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ORIGINAL ARTICLE Microvascular Decompression for Hemifacial Spasm: Evaluating Outcome Prognosticators Including the Value of Intraoperative Lateral Spread Response Monitoring and Clinical Characteristics in 293 Patients Parthasarathy D. Thirumala,*† Aalap C. Shah,* Tara N. Nikonow,* Miguel E. Habeych,* Jeffrey R. Balzer,*‡ Donald J. Crammond,* Lois Burkhart,* Yue-Fang Chang,* Paul Gardner,* Amin B. Kassam,* and Michael B. Horowitz* Abstract: Hemifacial spasm is a socially disabling condition that mani- fests as intermittent involuntary twitching of the eyelid and progresses to muscle contractions of the entire hemiface. Patients receiving microvas- cular decompression of the facial nerve demonstrate an abnormal lateral spread response (LSR) in peripheral branches during facial electromyo- graphy. The authors retrospectively evaluate the prognostic value of preoperative clinical characteristics and the efficacy of intraoperative monitoring in predicting short- and long-term relief after microvascular decompression for hemifacial spasm. Microvascular decompression was performed in 293 patients with hemifacial spasm, and LSR was recorded during intraoperative facial electromyography monitoring. In 259 (87.7%) of the 293 patients, the LSR was attainable. Patient outcome was evaluated on the basis of whether the LSR disappeared or persisted after decompression. The mean follow-up period was 54.5 months (range, 9 –102 months). A total of 88.0% of patients experienced immediate postoperative relief of spasm; 90.8% had relief at discharge, and 92.3% had relief at follow-up. Preoperative facial weakness and platysmal spasm correlated with persistent postoperative spasm, with similar trends at follow-up. In 207 patients, the LSR disappeared intraoperatively after decompression (group I), and in the remaining 52 patients, the LSR persisted intraoperatively despite decompression (group II). There was a significant difference in spasm relief between both groups within 24 hours of surgery (94.7% vs. 67.3%) (P 0.0001) and at discharge (94.2% vs. 76.9%) (P 0.001), but not at follow-up (93.3% vs. 94.4%) (P 1.000). Multivariate logistic regression analysis demonstrated indepen- dent predictability of residual LSR for present spasm within 24 hours of surgery and at discharge but not at follow-up. Facial electromyography monitoring of the LSR during microvascular decompression is an effec- tive tool in ensuring a complete decompression with long-lasting effects. Although LSR results predict short-term outcomes, long-term outcomes are not as reliant on LSR activity. Key Words: HFS, Spasm, LSR, MVD, Decompression, BT, Facial nerve, CN VII, Monitoring. (J Clin Neurophysiol 2011;28: 56 –66) H emifacial spasm (HFS) is a condition involving involuntary, repetitive, unilateral contraction of the muscles innervated by the facial nerve (cranial nerve [CN] VII). Typical HFS is caused by facial nerve irritation secondary to vascular compres- sion at the root exit zone (RExZ), leading to involuntary, inter- mittent spasms beginning at the orbicularis oculi muscle and progressing down to the mentalis muscle. Neurophysiologic investigations have provided insight into the underlying mechanisms responsible for the abnormal muscle response, which appears as the lateral spread response (LSR) during routine intraoperative monitoring. Previous neurophysio- logic studies (Nielsen, 1985) have demonstrated demyelination/ axonal injury and hyperexcitability of the facial motonucleus, as being responsible for the residual LSR. In a rat model, Kuroki and Moller (1994) showed that the facial motonucleus was involved in HFS, but previous injury causing demyelination (eg, pulsatile compression near the RExZ) was also required (Ruby and Jannetta, 1975). It is feasible that HFS is a total of the electrophysiologic phenomenon between the facial motonucleus, given the facilitated orthodromic activity in peripheral branches of CN VII, and demyelination. Nonsurgical treatments, such as medications and local intramuscular botulinum toxin (BT) injections, have been inef- fective as long-term solutions for HFS. The only method for providing a long-term cure has been retromastoid craniotomy and facial nerve microvascular decompression (MVD), which has proved effective in curing 90% of patients (Moller and Jan- netta, 1984). During surgery, concurrent monitoring of brainstem auditory evoked responses is routinely used to detect eighth nerve dysfunction (Haines and Torres, 1991; Yamashita et al., 2002). The eighth cranial nerve (vestibulocochlear nerve) enables the patient to hear and is pertinent to maintaining balance and body position. Another important monitoring tool is intraoperative electromyography and recording of LSR, which can help sur- geons to determine whether adequate decompression has been achieved. LSRs elicited by stimulation of the facial nerve branches denote the electrophysiologic perturbations consistent with HFS. When the offending vasculature is moved off the facial nerve, the LSR is known to disappear or become markedly attenuated. However, the practical value of LSR, as a predictor of surgical outcome and long-term prognosis, remains controversial. A retrospective study focusing on three time points (post- operative, discharge, and follow-up) was conducted on 293 patients who underwent MVD as a treatment for HFS. The study From the *Departments of Neurological Surgery, †Neurology, and ‡Neuro- science, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania, 15213, U.S.A. Address correspondence and reprint requests to Parthasarathy D. Thirumala, M.D., Center for Clinical Neurophysiology, UPMC Department of Neurosur- gery, UPMC Presbyterian, Suite B-400, 200 Lothrop Street, Pittsburgh, PA 15213, U.S.A.; e-mail: thirumalapd@upmc.edu. Copyright © 2011 by the American Clinical Neurophysiology Society ISSN: 0736-0258/11/2801-0056 Journal of Clinical Neurophysiology • Volume 28, Number 1, February 2011 56
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  • ORIGINAL ARTICLE

    Microvascular Decompression for Hemifacial Spasm: EvaluatingOutcome Prognosticators Including the Value of Intraoperative

