We have used short latency somatosensory evoked potential (SEP) in 108
patients with liver cirrhosis caused by viral hepatitis to evaluate h
epatic encephalopathy. Short-latency SEPs were recorded by the MEM-410
4 apparatus (Nihon Kohden Inc., Tokyo) in response to median nerve sti
mulation. For a precise analysis of the early components, we averaged
1000 responses during a 30-msec period. Early SEP components were prol
onged in patients with decompensated, but not in those with compensate
d, cirrhosis. We also examined the relationship between consciousness
level and interpeak latency (IPL) N13-N20 of SEP and between conscious
ness level and electroencephalograph in 51 patients among 108 patients
with liver cirrhosis. The IPL N13-N20 was prolonged in the decompensa
ted stage with normal consciousness, but EEG findings had not deterior
ated in this stage. EEG grade became worse in the stage of abnormal co
nsciousness. The prolongation of the IPL N13-N20 was attributed to the
central conduction impairment. We postulate that subcortical impairme
nt may occur in patients with subclinical hepatic encephalopathy, when
the cortex is little affected.