Flash visual potentials (FEPs), somatosensory evoked potentials (SEPs) and auditory brainstem responses (ABR) were recorded in a 66-year-old patient presenting with clinical, EEG and CT brain scan features of herpes simplex encephalitis (HSE). At the time of evoked potential study (10 days after onset of the disease) the patient was treated with iv barbiturate on controlled respiration (lidocaine and phenytoin were not utilized); core temperature was 37 degrees C and pupils were dilated and nonreactive. Cortical FEPs were not recognizable on 02 lead, whereas they were clearly evident on 01 with normal latency of early N1, P1, N2 waves and delayed P2 component. SEPs showed normal peripheral and central conduction times, but N20 peak was bilaterally absent with unrecognizable (on P3) or delayed (on P4) N33 wave. No ABR (including wave I) were found on stimulation of the right ear, whereas delayed wave V with prolonged interpeak I-V latency was found on stimulation of the left ear. In conclusion, changes in sensory evoked potentials in HSE seem to be caused either by necrotic-hemorrhagic damage (with the disappearance of some cortical responses), by coma (with alterations in middle-latency cortical responses) and by increased intracranial pressure (with subsequent ABR abnormalities).