    Lateral Spread Response Monitoring and Clinical Characteristics in293 Patients

    Parthasarathy D. Thirumala,* Aalap C. Shah,* Tara N. Nikonow,* Miguel E. Habeych,* Jeffrey R. Balzer,*Donald J. Crammond,* Lois Burkhart,* Yue-Fang Chang,* Paul Gardner,* Amin B. Kassam,*

    and Michael B. Horowitz*

    Abstract: Hemifacial spasm is a socially disabling condition that mani-fests as intermittent involuntary twitching of the eyelid and progresses tomuscle contractions of the entire hemiface. Patients receiving microvas-cular decompression of the facial nerve demonstrate an abnormal lateralspread response (LSR) in peripheral branches during facial electromyo-graphy. The authors retrospectively evaluate the prognostic value ofpreoperative clinical characteristics and the efficacy of intraoperativemonitoring in predicting short- and long-term relief after microvasculardecompression for hemifacial spasm. Microvascular decompression wasperformed in 293 patients with hemifacial spasm, and LSR was recordedduring intraoperative facial electromyography monitoring. In 259(87.7%) of the 293 patients, the LSR was attainable. Patient outcome wasevaluated on the basis of whether the LSR disappeared or persisted afterdecompression. The mean follow-up period was 54.5 months (range,9 102 months). A total of 88.0% of patients experienced immediatepostoperative relief of spasm; 90.8% had relief at discharge, and 92.3%had relief at follow-up. Preoperative facial weakness and platysmalspasm correlated with persistent postoperative spasm, with similar trendsat follow-up. In 207 patients, the LSR disappeared intraoperatively afterdecompression (group I), and in the remaining 52 patients, the LSRpersisted intraoperatively despite decompression (group II). There was asignificant difference in spasm relief between both groups within 24hours of surgery (94.7% vs. 67.3%) (P 0.0001) and at discharge (94.2%vs. 76.9%) (P 0.001), but not at follow-up (93.3% vs. 94.4%) (P 1.000). Multivariate logistic regression analysis demonstrated indepen-dent predictability of residual LSR for present spasm within 24 hours ofsurgery and at discharge but not at follow-up. Facial electromyographymonitoring of the LSR during microvascular decompression is an effec-tive tool in ensuring a complete decompression with long-lasting effects.Although LSR results predict short-term outcomes, long-term outcomesare not as reliant on LSR activity.

    Key Words: HFS, Spasm, LSR, MVD, Decompression, BT, Facial nerve,CN VII, Monitoring.

    (J Clin Neurophysiol 2011;28: 5666)

    Hemifacial spasm (HFS) is a condition involving involuntary,repetitive, unilateral contraction of the muscles innervatedby the facial nerve (cranial nerve [CN] VII). Typical HFS iscaused by facial nerve irritation secondary to vascular compres-sion at the root exit zone (RExZ), leading to involuntary, inter-mittent spasms beginning at the orbicularis oculi muscle andprogressing down to the mentalis muscle.

    Neurophysiologic investigations have provided insight intothe underlying mechanisms responsible for the abnormal muscleresponse, which appears as the lateral spread response (LSR)during routine intraoperative monitoring. Previous neurophysio-logic studies (Nielsen, 1985) have demonstrated demyelination/axonal injury and hyperexcitability of the facial motonucleus, asbeing responsible for the residual LSR. In a rat model, Kurokiand Moller (1994) showed that the facial motonucleus wasinvolved in HFS, but previous injury causing demyelination (eg,pulsatile compression near the RExZ) was also required (Rubyand Jannetta, 1975). It is feasible that HFS is a total of theelectrophysiologic phenomenon between the facial motonucleus,given the facilitated orthodromic activity in peripheral branchesof CN VII, and demyelination.

    Nonsurgical treatments, such as medications and localintramuscular botulinum toxin (BT) injections, have been inef-fective as long-term solutions for HFS. The only method forproviding a long-term cure has been retromastoid craniotomy andfacial nerve microvascular decompression (MVD), which hasproved effective in curing 90% of patients (Moller and Jan-netta, 1984). During surgery, concurrent monitoring of brainstemauditory evoked responses is routinely used to detect eighth nervedysfunction (Haines and Torres, 1991; Yamashita et al., 2002).The eighth cranial nerve (vestibulocochlear nerve) enables thepatient to hear and is pertinent to maintaining balance and bodyposition. Another important monitoring tool is intraoperativeelectromyography and recording of LSR, which can help sur-geons to determine whether adequate decompression has beenachieved. LSRs elicited by stimulation of the facial nervebranches denote the electrophysiologic perturbations consistentwith HFS. When the offending vasculature is moved off the facialnerve, the LSR is known to disappear or become markedlyattenuated. However, the practical value of LSR, as a predictor ofsurgical outcome and long-term prognosis, remains controversial.

    A retrospective study focusing on three time points (post-operative, discharge, and follow-up) was conducted on 293patients who underwent MVD as a treatment for HFS. The study

    From the *Departments of Neurological Surgery, Neurology, and Neuro-science, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania,15213, U.S.A.

    Address correspondence and reprint requests to Parthasarathy D. Thirumala,M.D., Center for Clinical Neurophysiology, UPMC Department of Neurosur-gery, UPMC Presbyterian, Suite B-400, 200 Lothrop Street, Pittsburgh, PA15213, U.S.A.; e-mail: thirumalapd@upmc.edu.

    Copyright 2011 by the American Clinical Neurophysiology SocietyISSN: 0736-0258/11/2801-0056

    Journal of Clinical Neurophysiology Volume 28, Number 1, February 201156

  • investigated the efficacy of intraoperative monitoring in predict-ing spasm persistence or resolution and identified clinical char-acteristics that can potentially predict surgical outcome.

