J Neurosurg 74:254-257, 1991
Intraoperative monitoring of the facial nerve during decompressive surgery for hemifacial spasm STEPHEN J. HAINES, M.D., AND FERNANDO TORRES, M.D.
Departments of Neurosurgery and Neurology, University of Minnesota Health Science Center, Minneapolis, Minnesota I In 11 consecutive patients, intraoperative electromyographic (EMG) recordings were made from the facial muscles during microvascular decompression for hemifacial spasm. In one patient, recordings could not be obtained for technical reasons, and two patients had no abnormality. In the remaining eight patients, the abnormal response resolved before decompression in two, resolved immediately at the time of decompression in five, and failed to resolve in one. All patients were relieved of their hemifacial spasm. In the five patients whose abnormalities resolved at the time of decompression, there was a precise intraoperative correlation between decompression of the nerve and disappearance of the abnormal EMG response. In three cases, this was a useful guide to the need to decompress more than one vessel. These results confirm the findings of Moller and Jannetta, support the use of this technique for intraoperative monitoring of facial nerve decompression procedures, and provide strong circumstantial evidence that vascular cross-compression is an impor-
tant etiological factor in hemifacial spasm. KEY WORDS
* hemifacial spasm
intraoperative monitoring • electromyography
•
facial nerve
M
OLLER and
Jannetta" have reported a series of observations on intraoperative facial electromyographic (EMG) recordings obtained during microvascular decompression for hemifacial spasm. These observations have suggested that this method of monitoring provides a useful way of confirming complete facial nerve decompression intraoperatively. In addition, it shows evidence that the actual vascular compression of the nerve is an important factor in the production of hemifacial spasm. To our knowledge, independent confirmation of these observations has not been recorded. In this paper we report our experience with this technique in 11 patients.
current at a rate of 5.1 stimuli/sec were applied alternately to the marginal mandibular and the temporal branches of the facial nerve on the side of hemifacial spasm. Bipolar stimulation was performed with the two electrodes about 1 cm apart. Electromyographic potentials were recorded from both the orbicularis oculi and mentalis muscles with each stimulus. Recording was bipolar, with an interelectrode distance of about 1 cm. The recording electrodes were located at a distance of about 4 cm from the stimulating electrodes. Recordings were made at each stage of the decompressive operation. Results
Clinical Material and Methods The technique is essentially that described by Moller and Jannetta.' Anesthesia was induced with thiopental, and a single dose of a short-acting neuromuscular blocking agent (vecuronium bromide) was given. Stimulating needle electrodes were inserted intradermally over the marginal mandibular and temporal branches of the facial nerve. Recording needle electrodes were inserted into the mentalis muscle and the orbicularis oculi muscle on the same side. The absence of muscle relaxant was confirmed with a peripheral nerve stimulator placed over the ulnar or medial nerve. Squarewave stimuli of 100 Atsec duration and a 3- to 5-mAmp 254
Recording has been attempted in 11 patients (Table 1). In one patient, equipment problems prevented satisfactory recording. In two patients, orthodromic responses to stimulation were recorded but no abnormal antidromic response could be identified. In the remaining eight patients, the abnormal response described by Moller and Jannetta was present. This consisted of a response in the muscles supplied by the unstimulated branch of the facial nerve. The latency between the stimulus and the response of the antidromically stimulated muscle is approximately 13 cosec. In two patients, the abnormal response disappeared prior to decompression of the nerve: this occurred upon opening J Neurosurg. / Volume 74 / February, 1991
Facial nerve monitoring in hemifacial spasm surgery TABLE 1 Results cif intraoperative neurophysiologic recording Result
technical failure normal response resolution of abnormal response before decompression after decompression not achieved
FIG. 1. Intraoperative electromyographic recordings from the orbicularis oculi muscle during stimulation of the marginal mandibular branch of the facial nerve. Progressive disappearance of the abnormal response of 1 3-msec approximate latency is shown as the operation progresses and all vessels compressing the facial nerve are mobilized.
