THE CEREBRAL-CORTEX IS DAMAGED IN CHRONIC-ALCOHOLICS

There is some controversy in the literature concerning whether chronic alcohol consumption damages the cerebral cortex. White decreased neur onal density in specific cortical regions is well described in chronic alcoholics, a recent study by Badsberg Jensen and Pakkenberg(5) using unbiased stereological methods questions whether neurodegeneration oc curs. In order to assess selective neurodegeneration in the cerebral c ortex of chronic alcoholics, regional volumes and unbiased estimates o f regional neuronal number (including neuronal identification with cal cium-binding proteins) were calculated for 14 chronic alcoholics and 2 1 controls. Cases were carefully screened to exclude any interfering p athologies. Lifetime and maximum daily alcohol consumption was determi ned, and homogeneous groups were identified (four chronic alcoholics w ith Wernicke's encephalopathy and Korsakoff's psychosis, four chronic alcoholics with Wernicke's encephalopathy alone, six chronic alcoholic s without Wernicke's encephalopathy or Korsakoff's psychosis, and 21 c ontrols). Brain volume analysis revealed that discrete regions were si gnificantly smaller in the chronic alcoholics compared to controls. As previously shown, white matter regions (particularly in the frontal l obe) were the most significantly reduced in volume. Alcoholics with We rnicke's encephalopathy (either alone or in combination with Korsakoff 's psychosis) had significantly smaller white matter volumes than cont rols or alcoholics without these complications. Medial temporal lobe r egions and the thalamus were also reduced in volume. Regression analys es revealed that the volume of both the white matter and thalamus nega tively correlated with alcohol consumption. Consistent with the interp retation of previous neuronal density studies, selective neuronal loss was found in the superior frontal association cortex of chronic alcoh olics, while no loss occurred from the motor cortex. The number of par valbumin-, calbindin- and calretinin-immunoreactive neurons was found to be unaltered in chronic alcoholics, suggesting that the neurodegene ration is confined to the non-GABAergic pyramidal neurons. As neurodeg eneration was observed in all alcoholic groups, damage to the frontal association cortex is not restricted to alcoholics with the amnesia of Korsakoff's psychosis. These results are consistent with the notion t hat chronic alcohol consumption is associated with selective neuronal vulnerability. The selective frontal neurodegeneration and the frontal focus of white matter atrophy are supported by neuropsychological, re gional blood flow, and magnetic resonance imaging studies of frontal l obe dysfunction in chronic alcoholics and may correlate with abnormali ties in working memory. (C) 1997 IBRO. Published by Elsevier Science L td.