Brain impairment in well‐nourished chronic alcoholics is related to ethanol intake

Abstract

To determine the influence of chronic ethanol intake on the central nervous system, we studied 40 asymptomatic, well-nourished, chronic alcoholics (mean age, 42.6 +/- 9.1 years) and 20 age-, sex-, and education-matched control subjects. Studies included neuropsychological testing, visual and short-latency auditory evoked potentials, and morphometric analysis of computed tomography scans. The mean daily ethanol consumption of the alcoholics was 204 gm over an average of 26.4 years. Compared to control subjects, chronic alcoholics exhibited a significant prolongation of the P100 latency of visual evoked potentials, and a prolongation and reduction in the amplitude of the latency of the V wave of short-latency auditory evoked potentials. These abnormalities were related to the lifetime dose of ethanol consumed. Brain morphometric analysis showed that alcoholics had a significantly greater degree of brain shrinkage with age, compared to control subjects. The cortical atrophy index correlated significantly with the lifetime ethanol consumption. Neuropsychological testing in alcoholics compared to controls revealed a significant impairment of frontal skills that was related to age, degree of scholarship, and the presence of frontal atrophy. In conclusion, well-nourished chronic alcoholics exhibited significant brain impairment, as demonstrated by neuropsychological testing, evoked potentials, and brain morphometric analysis, which was correlated with the lifetime dose of ethanol consumed.

Chronic alcoholism: Insights from neurophysiology

“…Chronic alcoholism leads to delayed latency [16], reduced amplitude [19] and abnormal topography [103] of this component. These aberrant findings seem to be associated with the lifetime dose of ethanol consumed [112] and to disappear after a period of abstinence [19]. A recent study by Maurage et al [13] confirmed and expanded these results to complex stimuli (namely faces).…”

“…However, repeated intake of high doses of alcohol can affect nearly every organ system, especially the gastrointestinal tract (e.g., liver cirrhosis, pancreatitis), the cardiovascular system (e.g., low-grade hypertension, elevated risk of heart disease), and the peripheral nervous system (e.g., muscle weakness, paraesthesias and decreased peripheral sensation). Moreover, it is well established that, because of alcohol neurotoxicity, chronic alcoholism leads to deleterious effects on the central nervous system (CNS), such as brain atrophy and/or dysfunction [44,156], these brain impairments being correlated with the lifetime dose of ethanol consumed [112]. Improvements in neuroimaging technology have contributed significantly to our understanding of these effects, revealing alcoholic-specific changes in the CNS associated with neuropsychological abnormalities.…”

Event-Related Brain Potentials in Psychopathology: Clinical and cognitive perspectives

“…These abnormalities were related to the lifetime consumption of ethanol (Nicolas et al, 1997), and improvement of P100 abnormalities have been found after a period of abstinence (Chan et al, 1986). Consequently, the hypothesis made for schizophrenia, namely that the P300 reduction may be caused by earlier sensory deficit, could also be suggested for alcoholism.…”

“…Several studies have demonstrated that alcoholics exhibit increased latency of short auditory evoked potentials, such as delayed peak V and an increase in the III-V and I-V intervals of the auditory brainstem potential and increased P100 latency of visual evoked potential (Cadaveira, Grau, Roso, & Sanchez-Turet, 1991;Chan, Mc Leod, Tuck, Walsh, & Feary, 1986;Nicolas et al, 1997) (the P100 component is largest over the occipital regions and it represents the activation of the area 17 in the visual cortex). These abnormalities were related to the lifetime consumption of ethanol (Nicolas et al, 1997), and improvement of P100 abnormalities have been found after a period of abstinence (Chan et al, 1986).…”

Zusammenhänge zwischen Alkohol- resp. Zigarettenkonsum und der kognitiven Leistungsfähigkeit bei Alkoholabhängigen. Ein Vergleich des Konsumverhaltens vor der stationären Behandlung mit der kognitiven Leistung nach Klinikeintritt

“…Keywords [6][7][8][9][10], verglichen den aktuellen Alkoholkonsum mit dem lebenszeitlichen Gesamt-konsum [11] oder befassten sich explizit mit Geschlechtsdifferenzen [12]. Durch vermehrte Anstrengung können die Betroffenen die kognitiven Beeinträchtigungen teilweise kompensieren.…”