions and he classified it in to five subtypes namely,delirium, epileptiform excitement, twilight state, hallucinosis and amentia. Eugine bleuler offered very coherent definition of ‘chronic brain syndrome’ and correlated with cerebral disorders of various causes. His son Manfred Bleuler described altered emotional responses such as apathy and irritability, defective control of impulse expression and increased or reduced intensity of various biological drives occurring in the organic brain disorders.

Definition

Organic Mental Disorders comprises “a range of mental disorders grouped together on the basis of their common, demonstrable etiology in cerebral disease, brain injury, or other insult leading to cerebral dysfunction” (World Health Organization, 1992).

Four criteria for Organic Mental Disorders:

(1) Evidence of cerebral disease, damage, or dysfunction, or of systemic physical disease, known to be associated with one of the listed syndromes

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

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

(4) Absence of evidence to suggest an alternative cause of the mental syndrome (such as a strong family history or precipitating stress).

ICD 10 Classification of Organic Mental Disorders

F00-F09

Organic, including symptomatic, mental disorders

F00 Dementia in Alzheimer's disease

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

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

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

F00.8 Dementia in Alzheimer's disease, unspecified

F01 Vascular dementia

F01.0 Vascular dementia of acute onset

F01.1 Multi-infarct dementia

F01.2 Subcortical vascular dementia

F01.3 Mixed cortical and subcortical vascular dementia

F01.8 Other vascular dementia

F01.9 Vascular dementia, unspecified

F02 Dementia in other diseases classified elsewhere

F02.0 Dementia in Pick's disease

F02.1 Dementia in Creutzfeldt-Jakob disease

F02.2 Dementia in Huntington's disease

F02.3 Dementia in Parkinson's disease

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

F02.8 Dementia in other specified diseases classified elsewhere

F03 Unspecified dementia

A fifth character may be used to specify dementia in F00-F03, as follows:

.x0 Without additional symptoms

.x1 With other symptoms, predominantly delusional

.x2 With other symptoms, predominantly hallucinatory

.x3 With other symptoms, predominantly depressive

.x4 With other mixed symptoms

A sixth character may be used to indicate the severity of the dementia:

.xx0 Mild

.xx1 Moderate

.xx2 Severe

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

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

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

F06.0 Organic hallucinosis

F06.1 Organic catatonic disorder

F06.2 Organic delusional [schizophrenia-like] disorder

F06.3 Organic mood [affective] disorder

.30 Organic manic disorder

.31 Organic bipolar disorder

.32 Organic depressive disorder

.33 Organic mixed affective disorder

F06.4 Organic anxiety disorder

F06.5 Organic dissociative disorder

F06.6 Organic emotionally labile [asthenic] disorder

F06.7 Mild cognitive disorder

.70 Not associated with a physical disorder

.71 Associated with a physical disorder

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

F06.9 Unspecified mental disorder due to brain damage and dysfunction and to physical disease

F07 Personality and behavioural disorders due to brain disease, damage and dysfunction

F07.0 Organic personality disorder

F07.1 Postencephalitic syndrome

F07.2 Postconcussional syndrome

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

F07.9 Unspecified mental disorder due to brain disease, damage and dysfunction

F09 Unspecified organic or symptomatic mental disorder

ETIOLOGY

•      Brain injury caused by trauma

Bleeding into the brain (intracerebral hemorrhage)

Bleeding into the space around the brain (subarachnoid hemorrhage)

Blood clot causing pressure on brain (chronic subdural hematoma)

Concussion

•      Breathing conditions

–     Low oxygen in the body (hypoxia)

–     High carbon dioxide levels in the body (hypercapnia)

•      Cardiovascular disorders

–     Abnormal heart rhythm (arrhythmias)

–     Brain injury due to high blood pressure (hypertensive brain injury)

–     Dementia due to many strokes (multi-infarct dementia)

–     Heart infections (endocarditis, myocarditis)

–     Stroke

–     Transient ischemic attack (TIA)

•      Degenerative disorders

–     Creutzfeldt-Jacob disease

–     Diffuse Lewy Body disease

–     Huntington's disease

–     Multiple sclerosis

–     Normal pressure hydrocephalus

–     Parkinson's disease

–     Pick's disease

•      Senile dementia, Alzheimer's type

•      Dementia due to metabolic causes

•      Drug and alcohol-related conditions

–     Alcohol withdrawal state

–     Intoxication, drug abuse, or alcohol use

–     Long-term effects of alcohol, Wernicke-Korsakoff syndrome

•      Withdrawal from drugs (especially sedative-hypnotics and corticosteroids)

•      Infections

–     Any sudden onset (acute) or long-term (chronic) infection

–     Blood poisoning (septicemia)

–     Swelling of the brain (encephalitis)

–     Swelling of the lining of the brain and spinal cord (meningitis)

•      Other medical disorders

–     Cancer

–     Kidney disease

–     Liver disease

–     Thyroid disease (high or low)

–     Vitamin deficiency (B12 and others)

DEMENTIA

Dementia is defined as a progressive impairment of cognitive functions occurring in clear consciousness (i.e., in the absence of delirium). Dementia consists of a variety of symptoms that suggest chronic and widespread dysfunction. Global impairment of intellect is the essential feature, manifested as difficulty with memory, attention, thinking, and comprehension. Other mental functions can often be affected, including mood, personality, judgment, and social behavior. Although specific diagnostic criteria are found for various dementias, such as Alzheimer's disease or vascular dementia, all dementias have certain common elements that result in significant impairment in social or occupational functioning and cause a significant decline from a previous level of functioning.

The critical clinical points of dementia are the identification of the syndrome and the clinical workup of its cause. The disorder can be progressive or static, permanent or reversible. An underlying cause is always assumed, although, in rare cases, it is impossible to determine a specific cause. The potential reversibility of dementia is related to the underlying pathological condition and to the availability and application of effective treatment. Approximately 15 percent of people with dementia have reversible illnesses if treatment is initiated before irreversible damage takes place.

Epidemiology

With the aging population, the prevalence of dementia is rising. The prevalence of moderate to severe dementia in different population groups is approximately 5 percent in the general population older than 65 years of age, 20 to 40 percent in the general population older than 85 years of age, 15 to 20 percent in outpatient general medical practices, and 50 percent in chronic care facilities.

Of all patients with dementia, 50 to 60 percent have the most common type of dementia, dementia of the Alzheimer's type (Alzheimer's disease). Dementia of the Alzheimer's type increases in prevalence with increasing age. For persons aged 65 years, men have a prevalence rate of 0.6 percent and women of 0.8 percent. At age 90, rates are 21 percent. For all these figures, 40 to 60 percent of cases are moderate to severe. The rates of prevalence (males to females) are 11 and 14 percent at age 85, 21 and 25 percent at age 90, and 36 and 41 percent at age 95. Patients with dementia of the Alzheimer's type occupy more than 50 percent of nursing home beds. More than 2 million persons with dementia are cared for in these homes. By 2050, current predictions suggest that there will be 14 million Americans with Alzheimer's disease and, therefore, more than 18 million people with dementia.

The second most common type of dementia is vascular dementia, which is causally related to cerebrovascular diseases. Hypertension predisposes a person to the disease. Vascular dementias account for 15 to 30 percent of all dementia cases. Vascular dementia is most common in persons between the ages of 60 and 70 and is more common in men than in women. Approximately 10 to 15 percent of patients have coexisting vascular dementia and dementia of the Alzheimer's type.

Other common causes of dementia, each representing 1 to 5 percent of all cases, include head trauma, alcohol-related dementias, and various movement disorder-related dementias, such as Huntington's disease and Parkinson's disease. Because dementia is a fairly general syndrome, it has many causes, and clinicians must embark on a careful clinical workup of a patient with dementia to establish its cause.

Etiology

The most common causes of dementia in individuals older than 65 years of age are (1) Alzheimer's disease; (2) vascular dementia and, (3) mixed vascular and Alzheimer's dementia. Other illnesses that account for approximately 10 percent include Lewy body dementia; Pick's disease; frontotemporal dementias; normal pressure hydrocephalus (NPH); alcoholic dementia; infectious dementia, such as human immunodeficiency virus (HIV) or syphilis; and Parkinson's disease. Many types of dementias evaluated in clinical settings can be attributable to reversible causes, such as metabolic abnormalities (e.g., hypothyroidism), nutritional deficiencies (e.g., vitamin B₁₂ or folate deficiencies), or dementia syndrome caused by depression.