    METHODS

    Microvascular DecompressionBetween January 2000 and December 2007, our center

    performed 326 retromastoid MVD procedures for HFS. Preoper-atively, all patients received a cranial MRI, audiometry, andfacial EMG testing. Decompression was achieved by placingTeflon pledgets between the facial nerve as it exited the brain-stem and the offending vessels, and/or by elevating and cauter-izing compressive veins that could not be safely decompressedwith Teflon. During surgery, facial EMG monitoring was per-formed from the initiation of general anesthesia until the time ofdural closure. Stimulating needle electrodes were inserted intra-dermally over the zygomatic branches of the facial nerve at themiddle point of a line between the ipsilateral tragus and externalcanthus of the eye. A 0.2- to 0.3-millisecond pulse wave with anintensity of 5 to 25 mV was applied. On stimulation of thezygomatic branch, which primarily innervated the orbicularisoculi muscle, the team recorded and reviewed the evoked LSRthat appeared in the other facial muscles via peripheral branches,including the frontalis (temporal), orbicularis oris (buccal) andmentalis (marginal mandibular) muscles (Fig. 1). The eighthcranial nerve (CN VIII) function was concurrently monitored bylooking for waveform shifts during the recording of brainstemauditory evoked responses. In some cases, use of neuromuscularblockade during anesthesia led to alterations in the LSR phenom-enon due to muscular paralysis. Therefore, the anesthesiologistused a technique that maintained the train-of-four ratio at a levelof at least 0.75. When complete decompression was achieved, theLSR was found to disappear in most patients. When the LSRpersisted or simply decreased in amplitude, the surgeon lookedagain for persistent arterial or venous compression. Residual LSRwas characterized as either an LSR that returned after initiallydisappearing during the procedure (after disappearing [AD]) oran LSR that persisted relatively unchanged throughout the de-compression (never disappearing [ND]) (Fig. 2). After confirm-ing that there were no further offending vessels, the surgeonterminated the procedure and closed the craniotomy in a routinefashion.

    Data Collection and AnalysisA retrospective study was conducted with Institutional

    Review Board approval from the University of Pittsburgh (IRB #:PR008120394). Of 326 MVD procedures, data were collected

    from 322 operations performed on 293 patients with HFS; 29operations were reexploration surgeries due to persistent orrecurrent spasm. The patient population consisted of 103 men and190 women ranging in age from 17 to 82 years (mean: 52.25years). Clinical outcome data were obtained immediately afterthe operation, at discharge (mean: 3.91 1.98 days), and at afollow-up phone call during June 2008. Follow-up data werecollected from 208 patients who had a minimum follow-up periodof 9 months (mean: 54.5 27.8 months). We attempted tocontact every patient identified during the record screening toobtain information regarding the patients present spasm statusand operative complications and to confirm the accuracy of datacollected from clinical notes and statements. Outcomes weredivided into two categories: success (spasm relief) and failure(persistent spasm). Postoperative success was defined as com-plete spasm resolution with no residual twitching within 24 hoursof operation and no more than two episodes of residual eyetwitching before discharge. At follow-up, complete relief wasdefined as the reported absence of HFS, allowing for residual eyetwitching at a frequency no more than one episode per month.Patients who experienced waxing and waning symptoms wereasked to rate the frequency and severity of their current symp-toms on a 1 to 10 scale. Patients were instructed to consider theirpreoperative symptoms as a 10 and rate their current symptoms incomparison to that value. Patients who reported spasm withfrequency and severity 3 on a 10 scale when compared withtheir preoperative spasm were considered to have persistentspasm. To minimize bias, an investigator other than the operatingsurgeons and neurophysiologists conducted all of the telephoneinterviews. Also, investigators responsible for collecting patientdata at all three time points were blinded to LSR results.

    Statistical analyses were performed using SAS version 9.1.3(SAS Institute, Cary, NC). Continuous variables were presented asmean standard deviation and categorical variables as frequency(%). Group differences in demographic, clinical characteristics, andoutcomes were assessed using t tests, 2 tests, and Fisher exact testswhen appropriate. Logistic regression models were conducted toevaluate the association of LSR and outcome at each time pointwhile adjusting for age, gender, prior BT use, platysmal spasm,preoperative facial weakness, and side of spasm. P 0.05 wasconsidered as statistically significant.

    RESULTS

    DemographicsMean patient age was 52.25 12.05 years (range, 1782

    years), with women to men ratio being 1.8:1. No patients exhibited

    FIGURE 1. A, Branches of the facial nerve (CNVII); cervical branch not depicted. B, Monitoringfor the paradoxical lateral spread response (LSR).The zygomatic branch is stimulated (STIM), andan evoked EMG response can be recorded in theorbicularis oculi (REC 1). In patients with HFS, anabnormal evoked response, the LSR, can be seenin the mentalis muscle (REC 2). T, temporal; Z,zygomatic; B, buccal; M, marginal mandibular.

    Journal of Clinical Neurophysiology Volume 28, Number 1, February 2011 Microvascular Decompression for Hemifacial Spasm

    Copyright 2011 by the American Clinical Neurophysiology Society 57

  • bilateral HFS (see Appendix, Table A2). The mean follow-up periodwas 54.5 27.8 months (range: 9102 months) (Table 1).

    Medical HxMedical and surgical histories were obtained from each

    patient undergoing MVD. Twenty-two patients underwent a priorMVD at an outside institution. Two hundred seventeen patients(74.6%) received prior BT treatment, with the average timebetween the last injection and the most recent operation being 12months (range: 1 49 months). Patients who underwent BT treat-ment did so over a variable period (average: 4.23 years, range: 2months14 years). Common medications used to control HFSsymptoms, including anticonvulsants and antipsychotics, arelisted separately (see Appendix, Fig. A2). There was no genderbias regarding patients undergoing prior BT treatment (P 0.561).

    Preoperative CharacteristicsSeven patients had evidence of a Chiari I malformation on

    radiographic imaging. Nine patients had symptoms of atypical HFS(spasms began in the buccal-oral muscles and then progressed toinvolve the orbicularis oculi muscle). Sixty-seven (22.8%) pa-tients exhibited moderate-to-severe preoperative facial weakness,as determined by the House-Brackmann score (House and Brack-mann, 1985) (grade III and higher). Of note, patients with priorBT treatment were significantly more likely to demonstratemoderate-to-severe preoperative facial weakness (P 0.01). Onehundred thirty-seven (49.6%) patients had platysmal spasm, while187 (85.8%) exhibited tonus (frequent eyelid locking), signs associatedwith an extended spasm history. One hundred twenty-six (43.0%)patients reported specific triggers that would initiate spasms. Thirty-six(12.3%) patients demonstrated functional hearing loss, as determinedby the pure tone average during preoperative audiograms.

    FIGURE 2. Recording of the stimulus-evoked EMG responses from two different patients at the orbicularis oculi (A) and men-talis (B) muscles in response to stimulation of the zygomatic branch of the facial nerve. On decompression (arrow; A), theparadoxical LSR (mentalis) becomes variable in amplitude and morphology (after disappearing) and on complete decompres-sion (B), the LSR eventually disappears with no significant change observed from the oculi muscle group.

