Search Results

You are looking at 1 - 4 of 4 items for

  • Author or Editor: Marshall F. Wilkinson x
Clear All Modify Search
Restricted access

Marshall F. Wilkinson and Anthony M. Kaufmann

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 µV (p ≤ 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.

Restricted access

David B. MacDonald

Full access

Marshall F. Wilkinson, Tumul Chowdhury, W. Alan Mutch and Anthony M. Kaufmann

OBJECTIVE

Hemifacial spasm (HFS) is a cranial nerve hyperactivity disorder characterized by unique neurophysiological features, although the underlying pathophysiology remains disputed. In this study, the authors compared the effects of desflurane on facial motor evoked potentials (MEPs) from the spasm and nonspasm sides of patients who were undergoing microvascular decompression (MVD) surgery to test the hypothesis that HFS is associated with a central elevation of facial motor neuron excitability.

METHODS

Facial MEPs were elicited in 31 patients who were undergoing MVD for HFS and were administered total intravenous anesthesia (TIVA) with or without additional desflurane, an inhaled anesthetic known to centrally suppress MEPs. All measurements were completed before dural opening while a consistent mean arterial blood pressure was maintained and electroencephalography was performed. The activation threshold voltage and mean amplitudes of the MEPs from both sides of the face were compared.

RESULTS

There was a significantly lower mean activation threshold of facial MEPs on the spasm side than on the nonspasm side (mean ± SD 162.9 ± 10.1 vs 198.3 ± 10.1 V, respectively; p = 0.01). In addition, MEPs were also elicited more readily when single-pulse transcranial electrical stimulation was used on the spasm side (74% vs 31%, respectively; p = 0.03). Although desflurane (1 minimum alveolar concentration) suppressed facial MEPs on both sides, the suppressive effects of desflurane were less on the spasm side than on the nonspasm side (59% vs 79%, respectively; p = 0.03), and M waves recorded from the mentalis muscle remained unchanged, which indicates that desflurane did not affect the peripheral facial nerve or neuromuscular junction.

CONCLUSIONS

Centrally acting inhaled anesthetic agents can suppress facial MEPs and therefore might interfere with intraoperative monitoring. The elevated motor neuron excitability and differential effects of desflurane between the spasm and nonspasm sides support a mechanism of central pathophysiology in HFS.

Clinical trial registration no.: B2012:099 (clinicaltrials.gov)

Restricted access

Sedat Ulkatan, Vedran Deletis and Isabel Fernandez-Conejero