the dura in one and after gentle cerebellar retraction was begun in the other. In one patient, the abnormalities did not disappear despite decompression of all visible compressing vessels. In the remaining five patients, the abnormality did not disappear until a complete microvascular decompression of the facial nerve had been accomplished. In three of these five cases, more than one vessel was cross-compressing the facial nerve, and complete disappearance of the abnormal EMG potentials did not occur until all vessels had been decompressed. Figure 1 shows progressive disappearance of the abnormal response as each of four corn-
No. of Cases 2 2 5
pressing vessels were lifted off the facial nerve in one of these patients. Figures 2, 3, and 4 depict tracings correlated with intraoperative photographs showing compressing vessels. In several cases, the vessel was repeatedly separated from the nerve and then allowed to return to its original position. The abnormal responses disappeared immediately with decompression and returned each time the vessel was replaced (Fig. 5). Hemifacial spasm has been relieved in all patients with a follow-up period of 3 months to 3 years. Two patients have complained of transient episodes of mild twitching in the orbicularis oculi muscle which has resolved spontaneously. The one patient in whom the abnormal response did not disappear, despite apparently adequate decompression, had persistent hemifacial spasm for 6 days postoperatively. The spasm then resolved completely and has remained absent. All other patients were free of spasm immediately after surgery. Discussion We have confirmed the findings of Moller and Jannetta that, in patients with hemifacial spasm, there is
FIG. 2. Upper: Intraoperative electromyographic recording after dural opening but before facial nerve decompression for hemifacial spasm. Lower: Drawing (left) and operative photograph (right) illustrate the compressing vessels as seen through the operating microscope.
J. Neurosurg, / Volume 74 /February, 1991
255
S. J. Haines and F. Torres FIG. 3. Upper: Intraoperative electromyographic recording after mobilization of one of two cross-compressing vessels. There is actually an increase in the amplitude of the abnormal potential. Lower.. Drawing (left) and operative photograph (right) showing the vessel held away from the facial nerve with a microdissector.
an abnormality in the facial nerve or its nucleus which allows the stimulus applied to one branch of the facial nerve to spread to other branches of that same nerve. In most cases, this abnormality disappears immediately upon microvascular decompression of the facial nerve as it exits the brain stem. Moller and Jannetta 3 have
speculated that the vascular compressive lesion produces antidromic activity which alters the excitability of the facial nucleus. They believe that the fact that lateral spread is also seen after stimulation of the supraorbital nerve further implicates the facial nucleus in the disease.' While the present observations do not provide FIG. 4, Upper: Intraoperative electromyographic recording after nerve decompression is completed. No abnormality persists although the orthodromic response in the orbicularis oculi muscle is unchanged. Lower: Drawing (left) and operative photograph (right) showing both vessels held away from the nerve.
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J. Neurosurg. / Volume 74 / February, 1991
Facial nerve monitoring in hemifacial spasm surgery
FIG. 5. Repeated intraoperative electromyographic recordings from the mentalis muscle during stimulation of the temporal branch of the facial nerve. The abnormal potential, which disappears when the compressing vessel is held away
from the nerve, returns when the vessel is replaced and again
disappears when the vessel is mobilized.
direct evidence of the specific site and nature of the abnormality, they provide strong evidence that the abnormality is immediately reversible at the time of surgery and this is strong circumstantial evidence that vascular compression plays an important role in the production of hemifacial spasm. The disappearance of the abnormality in some cases before decompression is accomplished is not inconsistent with this hypothesis. It is certainly possible that the removal of cerebrospinal fluid and retraction of the cerebellum could cause a shift in the neurovascular relationship temporarily equivalent to decompression. Placement of the Teflon felt pledget would then maintain the decompression permanently. The etiology and basic pathophysiology of microvascular compression syndromes such as trigeminal neuralgia and hemifacial spasm remain controversial. Recently, Adams' reviewed the literature on this subject; he was very critical of the concept but did not provide an explanation for the findings in hemifacial spasm. It would be most interesting to examine the response of the EMG abnormalities to the non-decompressive operation which he has performed for hemifacial spasm. Adams argues that the effectiveness of the vascular decompression procedure reported by Moller and Jannetta is due to manipulation and secondary trauma to the nerve. He thinks that this trauma may cause the symptoms to disappear, but he does not explain why the nerves in both hemifacial spasm and trigeminal neuralgia function normally after suffering mechanical trauma in addition to whatever initially caused the symptoms. He also does not explain the observation that facial weakness often resolves after decompression. He claims that the fact that sectioning the nerves also makes the symptoms disappear is an argument against