    P. D. Thirumala et al. Journal of Clinical Neurophysiology Volume 28, Number 1, February 2011

    Copyright 2011 by the American Clinical Neurophysiology Society58

  • Operative FindingsIntraoperative Remarks

    The vessels compressing the RExZ, as identified by thesurgeon, are summarized in Table 2. A majority (70.7%) of patientshad multiple compressing vessels. Of 21 patients (7.2%) requiring atwo-stage operation, 13 exhibited marked (2 milliseconds) shiftedbrainstem auditory evoked responses during the first operation,which prompted the surgeon to terminate the procedure. Fourpatients had a planned staged procedure because of a preexistingChiari I malformation (Chiari I decompressed during the first stage),while three other patients demonstrated dangerous cerebellar swell-ing during the first operation, which necessitated procedure termi-nation and repeat surgery. During one operation, equipment mal-function necessitated procedure termination and a second-stagesurgery.

    Operative OutcomesFacial spasm resolved in 257 patients (88.0%) within 24

    hours of MVD (Table 3). Success rate increased to 90.8% at the timeof discharge (3.91 1.98 days). Twenty-nine patients had persistentor recurrent spasm and underwent reexplorative surgery; resultswere similar to those of first-time patients undergoing MVD at eachtime point (see Appendix, Tables A4 and A5). It is noteworthy that18 patients with immediate postoperative spasm experienced com-plete relief at discharge, and 10 patients with postoperative relief had

    spasm recurrence by discharge. Among patients with follow-up data,only 16 patients (7.7%) had not experienced marked relief despiteMVD. Of these 16 patients, 12 reported that their spasm hadrecurred during the follow-up time period, despite having completepostoperative relief. An additional 16 patients who were dischargedwith persistent spasm reported complete relief at follow-up (54.5 27.8 months). Although no significant gender differences werepresent when comparing outcomes within 24 hours of surgery (P 0.376), a greater proportion of men had spasm resolution at dis-charge (95.2% vs. 88.4%) (P 0.056). However, there was asignificant gender difference in spasm relief at follow-up (98.7% vs.88.7%) (P 0.01) (Fig. 3). When dividing patients by age 50years and 50 years, younger patients had a slightly higher yetstatistically insignificant relief rate (see Appendix, Table A1).

    Among patients with preoperative platysmal spasm, 22(16.1%) experienced HFS 24 hours after the surgery. This rate wassignificantly greater than those without platysmal spasm (P 0.022). There was a similar but statistically insignificant trend atdischarge and at follow-up. Preoperative facial weakness also influ-enced operative outcome; patients with a H-B grade III or IV(moderate-to-severe) facial palsy were more likely to demonstratepersistent spasm than those with a grade I or II (mild) facial palsywithin 24 hours of the surgery (P 0.012) and at discharge (P 0.016). Prior BT treatment did not predict a poor surgical outcomewithin 24 hours after the operation or at discharge. However, at thetime of follow-up, 15 patients with a history of BT treatmentreported persistent or recurrent spasm, whereas only one patientwithout prior BT continued to experience spasm (P 0.076). Therewas no significant correlation between spasm laterality, preoperative

    FIGURE 3. Outcome as a factor of demographics (age andgender). *P 0.05.

    TABLE 1. Summary of Demographic and ClinicalCharacteristics

    Variable n (%)

    No. cases 293 (100.0)

    Discharge data available 292 (99.7)

    Follow-up available 208 (70.9)

    Mean discharge time (days) 3.91 1.98

    Mean follow-up time (years) 4.54 2.32

    Mean age at operation (years) 52.25 12.25

    Gender

    Female 190 (64.8)

    Male 103 (35.2)

    Spasm presentation

    Left:right 164:129

    Preoperative Botox usage 217 (74.6)

    Tonus 187 (85.8)

    Platysmal spasm 137 (49.6)

    Specific triggers 126 (43.0)

    TABLE 2. Compressing Vasculature Seen Near Facial NerveRoot Exit Zone During Operation

    Compressing Vessel n (%)

    AICA 147 (50.2)

    PICA 132 (45.1)

    VA 82 (28.0)

    Unnamed artery 58 (19.8)

    Vein 124 (42.3)

    Perforator 58 (19.8)

    AICA, anterior inferior cerebellar artery; PICA, posterior inferior cerebellar artery;VA, vertebral artery.

    TABLE 3. Hemifacial Spasm ResolutionRatesMicrovascular Decompression of the Facial Nerve(CN VII)

    Postoperative Discharge Follow-Up

    All subjects 88.0 (257) 90.8 (265) 92.3 (192)

    Gender

    Male 90.3 (93) 95.2 (98) 98.7 (74)

    Female 86.8 (164) 88.4 (167) 88.7 (118)

    P 0.376 0.056 0.010Age

    50 90.4 (103) 91.2 (104) 93.2 (69)

    50 86.5 (154) 90.5 (161) 91.8 (123)

    P 0.325 0.823 0.707

    Values are presented as % (n). Bold indicates statistical significance.

    Journal of Clinical Neurophysiology Volume 28, Number 1, February 2011 Microvascular Decompression for Hemifacial Spasm

    Copyright 2011 by the American Clinical Neurophysiology Society 59

  • tonus, or type of decompressed vasculature and outcome at any ofthe time points.

    Intraoperative Lateral Spread MonitoringCategorizing LSR at Termination of MVD

    Data regarding intraoperative monitoring of the LSR duringMVD were available for 259 (87.4%) of the 293 patients. LSR onother 12.3% of patients was collected but could not be located forreview at the time of this study. We divided these 259 patients intotwo groups, according to the disappearance (group I: LSR 0) orpersistence (group II: LSR 0) of facial EMG activity immediatelyafter decompression (see Appendix, Fig. A1). Demographic datawere not significantly different between groups (Table 4). LSRdisappearance (group I) was observed after facial nerve decompres-sion in 207 of 259 patients (79.9%). Fifty-two patients (20.1%) hadresidual LSR postoperatively (group II). Five of these patients hadan LSR amplitude increase when compared with baseline.