Etiologies of Dementia

Degenerative dementias
   Alzheimer's disease
   Frontotemporal dementias (e.g., Pick's disease)
   Parkinson's disease
   Lewy body dementia
   Idiopathic cerebral ferrocalcinosis (Fahr's disease)
   Progressive supranuclear palsy
Miscellaneous
   Huntington's disease
   Wilson's disease
   Metachromatic leukodystrophy
   Neuroacanthocytosis
Psychiatric
   Pseudodementia of depression
   Cognitive decline in late-life schizophrenia
Physiologic
   Normal pressure hydrocephalus
Metabolic
   Vitamin deficiencies (e.g., vitamin B₁₂, folate)
   Endocrinopathies (e.g., hypothyroidism)
   Chronic metabolic disturbances (e.g., uremia)
Tumor
   Primary or metastatic (e.g., meningioma or metastatic breast or lung cancer)
Traumatic
   Dementia pugilistica, posttraumatic dementia
   Subdural hematoma
Infection
   Prion diseases (e.g., Creutzfeldt-Jakob disease, bovine spongiform encephalitis)
   Acquired immune deficiency syndrome (AIDS)
   Syphilis
Cardiac, vascular, and anoxia
   Infarction (single or multiple or strategic lacunar)
   Binswanger's disease (subcortical arteriosclerotic encephalopathy)
   Hemodynamic insufficiency (e.g., hypoperfusion or hypoxia)
Demyelinating diseases
   Multiple sclerosis
Drugs and toxins
   Alcohol
   Heavy metals
   Irradiation
   Pseudodementia due to medications (e.g., anticholinergics)
   Carbon monoxide

Clinical features

Memory impairment is generally a prominent early symptom of dementia. Individuals with dementia have difficulty learning new material. In more severe dementia, individuals also forget previously learned material, including the names of loved ones. Individuals with dementia may have difficulty with spatial tasks, such as navigating around the house or in the immediate neighborhood. Poor judgment and poor insight are also common. In order to make a diagnosis of dementia, these cognitive deficits must be sufficiently severe to cause impairment in occupational or social functioning and must represent a decline from a previous level of functioning. The order of onset and relative prominence of the cognitive disturbances and associated symptoms vary with the specific type of dementia.

Other symptoms of dementia include disinhibited behavior, including making inappropriate jokes, neglecting personal hygiene, exhibiting undue familiarity with strangers, or disregarding conventional rules of social conduct. Suicidal behavior may occur in mildly impaired individuals, who are more likely to have insight into their deficits. Anxiety is fairly common, and some patients manifest "catastrophic reactions," overwhelming emotional responses to relatively minor stressors such as changes in routine or environment. Depressed mood and sleep disturbances are common. Delusions of persecution and misidentification, and hallucinations, most commonly in the visual modality, could be present. Some patients exhibit sundowning, a peak period of agitation during the evening hours. Dementia is sometimes accompanied by motor disturbances, which may include gait difficulties, slurred speech, and a variety of abnormal movements. Other neurological symptoms, such as myoclonus and seizures, may also occur.

ICD 10 Classification of dementia

F00 Dementia in Alzheimer's disease

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

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

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

F00.8 Dementia in Alzheimer's disease, unspecified

F01 Vascular dementia

F01.0 Vascular dementia of acute onset

F01.1 Multi-infarct dementia

F01.2 Subcortical vascular dementia

F01.3 Mixed cortical and subcortical vascular dementia

F01.8 Other vascular dementia

F01.9 Vascular dementia, unspecified

F02 Dementia in other diseases classified elsewhere

F02.0 Dementia in Pick's disease

F02.1 Dementia in Creutzfeldt-Jakob disease

F02.2 Dementia in Huntington's disease

F02.3 Dementia in Parkinson's disease

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

F02.8 Dementia in other specified diseases classified elsewhere

F03 Unspecified dementia

A fifth character may be used to specify dementia in F00-F03, as follows:

.x0 Without additional symptoms

.x1 With other symptoms, predominantly delusional

.x2 With other symptoms, predominantly hallucinatory

.x3 With other symptoms, predominantly depressive

.x4 With other mixed symptoms

A sixth character may be used to indicate the severity of the dementia:

.xx0 Mild

.xx1 Moderate

.xx2 Severe

INVESTIGATIONS

Investigation of dementia is important primarily to exclude reversible causes of cognitive deterioration:

Perform a midstream urine test if delirium is a possibility.

Blood tests:

• FBC, ESR, CRP - anaemia, vasculitis
• T4 and TSH - hypothyroidism
• biochemical screen - hypercalcium or hypocalcaemia
• urea and creatinine - renal failure, dialysis dementia
• glucose
• B12 and folate - vitamin deficiency dementia
• clotting and albumin - liver function

Other possible blood tests (though not routinely requested in primary care) include:

• syphilis serology
• HIV - if in young person
• caeruloplasmin - Wilson's disease

Conduct investigations such as chest X-ray or electrocardiogram (ECG) as determined by clinical presentation.

Other possible specialist investigations include:

• cerebrospinal fluid examination if Creutzfeldt-Jakob disease (CJD) or other forms of rapidly progressive dementia are suspected
• electroencephalography (EEG) - not routinely indicated

consider in:

• suspected delirium, frontotemporal dementia or CJD
• associated seizure disorder in those with dementia
• brain biopsy
• consider only if a potentially reversible cause is suspected that cannot be diagnosed in any other way
• imaging
• use structural imaging to exclude other cerebral pathologies and help establish the subtype of dementia
• imaging may help to identify treatable causes such as subdural haematoma, normal pressure hydrocephalus, cerebral tumours
• Prefer MRI to assist with early diagnosis and detect subcortical vascular changes. However, CT scanning could be used
• priority for CT scan should be given to the following
• atypical presentation
• rapid unexplained deterioration
• unexplained focal neurological signs or symptoms
• history of recent head injury
• urinary incontinence
• gait ataxia early in the illness (2)
• take specialist advice when interpreting scans in people with learning disabilities
• use perfusion hexamethylpropyleneamine oxime (HMPAO) single-photon emission computed tomography (SPECT) to help differentiate Alzheimer's disease, vascular dementia and frontotemporal dementia
• the test is not useful in people with Down's syndrome, who may have SPECT abnormalities resembling Alzheimer's disease throughout life
• if HMPAO SPECT is unavailable, consider 2-[18F]fluoro-2-deoxy-D-glucose positron emission tomography (FDG PET) as an alternative
• use dopaminergic iodine-123-radiolabelled 2b-carbomethoxy-3b-(4-iodophenyl)-N-(3-fluoropropyl) nortropane (FP-CIT) SPECT to confirm suspected dementia with Lewy bodies (DLB)

Genetic testing – can be offered to patients or to their unaffected relatives if a genetic cause is suspected (1).

DEMENTIA OF THE ALZHEIMER'S TYPE

In 1907, Alois Alzheimer first described the condition that later assumed his name. He described a 51-year-old woman with a 4¹/₂-year course of progressive dementia. The final diagnosis of Alzheimer's disease requires a neuropathological examination of the brain; nevertheless, dementia of the Alzheimer's type is commonly diagnosed in the clinical setting after other causes of dementia have been excluded from diagnostic consideration.

Genetic Factors

Although the cause of dementia of the Alzheimer's type remains unknown, progress has been made in understanding the molecular basis of the amyloid deposits that are a hallmark of the disorder's neuropathology. Some studies have indicated that as many as 40 percent of patients have a family history of dementia of the Alzheimer's type; thus, genetic factors are presumed to play a part in the development of the disorder, at least in some cases. Additional support for a genetic influence is the concordance rate for monozygotic twins, which is higher than the rate for dizygotic twins (43 percent vs. 8 percent, respectively). In several well-documented cases, the disorder has been transmitted in families through an autosomal dominant gene, although such transmission is rare. Alzheimer's type dementia has shown linkage to chromosomes 1, 14, and 21.

Amyloid Precursor Protein

The gene for amyloid precursor protein is on the long arm of chromosome 21. The process of differential splicing yields four forms of amyloid precursor protein. The β/A4 protein, the major constituent of senile plaques, is a 42-amino acid peptide that is a breakdown product of amyloid precursor protein. In Down syndrome (trisomy 21) are found three copies of the amyloid precursor protein gene, and in a disease in which a mutation is found at codon 717 in the amyloid precursor protein gene, a pathological process results in the excessive deposition of β/A4 protein. Whether the processing of abnormal amyloid precursor protein is of primary causative significance in Alzheimer's disease is unknown, but many research groups are studying both the normal metabolic processing of amyloid precursor protein and its processing in patients with dementia of the Alzheimer's type in an attempt to answer this question.

Multiple E4 Genes

One study implicated gene E4 in the origin of Alzheimer's disease. People with one copy of the gene have Alzheimer's disease three times more frequently than do those with no E4 gene, and people with two E4 genes have the disease eight times more frequently than do those with no E4 gene. Diagnostic testing for this gene is not currently recommended because it is found in persons without dementia and not found in all cases of dementia.

Neuropathology

The classic gross neuroanatomical observation of a brain from a patient with Alzheimer's disease is diffuse atrophy with flattened cortical sulci and enlarged cerebral ventricles. The classic and pathognomonic microscopic findings are senile plaques, neurofibrillary tangles, neuronal loss (particularly in the cortex and the hippocampus), synaptic loss (perhaps as much as 50 percent in the cortex), and granulovascular degeneration of the neurons. Neurofibrillary tanglesare composed of cytoskeletal elements, primarily phosphorylated tau protein, although other cytoskeletal proteins are also present. Neurofibrillary tangles are not unique to Alzheimer's disease; they also occur in Down syndrome, dementia pugilistica (punch-drunk syndrome), Parkinson-dementia complex of Guam, Hallervorden-Spatz disease, and the brains of normal people as they age. Neurofibrillary tangles are commonly found in the cortex, the hippocampus, the substantia nigra, and the locus ceruleus.

