Also known as alcohol-induced persisting dementia, alcohol-related dementia falls within the categories of both alcohol-related disorders and substance-induced persisting dementias. Prevalence rates differ considerably according to the population studied and the diagnostic criteria used, although alcohol related dementia has been estimated to account for approximately 4 percent of dementias. Milder forms of cognitive impairment are also frequently associated with chronic alcohol abuse, but typically do not result in prolonged, irreversible cognitive deficit upon cessation.
The causal relationship between alcohol use and dementia is complicated and controversy exists in the literature. Alcohol, or its metabolite acetaldehyde, may have direct CNS neurotoxic effects. Dementia may also result from thiamine deficiency and subsequent cortical neuronal loss. In 1881, Wernicke described a syndrome in alcoholics that consisted of abrupt onset confusion, accompanied by ataxia and abnormal eye movements, which begin with nystagmus and lateral rectus or horizontal gaze paresis and progress to complete ophthalmoplegia, usually with pupillary sparing. This syndrome became known as Wernicke’s encephalopathy. Several years later, Korsakoff reported on an amnestic state with confabulation that appeared to frequently follow the encephalopathy. It has since become clear that chronic alcohol abuse impairs gastrointestinal absorption of thiamine, and the resultant thiamine deficiency is the major factor in producing Wernicke’s encephalopathy and Korsakoff’s psychosis. In addition, alcoholism frequently results in liver disease, which in turn affects thiamine homeostasis, and may also directly cause neurotoxicity and cognitive impairment. Questions remain, however, as to whether dementia represents a distinct pathophysiological entity, or is rather part of the constellation of symptoms seen in chronic alcohol abuse associated with liver disease and thiamine deficiency. Recent evidence suggests that alcoholic brain damage and subsequent cognitive dysfunction may be the result of a combination of direct neurotoxic insult and the metabolic effects of thiamine deficiency and liver disease.
In order to make the diagnosis of alcohol-induced persisting dementia, the criteria for dementia (Table 1) must be met. Because amnesia may also occur in the context Korsakoff’s psychosis, it is important to distinguish between memory impairment accompanied by other cognitive deficits (i.e., dementia) and amnesia due to thiamine deficiency. To complicate matters, however, there is also evidence that other cognitive functions such as attention and concentration may also be impaired in Wernicke-Korsakoff syndrome. In addition, alcohol abuse is frequently associated with mood changes, so poor concentration and other cognitive symptoms often observed in the context of a major depression must also be ruled-out.
Mild cognitive impairments may also exist in patients with alcohol dependence without fully meeting criteria for dementia. Recent theories have suggested that dementia may actually result from the combined effects of Korsakoff-like amnesia and the milder cognitive impairments characteristic of chronic alcohol use. These patients tend to have problem-solving and planning difficulties, and perceptual-motor dysfunction, but verbal and overall IQs generally remain within the normal range. Patients with milder alcohol-related cognitive impairment may also improve significantly with sustained abstinence. Alcohol-induced persisting dementia, on the other hand, has more global and prolonged deficits.
Descriptions of alcohol related dementia in the literature have reported many features that include memory impairment, slow mentation, disorganized thought, poor attention, impaired judgment, and disorientation. Other psychiatric symptoms may include mood lability, impulsivity, behavioral disinhibition, irritability, aggression, apathy, and paranoid ideation. In 1941, Wechsler noted that alcoholics had difficulty with abstraction, learning new material, and organizing complex perceptions. Since then, others have replicated these findings and shown deficits to be accompanied by a relative preservation of verbal abilities. Symptoms tend to develop gradually, and this may be one way, albeit unreliably, to distinguish dementia from Wernicke-Korsakoff syndrome.
The diagnosis of alcohol-induced persisting dementia is made based on clinical evaluation. There are no pathognomonic findings and neuroimaging studies show only nonspecific neuroanatomical changes. The most common findings on CT or MRI are cerebral atrophy and ventricular enlargement with widening of the cerebral sulci, although the relationship between radiologic abnormalities and dementia is unclear. Furthermore, enlarged ventricles and widened sulci have also been found in alcohol dependence without cognitive impairment. The treatment of alcohol-induced dementia consists mainly of abstinence, although cognitive deficits persist despite cessation of drinking. Adequate nutrition and the treatment of underlying or comorbid psychiatric and medical illness are crucial.