I Neurosurg. / toluene 74 / February, 1991
the vascular compression hypothesis because "inevitably, the possibility arises that the effect of microvascular decompression is by the way of trauma." It is hard to explain why a definitive trauma (section) would cause complete dysfunction, while a milder one would restore normal function. In addition, the traumatic hypothesis cannot explain the disappearance and reappearance of the phenomenon with repeated intraoperative decompression. The data presented by Moller and Jannetta' suggest that failure to relieve the neurophysiological abnormality during surgery is associated with a relatively poor prognosis for relief of hemifacial spasm. In our patient in whom the abnormality was not relieved intraoperatively, although her spasm has resolved, it persisted unusually long postoperatively. It is too early to know if this relief will be long-lasting. This finding is consistent, however, with an association between the electrophysiological and clinical findings. We believe that these observations justify the use of this technique as a method for monitoring the completeness of decompression during microvascular decompression for hemifacial spasm. Further support to justify the use of this technique is given by the finding that in three of our cases it was a useful guide to the need to decompress more than one vessel. Acknowledgments We would like to acknowledge the secretarial assistance of Susan Whaley and technical assistance of Connie Erickson, R.EEGT, in obtaining the reports. References 1. Adams CBT: Microvascular compression: an alternative view and hypothesis. J Neurosurg 70:1-12, 1989 2. Moller AR, Jannetta PJ: Hemifacial spasm: results of electrophysiologic recording during microvascular decompression operations. Neurology 35:969-974, 1985 3. Moller AR, Jannetta PJ: Microvascular decompression in hemifacial spasm: intraoperative electrophysiological observations. Neurosurgery 16:612-618, 1985 4. Moller AR, Jannetta PJ: Monitoring the facial EMG responses during microvascular decompression operations for hemifacial spasm. J Neurosurg 66:681-685,
1987 5. Moller AR, Jannetta PJ: Physiological abnormalities in hemifacial spasm studied during microvascular decompression operations. Exp Neural 93:584-600, 1986
Manuscript received March 27, 1990. Accepted in final form August 13, 1990. Address reprint requests to: Stephen J. Haines, M.D., Department of Neurosurgery, 420 Delaware Street SE, Box 96 UMHC, Minneapolis, Minnesota 55455.
257
Intraoperative monitoring of the facial nerve during decompressive surgery for hemifacial spasm STEPHEN J. HAINES, M.D., AND FERNANDO TORRES, M.D.
Departments of Neurosurgery and Neurology, University of Minnesota Health Science Center, Minneapolis, Minnesota I In 11 consecutive patients, intraoperative electromyographic (EMG) recordings were made from the facial muscles during microvascular decompression for hemifacial spasm. In one patient, recordings could not be obtained for technical reasons, and two patients had no abnormality. In the remaining eight patients, the abnormal response resolved before decompression in two, resolved immediately at the time of decompression in five, and failed to resolve in one. All patients were relieved of their hemifacial spasm. In the five patients whose abnormalities resolved at the time of decompression, there was a precise intraoperative correlation between decompression of the nerve and disappearance of the abnormal EMG response. In three cases, this was a useful guide to the need to decompress more than one vessel. These results confirm the findings of Moller and Jannetta, support the use of this technique for intraoperative monitoring of facial nerve decompression procedures, and provide strong circumstantial evidence that vascular cross-compression is an impor-
tant etiological factor in hemifacial spasm. KEY WORDS
* hemifacial spasm
intraoperative monitoring • electromyography
•
facial nerve
M
OLLER and
Jannetta" have reported a series of observations on intraoperative facial electromyographic (EMG) recordings obtained during microvascular decompression for hemifacial spasm. These observations have suggested that this method of monitoring provides a useful way of confirming complete facial nerve decompression intraoperatively. In addition, it shows evidence that the actual vascular compression of the nerve is an important factor in the production of hemifacial spasm. To our knowledge, independent confirmation of these observations has not been recorded. In this paper we report our experience with this technique in 11 patients.