Senile plaques, also referred to as amyloid plaques, more strongly indicate Alzheimer's disease, although they are also seen in Down syndrome and, to some extent, in normal aging. Senile plaques are composed of a particular protein, β/A4, and astrocytes, dystrophic neuronal processes, and microglia. The number and the density of senile plaques present in postmortem brains have been correlated with the severity of the disease that affected the persons.

Neurotransmitters

The neurotransmitters that are most often implicated in the pathophysiological condition of Alzheimer's disease are acetylcholine and norepinephrine, both of which are hypothesized to be hypoactive in Alzheimer's disease. Several studies have reported data consistent with the hypothesis that specific degeneration of cholinergic neurons is present in the nucleus basalis of Meynert in persons with Alzheimer's disease. Other data supporting a cholinergic deficit in Alzheimer's disease demonstrate decreased acetylcholine and choline acetyltransferase concentrations in the brain. Choline acetyltransferase is the key enzyme for the synthesis of acetylcholine, and a reduction in choline acetyltransferase concentration suggests a decrease in the number of cholinergic neurons present. Additional support for the cholinergic deficit hypothesis comes from the observation that cholinergic antagonists, such as scopolamine and atropine, impair cognitive abilities, whereas cholinergic agonists, such as physostigmine and arecoline, enhance cognitive abilities. Decreased norepinephrine activity in Alzheimer's disease is suggested by the decrease in norepinephrine-containing neurons in the locus ceruleus found in some pathological examinations of brains from persons with Alzheimer's disease. Two other neurotransmitters implicated in the pathophysiological condition of Alzheimer's disease are the neuroactive peptides somatostatin and corticotropin; decreased concentrations of both have been reported in persons with Alzheimer's disease.

Other Causes

Another theory to explain the development of Alzheimer's disease is that an abnormality in the regulation of membrane phospholipid metabolism results in membranes that are less fluid that is, more rigid than normal. Several investigators are using molecular resonance spectroscopic imaging to assess this hypothesis directly in patients with dementia of the Alzheimer's type. Aluminum toxicity has also been hypothesized to be a causative factor, because high levels of aluminum have been found in the brains of some patients with Alzheimer's disease; but this is no longer considered a significant etiological factor. Excessive stimulation by the transmitter glutamate that may damage neurons is another theory of causation.

Familial Multiple System Taupathy with Presenile Dementia

A recently discovered type of dementia, familial multiple system taupathy, shares some brain abnormalities found in people with Alzheimer's disease. The gene that causes the disorder is thought to be carried on chromosome 17. The symptoms of the disorder include short-term memory problems and difficulty maintaining balance and walking. The onset of disease occurs in the 40s and 50s, and persons with the disease live an average of 11 years after the onset of symptoms.

As in patients with Alzheimer's disease, tau protein builds up in neurons and glial cells of persons with familial multiple system taupathy. Eventually, the protein buildup kills brain cells. The disorder is not associated with the senile plaques seen with Alzheimer's disease.

VASCULAR DEMENTIA

The primary cause of vascular dementia (multi-infarct dementia), is presumed to be multiple areas of cerebral vascular disease, resulting in a symptom pattern of dementia. Vascular dementia most commonly is seen in men, especially those with preexisting hypertension or other cardiovascular risk factors. The disorder affects primarily small- and medium-sized cerebral vessels, which undergo infarction and produce multiple parenchymal lesions spread over wide areas of the brain. The causes of the infarctions can include occlusion of the vessels by arteriosclerotic plaques or thromboemboli from distant origins (e.g., heart valves). An examination of a patient may reveal carotid bruits, fundoscopic abnormalities, or enlarged cardiac chambers

Binswanger's Disease

Binswanger's disease, also known as subcortical arteriosclerotic encephalopathy, is characterized by the presence of many small infarctions of the white matter that spare the cortical regions. Although Binswanger's disease was previously considered a rare condition, the advent of sophisticated and powerful imaging techniques, such as magnetic resonance imaging (MRI), has revealed that the condition is more common than previously thought.

Pick's Disease

In contrast to the parietal-temporal distribution of pathological findings in Alzheimer's disease, Pick's disease is characterized by a preponderance of atrophy in the frontotemporal regions. These regions also have neuronal loss, gliosis, and neuronal Pick's bodies, which are masses of cytoskeletal elements. Pick's bodies are seen in some postmortem specimens but are not necessary for the diagnosis. The cause of Pick's disease is unknown, but the disease constitutes approximately 5 percent of all irreversible dementias. It is most common in men, especially those who have a first-degree relative with the condition. Pick's disease is difficult to distinguish from dementia of the Alzheimer's type, although the early stages of Pick's disease are more often characterized by personality and behavioral changes, with relative preservation of other cognitive functions, and it typically begins before 75 years of age. Familial cases may have an earlier onset, and some studies have shown that approximately one half of the cases of Pick's disease are familial.

Lewy Body Disease

Lewy body disease is a dementia clinically similar to Alzheimer's disease and often characterized by hallucinations, parkinsonian features, and extrapyramidal signs. Lewy inclusion bodies are found in the cerebral cortex. The exact incidence is unknown. These patients show marked adverse effects when given antipsychotic medications.

Huntington's Disease

Huntington's disease is classically associated with the development of dementia. The dementia seen in this disease is the subcortical type of dementia, characterized by more motor abnormalities and fewer language abnormalities than in the cortical type of dementia. The dementia of Huntington's disease exhibits psychomotor slowing and difficulty with complex tasks, but memory, language, and insight remain relatively intact in the early and middle stages of the illness. As the disease progresses, however, the dementia becomes complete; the features distinguishing it from dementia of the Alzheimer's type are the high incidence of depression and psychosis, in addition to the classic choreoathetoid movement disorder.

HIV-Related Dementia

Encephalopathy in HIV infection is associated with dementia and is termed acquired immune deficiency syndrome (AIDS) dementia complex, or HIV dementia. Patients infected with HIV experience dementia at an annual rate of approximately 14 percent. An estimated 75 percent of patients with AIDS have involvement of the central nervous system (CNS) at the time of autopsy. The development of dementia in people infected with HIV is often paralleled by the appearance of parenchymal abnormalities in MRI scans. Other infectious dementias are caused by Cryptococcus or Treponema pallidum.

The diagnosis of AIDS dementia complex is made by confirmation of HIV infection and exclusion of alternative pathology to explain cognitive impairment. The American Academy of Neurology AIDS Task Force developed research criteria for the clinical diagnosis of CNS disorders in adults and adolescents. The AIDS Task Force criteria for AIDS dementia complex require laboratory evidence for systemic HIV, at least two cognitive deficits, and the presence of motor abnormalities or personality changes. Personality changes may be manifested by apathy, emotional lability, or behavioral disinhibition. As with the DSM-IV-TR, the AIDS Task Force criteria also require the absence of clouding of consciousness or evidence of another etiology that could produce the cognitive impairment. Cognitive, motor, and behavioral changes are assessed using physical, neurological, and psychiatric examinations, in addition to neuropsychological testing.

Head Trauma-Related Dementia

Dementia can be a sequela of head trauma. The so-called punch-drunk syndrome occurs in boxers after repeated head trauma over many years. It is characterized by emotional labiality, dysarthria, and impulsivity.

Diagnosis and Clinical Features

The dementia diagnoses in DSM-IV-TR are dementia of the Alzheimer's type, vascular dementia, dementia due to other general medical conditions, substance-induced persisting dementia, dementia due to multiple etiologies, and dementia not otherwise specified.

The diagnosis of dementia is based on the clinical examination, including a mental status examination, and on information from the patient's family, friends, and employers. Complaints of a personality change in a patient older than age 40 suggest that a diagnosis of dementia should be carefully considered.

Clinicians should note patients' complaints about intellectual impairment and forgetfulness as well as evidence of patients' evasion, denial, or rationalization aimed at concealing cognitive deficits. Excessive orderliness, social withdrawal, or a tendency to relate events in minute detail can be characteristic, and sudden outbursts of anger or sarcasm can occur. Patients' appearance and behavior should be observed. Lability of emotions, sloppy grooming, uninhibited remarks, silly jokes, or a dull, apathetic, or vacuous facial expression and manner suggest the presence of dementia, especially when coupled with memory impairment.

Memory impairment is typically an early and prominent feature in dementia, especially in dementias involving the cortex, such as dementia of the Alzheimer's type. Early in the course of dementia, memory impairment is mild and usually most marked for recent events; people forget telephone numbers, conversations, and events of the day. As the course of dementia progresses, memory impairment becomes severe, and only the earliest learned information (e.g., a person's place of birth) is retained.

Psychiatric and Neurological Changes

Personality

Changes in the personality of a person with dementia are especially disturbing for their families. Preexisting personality traits may be accentuated during the development of a dementia. Patients with dementia may also become introverted and seem to be less concerned than they previously were about the effects of their behavior on others. Persons with dementia who have paranoid delusions are generally hostile to family members and caretakers. Patients with frontal and temporal involvement are likely to have marked personality changes and may be irritable and explosive.

