Marshall F Wilkinson1, Anthony M Kaufmann. 1. Centre for Cranial Nerve Disorders, Division of Neurosurgery, University of Manitoba, Winnipeg, Manitoba, Canada. mwilkinson@exchange.hsc.mb.ca
Abstract
OBJECT: Hemifacial spasm (HFS) is thought to be due to a hyperactive facial motor nucleus consequent to chronic neurovascular contact. The lateral spread (LS) response is presumed to reflect changes in facial motor neuron excitability. Facial muscle motor evoked potentials (MEPs) use the same efferent pathway as LS, therefore the authors speculated that these potentials should reflect differences consistent with changes at the facial motor nucleus level. METHODS: Monitoring of LS and bilateral facial MEP was performed in 10 consecutive patients undergoing MVD for HFS. Ipsilateral facial MEPs were monitored in 17 patients undergoing MVD for trigeminal neuralgia (TN). Latency, amplitude, and duration of the MEPs were compared before and after MVD. Following MVD the duration of ipsilateral MEPs decreased from 17.6 +/- 1.2 to 7.6 +/- 0.7 msec and their amplitude decreased from 269.9 +/- 66.3 to 76.5 +/- 26.2 microV (p < or = 0.01). These changes were consequent to the abolition of LS in eight of 10 patients and an approximately 50% reduction in two patients. The relationship between the reduction in MEPs and changes in LS was significant (p < 0.01). Control facial muscle MEPs (nonspastic side in patients with HFS and in those with TN) did not change significantly during the MVD procedure. Spasms were alleviated in nine of 10 patients, and there was no indication of facial nerve damage intraoperatively or postoperatively. CONCLUSIONS: Facial muscle MEPs represent a novel tool for studying the neurophysiological mechanisms of HFS in particular and monitoring the facial nerve in general. Data in this study support the hypothesis that the development of HFS and its alleviation with MVD are related to changes in facial motor nucleus activity.
OBJECT: Hemifacial spasm (HFS) is thought to be due to a hyperactive facial motor nucleus consequent to chronic neurovascular contact. The lateral spread (LS) response is presumed to reflect changes in facial motor neuron excitability. Facial muscle motor evoked potentials (MEPs) use the same efferent pathway as LS, therefore the authors speculated that these potentials should reflect differences consistent with changes at the facial motor nucleus level. METHODS: Monitoring of LS and bilateral facial MEP was performed in 10 consecutive patients undergoing MVD for HFS. Ipsilateral facial MEPs were monitored in 17 patients undergoing MVD for trigeminal neuralgia (TN). Latency, amplitude, and duration of the MEPs were compared before and after MVD. Following MVD the duration of ipsilateral MEPs decreased from 17.6 +/- 1.2 to 7.6 +/- 0.7 msec and their amplitude decreased from 269.9 +/- 66.3 to 76.5 +/- 26.2 microV (p < or = 0.01). These changes were consequent to the abolition of LS in eight of 10 patients and an approximately 50% reduction in two patients. The relationship between the reduction in MEPs and changes in LS was significant (p < 0.01). Control facial muscle MEPs (nonspastic side in patients with HFS and in those with TN) did not change significantly during the MVD procedure. Spasms were alleviated in nine of 10 patients, and there was no indication of facial nerve damage intraoperatively or postoperatively. CONCLUSIONS: Facial muscle MEPs represent a novel tool for studying the neurophysiological mechanisms of HFS in particular and monitoring the facial nerve in general. Data in this study support the hypothesis that the development of HFS and its alleviation with MVD are related to changes in facial motor nucleus activity.
Authors: Maura K Cosetti; Ming Xu; Andrew Rivera; Daniel Jethanamest; Maggie A Kuhn; Aleksandar Beric; John G Golfinos; J Thomas Roland Journal: J Neurol Surg B Skull Base Date: 2012-10