current at a rate of 5.1 stimuli/sec were applied alternately to the marginal mandibular and the temporal branches of the facial nerve on the side of hemifacial spasm. Bipolar stimulation was performed with the two electrodes about 1 cm apart. Electromyographic potentials were recorded from both the orbicularis oculi and mentalis muscles with each stimulus. Recording was bipolar, with an interelectrode distance of about 1 cm. The recording electrodes were located at a distance of about 4 cm from the stimulating electrodes. Recordings were made at each stage of the decompressive operation. Results
Clinical Material and Methods The technique is essentially that described by Moller and Jannetta.' Anesthesia was induced with thiopental, and a single dose of a short-acting neuromuscular blocking agent (vecuronium bromide) was given. Stimulating needle electrodes were inserted intradermally over the marginal mandibular and temporal branches of the facial nerve. Recording needle electrodes were inserted into the mentalis muscle and the orbicularis oculi muscle on the same side. The absence of muscle relaxant was confirmed with a peripheral nerve stimulator placed over the ulnar or medial nerve. Squarewave stimuli of 100 Atsec duration and a 3- to 5-mAmp 254
Recording has been attempted in 11 patients (Table 1). In one patient, equipment problems prevented satisfactory recording. In two patients, orthodromic responses to stimulation were recorded but no abnormal antidromic response could be identified. In the remaining eight patients, the abnormal response described by Moller and Jannetta was present. This consisted of a response in the muscles supplied by the unstimulated branch of the facial nerve. The latency between the stimulus and the response of the antidromically stimulated muscle is approximately 13 cosec. In two patients, the abnormal response disappeared prior to decompression of the nerve: this occurred upon opening J Neurosurg. / Volume 74 / February, 1991
Facial nerve monitoring in hemifacial spasm surgery TABLE 1 Results cif intraoperative neurophysiologic recording Result
technical failure normal response resolution of abnormal response before decompression after decompression not achieved
FIG. 1. Intraoperative electromyographic recordings from the orbicularis oculi muscle during stimulation of the marginal mandibular branch of the facial nerve. Progressive disappearance of the abnormal response of 1 3-msec approximate latency is shown as the operation progresses and all vessels compressing the facial nerve are mobilized.
the dura in one and after gentle cerebellar retraction was begun in the other. In one patient, the abnormalities did not disappear despite decompression of all visible compressing vessels. In the remaining five patients, the abnormality did not disappear until a complete microvascular decompression of the facial nerve had been accomplished. In three of these five cases, more than one vessel was cross-compressing the facial nerve, and complete disappearance of the abnormal EMG potentials did not occur until all vessels had been decompressed. Figure 1 shows progressive disappearance of the abnormal response as each of four corn-
No. of Cases 2 2 5
pressing vessels were lifted off the facial nerve in one of these patients. Figures 2, 3, and 4 depict tracings correlated with intraoperative photographs showing compressing vessels. In several cases, the vessel was repeatedly separated from the nerve and then allowed to return to its original position. The abnormal responses disappeared immediately with decompression and returned each time the vessel was replaced (Fig. 5). Hemifacial spasm has been relieved in all patients with a follow-up period of 3 months to 3 years. Two patients have complained of transient episodes of mild twitching in the orbicularis oculi muscle which has resolved spontaneously. The one patient in whom the abnormal response did not disappear, despite apparently adequate decompression, had persistent hemifacial spasm for 6 days postoperatively. The spasm then resolved completely and has remained absent. All other patients were free of spasm immediately after surgery. Discussion We have confirmed the findings of Moller and Jannetta that, in patients with hemifacial spasm, there is
FIG. 2. Upper: Intraoperative electromyographic recording after dural opening but before facial nerve decompression for hemifacial spasm. Lower: Drawing (left) and operative photograph (right) illustrate the compressing vessels as seen through the operating microscope.
J. Neurosurg, / Volume 74 /February, 1991
255
S. J. Haines and F. Torres FIG. 3. Upper: Intraoperative electromyographic recording after mobilization of one of two cross-compressing vessels. There is actually an increase in the amplitude of the abnormal potential. Lower.. Drawing (left) and operative photograph (right) showing the vessel held away from the facial nerve with a microdissector.
an abnormality in the facial nerve or its nucleus which allows the stimulus applied to one branch of the facial nerve to spread to other branches of that same nerve. In most cases, this abnormality disappears immediately upon microvascular decompression of the facial nerve as it exits the brain stem. Moller and Jannetta 3 have
speculated that the vascular compressive lesion produces antidromic activity which alters the excitability of the facial nucleus. They believe that the fact that lateral spread is also seen after stimulation of the supraorbital nerve further implicates the facial nucleus in the disease.' While the present observations do not provide FIG. 4, Upper: Intraoperative electromyographic recording after nerve decompression is completed. No abnormality persists although the orthodromic response in the orbicularis oculi muscle is unchanged. Lower: Drawing (left) and operative photograph (right) showing both vessels held away from the nerve.
