Also discussed in Chap. 40 are alcoholic cerebellar degeneration and Marchiafava-Bignami disease. The former is almost certainly of nutritional origin; in the latter a nutritional–metabolic etiology seems likely but has not been established. Central pontine myelinolysis, although frequently observed in alcoholics, is more appropriately considered with the acquired metabolic disorders, usually the too rapid correction of hyponatremia (see Chap. 39). Certain disorders of skeletal and cardiac muscle associated with alcoholism (acute alcoholic myopathy and cardiomyopathy) are described in Chap. 45, with the myopathies caused by drugs and toxins. There remain to be discussed several diverse disorders that have been attributed to alcoholism but whose causal relationship to alcohol abuse, nutritional deficiency, or some other relevant factor is not clear.
The term alcoholic dementia is used widely and often indiscriminately to designate a presumably distinctive form of dementia that is attributable to the chronic, direct effects of alcohol on the brain. Unfortunately, a syndrome subsumed under the title of alcoholic dementia and its many synonyms that appear in the older literature (alcoholic deteriorated state, chronic alcoholic psychosis, chronic or organic brain syndrome due to alcohol) has never been delineated satisfactorily, either clinically or pathologically. In the Comprehensive Textbook of Psychiatry, it has been defined as “a gradual disintegration of personality structure, with emotional lability, loss of control, and dementia” (Sadock and Sadock). Purported examples of this state show a remarkably diverse group of symptoms, including jealousy and suspiciousness; coarsening of moral fiber and other personality and behavioral disorders; deterioration of work performance, personal care, and living habits; and disorientation, impaired judgment, and defects of intellectual function, particularly of memory.
There have been many attempts to redefine alcoholic dementia. Cutting, as well as Lishman, expressed the view that the term Korsakoff psychosis should be limited to patients with a fairly pure disorder of memory of acute onset and that patients with more global symptoms of intellectual deterioration, of gradual evolution, be considered to have alcoholic dementia. These are rather weak diagnostic criteria. As pointed out in Chap. 40, Korsakoff psychosis may have an insidious onset and gradual progression, and patients with this disorder, in addition to an amnesic defect, characteristically show disturbances of cognitive functions that depend little or not at all on memory. More importantly, in none of the patients designated by these authors as having alcoholic dementia was there a neuropathologic examination, without which the clinical assessment must remain arbitrary and imprecise.
The pathologic changes that purportedly underlie primary alcoholic dementia are even less precisely defined than the clinical syndrome. Courville, whose writings have been quoted most frequently in this respect, described a series of cerebral cortical changes that he attributed to the toxic effects of alcohol. Some of them turn out on close inspection to be quite nonspecific, reflecting nothing more than the effects of aging or the insignificant artifacts of tissue fixation and staining. Harper and Blumbergs, and subsequently Harper and Kril, reported that the mean brain weight is decreased in alcoholics and the pericerebral space is increased in volume—findings that do no more than confirm the brain shrinkage that is readily demonstrable by brain imaging studies in many alcoholics and is to some extent reversible with sustained abstinence (see later).