    There was no statistically significant difference betweengroup I and II with regard to laterality, compressing vasculature,

    history of BT injections, or tonus/platysma involvement (Fig. 3).Although no statistical difference existed with regard to preoperativefacial weakness, we observed an increasing proportion of patientswith greater degrees of preoperative paresis having postoperativeresidual LSR (grade I, II: 15.5%; grade III: 17.0%; grade IV:40.0%). More patients requiring venous decompression had residualpostdecompression LSR (51.9%) than did those without venousinvolvement (42.0%) (P 0.199). Reexploration patients (includingoperations at our institution) were more likely to have LSR resolu-tion at MVD termination (85.1%) when compared with first-timeoperations (78.8%) (P 0.327).

    Outcomes: Short-Term Prognostic ValueWithin group I, (patients in whom the LSR disappeared after

    decompression), spasms completely disappeared postoperatively in195 of 207 patients; LSR monitoring therefore had a negativepredictive value (NPV; proportion of patients without residual LSRthat are spasm-free) of 94.7%. In contrast, only 67.3% of group IIpatients (patients in whom residual LSR was present after decom-pression) experienced immediate postoperative relief; the positivepredictive value (proportion of patients with residual LSR that havepersistent spasm) was 32.7% (Fig. 4). The specificity and sensitivityof intraoperative LSR monitoring for predicting postoperative sur-gical outcome were 60.7% and 84.8%, respectively (see Appendix,Table A3).

    There was a statistically significant difference in the postop-erative spasm relief outcomes between the two groups (P 0.0001),a trend which was also evident at discharge (94.2% vs. 76.9%) (P 0.001). Five group II patients with postoperative spasm had com-plete relief by discharge. When 32 patients in group II weresubdivided by whether the residual LSR was present throughout theentire operation (ND), or returned after initially disappearing duringthe operation (AD), no statistically significant difference in out-comes was identified. All group II patients with follow-up datawhose LSR reappeared after initially resolving during the decom-pression (AD) described complete spasm relief at follow-up. Of sixgroup II patients whose residual LSR was persistent during theentirety of the decompression (ND), one patient declared persistentspasm at follow-up.

    When separating patients in groups I and II by BT history orgender, we found no differences from the outcomes seen when

    FIGURE 4. Clinical characteristics ofpatients without residual lateralspreads (group I: lateral spread re-sponse [LSR] 0) and with residuallateral spreads (group II: LSR 0) dur-ing intraoperative electromyography.AICA, anterior inferior cerebellar ar-tery; PICA, posterior inferior cerebellarartery; VA, vertebral artery.

    TABLE 4. Patients With Measured LSR: Demographics

    ParameterGroup I:LSR 0

    Group II:LSR >0 P

    No. patients 207 52

    Gender (M:F) 72:135 19:33 0.813

    Age 0.638

    Mean age (years) 51.9 52.8

    No. patients aged 50 years 85 19

    No. patients aged 50 years 122 33

    Operation 0.327

    First-time 167 45

    Reexploration 40 7

    Mean time to FUP (months) 57.1 51.1

    Residual LSR classification

    After disappearing 23

    Never disappearing 9

    LSR, lateral spread response; FUP, follow-up.

    P. D. Thirumala et al. Journal of Clinical Neurophysiology Volume 28, Number 1, February 2011

    Copyright 2011 by the American Clinical Neurophysiology Society60

  • comparing groups I and II as a whole. In patients without previousBT use (n 68), group I subjects (no postoperative LSR) weresignificantly more likely than those in group II (residual postoper-ative LSR) to have complete relief within 24 hours of the operation(96.3% vs. 50.0%) (P 0.0001) and at discharge (94.4% vs. 57.1%)(P 0.0002). This association was also true for patients withprevious BT injections (n 189) postoperatively, although with lessstatistical significance (94.1% vs. 75.7%) (P 0.002). However, theoutcomes of group I and II patients did not significantly differ atdischarge (94.1% vs. 83.8%) (P 0.081) when considering priorBT use (Fig. 5). Within the BT use subgroup, postoperative spasmdisappeared in three patients with residual LSR by the time ofdischarge. When separating patients by gender, the associationbetween residual LSR and persistent spasm was strongest within 24hours of the operation (men: P 0.0017; women: P 0.0001) andremained significant for women at the time of discharge (P 0.001).

    Outcomes: Long-Term Prognostic ValueAt the time of follow-up phone call with 208 patients, the

    outcomes between group I and II patients did not significantly differ(93.3% vs. 94.4%) (P 1.000), although the NPV of LSR moni-

    toring for long-term outcomes was 93.3%. There was no significantstatistical difference even when specifically considering patientswithout previous BT injections (P 0.688), female patients (P 1.000), and patients with recent follow-up (2 years) (P 0.402).

    Multivariate Logistic Regression ModelThe association between predisposing factors and spasm

    status at each time point was examined with a multivariate logisticregression model (Table 5). Predicting variables controlled forincluded residual LSR, gender, age (50 years or 50 years), priorBT treatment, platysmal spasm, preoperative facial weakness (H-Bgrade 0/I/II [absent/mild], or III/IV [moderate/severe]), and lateral-ity (left or right). Postoperatively, persistent spasm was associatedwith residual LSR (odds ratio [OR]: 9.59; 95% confidence interval[CI]: 3.7324.65; P 0.0001) and preoperative platysmal spasm(OR: 5.46; 95% CI: 1.8815.90; P 0.002). At discharge, residualLSR (OR: 5.50; 95% CI: 2.2113.73; P 0.001) and platysmalinvolvement (OR: 2.74; 95% CI: 1.037.27; P 0.043) were alsopredictive of present spasm. However, at follow-up, only preoper-ative platysmal spasm was associated with persistent spasm (OR:6.29; 95% CI: 1.2531.55; P 0.025). Men tended to report spasm

    FIGURE 5. MVD Outcomes at three major time points. A, Outcomes in patients without prior Botox treatment. B, Out-comes in patients with prior Botox treatment. C, Operative outcomes with respect to residual LSR status. ***P 0.0005;**P 0.005, when compared with patients without residual LSR.

