In order to test the hypothesis that Wernicke's encephalopathy is of t
opographic rather than of pathogenetic specifity we examined the brain
s of 49 patients without any evidence of chronic alcoholism. They had
died at least four days after an event of severe hypoxia-ischemia. The
y all showed extensive lesions in the cortex, in the thalamus and in o
ther regions. In 19 of them there was additional necrosis in the mamil
lary bodies which apparently was of the same age as the associated cor
tical and thalamic lesions and which could not be distinguished from W
ernicke's encephalopathy. In three of the 19 cases there was a total n
ecrosis within the mamillary bodies. By re-examining the mamillary bod
ies of 12 known alcoholics without any evidence for an ischemic impact
we could affirm that total necrosis may fit into the spectrum of Wern
icke's encephalopathy. Our findings demonstrate that the morphological
changes in the mamillary bodies due to thiamine deficiency and those
due to hypoxia-ischemia may be identical.