Neuropsychological Differences between Male Familial and Nonfamilial Alcoholics and Nonalcoholics

Abstract

The hypothesis was tested that neuropsychological differences exist between males who have an alcoholic parent, sister, or brother (FH+) versus those who do not (FH-). Neuropsychological tests measuring verbal, learning/memory, abstracting/problem solving, and perceptual-motor performance were given to four groups of middle-aged subjects: alcoholic FH+ (n = 41); alcoholic FH- (n = 27); nonalcoholic FH+ (n = 19); and nonalcoholic FH- (n = 43). FH+ subjects performed significantly poorer than FH- subjects on the abstracting/problem solving and perceptual-motor tasks, and approached significance on the verbal and learning/memory measures. Alcoholics performed more poorly than nonalcoholics on abstracting/problem solving and learning/memory tasks. There were no groups by family history significant interactions. From these results we suggest: a performance deficit in abstracting/problem solving and possibly learning/memory may antedate the alcoholic stage in FH+ individuals; alcoholism and positive family history of alcoholism have independent, additive deleterious effects on cognitive-perceptual functioning; and future neuropsychological studies of alcoholism should consider the frequency of FH+ and FH- individuals in both alcoholic and control groups.

Cognitive Dysfunction in Alcohol Withdrawal

“…Alcoholism has even been proposed as a cause of prema ture brain aging [5][6][7][8]; not only does this not account for the specificity or reversal of cognitive dysfunction, but there is also evidence that alcohol may not aggravate the effects of age [9], Correlation between degree of cognitive dysfunction and total alcohol intake is weak and inconsis tent [10,11]; an important parameter appears to be the frequency of alcoholic bingeing, which modulates the effects of the amount of alcohol absorbed during each epi sode [12,13], Emotional and mood disturbances, both primary and secondary, may also be involved. Some investigators be lieve that they aggravate cognitive dysfunction in alcohol ism, and that anxiety may be predictive of severe cogni tive impairment [14,15]; others consider that psychologi cal distress has no influence [12], Despite some evidence to the contrary [13], studies have indicated that cognitive dysfunction is more severe in patients with a family history of alcoholism [2,16]. This is supported by other data on inborn cognitive ability and a genetic predisposition to alcoholism.…”

“…This is supported by other data on inborn cognitive ability and a genetic predisposition to alcoholism. However, cog nitive and in particular psychomotor dysfunction, identi cal to that in alcoholics, is observed in the absence of alco holism in high-risk subjects: in sons of alcoholic fathers [16,17], subjects with an antisocial personality disorder [18] , or those with a residual attention deficit disorder [19] . However, although cognitive dysfunction may revert to normal following abstinence, recovery is rarely com plete and the residual dysfunction is usually psychomotor [20] , hence the hypothesis that frontal cognitive dysfunc tion is a predisposing factor for all 'behavioral disinhibition' syndromes, including alcohol abuse [21], Four two reasons, data on the frequency of cognitive dysfunction in alcoholics vary between studies: not only do study populations differ with respect to alcohol charac teristics and risk factors, but some studies have been con ducted less than 4 weeks after alcohol withdrawal, when the somatic, mood and emotional repercussions of with drawal may still be compounding and/or modifying pre existing cognitive dysfunction, whereas other studies have been conducted after a fairly prolonged period of absti nence, allowing for the recovery of some of the dysfunc tion caused by the direct effects of alcohol on the central nervous system.…”

Event-Related Oscillations in Offspring of Alcoholics: Neurocognitive Disinhibition as a Risk for Alcoholism

“…This view is strengthened by our finding that the OA group has a weaker fronto-parietal interaction as observed in the topography of slow alpha activity (8-9 Hz) (see Figure 4). It is also known that children of alcoholics, similar to adult alcoholics, manifest neuropsychological or cognitive deficits that precede the onset of alcoholism (Schaeffer et al 1984;Drejer et al 1985;Tarter et al 1989;Pihl et al 1990, Pihl andBruce 1995;Peterson et al 1992;Knop et al 1993). Therefore, we propose that the neuro-cognitive deficits observed in the OA group, as elicited by decreased P3 amplitude and weaker oscillatory responses in low frequency bands perhaps predispose these high risk individuals to develop alcoholism and related disorders.…”

Alexithymia in Males at High Genetic Risk for Alcoholism

“…Alcohol ics have also been found to be more autonomically reactive to stress than controls [Chandler et al, 1975;Coopersmith, 1964], A greater prevalence of psychosomatic symptoms has been found in daughters (not sons) of alcoholic fathers with extensive family histories of male alcoholism (type 2 familial alcoholism) [Cloninger et al, 1983], It is not completely clear why the sons in these families did not have more psychoso matic symptoms, except that their increased alcohol consumption may be prophylactic of such symptoms. Finally, concrete thinking, one of the features of alexithymia, has been well documented in alcoholics and their off spring [Gabrielli and Mednick, 1983;Schaeffer et al, 1984],…”