Mohammed T. Abou-Saleh

286 PRINCIPLES AND PRACTICE OF GERIATRIC PSYCHIATRYesters essential to CNS function. Thus, there are several possibleroutes to the production of brain damage in alcoholics. Further,these appear to be so interlinked that it may be unproductive totry and dissect the separate contribution of alcohol and thiaminedeficiency to brain damage. Rather, it appears that a combinationof malnutrition and alcohol intake can give rise to a range ofcognitive deficits, from mild cognitive impairment to severedementia, depending on the severity of the contributory abnormalmechanisms described by Butterworth.Although the evidence points to alcohol being neurotoxic, therelationship between this and cognitive impairment is not clear. Amajor drawback of neuropathological studies is that suchinferences have been either not possible or gleaned by retrospectivecase note analysis. In contrast, neuroimaging allows theprospective analysis of clinical features in relation to in vivo brainstructural and functional abnormalities. Well-controlled, prospectivestudies using both CT and MRI have reliably confirmedthe presence of cerebral shrinkage in alcoholics in life, involvingboth cortical grey and subcortical white matter 27–34 which aremore pronounced in older patients 35 and more apparent in thefrontal lobe 36,37 . The percentage of alcoholics with evidence ofcerebral atrophy on brain scans is far in excess of that noted inneuropathological studies 12 . This discrepancy is probablyexplained by the finding that brain changes are reversible withcontinuing abstinence 29,33,34,38–42 indicating that neuroimagingfindings do not accurately reflect the permanent neuropathologicalchanges previously described. Some studies have found thatthe neuroimaging changes worsen in patients who continue todrink 41,43,44 . A recent carefully controlled study, in which alcoholicmen and controls were followed over 5 years 45 found that agreater total alcohol consumption was associated with greaterdecrease in cortical grey matter, particularly in the frontal lobe.Thus, it is possible that prolonged alcohol ingestion leads toirreversible brain damage, which might be mirrored by irreversiblecognitive deficits.There is certainly no doubt that cognitive dysfunction can bewitnessed in uncomplicated alcoholics, even though these maynot reach the severity required for a diagnosis of dementia.Parsons 46 , following decades of his own research, concludes thatboth male and female sober adult alcoholics have deficits ontests of learning, memory, abstracting, problem-solving, perceptualanalysis and synthesis, and speed of information processing,which are equivalent to those found in patients with knownbrain dysfunction of a mild to moderate nature. Suchabnormalities can also be witnessed in adolescent alcoholics 47 .Further attempts to identify factors other than alcoholism toaccount for these differences have been unsuccessful 46 . It isnoticeable, however, that, like neuroimaging studies, thesedeficits are largely reversible over weeks or years of abstinence46,48 . This may explain why studies relating cognitive andstructural changes in alcoholics found weak and inconsistentcorrelations, the majority of which were explained mainly by ageand premorbid IQ 27–30,50 .Functional imaging studies have been a bit more fruitful in thisregard. One study found a reduction in overall cerebral glucoseutilization 51 but all other studies found specific regional changes.For example, Samson et al. 52 have shown a relative decrease inglucose utilization within the medial frontal cortex of six recentlydetoxified neurologically intact chronic alcoholics, and Gilman etal. 53 have also reported the same finding in 14 alcoholics studiedafter at least 27 days of abstinence. In the latter study, patientsmade errors on the category sorting test, a test of frontal lobefunction, and this correlated with glucose utilization in the medialfrontal cortex. However, in a small-scale follow-up study from thesame group, these deficits were partially reversible with abstinence54 and it is not clear whether they become irreversible withcontinued drinking.DISCUSSIONThere are several conclusions that can be made from these studiesconcerning the validity of alcoholic dementia. First, diffusecognitive impairment in alcoholic patients is common. It is anage-related phenomenon and the cognitive deficits are more mildthan in patients with neurodegenerative dementias. Alcohol itselfcan produce irreversible brain damage, mainly of white matterand the frontal association cortex, but most studies suggest thatfrank dementia cannot be ascribed entirely to alcohol neurotoxicity.Other causes should therefore be sought, most notablythiamine deficiency. In younger patients, alcohol alone can alsoproduce diffuse cognitive and cerebral abnormalities but these arelargely reversible with abstinence. It remains to be determinedwhich factors lead to the permanent alcohol-induced neuropathologyseen at post mortem.OTHER TOXIC DEMENTIAS IN THE ELDERLYThe acute and chronic psychiatric effects of ingestion of drugs ofabuse, including those most relevant to the elderly—barbituratesand benzodiazepines—have been extensively reviewed by Lishman55 . Suffice it to say that there is little evidence to suggest thatthese produce diffuse cognitive impairment. The neuropsychiatriceffects of long-term occupational solvent exposure is also relevantto the elderly. Although there is controversy concerning whethersolvents per se produce long-lasting effects, most studies findevidence for lasting neuropsychological abnormalities 56–59 . Ofparticular interest is that these studies also found that acombination of long-term solvent exposure and alcohol abuse isa particular risk factor for the development of dementia. Of finalrelevance to this age group is the identification of bismuthencephalopathy, which results from the over-ingestion of bismuth-containingcompounds commonly taken for gastricirritation and sold without prescription. Following an acuteorganic reaction characterized by delirium, seizures and neurologicalabnormalities, persistent sequelae of diffuse cognitiveimpairment and cerebral atrophy have been documented 60,61 .REFERENCES1. 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