Amnestic Disorders

Amnestic Disorders

The amnestic disorders are characterized by a disturbance in memory related to the direct effects of a general medical condi-tion or the persisting effects of a substance (American Psychiatric Association, 1994). The impairment should interfere with social and occupational functioning and represent a significant decline from the previous level of functioning. The amnestic disorders are differentiated on the basis of the etiology of the memory loss. These disorders should not be diagnosed if the memory deficit is a feature of a dissociative disorder, is associated with demen-tia, or occurs in the presence of clouded sensorium, as in delir-ium. Amnestic disorders are predominately comprised of those caused by a general medical condition or those whose etiology is substance-induced.

Epidemiology

The exact prevalence and incidence of the amnestic disorders are unknown (Kaplan et al., 1994). Memory disturbances related to specific conditions such as alcohol dependence and head trauma have been studied and these appear to be the two most common causes of amnestic disorders. Kaplan and coworkers (Torres et al., 2001) reported that in the hospital setting the incidence of alcohol-induced amnestic disorders is decreasing while that of amnestic disorders, secondary to head trauma, is on the rise. This may be related to rigorous efforts by hospital personnel to decrease the incidence of iatrogenic amnestic disorder by giving thiamine before glucose is administered to a patient with chronic alcohol dependence and nutritional deficiencies.

Etiology

Amnesia results from generally bilateral damage to the areas of the brain involved in memory. The areas and structures so in-volved include the dorsomedial and midline thalamic nuclei, such temporal lobe-associated structures as the hippocampus, amy-gdala and mamillary bodies. The left hemisphere may be more important than the right in the occurrence of memory disorders. Frontal lobe involvement may be responsible for such commonly seen symptoms as apathy and confabulation.

The specific causes of amnestic disorders include 1) sys-temic medical conditions such as thiamine deficiency; 2) brain conditions, including seizures, cerebral neoplasms, head injury, hypoxia, carbon monoxide poisoning, surgical ablation of tem-poral lobes, electroconvulsive therapy and multiple sclerosis; 3) altered blood flow in the vertebral vascular system, as in tran-sient global amnesia; and 4) effects of a substance (drug or alco-hol use and exposure to toxins).

Conditions that affect the temporal lobes such as herpes infection and Kluver–Bucy syndrome can produce amnesia. Among drugs that can cause amnestic disorders, triazolam has received the most attention, but all benzodiazepines can produce

memory impairment, with the dose utilized being the determin-ing factor (Kirk et al., 1990) (Table 32.12).

Clinical Features

Patients with amnestic disorder have impaired ability to learn new information (anterograde amnesia) or cannot remember ma-terial previously learned (retrograde amnesia). Memory for the event that produced the deficit (e.g., a head injury in a motor ve-hicle accident) may also be impaired.

Remote recall (tertiary memory) is generally good, so pa-tients may be able to relate accurately incidents that occurred during childhood but not remember what they had for breakfast. As illus-trated by such conditions as thiamine amnestic syndrome, immedi-ate memory is often preserved. In some instances, disorientation to time and place may occur, but disorientation to person is unusual.

The onset of the amnesia is determined by the precipitant and may be acute as in head injury or insidious as in poor nu-tritional states. DSM-IV characterizes short-duration amnestic disorder as lasting less than 1 month and long-duration disorder lasting 1 month or longer. Often individuals lack insight into the memory deficit and vehemently insist that their inaccurate re-sponses on a Mental Status Examination are correct.

Selected Amnestic Disorders

Blackouts

Blackouts are periods of amnesia for events that occur during heavy drinking (Tarter and Schneider, 1976). Typically, a person awakens the morning after consumption and does not remember what happened the night before. Unlike delirium tremens, which is related to chronicity of alcohol abuse, blackouts are more a measure of the amount of alcohol consumed at any one time. Thus, blackouts are common in binge pattern drinkers and may occur the first time a person ingests a large amount of alcohol. Blackouts are generally transient phenomena, but some patients may continue to have blackouts for weeks even after they have stopped using alcohol. These memory lapses are similar to black-outs experienced while using alcohol. With continued sobriety, the blackouts should end, but information forgotten during past blackouts is never remembered. Blackouts may also be produced by agents with cross-sensitivity to alcohol, such as benzodi-azepines. Blackouts should not be confused with alcohol-induced dementia, which presents with cortical atrophy on CT scans, as-sociated features of dementia and a usually irreversible course.

Korsakoff’s Syndrome

Korsakoff’s syndrome is an amnestic disorder caused by thia-mine deficiency. Although generally associated with alcohol abuse, it can occur in other malnourished states such as maras-mus, gastric carcinoma and HIV spectrum disease (Reulen et al., 1985; Victor, 1987). This syndrome is usually associated with Wernicke’s encephalopathy, which involves ophthalmoplegia, ataxia and confusion. Korsakoff’s syndrome is often associated with a neuropathy and occurs in about 85% of untreated patients with Wernicke’s disease (Kaplan et al., 1994). Complete recovery from Korsakoff’s syndrome is rare.

Head Injury

Head injuries can produce a wide variety of neurological and psy-chiatric disorders, even in the absence of radiological evidence of structural damage. Delirium, dementia, mood disturbances, behavioral disinhibition, alterations of personality and amnestic disorders may result (Torres et al., 2001). Amnesia in head injury is for events preceding the incident and the incident itself, lead-ing some physicians to consider these patients as having facti-tious disorders or being malingerers. The eventual duration of the amnesia is related to the degree of memory recovery that occurs in the first few days after the injury. Amnesia after head injury has become a popular plot device in novels and motion pictures, many of which are depictions that erroneously suggest that a sec-ond blow to the head is curative

Differential Diagnosis

Amnestic disorders must be differentiated from the less disrup-tive changes in memory that occur in normal aging, the memory impairment that is accompanied by other cognitive deficits in dementia, the amnesia that might occur with clouded conscious-ness in delirium, the stress-induced impairment in recall seen in dissociative disorders, and the inconsistent amnestic deficits seen in factitious disorder and malingering.

Treatment

As in delirium and dementia, the primary goal in the amnestic dis-orders is to discover and treat the underlying cause. Because some of these causes of amnestic disorder are associated with dangerous self-damaging behavior (e.g., suicide attempts by hanging, carbon monoxide poisoning, deliberate motor vehicle accidents, self-in-flicted gunshot wounds to the head and chronic alcohol abuse), some form of psychiatric involvement is often necessary. In the hospital, continuous reorientation by means of verbal redirection, clocks and calendars can allay the patient’s fears. Supportive indi-vidual psychotherapy and family counseling are beneficial.