Substance/ medication-induced major or mild NCD is characterized by neurocognitive impairments that persist beyond the usual duration of intoxication and acute withdrawal (Criterion B). Initially, these manifestations can reﬂect slow recovery of brain functions from a period of prolonged substance use, and improvements in neurocognitive as well as brain imaging indicators may be seen over many months. If the disorder continues for an extended period, persistent should be specified. The given substance and its use must be known to be capable of causing the observed impairments (Criterion C). While nonspecific decrements in a range of cognitive abilities can occur with nearly any substance of abuse and a variety of medications, some patterns occur more frequently with selected drug classes. For example, NCD due to sedative, hypnotic, or anxiolytic drugs (e.g., benzodiaz- epines, barbiturates) may show greater disturbances in memory than in other cognitive functions. NCD induced by alcohol frequently manifests with a combination of impair- ments in executive-function and memory and learning domains. The temporal course of the substance-induced NCD must be consistent with that of use of the given substance (Criterion D). In alcohol-induced amnestic confabulatory (Korsakoff’s) NCD, the features include prominent amnesia (severe difficulty learning new information with rapid forget- ting) and a tendency to confabulate. These manifestations may co—occur with signs of thi- amine encephalopathy (Wernicke’s encephalopathy) with associated features such as nystagmus and ataxia. Ophthalmoplegia of Wernicke’s encephalopathy is typically charac- terized by a lateral gaze paralysis.
In addition to or independent of the more common neurocognitive symptoms related to methamphetamine use (e.g., difficulties with learning and memory; executive func- tion), methamphetamine use can also be associated with evidence of vascular injury (e.g., focal weakness, unilateral incoordination, asymmetrical reﬂexes). The most common neu- rocognitive profile approximates that seen in vascular NCD.
Intermediate-duration NCD induced by drugs with central nervous system depressant effects may manifest with added symptoms of increased irritability, anxiety, sleep disturbance, and dysphoria. Intermediate-duration NCD induced by stimulant drugs may manifest with re- bound depression, hypersomnia, and apathy. In severe forms of substance/medication— induced major NCD (e.g., associated with long-term alcohol use), there may be prominent neuromotor features, such as incoordination, ataxia, and motor slowing. There may also be loss of emotional control, including aggressive or inappropriate affect, or apathy.
The prevalence of these conditions is not known. Prevalence figures for substance abuse are available, and substance/medication—induced major or mild NCDs are more likely in those who are older, have longer use, and have other risk factors such as nutritional deficits.
For alcohol abuse, the rate of mild NCD of intermediate duration is approximately 30%— 40% in the first 2 months of abstinence. Mild NCD may persist, particularly in those who do not achieve stable abstinence until after age 50 years. Major NCD is rare and may result from concomitant nutritional deficits, as in alcohol—induced amnestic confabulatory NCD.