Hallucinations and Delusions

An estimated 20 to 30 percent of patients with dementia (primarily patients with dementia of the Alzheimer's type) have hallucinations, and 30 to 40 percent have delusions, primarily of a paranoid or persecutory and unsystematized nature, although complex, sustained, and well-systematized delusions are also reported by these patients. Physical aggression and other forms of violence are common in demented patients who also have psychotic symptoms.

Mood

In addition to psychosis and personality changes, depression and anxiety are major symptoms in an estimated 40 to 50 percent of patients with dementia, although the full syndrome of depressive disorder may be present in only 10 to 20 percent. Patients with dementia also may exhibit pathological laughter or crying that is, extremes of emotions with no apparent provocation.

Cognitive Change

In addition to the aphasias in patients with dementia, apraxias and agnosias are common, and they are included as potential diagnostic criteria in DSM-IV-TR. Other neurological signs that can be associated with dementia are seizures, seen in approximately 10 percent of patients with dementia of the Alzheimer's type and in 20 percent of patients with vascular dementia, and atypical neurological presentations, such as nondominant parietal lobe syndromes. Primitive reflexes, such as the grasp, snout, suck, tonic-foot, and palmomental reflexes, may be present on neurological examination, and myoclonic jerks are present in 5 to 10 percent of patients.

Patients with vascular dementia may have additional neurological symptoms, such as headaches, dizziness, faintness, weakness, focal neurological signs, and sleep disturbances, possibly attributable to the location of the cerebrovascular disease. Pseudobulbar palsy, dysarthria, and dysphagia are also more common in vascular dementia than in other dementing conditions.

Catastrophic Reaction

Patients with dementia also exhibit a reduced ability to apply what Kurt Goldstein called the abstract attitude. Patients have difficulty generalizing from a single instance, forming concepts, and grasping similarities and differences among concepts. Furthermore, the ability to solve problems, to reason logically and to make sound judgments is compromised. Goldstein also described a catastrophic reaction marked by agitation secondary to the subjective awareness of intellectual deficits under stressful circumstances. Persons usually attempt to compensate for defects by using strategies to avoid demonstrating failures in intellectual performance; they may change the subject, make jokes, or otherwise divert the interviewer. Lack of judgment and poor impulse control appear commonly, particularly in dementias that primarily affect the frontal lobes. Examples of these impairments include coarse language, inappropriate jokes, neglect of personal appearance and hygiene, and a general disregard for the conventional rules of social conduct.

Sundowner Syndrome

Sundowner syndrome is characterized by drowsiness, confusion, ataxia, and accidental falls. It occurs in older people who are overly sedated and in patients with dementia who react adversely to even a small dose of a psychoactive drug. The syndrome also occurs in demented patients when external stimuli, such as light and interpersonal orienting cues, are diminished.

DIAGNOSITIC CRITERIA

1.      Dementia of the Alzheimer's Type

Diagnostic criteria for dementia of the Alzheimer's type emphasize the presence of memory impairment and the associated presence of at least one other symptom of cognitive decline (aphasia, apraxia, agnosia, or abnormal executive functioning). The diagnostic criteria also require a continuing and gradual decline in functioning, impairment in social or occupational functioning, and the exclusion of other causes of dementia. According to DSM-IV-TR, the age of onset can be characterized as early (at age 65 or younger) or late (after age 65) and any predominant behavioral symptom should be coded with the diagnosis, if appropriate.

2.      Vascular Dementia

The general symptoms of vascular dementia are the same as those for dementia of the Alzheimer's type, but the diagnosis of vascular dementia requires either clinical or laboratory evidence in support of a vascular cause of the dementia. Vascular dementia is more likely to show a decremental, stepwise deterioration than is Alzheimer's disease.

3.      Dementia Due to Other General Medical Conditions

The DSM-IV-TR lists six specific causes of dementia that can be coded directly: HIV disease, head trauma, Parkinson's disease, Huntington's disease, Pick's disease, and Creutzfeldt-Jakob disease. A seventh category allows clinicians to specify other non-psychiatric medical conditions associated with dementia.

4.      Substance-Induced Persisting Dementia

To facilitate the clinician's thinking about differential diagnosis, substance-induced persisting dementia is listed in two places in the DSM-IV-TR, with the dementias and with the substance-related disorders. The specific substances that DSM-IV-TR cross references are alcohol, inhalants, sedatives, hypnotics, or anxiolytics, and other or unknown substances.

5.      Alcohol-Induced Persisting Dementia

To make the diagnosis of alcohol-induced persisting dementia, the criteria for dementia must be met. Because amnesia can also occur in the context Korsakoff's psychosis, it is important to distinguish between memory impairment accompanied by other cognitive deficits (i.e., dementia) and amnesia caused by thiamine deficiency. To complicate matters, however, evidence also suggests that other cognitive functions, such as attention and concentration, may also be impaired in Wernicke-Korsakoff syndrome. In addition, alcohol abuse is frequently associated with mood changes, so poor concentration and other cognitive symptoms often observed in the context of a major depression must also be ruled out. Prevalence rates differ considerably according to the population studied and the diagnostic criteria used, although alcohol-related dementia has been estimated to account for approximately 4 percent of dementias.

INVESTIGATIONS

A comprehensive laboratory workup must be performed when evaluating a patient with dementia. The purposes of the workup are to detect reversible causes of dementia and to provide the patient and family with a definitive diagnosis. The range of possible causes of dementia mandates selective use of laboratory tests. The evaluation should follow informed clinical suspicion, based on the history and physical and mental status examination results. The continued improvements in brain imaging techniques, particularly MRI, have made differentiation between dementia of the Alzheimer's type and vascular dementia, in some cases, somewhat more straightforward than in the past. An active area of research is the use of single photon emission computed tomography (SPECT) to detect patterns of brain metabolism in various types of dementias; the use of SPECT images may soon help in the clinical differential diagnosis of dementing illnesses.

A general physical examination is a routine component of the workup for dementia. It may reveal evidence of systemic disease causing brain dysfunction, such as an enlarged liver and hepatic encephalopathy, or it may demonstrate systemic disease related to particular CNS processes. The detection of Kaposi's sarcoma, for example, should alert the clinician to the probable presence of AIDS and the associated possibility of AIDS dementia complex. Focal neurological findings, such as asymmetrical hyper reflexia or weakness, are seen more often in vascular than in degenerative disease. Frontal lobe signs and primitive reflexes occur in many disorders and often point to greater progression.

Course and Prognosis

The classic course of dementia is an onset in the patient's 50s or 60s, with gradual deterioration over 5 to 10 years, leading eventually to death. The age of onset and the rapidity of deterioration vary among different types of dementia and within individual diagnostic categories. The average survival expectation for patients with dementia of the Alzheimer's type is approximately 8 years, with a range of 1 to 20 years. Data suggest that in persons with an early onset of dementia or with a family history of dementia the disease is likely to have a rapid course. In a recent study of 821 persons with Alzheimer's disease, the median survival time was 3.5 years. Once dementia is diagnosed, patients must have a complete medical and neurological workup, because 10 to 15 percent of all patients with dementia have a potentially reversible condition if treatment is initiated before permanent brain damage occurs.

The most common course of dementia begins with a number of subtle signs that may, at first, be ignored by both the patient and the people closest to the patient. A gradual onset of symptoms is most commonly associated with dementia of the Alzheimer's type, vascular dementia, endocrinopathies, brain tumors, and metabolic disorders. Conversely, the onset of dementia resulting from head trauma, cardiac arrest with cerebral hypoxia, or encephalitis can be sudden. Although the symptoms of the early phase of dementia are subtle, they become conspicuous as the dementia progresses, and family members may then bring a patient to a physician's attention. People with dementia may be sensitive to the use of benzodiazepines or alcohol, which can precipitate agitated, aggressive, or psychotic behavior. In the terminal stages of dementia, patients become empty shells of their former selves profoundly disoriented, incoherent, amnestic, and incontinent of urine and feces.

With psychosocial and pharmacological treatment and possibly because of the self-healing properties of the brain, the symptoms of dementia may progress slowly for a time or may even recede somewhat. Symptom regression is certainly a possibility in reversible dementias (dementias caused by hypothyroidism, normal pressure hydrocephalus, and brain tumors) once treatment is initiated. The course of the dementia varies from a steady progression (commonly seen with dementia of the Alzheimer's type) to an incrementally worsening dementia (commonly seen with vascular dementia) to a stable dementia (as may be seen in dementia related to head trauma).

Psychosocial Determinants

The severity and course of dementia can be affected by psychosocial factors. The greater a person's premorbid intelligence and education, the better the ability to compensate for intellectual deficits. People who have a rapid onset of dementia use fewer defenses than do those who experience an insidious onset. Anxiety and depression can intensify and aggravate the symptoms. Pseudodementia occurs in depressed people who complain of impaired memory but, in fact, are suffering from a depressive disorder. When the depression is treated, the cognitive defects disappear.

