A. The development of memory impairment as manifested by impairment in the ability to learn new information or the inability to recall previously learned information.
B. The memory disturbance causes significant impairment in social or occupational functioning and represents a significant decline from a previous level of functioning.
D. There is evidence from the history, physical examination, or laboratory findings that the memory disturbance is etiologically related to the persisting effects of substance use (e.g., a drug of abuse, a medication).
The name of the diagnosis begins with the specific substance (e.g., alcohol, secobarbital) that is presumed to be causing the memory disturbance. When more than one substance is judged to play a significant role in the development of the memory disturbance, each should be listed separately (e.g., Alcohol-Induced Persisting Amnestic Disorder; Secobarbital-Induced Persisting Amnestic Disorder). If a substance is judged to be the etiological factor but the specific substance or class of substances is unknown, the diagnosis is Unknown Substance-Induced Persisting Amnestic Disorder.
Substance-Induced Persisting Amnestic Disorder can occur in association with the following classes of substances: alcohol, sedatives, hypnotics, and anxiolytics; and other or unknown substances.
Alcohol-Induced Persisting Amnestic Disorder is apparently due to the vitamin deficiency that is associated with prolonged, heavy ingestion of alcohol. Neurological disturbances such as peripheral neuropathy, cerebellar ataxia, and myopathy are among the associated features. Alcohol-Induced Persisting Amnestic Disorder due to thiamine deficiency (Korsakoff's syndrome) often follows an acute episode of Wenicke's encephalopathy, neurological condition manifested by confusion, ataxia, eye-movement abnormalities (gaze palsies, nystagmus), and other neurological signs. Gradually, these manifestations subside, but a major impairment of memory remains. If Wernicke's encephalopathy is treated early with large doses of thiamine, Alcohol-Induced Persisting Amnestic Disorder may not develop. Although age is not a specific etiological factor in the condition, individuals who develop Alcohol-Induced Persisting Amnestic Disorder generally have histories of many years of heavy alcohol use and are most often over age 40 years. Although the mode of onset is typically abrupt, some individuals may develop deficits insidiously over many years, due to repeated toxic and nutritional insults, prior to the emergence of a final, more dramatically impairing episode apparently related to thiamine deficiency. Once established, Alcohol-Induced Persisting Amnestic Disorder usually persists indefinitely, although there may be slight improvement over time and in a minority of the cases the condition can remit. Impairment is usually quite severe, and lifelong custodial care may be necessary. Sedative-, Hypnotic-, or Anxiolytic-Induced Persisting Amnestic Disorder can follow prolonged and heavy use of drugs from this class. The course is variable, and, unlike Alcohol-Induced Persisting Amnestic Disorder, full recovery can occur. Medications reported to cause amnestic disorders include anticonvulsants and intrathecal methotrexate. Toxins reported to evoke symptoms of amnesia include lead, mercury, carbon monoxide, organophosphate insecticides, and industrial solvents.