OBJECTIVE: We used the contingent negative variation (CNV), a slow negative shift in the human electroencephalogram, to investigate the effects of heavy chronic alcohol use on frontal lobe function. METHODS: Event-related potentials (ERPs) were recorded from 30 heavy drinkers (HD) and 30 age-, sex-, and education-matched light or non-drinkers (LD), using a classical two-stimulus reaction time (RT) paradigm. Structural magnetic resonance images and neuropsychological tests were also administered. RESULTS: The amplitude of the late CNV was significantly reduced in HD relative to light drinkers. Moreover, diminished CNV amplitudes in HD appear to be closely related to the amount of recent alcohol consumption. There were no significant differences in neuropsychological measures of frontal lobe function and frontal lobe volume between light and HD. However, in HD, reduced late CNV amplitudes were associated with decreased frontal lobe gray matter volume and poor performance on the Trail Making Test B. In LD but not in HD, late CNV amplitude correlated positively with RT, suggesting that the late CNV reflects some aspect of motor and cognitive preparation. CONCLUSIONS: The inverse relationships between frontal lobe gray matter volume, performance on the Trail Making Test B, and late CNV amplitude in HD suggest that the ERP abnormalities observed in the current study may be indices of alcohol-related damage to the frontal lobe. The lack of a significant relationship between CNV amplitude and RT in HD suggests that chronic heavy alcohol use may disrupt response preparation.
OBJECTIVE: We used the contingent negative variation (CNV), a slow negative shift in the human electroencephalogram, to investigate the effects of heavy chronic alcohol use on frontal lobe function. METHODS: Event-related potentials (ERPs) were recorded from 30 heavy drinkers (HD) and 30 age-, sex-, and education-matched light or non-drinkers (LD), using a classical two-stimulus reaction time (RT) paradigm. Structural magnetic resonance images and neuropsychological tests were also administered. RESULTS: The amplitude of the late CNV was significantly reduced in HD relative to light drinkers. Moreover, diminished CNV amplitudes in HD appear to be closely related to the amount of recent alcohol consumption. There were no significant differences in neuropsychological measures of frontal lobe function and frontal lobe volume between light and HD. However, in HD, reduced late CNV amplitudes were associated with decreased frontal lobe gray matter volume and poor performance on the Trail Making Test B. In LD but not in HD, late CNV amplitude correlated positively with RT, suggesting that the late CNV reflects some aspect of motor and cognitive preparation. CONCLUSIONS: The inverse relationships between frontal lobe gray matter volume, performance on the Trail Making Test B, and late CNV amplitude in HD suggest that the ERP abnormalities observed in the current study may be indices of alcohol-related damage to the frontal lobe. The lack of a significant relationship between CNV amplitude and RT in HD suggests that chronic heavy alcohol use may disrupt response preparation.