TREATMENT

The first step in the treatment of dementia is verification of the diagnosis. Accurate diagnosis is imperative, for the progression may be halted or even reversed if appropriate therapy is provided. Preventive measures are important, particularly in vascular dementia. Such measures might include changes in diet, exercise, and control of diabetes and hypertension. Pharmacological agents might include antihypertensive, anticoagulant, or antiplatelet agents. Blood pressure control should aim for the higher end of the normal range, because that has been demonstrated to improve cognitive function in patients with vascular dementia. Blood pressure below the normal range has been demonstrated to further impair cognitive function in the patient with dementia. The choice of antihypertensive agent can be significant in that β-adrenergic receptor antagonists have been associated with exaggeration of cognitive impairment. Angiotensin-converting enzyme (ACE) inhibitors and diuretics have not been linked to exaggeration of cognitive impairment and are thought to lower blood pressure without affecting cerebral blood flow, which is presumed to be correlated with cognitive function. Surgical removal of carotid plaques may prevent subsequent vascular events in carefully selected patients. The general treatment approach to patients with dementia is to provide supportive medical care, emotional support for the patients and their families, and pharmacological treatment for specific symptoms, including disruptive behavior.

Psychosocial Therapies

The deterioration of mental faculties has significant psychological meaning for patients with dementia. The experience of a sense of continuity over time depends on memory. Recent memory is lost before remote memory in most cases of dementia, and many patients are highly distressed by clearly recalling how they used to function while observing their obvious deterioration. At the most fundamental level, the self is a product of brain functioning. Patients' identities begin to fade as the illness progresses, and they can recall less and less of their past. Emotional reactions ranging from depression to severe anxiety to catastrophic terror can stem from the realization that the sense of self is disappearing.

Patients often benefit from a supportive and educational psychotherapy in which the nature and course of their illness are clearly explained. They may also benefit from assistance in grieving and accepting the extent of their disability and from attention to self-esteem issues. Any areas of intact functioning should be maximized by helping patients identify activities in which successful functioning is possible. A psychodynamic assessment of defective ego functions and cognitive limitations can also be useful. Clinicians can help patients find ways to deal with the defective ego functions, such as keeping calendars for Psychodynamic interventions with family members of patients with dementia may be of great assistance. Those who take care of a patient struggle with feelings of guilt, grief, anger, and exhaustion as they watch a family member gradually deteriorate. A common problem that develops among caregivers involves their self-sacrifice in caring for a patient. The gradually developing resentment from this self-sacrifice is often suppressed because of the guilt feelings it produces. Clinicians can help caregivers understand the complex mixture of feelings associated with seeing a loved one decline and can provide understanding as well as permission to express these feelings. Clinicians must also be aware of the caregivers' tendencies to blame themselves or others for patients' illnesses and must appreciate the role that patients with dementia play in the lives of family members.

Pharmacotherapy

Clinicians may prescribe benzodiazepines for insomnia and anxiety, antidepressants for depression, and antipsychotic drugs for delusions and hallucinations, but they should be aware of possible idiosyncratic drug effects in older people (e.g., paradoxical excitement, confusion, and increased sedation). In general, drugs with high anticholinergic activity should be avoided.

Donepezil, rivastigmine, galantamine, and tacrine are cholinesterase inhibitors used to treat mild to moderate cognitive impairment in Alzheimer's disease. They reduce the inactivation of the neurotransmitter acetylcholine and, thus, potentiate the cholinergic neurotransmitter, which in turn produces a modest improvement in memory and goal-directed thought. These drugs are most useful for persons with mild to moderate memory loss who have sufficient preservation of their basal forebrain cholinergic neurons to benefit from augmentation of cholinergic neurotransmission.

Donepezil is well tolerated and widely used. Tacrine is rarely used, because of its potential for hepatotoxicity. Fewer clinical data are available for rivastigmine and galantamine, which appear more likely to cause gastrointestinal (GI) and neuropsychiatric adverse effects than does donepezil. None of these medications prevents the progressive neuronal degeneration of the disorder.

Memantine protects neurons from excessive amounts of glutamate, which may be neurotoxic. The drug is sometimes combined with donepezil. It has been known to improve dementia.

Other Treatment Approaches

Other drugs being tested for cognitive-enhancing activity include general cerebral metabolic enhancers, calcium channel inhibitors, and serotonergic agents. Some studies have shown that selegiline (Eldepryl), a selective type B monoamine oxidase (MAO_B) inhibitor, may slow the advance of this disease. Ondansetron (Zofran), a 5-HT₃ receptor antagonist, is under investigation.

Estrogen replacement therapy may reduce the risk of cognitive decline in postmenopausal women; however, more studies are needed to confirm this effect. Complementary and alternative medicine studies of ginkgo biloba and other phytomedicinals to see if they have a positive effect on cognition. Reports have appeared of patients using nonsteroidal anti-inflammatory agents having a lower risk of developing Alzheimer's disease. Vitamin E has not been shown to be of value in preventing the disease.

Research study on dementia:

Ginkgo has been proposed as a treatment for Alzheimer's disease on the basis of positive preclinical results in mice and a 2006 study that found 160 mg of ginkgo extract as effective as a daily 5 mg dose of the cholinesterase inhibitor donepezil in human subjects. However, a 2008 randomized controlled clinical trial published in the International Journal of Geriatric Psychiatry found gingko ineffective at treating dementia in humans. A second randomized controlled trial, published in JAMA in 2009, similarly found no benefit from ginkgo in preventing cognitive decline or dementia. A more recent meta-analysis of nine studies of ginkgo for use in dementia concluded that it was more effective than placebo although, like other dementia drugs, the clinical significance of these moderate effects was difficult to quantify.

Nursing Diagnoses and Interventions Dementia and Amnestic Disorders

1.      Risk for trauma related to chronic alteration in structure or function of brain tissue, secondary to the aging process, multiple infarcts, HIV disease, head trauma, chronic substance abuse, or progressively dysfunctional physical conditions.

Goals/Objectives

Short-Term Goals

1. Client will call for assistance when ambulating or carrying out other activities.

2. Client will not experience physical injury.

Long-Term Goal

Client will not experience physical injury.

Interventions

1.  Assess client’s level of disorientation and confusion to determine specific requirements for safety.

2. Institute appropriate safety measures, such as the following:

a. Place furniture in room in an arrangement that best accommodates client’s disabilities.

b. Observe client behaviors frequently; assign staff on one-to one basis if condition warrants; accompany and assist client when ambulating; use wheelchair for transporting long distances.

c. Store items that client uses frequently within easy access.

d. Remove potentially harmful articles from client’s room: cigarettes, matches, lighters, sharp objects.

e. Remain with client while he or she smokes.

f. Pad side rails and headboard of client with seizure disorder. Institute seizure precautions as described in procedure manual of individual institution.

g. If client is prone to wander, provide an area within which wandering can be carried out safely.

3. Frequently orient client to reality and surroundings.

4. Use tranquilizing medications and soft restraints, as prescribed by physician, for client’s protection during periods of excessive hyperactivity.

5. Teach prospective caregivers methods that have been successful in preventing client injury.

2. Risk for self-directed or other-directed violence related to chronic alteration in structure or function of brain tissue, secondary to the aging process, multiple infarcts, HIV disease, head trauma, chronic substance abuse, or progressively dysfunctional physical condition resulting in the following symptoms: delusional thinking suspiciousness of others hallucinations illusions disorientation or confusion impairment of impulse control inaccurate perception of the environment body language- rigid posture, clenching of fists and jaw, hyperactivity, pacing, breathlessness, and threatening stances suicidal ideation, plan, available means cognitive impairment [ depressed mood]

Goals/Objectives

Short-Term Goals

1. Client will maintain agitation at manageable level so as not to become violent.

2. Client will not harm self or others.

Long-Term Goal

Client will not harm self or others.

Interventions

1. Assess client’s level of anxiety and behaviors that indicate the anxiety is increasing.

2. Maintain low level of stimuli in client’s environment (low lighting, few people, simple decor, low noise level).

3. Remove all potentially dangerous objects from client’s environment.

4. Have sufficient staff available to execute a physical confrontation, if necessary.

5. Maintain a calm manner with client. Attempt to prevent frightening the client unnecessarily. Provide continual reassurance and support.

6. Interrupt periods of unreality and reorient.

7. Use tranquilizing medications and soft restraints, as prescribed by physician

8. Sit with client and provide one-to-one observation if assessed to be actively suicidal.

Teach relaxation exercises to intervene in times of increasing anxiety.

10. Teach prospective caregivers to recognize client behaviors that indicate anxiety is increasing and ways to intervene before violence occurs.

3. DISTURBED THOUGHT PROCESSES related to Alteration in structure/function of brain tissue, secondary to advanced age /Vascular disease/ Hypertension /Cerebral hypoxia /Long-term abuse of mood- or behavior-altering substances /Exposure to environmental toxins/ Various other physical disorders that predispose to cerebral abnormalities.

Goals/Objectives

Short-Term Goal

Client will accept explanations of inaccurate interpretations within the environment within 5 days.

Long-Term Goal

With assistance from caregiver, client will be able to interrupt non reality-based thinking.

Interventions

1.      Frequently orient client to reality and surroundings. Allow client to have familiar objects around him or her. Use other items, such as clock, calendar, and daily schedules, to assist in maintaining reality orientation.

