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Organic mental disorders

AUTHOR: DR. SHAHUL AMEEN, M.D.

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2.4 AMNESTIC DISORDERS

Victor et al. (1971) defines the amnestic syndrome as an abnormal mental state in which memory and learning are affected out of all proportion to other cognitive functions in an otherwise alert and responsive patient. Amnestic disorders have been broadly classified into transient amnesias and persistent memory disorders. Transient amnesias include transient global amnesia, transient epileptic amnesia, posttraumatic amnesia and alcoholic blackouts, while persistent memory disorders include Korsakoff syndrome and amnestic syndromes that follow herpes encephalitis, severe hypoxia, vascular disorders or head injury (Kopelman, 2000).

Transient global amnesia (TGA)

TGA is a syndrome of severe, forgetful confusion characterized by memory loss and total disorientation except for self-identity, followed by gradual resolution within 24 hours. The memory loss includes a profound impairment of long-term episodic memory, while working memory is spared. TGA presumably results from transient dysfunction of the temporal lobes or diencephalons. Commonly, the presumed cause is transient ischemia (Plum, 1992). TGA may arise during coughing, exercise, sexual intercourse, driving, medical procedures or after severe emotional stress; and other known precipitants include seizures, migraine, and medications like sildenafil (Ullrich and Urion, 2003; Gandolfo et al., 2003).

Posttraumatic amnesia

TBI is the common cause of amnestic syndromes seen in clinical practice (Cummings and Mega, 2003). Duration of the coma after TBI is the best predictor of the severity of posttraumatic memory and cognitive deficits, and duration of post-traumatic amnesia is correlated with posttraumatic intellectual disorders (Levin, 1989).

Alcoholic blackouts

Alcoholic blackouts are among the most frequently reported symptoms in the progression of alcoholism, and are defined as the temporary, complete inability to form long-term memory as a result of a high blood alcohol level. Goodwin et al. (1969) described en bloc and fragmentary types of blackouts. The former are instances of full and permanent memory loss for intoxicated events, whereas the latter are episodes for which retrieval of experiences is facilitated by provision of cues. The risk of blackouts is associated with increased alcohol consumption, age of drinking onset, the number of alcoholic relatives, and the individual's capacity to control drinking behavior (Jennison and Johnson, 1994). Nelson et al. (2004) found evidence of a substantial genetic contribution to liability for alcohol-induced blackouts. Hypoglycemia may be another contributory factor to blackouts (Kopelman, 2000).

Korsakoff syndrome

Many cases of the Korsakoff syndrome are diagnosed following an acute Wernicke encephalopathy, but the disorder can also have an insidious onset and such cases are more likely to come to the attention of the psychiatrists (Kopelman, 2000). Patients with the syndrome have difficulty learning new information and usually have a retrograde amnesia that extends 3-20 years prior to the onset of the amnesia. Typically, patients remain amnestic for 1-3 months after onset and then begin to recover over a 1- to 10- month period. A personality change, usually emotional indifference or apathy, frequently accompanies the amnesia (Cummings and mega, 2003).

Management of amnesia

It has been observed that the natural history of many of the amnestic disorders, regardless of the cause, entails a gradual lessening of the severity of the retrograde and anterograde amnesia with time (Burke, 2001). Memory impairment in the Korsakoff syndrome has shown mild response to treatment with clonidine, methysergide, and methylphenidate (McEntee and Crook, 1990). Physostigmine has been found useful in cases with amnestic disorder due to herpes simplex encephalitis (Catsman-Berrevoets et al., 1986, Peters and Levin, 1977). Psychosocial approaches used in the management of amnesia are categorized as restorative therapies which attempt to bring back normal function by repeated training, and compensatory approaches which attempt to help the person overcome the deficit by the use of other intact cognitive abilities (Burke, 2001).

 
 
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