A 47-year-old-man lapsed into coma 12 h after liver transplantation, a
nd remained comatose until death 38 days later. Prior to transplantati
on he had repeated episodes of hepatic encephalopathy, but no fixed ne
urological signs. Autopsy revealed typical features of acquired hepato
cerebral degeneration with diffuse but patchy pseudolaminar cortical n
ecrosis, variable amount of neuronal loss in the cerebral cortex, basa
l ganglia and other areas, and proliferation of Alzheimer type II glia
. In addition, there was central pontine and extensive extrapontine my
elinolysis involving the lateral and medical geniculate bodies, the th
alamus, internal capsule, fornix, mamillothalamic tract, white matter
bundles in the caudate and pallidum, the oculomotor nuclei and the fol
iar white matter of the cerebellum. The distinction between myelinolyt
ic lesions and lesions due to hepatocerebral degeneration was not alwa
ys clear. Although neurological complications and brain lesions are ra
ther common after liver transplantation, there have been no reports of
acquired hepatocerebral degeneration in liver transplant recipients.
Our data lend support to the idea that a single prolonged comatose epi
sode, due to hepatic dysfunction, may induce permanent parenchymal bra
in damage.