2.      Teach prospective caregivers how to orient client to time, person, place, and circumstances, as required.

3.      Give positive feedback when thinking and behavior are appropriate, or when client verbalizes that certain ideas expressed are not based in reality.

4.      Use simple explanations and face-to-face interaction when communicating with client. Do not shout message into client’s ear.

5.      Express reasonable doubt if client relays suspicious beliefs in response to delusional thinking. Discuss with client the potential personal negative effects of continued suspiciousness of others. Reinforce accurate perception of people and situations.

6.      Do not permit rumination of false ideas. When this begins, talk to client about real people and real events.

7.      Close observation of client’s behavior is indicated if delusional thinking reveals an intention for violence.

4. SELF-CARE DEFICIT related to Disorientation/ Confusion/ Memory deficits as evidenced by Inability to fulfill ADLs

Goals/Objectives

Short-Term Goal

Client will participate in ADLs with assistance from caregiver.

Long-Term Goal

Client will accomplish ADLs to the best of his or her ability. Unfulfilled needs will be met by caregiver.

Interventions

1. Provide a simple, structured environment to minimize confusion:

a. Identify self-care deficits and provide assistance as required.

b. Allow plenty of time for client to perform tasks.

c. Provide guidance and support for independent actions by talking the client through the task one step at a time.

d. Provide a structured schedule of activities that does not change from day to day.

e. Ensure that ADLs follow home routine as closely as possible.

f. Provide for consistency in assignment of daily caregivers.

2. In planning for discharge:

a. Perform ongoing assessment of client’s ability to fulfill nutritional needs, ensure personal safety, follow medication regimen, and communicate need for assistance with those activities that he or she cannot accomplish independently.

b. Assess prospective caregivers’ ability to anticipate and fulfill client’s unmet needs. Provide information to assist caregivers with this responsibility. Ensure that caregivers are aware of available community support systems from which they can seek assistance when required.

5. DISTURBED SENSORY PERCEPTION related to Alteration in structure/function of brain tissue, secondary to Advanced age/ Vascular disease/ Hypertension/ Cerebral hypoxia/ Abuse of mood- or behavior-altering substances/ Exposure to environmental toxins/ Various other physical disorders that predispose to cerebral abnormalities as evidenced by Disorientation to time, place, person, or circumstances Inability to concentrate/ Visual and auditory distortions/Inappropriate responses/ Talking and laughing to self / suspiciousness/ Hallucinations

Goals/Objectives

Short-Term Goal

With assistance from caregiver, client will maintain orientation to time, place, person, and circumstances for specified period of time.

Long-Term Goal

Client will demonstrate accurate perception of the environment by responding appropriately to stimuli indigenous to the surroundings.

Interventions

1.      Decrease the amount of stimuli in the client’s environment (e.g., low noise level, few people, and simple decor).

2.      Do not reinforce the hallucination. Let client know that you do not share the perception. Maintain reality through reorientation and focus on real situations and people.

3.      Provide reassurance of safety if client responds with fear to inaccurate sensory perception.

4.      Correct client’s description of inaccurate perception, and describe the situation as it exists in reality.

5.      Allow for care to be given by same personnel on a regular basis, if possible.

6.      Teach prospective caregivers how to recognize signs and symptoms of client’s inaccurate sensory perceptions. Explain techniques they may use to restore reality to the situation.

6. Low self-esteem related to loss of independent functioning/ loss of capacity for remembering/ loss of capability for effective verbal communication as evidenced by withdraws into social isolation, lack of eye contact, excessive crying alternating with expressions of anger refusal to participate in therapies refusal to participate in own self-care activities becomes increasingly dependent on others to perform ADLs expressions of shame or guilt.

Goals/objectives

Short-Term Goal

Client will voluntarily spend time with staff and peers in dayroom activities within 1 week.

Long-Term Goal

By time of discharge, client will exhibit increased feelings of self worth as evidenced by voluntary participation in own self-care and interaction with others.

Interventions

1. Encourage client to express honest feelings in relation to loss of prior level of functioning. Acknowledge pain of loss. Support client through process of grieving.

2. Devise methods for assisting client with memory deficit.

Examples follow:

a. Name sign on door identifying client’s room.

b. Identifying sign on outside of dining room door.

c. Identifying sign on outside of restroom door.

d. Large clock, with oversized numbers and hands, appropriately placed.

e. Large calendar, indicating one day at a time, with month, day, and year identified in bold print.

f. Printed, structured daily schedule, with one copy for client and one posted on unit wall.

g. “News board” on unit wall where current national and local events may be posted.

3. Encourage client’s attempts to communicate. If verbalizations are not understandable, express to client what you think he or she intended to say. It may be necessary to reorient client frequently.

4. Encourage reminiscence and discussion of life review. Also discuss present-day events. Sharing picture albums, if possible, is especially good.

5. Encourage participation in group activities. Caregiver may need to accompany client at first, until he or she feels secure that the group members will be accepting, regardless of limitations in verbal communication.

6. Offer support and empathy when client expresses embarrassment at inability to remember people, events, and places. Focus on accomplishments.

7. Encourage client to be as independent as possible in self-care activities. Provide written schedule of tasks to be performed.

DELIRIUM

Delirium is defined by the acute onset of fluctuating cognitive impairment and a disturbance of consciousness. Delirium is a syndrome, not a disease, and it has many causes, all of which result in a similar pattern of signs and symptoms relating to the patient's level of consciousness and cognitive impairment.

Delirium is under recognized by health care workers. Part of the problem is that the syndrome has a variety of other names- Intensive care unit psychosis, Acute confessional state, Acute brain failure, Encephalitis, Encephalopathy, Toxic metabolic state, Central nervous system toxicity, Paraneoplastic limbic encephalitis, Sundowning, Cerebral insufficiency, Organic brain syndrome.

Epidemiology

Delirium is a common disorder. According to DSM-IV-TR, the point prevalence of delirium in the general population is 0.4 percent for people 18 years of age and older and 1.1 percent for people 55 and older. Approximately 10 to 30 percent of medically ill patients who are hospitalized exhibit delirium. Approximately 30 percent of patients in surgical intensive care units and cardiac intensive care units and 40 to 50 percent of patients who are recovering from surgery for hip fractures have an episode of delirium. The highest rate of delirium is found in postcardiotomy patients, more than 90 percent in some studies. An estimated 20 percent of patients with severe burns and 30 to 40 percent of patients with acquired immune deficiency syndrome (AIDS) have episodes of delirium while they are hospitalized. Delirium develops in 80 percent of terminally ill patients. The causes of postoperative delirium include the stress of surgery, postoperative pain, insomnia, pain medication, electrolyte imbalances, infection, fever, and blood loss.

Clinical features

• Impairment of consciousness is the key feature that separates delirium from most other psychiatric disorders. There is a continuum between mild impairment of consciousness and near unconsciousness. There is fluctuation in intensity, and symptoms are often worse at night. The patient may be unmistakably drowsy, but milder states are easy to miss, especially by those who are unfamiliar with the patient's normal intellectual performance. They may be apparent only in reduced or slowed performance on bedside cognitive testing. There is disorientation in time, place, and the identity of other people .
• Appearance and behaviour: the patient looks unwell and behaviour may be marked by agitation or hypoactivity, by a fluctuation between these states, or by a mixture of them—for example, a drowsy patient plucking aimlessly at the bedclothes.
• Mood is frequently labile, with perplexity, intermittent periods of anxiety or depression, or occasionally of other mood states such as elation and irritability. Usually, the mood states have an empty and transitory quality.
• Speech: the patient may mumble and be incoherent.
• Perception: visual perception is the modality most often affected. Illusions and misinterpretations are frequent. For example, a patient may become agitated and fearful, believing that a shadow in a dark room is actually an attacker. Visual hallucinations also occur. The small living creatures which may be seen in delirium tremens are the best-known example. Auditory and tactile hallucinations also occur. Complex sensory distortions, such as colours being experienced as tastes, would suggest intoxication with hallucinogens.
• Cognition: there are abnormalities in all areas of cognitive function. Memory registration, retention, and recall are all affected. Mild cases may show their most pronounced abnormalities in slow performance on tasks or in the wandering of attention away from the task at hand.
• Orientation: in obvious cases, orientation in person, time, and place will all be disturbed. Milder degrees of disorientation will need to be interpreted in the context of the individual patient. For example, it may be considered not abnormal for a person who has been seriously ill in hospital for a long time to be unaware of the day of the month.
• Concentration is impaired, for example, on tests such as ‘serial sevens' or ‘days of the week backwards'.
• Memory disturbances are seen, with impaired registration (e.g. digit span), short-term recall (e.g. name and address), and long-term recall (e.g. current news items). After recovery from the illness there is usually (but not always) amnesia for the illness.
• Insight is usually impaired. The patient will have no understanding of why a psychiatric assessment has been requested.