    TABLE 5. Logistic Regression Analysis of the Association Between Perioperative Risk Factors and Spasm Persistence

    Postoperative Discharge Follow-Up

    OR (95% CI) P OR (95% CI) P OR (95% CI) P

    Residual LSR 9.59 (3.7324.65) 0.0001 5.50 (2.2113.73) 0.001 1.03 (0.195.43) 0.977

    Gender 0.75 (0.282.03) 0.572 0.43 (0.141.27) 0.127 0.13 (0.021.07) 0.058

    Age 50 years 1.93 (0.715.21) 0.197 1.04 (0.422.61) 0.931 1.37 (0.365.15) 0.643

    Prior BT use 0.42 (0.151.18) 0.098 0.41 (0.151.12) 0.081 3.03 (0.3426.92) 0.321

    Platysmal spasm 5.46 (1.8815.90) 0.002 2.74 (1.037.27) 0.043 6.29 (1.2531.55) 0.025Weakness (H-B III, IV) 1.86 (0.675.19) 0.238 1.65 (0.584.65) 0.347 0.21 (0.021.77) 0.150

    Left-sided spasm 0.74 (0.291.91) 0.537 0.95 (0.382.38) 0.907 1.35 (0.384.79) 0.641

    Reference group: gender (female), age 50 years, no prior BT use, no platysmal spasm, H-B score 0/I/II (none or mild weakness), left-sided spasm.LSR, lateral spread response; BT, botulinum toxin; OR, odds ratio; CI, confidence interval. Bold indicates statistical significance.

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  • less frequently than women (OR: 0.13; 95% CI: 0.021.07; P 0.058).

    DISCUSSIONCN VII MVD is an effective treatment for HFS. In our

    experience with 326 operations, postoperative outcomes, with re-spect to demographic variables, concurred with the results of pre-vious studies (Barker et al., 1995; Ishikawa et al., 2001; Lovely etal., 1998) Men demonstrate a greater relief rate compared withwomen, a trend that was especially apparent at the time of follow-up, and patients aged 50 years and older at the time of operationhave a similar resolution rate to that of younger patients (Shin et al.,1997). Although a majority of patients presented with left-sidedspasm, laterality did not affect outcome. Outcome was not contin-gent on vessel type, although multiple vessels were frequently seencompressing the nerve. Excellent outcomes were achieved in themajority of patients within 24 hours of surgery (88.0% spasm-free).Eight additional patients achieved complete relief during their inpa-tient stay, increasing the resolution rate to 90.8% at discharge. Only16 patients with follow-up (7.7%) had symptoms, demonstrating thelong-lasting effects of MVD. The delayed spasm resolution may beattributed to the time required for remyelination of the damagedarea, as well as the return of normal excitability of the facialmotonucleus (Ishikawa, et al., 1997; Moller and Jannetta, 1985,a,b;Yamashita et al., 2001).

    Facial EMG monitoring aids in the perioperative diagnosis ofHFS and has been considered by us to be a valuable intraoperativetool in ensuring a meticulous CN VII decompression. Pulsatilecompression at the CN VII RExZ leads to the LSR (Ishikawa et al.,1996b; Jannetta et al., 1970; Moller and Jannetta, 1986). In line withrecent studies (Isu et al., 1996; Kong et al., 2007; Sekula et al., 2009;Shin et al., 1997) demonstrating the usefulness of intraoperativeLSR monitoring, we found that the disappearance of LSR at the endof MVD was predictive of spasm relief both immediately after thesurgery (NPV 94.7%) and at discharge. This finding was also truewhen focusing on individual genders and BT history, although theshort-term correlation was weaker for those with prior BT injections.In light of the excellent surgical outcomes in 90% of patients atdischarge, we believe that intraoperative monitoring is an effectivetool in identifying culprit vessels. Given the significant negativepredictive value of LSR monitoring, the surgeon can be reassuredthat an adequate decompression has been achieved and avoid un-necessary operation time and resultant complications, especiallywhen multiple vessels are involved. However, we did find thatseveral patients with residual LSR were spasm-free after the surgery,reducing the positive predictive value of LSR monitoring for short-term outcomes. This appeared to be more common when the nervewas found to be compressed by veins.

    In five patients with residual LSR and immediate postopera-tive spasm, symptoms disappeared by the time of discharge. Severalmore reported relief at follow-up, which detracted from the positivepredictive value of LSR for long-term outcomes. All patients withfollow-up data whose residual LSR reappeared after initially disap-pearing (AD) were spasm-free at follow-up, whereas only onepatient with persistent intraoperative LSR (ND) had refractoryspasm. A returning LSR (AD) may be the factor of additional minorvessel or dural involvement that resolves after hospital stay. Of note,when the LSR is found to reappear after initially disappearing, thesurgeon will make the decision whether to continue surgery and lookfor additional compressing vasculature. Therefore, the proportion ofpatients with postoperative residual LSR at our center is compara-tively less because several potential AD cases were resolved afterfurther investigation into the compression. A persistent intraopera-tive LSR (ND), although not significantly predictive of spasm at

    follow-up, could also be indicative of a different pathology for thepatients spasm or an incomplete decompression. It is hypothesizedthat delayed LSR resolution is due to a variable duration forrestoration of CN VII firing thresholds or remyelination in differentpatients (Goto et al., 2002; Huang et al., 1992; Ishikawa 2001; Li,2005). In addition, BT-induced and postoperative facial weaknesscan make it difficult to ascertain spasm status in patients with subtlebut persistent symptoms, detracting from the predictive value of theLSR in these subgroups.

    Some authors have described the significant predictive valueof the LSR for outcomes at 1-year follow-up (Kong et al., 2007;Moller and Jannetta, 1987), whereas others question its value (Ha-tem et al., 2001; Joo et al., 2008; Kiya et al., 2001). We, too,investigated the predictive value of the LSR on long-term outcomesin our series. Our follow-up data were collected from patients witha mean follow-up period of 54.5 months, whereas prior studiesdocument relatively short-term follow-up, with a mean period 1year (Sekula et al., 2009). Although we did not find a significantstatistical correlation, LSR resolution was predictive of spasm reliefat follow-up (NPV 93.3%). However, residual LSR does notalways correlate with a poor outcome because it may take severalmonths for nerve excitability to normalize.

