As the etiologies of various dementing illnesses have been elucidated and treatments developed, the prevalence and impact of these illnesses have changed. For example, general paralysis of the insane (now termed neurosyphilis) was described by Thomas Willis in 1672 as a syndrome beginning with mania and followed by dementia and paralysis, but the paralysis was thought to be a late, nonspecific concomitant of mental disease. In 1826, Bayle recognized the entire cluster of signs and symptoms as a specific entity. The relationship of this syndrome to syphilis was hotly debated until 1913, when the spirochete Treponema pallidum was demonstrated in the brains of persons with general paresis by Noguchi and Moore, and the term neurosyphilis came into use (Henry 1941). Since the 1940s, with the widespread use of serological tests to detect early syphilis and the availability of penicillin for treatment, neurosyphilis has become relatively rare in the United States. In fact, the rate of first admissions to psychiatric hospitals because of neurosyphilis fell from 4.3/ 100,000 population in 1946 to 0.4/100,00 in 1960 (Adams and Victor 1989, p. 573).

The prevalence and impact of dementia due to metabolic causes have also changed as a result of medical discoveries. Wilson disease is now treatable, the dementia of AIDS (acquired immunodeficiency syndrome) is largely preventable, and obstructive hydrocephalus due to meningitis can be relieved surgically. Early conjectures about the relationship between alcohol consumption and dementia may have implicated the wrong agent. Despite the association of dementia with repeated episodes of delirium tremens noted in the 19th century (Wilson 1886), Victor et al. (1989) found no evidence for direct toxicity of alcohol at postmortem examination of persons diagnosed during life as having alcoholic dementia. Instead, they demonstrated the stigmata of the thiamin deficiency-related Wernicke syndrome and other unrelated conditions, including trauma and Alzheimer disease. Thus, the primary cause of dementia in alcoholics appears to be malnutrition rather than the direct toxic effect of alcohol on the brain.

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Myron F. Weiner, M.D.
Clinical Professor of Psychiatry and Neurology,
Aradine S. Ard Chair in Brain Science,
Dorothy L. and John P. Harbin Chair in Alzheimer’s Disease Research,
University of Texas Southwestern Medical Center at Dallas, Texas
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