COMMON CAUSES OF DELIRIUM

Central nervous system disorder Seizure (postictal, nonconvulsive status, status) Migraine Head trauma, brain tumor, subarachnoid hemorrhage, subdural, epidural hematoma, abscess, intracerebral hemorrhage, cerebellar hemorrhage, nonhemorrhagic stroke,transientischemia Metabolic disorder Electrolyte abnormalities Diabetes, hypoglycemia, hyperglycemia, or insulin resistance Systemic illness Infection (e.g., sepsis, malaria, erysipelas, viral, plague, Lyme disease, syphilis,abscess)Trauma Change in fluid status (dehydration or volume overload) Nutritional deficiency Burns Uncontrolled pain Heat stroke High altitude (usually >5,000 m) Medications Pain medications (e.g., postoperative meperidine or morphine Antibiotics, antivirals,andantifungals Steroids Anesthesia Cardiac medications Antihypertensives Antineoplastic agents Anticholinergic agents Neuroleptic malignant syndrome Serotonin syndrome Over-the-counter preparations Herbals, teas, and nutritional supplements Botanicals Jimsonweed, oleander, foxglove, hemlock, dieffenbachia Cardiac Cardiac failure, arrhythmia, myocardial infarction, cardiac assist device, cardiac surgery Pulmonary Chronic obstructive pulmonary disease, hypoxia, SIADH, acid base disturbance Endocrine Adrenal crisis or adrenal failure, thyroid abnormality, parathyroid abnormality Hematological Anemia, leukemia, blood dyscrasia, stem cell transplant Renal Renal failure, uremia, SIADH Hepatic Hepatitis, cirrhosis, hepatic failure Neoplasm Neoplasm (primary brain, metastases, paraneoplastic syndrome) Drugs of abuse Intoxication and withdrawal Toxins Intoxication and withdrawal Heavy metals and aluminum

Classification

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

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.

Treatment

In treating delirium, the primary goal is to treat the underlying cause. When the underlying condition is anticholinergic toxicity, the use of physostigmine salicylate , 1 to 2 mg intravenously or intramuscularly, with repeated doses in 15 to 30 minutes may be indicated. The other important goal of treatment is to provide physical, sensory, and environmental support. Physical support is necessary so that delirious patients do not get into situations in which they may have accidents. Patients with delirium should be neither sensory deprived nor overly stimulated by the environment. They are usually helped by having a friend or relative in the room or by the presence of a regular sitter. Familiar pictures and decorations, the presence of a clock or a calendar, and regular orientations to person, place, and time help make patients with delirium comfortable. Delirium can sometimes occur in older patients wearing eye patches after cataract surgery (black-patch delirium). Such patients can be helped by placing pinholes in the patches to let in some stimuli or by occasionally removing one patch at a time during recovery.

Pharmacotherapy

The two major symptoms of delirium that may require pharmacological treatment are psychosis and insomnia. A commonly used drug for psychosis is haloperidol. Depending on a patient's age, weight, and physical condition, the initial dose may range from 2 to 6 mg intramuscularly, repeated in an hour if the patient remains agitated. As soon as the patient is calm, oral medication in liquid concentrate or tablet form should begin. Two daily oral doses should suffice, with two thirds of the dose being given at bedtime. To achieve the same therapeutic effect, the oral dose should be approximately 1.5 times the parenteral dose. The effective total daily dose of haloperidol may range from 5 to 40 mg for most patients with delirium.

Droperidol is a butyrophenone available as an alternative intravenous formulation, although careful monitoring of the electrocardiogram may be prudent with this treatment.

Phenothiazines should be avoided in delirious patients because these drugs are associated with significant anticholinergic activity.

Use of second-generation antipsychotics, such as risperidone, clozapine, olanzapine, quetiapine, ziprasidone, and aripiprazole, may be considered for delirium management, but clinical trial experience with these agents for delirium is limited. Ziprasidone appears to have an activating effect and may not be appropriate in delirium management. Olanzapine is available for intramuscular (IM) use and as a rapidly disintegrating oral preparation. These routes of administration may be preferable for some patients with delirium who are poorly compliant with medications or who are too sedated to safely swallow medications. For patients with Parkinson's disease and delirium who require antipsychotic medications, clozapine or quetiapine have some support in the literature and are less likely to exacerbate parkinsonian symptoms.

Insomnia is best treated with benzodiazepines with short or intermediate half-lives (e.g., lorazepam 1 to 2 mg at bedtime). Benzodiazepines with long half-lives and barbiturates should be avoided unless they are being used as part of the treatment for the underlying disorder (e.g., alcohol withdrawal). There have been case reports of improvement in or remission of delirious states caused by intractable medical illnesses with electroconvulsive therapy (ECT); however, routine consideration of ECT for delirium is not advised. If delirium is caused by severe pain or dyspnea, a physician should not hesitate to prescribe opioids for both their analgesic and sedative effects.

AMNESTIC DISORDERS

The amnestic disorders are a broad category that includes a variety of diseases and conditions that present with an amnestic syndrome. The syndrome is defined primarily by impairment in the ability to create new memories. Three variations of the amnestic disorder diagnosis, differing in etiology, are offered: amnestic disorder caused by a general medical condition (e.g., head trauma), substance-induced persisting amnestic disorder (e.g., caused by carbon monoxide poisoning or chronic alcohol consumption), and amnestic disorder not otherwise specified for cases in which the etiology is unclear. The two modifiers are (1) transient, for duration less than 1 month, and (2) chronic, for conditions extending beyond 1 month.

Epidemiology

No adequate studies have reported on the incidence or prevalence of amnestic disorders. Amnesia is most commonly found in alcohol use disorders and in head injury. In general practice and hospital settings, the frequency of amnesia related to chronic alcohol abuse has decreased, and the frequency of amnesia related to head trauma has increased.

Causes of Amnestic Disorders

Systemic medical conditions
   Thiamine deficiency (Korsakoff's syndrome)
Hypoglycemia
Primary brain conditions
   Seizures
   Head trauma (closed and penetrating)
   Cerebral tumors (especially thalamic and temporal lobe)
   Cerebrovascular diseases (especially thalamic and temporal lobe)
   Surgical procedures on the brain
   Encephalitis due to herpes simplex
   Hypoxia (including nonfatal hanging attempts and carbon monoxide poisoning)
   Transient global amnesia
   Electroconvulsive therapy
   Multiple sclerosis
Substance-related causes
   Alcohol use disorders
   Neurotoxins
   Benzodiazepines (and other sedative-hypnotics)
   Many over-the-counter preparations

DIAGNOSTIC CRITERIA- ICD 10

A. Memory impairment, manifest in both:

(1) A defect of recent memory (impaired learning of new material), to a degree sufficient to interfere with daily living; and

(2) A reduced ability to recall past experiences.

B. Absence of:

(1) A defect in immediate recall (as tested, for example, by the digit span);

(2) Clouding of consciousness and disturbance of attention, as defined in FO5, criterion A;

(3) Global intellectual decline (dementia).

C. Objective evidence (physical & neurological examination, laboratory tests) and/or history of an insult to or a disease of the brain (especially involving bilaterally the diencephalic and medial temporal structures but other than alcoholic encephalopathy) that can reasonably be presumed to be responsible for the clinical manifestations described under A.

Comments: Associated features, including confabulations, emotional changes (apathy, lack of initiative), and lack of insight, are useful additional pointers to the diagnosis but are not invariably present.

CLINICAL FEATURES

The central symptom of amnestic disorders is the development of a memory disorder characterized by impairment in the ability to learn new information (anterograde amnesia) and the inability to recall previously remembered knowledge (retrograde amnesia). The symptom must result in significant problems for patients in their social or occupational functioning. The time in which a patient is amnestic can begin directly at the point of trauma or include a period before the trauma. Memory for the time during the physical insult (e.g., during a cerebrovascular event) may also be lost.

Short-term and recent memory are usually impaired. Patients cannot remember what they had for breakfast or lunch, the name of the hospital, or their doctors. In some patients, the amnesia is so profound that the patient cannot orient him-or-herself to city and time, although orientation to person is seldom lost in amnestic disorders. Memory for over learned information or events from the remote past, such as childhood experiences, is good; but memory for events from the less remote past (over the past decade) is impaired. Immediate memory (tested, for example, by asking a patient to repeat six numbers) remains intact. With improvement, patients may experience a gradual shrinking of the time for which memory has been lost, although some patients experience a gradual improvement in memory for the entire period.

The onset of symptoms can be sudden, as in trauma, cerebrovascular events, and neurotoxic chemical assaults, or gradual, as in nutritional deficiency and cerebral tumors. The amnesia can be of short duration  or of long duration .

A variety of other symptoms can be associated with amnestic disorders. For patients with other cognitive impairments, a diagnosis of dementia or delirium is more appropriate than a diagnosis of an amnestic disorder. Both subtle and gross changes in personality can accompany the symptoms of memory impairment in amnestic disorders. Patients may be apathetic, lack initiative, have unprovoked episodes of agitation, or appear to be overly friendly or agreeable. Patients with amnestic disorders can also appear bewildered and confused and may attempt to cover their confusion with confabulatory answers to questions. Characteristically, patients with amnestic disorders do not have good insight into their neuropsychiatric conditions.