    Therefore, we recognize the importance of intraoperativeLSR monitoring and agree with prior studies that recommendpostoperative facial EMG testing. In addition to detecting when theLSR is fully normalized, postoperative testing can confirm thatHFS-related complexes, synkinesis, and cross talk are eliminatedand can thus be helpful in determining prognosis of persistentspasm, ascertaining recurrence, and planning for reexploration. Kimand Fukushima (1984) showed that synkinesis remains in the orbic-ularis oris and mentalis muscles on postoperative facial EMGmonitoring 10 days after surgery. In evaluating outcomes after MVDfor HFS, it is therefore important to continue observing patients withpersistent spasm and discuss the likelihood of delayed resolutionwith the patient before considering reoperation. This can be difficultin practice because the refractory symptoms can be debilitating tothe already anxious patient, and there is no guarantee of resolutioneven after 1 year. Also, early reoperation has been found to correlatewith better outcomes compared with patients receiving late reopera-tions in one study (Engh et al., 2005), but complication rates foradditional MVD operations need to be considered. Other institutionshave advocated waiting 1 to 2 years before considering reoperation(Goto et al., 2002; Ishikawa et al., 2001; Li et al., 2005). RepeatEMGs may provide more insight into the neurophysiologic status ofpatients with persistent spasm and can be implemented beforereoperation.

    The use of BT injections has long been advocated as a quick,noninvasive treatment for HFS, as well as blepharospasm (Laskawi,2008), dystonias (Benecke and Dressler, 2007), and various otherdisorders involving muscle overactivity. However, BT frequentlyresults in facial paresis (Yamashita et al., 2002). Patients also tendto become refractory to treatment, requiring larger and more fre-quent toxin doses over time, resulting in recurrent spasms. It issignificant that almost three quarters of patients who underwentMVD have tried and been unsuccessful with BT in the past. Thisrepresents a larger proportion of patients who tried BT comparedwith that of previous series (Yamashita et al., 2002), pointing toincreasing popularity. Although a statistically insignificant trend, theobservation that 15 of 16 patients expressing persistent spasm atfollow-up had received preoperative BT injections raises the issuethat this drug may predispose a patient to recurrent spasm. We alsofound that severe preoperative facial weakness, which can occurafter repeated BT treatment (House-Brackmann grade III or greater),is predictive of poor surgical outcome. To explain these findings, it

    P. D. Thirumala et al. Journal of Clinical Neurophysiology Volume 28, Number 1, February 2011

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  • is possible that paretic muscles (including those with weaknesssecondary to BT injections) have lower thresholds for firing duringa period of spasmodic activity. A recent study suggests the HFSleads to mild facial nerve injury, which leads to greater vulnerabilityto BT injections (Misawa et al., 2008).

    In addition to preoperative paresis, involvement of theplatysma muscle is another indicator of long-standing and severespasm. Preoperative platysma muscle spasm was also found tocorrelate with poor outcome within 24 hours of surgery. In theunivariate analyses, platysmal involvement did not correlate withspasm at discharge or follow-up, suggesting that the normal firingactivity in different branches of CN VII is not immediately restoredafter decompression. However, we found a significant associationbetween platysmal spasm and postsurgical spasm status when con-trolling for other perioperative characteristics in the multivariateanalyses. Therefore, patients with these progressive symptoms arestrongly encouraged to seek neurologic consultation and considerMVD to improve their prognosis after surgery.

    Study limitations include the inherent bias in evaluating LSRmonitoring, which was actively being used to make intraoperativedecisions, along with the absence of a control group. In addition, theall-or-nothing nature of the LSR categorization (LSR 0 or LSR0) may account for some of the patients with persistent LSR butresolved spasm; even 95% disappearance of LSR was consideredLSR persistence in this study. Finally, follow-up data may beproblematic because some patients may not be objective about theirclinical condition. Further investigations, which decrease the reli-ance on self-interpretation of surgical results, would be beneficial.

    CONCLUSIONSMVD for HFS is an effective treatment that can offer perma-

    nent symptom resolution. We identified preoperative clinical char-acteristics that affect outcome after MVD. Pertinent findings of thisstudy include the following:

    1. Men expressed a greater relief rate compared with women atfollow-up (P 0.01).

    2. A BT treatment history, which was positive in three quarters ofpatients, was associated with preoperative facial weakness(P 0.01) and was also common in patients reporting spasmat follow-up (P 0.076).

    3. Preoperative facial weakness correlated with persistent spasmwithin 24 hours of operation (P 0.012) and at discharge(P 0.016), with a similar trend at the time of follow-up (P 0.056).

    4. Preoperative platysmal spasm correlated with persistent spasmwithin 24 hours of operation (P 0.022) and exhibited asimilar trend at the time of follow-up (P 0.069). Whencontrolling for other perioperative characteristics, we found asignificant association of preoperative platysmal involvementwith poor postoperative surgical outcome (OR: 5.46; 95% CI:1.8815.90; P 0.002), positive spasm status at discharge(OR: 2.74; 95% CI: 1.037.27; P 0.043), and persistent orrecurrent spasm at follow-up (OR: 6.29; 95% CI: 1.2531.55;P 0.025). It is recommended that patients with progressivesymptoms (affecting multiple facial muscle groups) considerMVD and undergo surgery before muscles of the lower faceand neck become involved.

    5. LSR monitoring was predictive of surgical outcomes within 24hours of operation (P 0.0001) and at discharge (P 0.001).When we adjusted for clinical and demographic variables, wefound residual LSR to be significantly predictive of persistentpostoperative spasm (OR: 9.59; 95% CI: 3.7324.65; P 0.0001) and spasm at discharge (OR: 5.50; 95% CI: 2.2113.73; P 0.001).

    6. Although LSR monitoring was not statistically associated withlong-term reported outcomes (P 1.00), postoperative LSRresolution was predictive of long-term spasm relief (NPV:93.3%).

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  • APPENDIX

    FIGURE A1. LSR, lateral spread response; ND, never disap-pearing; AD, after disappearing.

    FIGURE A2. Common medicationsof patients referred for microvascu-lar decompression.

