Physiological abnormalities in hemifacial spasm studied during microvascular decompression operations.

The pathophysiology of hemifacial spasm was studied using electrophysiologic recordings made during neurosurgical operations to relieve it by microvascular decompression of the facial nerve near its entrance into the brain stem. Electrical stimulation of the temporal or the marginal mandibular branch of the facial nerve resulted in a response not only from the muscles that were innervated by the branch of the facial nerve that was stimulated, but also from other muscles, as evidenced by EMG recordings. This "lateral spread" of antidromic activity was facilitated by stimulation at a high rate (50 pps): the response increased five- to tenfold within a few seconds. When the repetition rate was reduced to the initial low stimulus rate (2 to 5 pps), facilitation continued for periods lasting from a few seconds to several minutes. The amplitude of the response of the supraorbital reflex (blink reflex), which can be elicited in patients with hemifacial spasm intraoperatively on the affected side despite the use of inhalation anesthesia, also increased after brief stimulation at a high rate (50 pps). After the facial nerve had been decompressed, both the lateral spread response and the blink reflex response were absent. These results support the hypothesis that hemifacial spasm is the result of hyperexcitability of the facial motor nucleus and facilitation of cross-transmissions between cells in the nucleus that innervate different parts of the face.