SUBTYPES:

Cerebrovascular Diseases

Cerebrovascular diseases affecting the hippocampus involve the posterior cerebral and basilar arteries and their branches. Infarctions are rarely limited to the hippocampus; they often involve the occipital or parietal lobes. Thus, common accompanying symptoms of cerebrovascular diseases in this region are focal neurological signs involving vision or sensory modalities. Cerebrovascular diseases affecting the bilateral medial thalamus, particularly the anterior portions, are often associated with symptoms of amnestic disorders. A few case studies report amnestic disorders from rupture of an aneurysm of the anterior communicating artery, resulting in infarction of the basal forebrain region.

Multiple Sclerosis

The pathophysiological process of multiple sclerosis involves the seemingly random formation of plaques within the brain parenchyma. When the plaques occur in the temporal lobe and the diencephalic regions, symptoms of memory impairment can occur. In fact, the most common cognitive complaints in patients with multiple sclerosis involve impaired memory, which occurs in 40 to 60 percent of patients. Characteristically, digit span memory is normal, but immediate recall and delayed recall of information are impaired. The memory impairment can affect both verbal and nonverbal material.

Korsakoff's Syndrome

Korsakoff's syndrome is an amnestic syndrome caused by thiamine deficiency, most commonly associated with the poor nutritional habits of people with chronic alcohol abuse. Other causes of poor nutrition (e.g., starvation), gastric carcinoma, hemodialysis, hyperemesis gravidarum, prolonged intravenous hyperalimentation, and gastric plication can also result in thiamine deficiency. Korsakoff's syndrome is often associated with Wernicke's encephalopathy, which is the associated syndrome of confusion, ataxia, and ophthalmoplegia. In patients with these thiamine deficiency-related symptoms, the neuropathological findings include hyperplasia of the small blood vessels with occasional hemorrhages, hypertrophy of astrocytes, and subtle changes in neuronal axons. Although the delirium clears up within a month or so, the amnestic syndrome either accompanies or follows untreated Wernicke's encephalopathy in approximately 85 percent of all cases.

Patients with Korsakoff's syndrome typically demonstrate a change in personality as well, such that they display a lack of initiative, diminished spontaneity, and a lack of interest or concern. These changes appear frontal lobe-like, similar to the personality change ascribed to patients with frontal lobe lesions or degeneration. Indeed, such patients often demonstrate executive function deficits on neuropsychological tasks involving attention, planning, set shifting, and inferential reasoning consistent with frontal pattern injuries. For this reason, Korsakoff's syndrome is not a pure memory disorder, although it certainly is a good paradigm of the more common clinical presentations for the amnestic syndrome.

The onset of Korsakoff's syndrome can be gradual. Recent memory tends to be affected more than is remote memory, but this feature is variable. Confabulation, apathy, and passivity are often prominent symptoms in the syndrome. With treatment, patients may remain amnestic for up to 3 months and then gradually improve over the ensuing year. Administration of thiamine may prevent the development of additional amnestic symptoms, but the treatment seldom reverses severe amnestic symptoms once they are present. Approximately one third to one fourth of all patients recover completely, and approximately one fourth of all patients have no improvement of their symptoms.

Alcoholic Blackouts

Some persons with severe alcohol abuse may exhibit the syndrome commonly referred to as an alcoholic blackout. Characteristically, these persons awake in the morning with a conscious awareness of being unable to remember a period the night before during which they were intoxicated. Sometimes, specific behaviors (hiding money in a secret place and provoking fights) are associated with the blackouts.

Electroconvulsive Therapy

Electroconvulsive therapy (ECT) treatments are usually associated with retrograde amnesia for a period of several minutes before the treatment and anterograde amnesia after the treatment. The anterograde amnesia usually resolves within 5 hours. Mild memory deficits may remain for 1 to 2 months after a course of ECT treatments, but the symptoms are completely resolved 6 to 9 months after treatment.

Head Injury

Head injuries (both closed and penetrating) can result in a wide range of neuropsychiatric symptoms, including dementia, depression, personality changes, and amnestic disorders. Amnestic disorders caused by head injuries are commonly associated with a period of retrograde amnesia leading up to the traumatic incident and amnesia for the traumatic incident itself. The severity of the brain injury correlates somewhat with the duration and severity of the amnestic syndrome, but the best correlate of eventual improvement is the degree of clinical improvement in the amnesia during the first week after the patient regains consciousness.

Transient Global Amnesia

Transient global amnesia is characterized by the abrupt loss of the ability to recall recent events or to remember new information. The syndrome is often characterized by mild confusion and a lack of insight into the problem, a clear sensorium, and, occasionally, the inability to perform some well-learned complex tasks. Episodes last from 6 to 24 hours. Studies suggest that transient global amnesia occurs in 5 to 10 cases per 100,000 persons per year; although, for patients older than age 50, the rate may be as high as 30 cases per 100,000 persons per year. The pathophysiology is unknown, but it likely involves ischemia of the temporal lobe and the diencephalic brain regions. Several studies of patients with single photon emission computed tomography (SPECT) have shown decreased blood flow in the temporal and parietotemporal regions, particularly in the left hemisphere. Patients with transient global amnesia almost universally experience complete improvement, although one study found that approximately 20 percent of patients may have recurrence of the episode, and another study found that approximately 7 percent of patients may have epilepsy. Patients with transient global amnesia have been differentiated from patients with transient ischemic attacks in that fewer patients have diabetes, hypercholesterolemia, and hypertriglyceridemia, but more have hypertension and migrainous episodes.

PATHOLOGY AND LABORATORY EXAMINATION

Laboratory findings diagnostic of anmestic disorder may be obtained using quantitative neuropsychological testing. Standardized tests also are available to assess recall of well-known historical events or public figures, to characterize an individual's inability to remember previously learned information. Performance on such tests varies among individuals with amnestic disorder. Subtle deficits in other cognitive functions may be noted in individuals with amnestic disorder. Memory deficits, however, constitute the predominant feature of the mental status examination and account largely for any functional deficits. No specific or diagnostic features are detectable on imaging studies such as magnetic resonance imagery (MRI) or computed tomography (CT). Damage of mid temporal lobe structures are common, however, and may be reflected in enlargement of third ventricle or temporal horns or in structural atrophy detected by MRI.

Course and Prognosis

The course of an amnestic disorder depends on its etiology and treatment, particularly acute treatment. Generally, the amnestic disorder has a static course. Little improvement is seen over time, but also no progression of the disorder occurs. The exceptions are the acute amnesias, such as transient global amnesia, which resolves entirely over hours to days, and the amnestic disorder associated with head trauma, which improves steadily in the months subsequent to the trauma. Amnesia secondary to processes that destroy brain tissue, such as stroke, tumor, and infection, are irreversible, although, again, static, once the acute infection or ischemia has been staunched.

Treatment

The primary approach to treating amnestic disorders is to treat the underlying cause. Although a patient is amnestic, supportive prompts about the date, the time, and the patient's location can be helpful and can reduce the patient's anxiety. After resolution of the amnestic episode, psychotherapy of some type (cognitive, psychodynamic, or supportive) may help patients incorporate the amnestic experience into their lives.

Psychotherapy

Psychodynamic interventions may be of considerable value for patients who have amnestic disorders that result from insults to the brain. Understanding the course of recovery in such patients helps clinicians to be sensitive to the narcissistic injury inherent in damage to the central nervous system.

The first phase of recovery, in which patients are incapable of processing what happened because the ego defenses are overwhelmed, requires clinicians to serve as a supportive auxiliary ego who explains to a patient what is happening and provides missing ego functions. In the second phase of recovery, as the realization of the injury sets in, patients may become angry and feel victimized by the malevolent hand of fate. They may view others, including the clinician, as bad or destructive, and clinicians must contain these projections without becoming punitive or retaliatory. Clinicians can build a therapeutic alliance with patients by explaining slowly and clearly what happened and by offering an explanation for a patient's internal experience. The third phase of recovery is integrative. As a patient accepts what has happened, a clinician can help the patient form a new identity by connecting current experiences of the self with past experiences. Grieving over the lost faculties may be an important feature of the third phase.

Most patients who are amnestic because of brain injury engage in denial. Clinicians must respect and empathize with the patient's need to deny the reality of what has happened. Insensitive and blunt confrontations destroy any developing therapeutic alliance and can cause patients to feel attacked. In a sensitive approach, clinicians help patients accept their cognitive limitations by exposing them to these deficits bit by bit over time. When patients fully accept what has happened, they may need assistance in forgiving themselves and any others involved, so that they can get on with their lives. Clinicians must also be wary of being seduced into thinking that all of the patient's symptoms are directly related to the brain insult. An evaluation of preexisting personality disorders, such as borderline, antisocial, and narcissistic personality disorders, must be part of the overall assessment; many patients with personality disorders place themselves in situations that predispose them to injuries. These personality features may become a crucial part of the psychodynamic psychotherapy.

Recently, centers for cognitive rehabilitation have been established whose rehabilitation-oriented therapeutic milieu is intended to promote recovery from brain injury, especially that from traumatic causes. Despite the high cost of extended care at these sites, which provide both long-term institutional and daytime services, no data have been developed to define therapeutic effectiveness for the heterogeneous groups of patients who participate in such tasks as memory retaining.

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