Pathologic and pathophysiologic findings in hemifacial spasm are reviewed in connection with recent theoretical and experimental studies of ectopic/ephaptic excitation. The intracranial segment of the normal facial nerve is ensheathed by an arachnoid membrane only and shows no fascicular organization. In hemifacial spasm, this segment shows signs of demyelination. Several electrical phenomena relating to ectopic excitation, ephaptic transmission between facial nerve fibers, and autoexcitation can be reproduced in clinical electrophysiologic studies of hemifacial spasm. These abnormalities gradually disappear after facial nerve decompression in the cerebellopontine recess. It is concluded that the normal facial nerve is vulnerable to minor compression, the primary pathophysiologic mechanism in hemifacial spasm is ectopic/ephaptic excitation due to compression and demyelination of the intracranial segment of the facial nerve, and the facial nerve in hemifacial spasm is a useful model for the study of ephaptic transmission, which has provided new information about the resolution of abnormal electrical events after decompression.