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Organic Disorders

Dr. Mushtaq Talib

Organic psychiatry(Neuropsychiatry)

Comprises psychiatric disorders that arise from demonstrable abnormalities of brain structure and function.
Cognitive impairments are the most prominent feature, especially in dementia and delirium.
But , behavioral and emotional disturbances are also common, and may be the sole manifestations.

Classification

Delirium
Dementia
Amnestic ( or amnesic) syndromes
Epilepsy
Head injury
Other neuro-psychiatric disorders( focal cerebral syndromes, infections, tumors, and multiple sclerosis)
Secondary or symptomatic neuro-psychiatric disorders ( due to other disease in the body)

Amnestic syndromes

Amnesia is loss of memory, and amnestic syndromes (disorders) are those in which memory is specifically and persistently affected.
Amnestic disorder( by DSM IV) is defined as a specific impairment of episodic memory, manifesting as inability to learn new information( anterograde amnesia) and to recall past events( retrograde amnesia) accompanied by significant impairment in social or occupational functioning and with evidence of a general medical condition” etiologically related to memory impairment”.


Causes of amnesia
Transient:
• Transient global amnesia
• Transient epileptic amnesia
• Head injury
• Alcoholic blackouts
• Post-electroconvulsive therapy
• Posttraumatic stress disorder (PTSD)
• Psychogenic fugue

Causes of amnesia

Permanent:
• Korsakov (Korsakoff) syndrome
• Encephalitis
• Posterior cerebral artery and thalamic strokes
• Head injury

Clinical features

The cardinal feature is profound deficit of episodic memory
Disorientation for time,
loss of autobiographical information
Severe anterograde amnesia for verbal and visual material
Lack of insight to the amnesia
Confabulation: gaps in memory are filled by a vivid and detailed wholly fictitious account of recent activities which the patient believes to be true.


Etiology
Lesions in the medial thalamus, other midline diencephalic structures , or medial temporal lobes.
Korsakov syndrome: which usually follows an acute neurological syndrome called Wernicke’s encephalopathy. This is caused by thiamin deficiency ,secondary to alcohol abuse, although it occasionally results from hyperemesis gravidarum and severe malnutrition.

Investigations

Inquire about alcohol abuse
Reduced red cell transketolase level ( marker of thiamin deficiency)
Brain MRI: increased MRI signal in midline structures

Management

Korsakov syndrome should be assumed to be the cause of amnestic syndrome until another etiology is demonstrated
Urgent treatment with thiamin should be started without waiting the results of investigations (parenteral thiamine)
Rehydration
General nutritional support
Treatment of alcohol withdrawal
Rehabilitation and support

Transient global amnesia

Sudden onset of isolated anterograde amnesia in a clear sensorium generally lasting for less than 24 hours
Due to dysfunction of the circuits mediating episodic memory
Needs to be considered in the differential diagnosis of paroxysmal neurological and psychiatric conditions that occur in middle and late life.


Delirium
Characterized by global impairment of consciousness ( clouding of consciousness) ,resulting in reduced levels of alertness, attention, and perception of the environment.
It occurs in 15-30% of patients in general medical or surgical wards.
Other terms: acute confusional state, acute organic syndrome, acute brain failure

Clinical features

The cardinal feature is disturbed consciousness
Manifested as drowsiness, decreased awareness of surroundings
Disorientation in time and place, and distractibility
In most severe cases ;patient may be unresponsive( stuporose)
May start as mental slowness, distractibility, perceptual anomalies, and disorganization of the sleep-wake cycle.

Clinical features

Symptoms vary at different times of the day and between different patients
Symptoms are worse at night
Some patients are hyperactive ,restless, irritable and have psychotic symptoms
Some are hypoactive with psychomotor retardation and perseveration.
Repetitive ,purposeless movements are common in both forms
Thinking is slow

Clinical features

Ideas of reference and delusions are common but usually transient
Illusions , misinterpretations and visual hallucinations sometimes with fantastic contents
Anxiety ,depression, and emotional lability are common
Patients may appear frightened and perplexed
Attention and registration are often impaired and on recovery there is usually amnesia for the period of the delirium.


Etiology
Old age, frailty, and prior medical and neurological disorders lower the threshold for developing delirium.
The patho-physiological basis of delirium is unclear.
The neurotransmitters dopamine and acetylcholine are implicated.

Causes of delirium

Drugs : alcohol intoxication, withdrawal, opiates, drugs with anticholinergic properties, any sedative, digoxin, diuretics, lithium, and steroids.
Medical conditions: febrile illness, septicaemia, organ failure( cardiac, renal, hepatic), hypo or hyperglycaemia, post-operative hypoxia, thiamine deficiency
Neurological conditions: epileptic seizure, head injury, space occupying lesion, encephalitis ,cerebral hemorrhage.
Others : constipation, dehydration, pain, sensory deprivation.

Management

Delirium is a medical emergency
It is very essential to identify and treat the cause
Drugs (side effect or withdrawal) should be suspected until there is evidence of another cause.
While doing investigations, measures should be taken to decrease distress and control agitation
These include: frequent explanation, reorientation, and reassurance.
Nursing : minimal number of nurses, quite room , good lightening, relatives should be encouraged to visit regularly.

Drug treatment

Medications to control agitation and distress and permit adequate sleep
Drug of choice is usually an antipsychotic
Haloperidol is conventionally used (2-10 mg/day)
Antipsychotics should be avoided in alcohol withdrawal and epilepsy because of the risk of seizure.
All sedative drugs should be used sparingly in liver failure because of the danger of precipitating hepatic coma.



رفعت المحاضرة من قبل: AyA Abdulkareem
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