CORTICAL AND SUBCORTICAL WHITE-MATTER DAMAGE WITHOUT WERNICKES ENCEPHALOPATHY AFTER RECOVERY FROM THIAMINE-DEFICIENCY IN THE RAT

The relative etiologic roles of ethanol and thiamine deficiency in the cortical atrophy and loss of cerebral white matter in chronic alcohol ics are uncertain, The present study examined the distribution of dege nerating axons within cortical and subcortical tracts 1 week after rec overy from early to late symptomatic stages of thiamine deficiency in the absence of ethanol in Sprague-Dawley rats, The brains of rats expo sed to an early symptomatic stage of pyrithiamine-induced thiamine def iciency, 12-13 days of treatment, contained degenerating axons in corp us callosum, anterior commissure, external and internal capsules, opti c and olfactory tracts, and fornix and mammillothalamic tracts, A dens e pattern of degenerating axons was evident in layers III-IV of fronta l and parietal cortex, Less intense and more evenly distributed degene rating axons were present in layers IV-VI of frontal, parietal, cingul ate, temporal, retrosplenial, occipital, and granular insular cortex. Neuronal counts in mammillary body nuclei and areal measurements of th e mammillary body were unchanged from controls and the thalamus was re latively undamaged. In animals reversed at later and more advanced sym ptomatic stages of thiamine deficiency, 14-15 days of treatment, degen erating axons were found in other cortical regions and hippocampus and there was extensive neuronal loss and gliosis within mammillary body and medial thalamus. These results demonstrate that a single episode o f thiamine deficiency can selectively damage cortical white matter tra cts while sparing the thalamus and mammillary body and may be a critic al factor responsible for the pathological and behavioral changes obse rved in alcoholics without Wernicke's encephalopathy.