256
J. Neurosurg. / Volume 74 / February, 1991
Facial nerve monitoring in hemifacial spasm surgery
FIG. 5. Repeated intraoperative electromyographic recordings from the mentalis muscle during stimulation of the temporal branch of the facial nerve. The abnormal potential, which disappears when the compressing vessel is held away
from the nerve, returns when the vessel is replaced and again
disappears when the vessel is mobilized.
direct evidence of the specific site and nature of the abnormality, they provide strong evidence that the abnormality is immediately reversible at the time of surgery and this is strong circumstantial evidence that vascular compression plays an important role in the production of hemifacial spasm. The disappearance of the abnormality in some cases before decompression is accomplished is not inconsistent with this hypothesis. It is certainly possible that the removal of cerebrospinal fluid and retraction of the cerebellum could cause a shift in the neurovascular relationship temporarily equivalent to decompression. Placement of the Teflon felt pledget would then maintain the decompression permanently. The etiology and basic pathophysiology of microvascular compression syndromes such as trigeminal neuralgia and hemifacial spasm remain controversial. Recently, Adams' reviewed the literature on this subject; he was very critical of the concept but did not provide an explanation for the findings in hemifacial spasm. It would be most interesting to examine the response of the EMG abnormalities to the non-decompressive operation which he has performed for hemifacial spasm. Adams argues that the effectiveness of the vascular decompression procedure reported by Moller and Jannetta is due to manipulation and secondary trauma to the nerve. He thinks that this trauma may cause the symptoms to disappear, but he does not explain why the nerves in both hemifacial spasm and trigeminal neuralgia function normally after suffering mechanical trauma in addition to whatever initially caused the symptoms. He also does not explain the observation that facial weakness often resolves after decompression. He claims that the fact that sectioning the nerves also makes the symptoms disappear is an argument against
I Neurosurg. / toluene 74 / February, 1991
the vascular compression hypothesis because "inevitably, the possibility arises that the effect of microvascular decompression is by the way of trauma." It is hard to explain why a definitive trauma (section) would cause complete dysfunction, while a milder one would restore normal function. In addition, the traumatic hypothesis cannot explain the disappearance and reappearance of the phenomenon with repeated intraoperative decompression. The data presented by Moller and Jannetta' suggest that failure to relieve the neurophysiological abnormality during surgery is associated with a relatively poor prognosis for relief of hemifacial spasm. In our patient in whom the abnormality was not relieved intraoperatively, although her spasm has resolved, it persisted unusually long postoperatively. It is too early to know if this relief will be long-lasting. This finding is consistent, however, with an association between the electrophysiological and clinical findings. We believe that these observations justify the use of this technique as a method for monitoring the completeness of decompression during microvascular decompression for hemifacial spasm. Further support to justify the use of this technique is given by the finding that in three of our cases it was a useful guide to the need to decompress more than one vessel. Acknowledgments We would like to acknowledge the secretarial assistance of Susan Whaley and technical assistance of Connie Erickson, R.EEGT, in obtaining the reports. References 1. Adams CBT: Microvascular compression: an alternative view and hypothesis. J Neurosurg 70:1-12, 1989 2. Moller AR, Jannetta PJ: Hemifacial spasm: results of electrophysiologic recording during microvascular decompression operations. Neurology 35:969-974, 1985 3. Moller AR, Jannetta PJ: Microvascular decompression in hemifacial spasm: intraoperative electrophysiological observations. Neurosurgery 16:612-618, 1985 4. Moller AR, Jannetta PJ: Monitoring the facial EMG responses during microvascular decompression operations for hemifacial spasm. J Neurosurg 66:681-685,
1987 5. Moller AR, Jannetta PJ: Physiological abnormalities in hemifacial spasm studied during microvascular decompression operations. Exp Neural 93:584-600, 1986
Manuscript received March 27, 1990. Accepted in final form August 13, 1990. Address reprint requests to: Stephen J. Haines, M.D., Department of Neurosurgery, 420 Delaware Street SE, Box 96 UMHC, Minneapolis, Minnesota 55455.
257