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    Copyright 2011 by the American Clinical Neurophysiology Society64

  • TABLE A1. Microvascular Decompression Success Rate byGender-Age Subgroups

    Age (Years) Male (%) Female (%)

    Postoperative

    50 86.4 95.3

    50 91.1 88.7

    P 0.676 0.163

    Discharge

    50 90.9 98.4

    50 91.1 90.1

    P 0.999 0.065

    Follow-up

    50 100.0 97.5

    50 96.9 90.4

    P 0.999 0.228

    TABLE A2. Microvascular DecompressionDemographics

    Parameter Male Female

    Mean age (years) 53.2 50.9

    No. patients postoperative 75 148

    % patients with follow-up data (n) 68.0 (51) 66.2 (98)

    Mean time to follow-up (months) 66.1 70.7

    % with recorded (n) 84.0 (63) 89.2 (132)

    % with repeat operations (n) 12.0 (9) 18.2 (27)

    TABLE A3. Predictive Value of Intraoperative Lateral SpreadMonitoring on Spasm Relief During MicrovascularDecompression, by Time Point

    Parameter Postoperative Discharge Follow-Up

    2 test P 0.0001 P 0.001 P 1.00

    Sensitivity* 60.7 50.0 16.7

    Specificity 84.8 82.9 80.5

    Positive predictive value 32.7 23.1 5.6

    Negative predictive value 94.7 94.2 93.3

    Values are presented as %.*Proportion of patients with postoperative spasm that exhibit residual LSR at end

    of MVD.Proportion of patients without postoperative spasm that exhibit disappearance of

    LSR at end of MVD.Proportion of patients with residual LSR at end of MVD that exhibit postoperative

    persistent spasm.Proportion of patients with disappearance of LSR at end of MVD that are without

    postoperative spasm.LSR, lateral spread response; MVD, microvascular decompression.

    TABLE A4. Reexploration Surgeries (University ofPittsburgh Medical Center)

    nNo. PatientsWith Spasm

    Time since previous MVD (n 29)

    1 month 16 2

    1 year 8 0

    1 year 5 0

    Time since recurrence (n 17)

    1 week 9 1

    1 week 8 0

    MVD, microvascular decompression.

    TABLE A5. Prognosis of First-Time vs. ReexplorationPatients

    Outcome

    First-Time

    PatientReexploration

    Patient P

    Redo:Other

    Institution

    Redo:WithinUPMC P

    Postoperative 87.6 90.2 0.597 86.4 (19) 93.1 (27) 0.641

    Discharge 91.6 86.3 0.283 90.9 (20) 82.8 (24) 0.684

    Follow-up 93.6 85.7 0.155 78.6 (11) 90.5 (19) 0.369

    Values are presented as % or % (n).UPMC, University of Pittsburgh Medical Center.

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  • REFERENCESBarker FG II, Jannetta PJ, Bissonette DJ, et al. Microvascular decompression for

    hemifacial spasm. J Neurosurg. 1995;82:201210.Benecke R, Dressler D. Botulinum toxin treatment of axial and cervical dystonia.

    Disabil Rehabil. 2007;29:17691777.Eekhof JL, Aramideh M, Speelman JD, et al. Blink reflexes and lateral spreading

    in patients with synkinesia after Bells Palsy and in hemifacial spasm. EurNeurol. 2000;43:141146.

    Engh JA, Horowitz M, Burkhart L, et al. Repeat microvascular decompression forhemifacial spasm. J Neurol Neurosurg Psychiatry. 2005;76:15741580.

    Esteban A, Molina-Negro P. Primary hemifacial spasm: a neurophysiologicalstudy. J Neurol Neurosurg Psychiatry. 1989;49:5863.

    Frueh BR, Preston RA, Musch DC. Facial nerve injury and hemifacial spasm.Am J Ophthalmol. 1990;110:421423.

    Goto Y, Matsushima T, Natori Y, et al. Delayed effects of the microvasculardecompression on hemifacial spasm: a retrospective study of 131 consecu-tive operated cases. Neurol Res. 2002;24:296300.

    Haines SJ, Torres F. Intra-operative monitoring of the facial nerve during decompres-sive surgery for hemifacial spasm. J Neurosurg. 1991;74:254257.

    Hatem J, Sindou M, Vial C. Intra-operative monitoring of facial EMG responsesduring microvascular decompression for hemifacial spasm. Prognostic valuefor long-term outcome: a study in a 33-patient series. Br J Neurosurg.2001;15:496499.

    Hopf HC, Lowitzsch K. Hemifacial spasm: location of the lesion by electrophys-iological means. Muscle Nerve. 1982;5:S84S88.

    House JW, Brackmann DE. Facial nerve grading system. Otolaryngol Head NeckSurg. 1985;93:146147.

    Huang CI, Chen IH, Lee LS. Microvascular decompression for hemifacial spasm:analyses of operative findings and results in 310 patients. Neurosurgery.1992;30:5357.

    Ishikawa M, Nakanishi T, Takamiya Y, Namiki J. Delayed resolution of residualhemifacial spasm after microvascular decompression operations. Neurosurgery.2001;49:847856.

    Ishikawa M, Ohira T, Namiki J, et al. Electrophysiological investigation ofhemifacial spasm: F-wave of the facial muscles. Acta Neurochir (Wien).1996a;138:2432.

    Ishikawa M, Ohira T, Namiki J, et al. Abnormal muscle response (lateral spread)and F-wave in patients with hemifacial spasm. J Neurol Sci. 1996b;137:109116.

    Ishikawa M, Ohira T, Namiki J, et al. Electrophysiological investigations ofhemifacial spasm after microvascular decompression: F waves of the facialmuscles, blink reflexes, and abnormal muscle responses. J Neurosurg.1997;86:654661.

    Isu T, Kamada K, Mabuchi S, et al. Intra-operative monitoring by facial electro-myographic responses during microvascular decompressive surgery forhemifacial spasm. Acta Neurochir (Wien). 1996;138:1923.

    Jannetta PJ, Hackett E, Ruby JR. Electromyographic and electron microscopiccorrelates in hemifacial spasm treated by microsurgical relief of neurovas-cular compression. Surg Forum. 1970;21:449451.

    Joo WI, Lee KJ, Park HK, et al. Prognostic value of intra-operative lateral spreadresponse monitoring during microvascular decompression in patients withhemifacial spasm. J Clin Neurosci. 2008;15:13351339.

    Kim P, Fukushima T. Observations on synkinesis in patients with hemifacialspasm: effect of microvascular decompression and etiological considerations.J Neurosurg. 1984;60:821827.

    Kiya N, Bannur U, Yamauchi A, et al. Monitoring of facial evoked EMG forhemifacial spasm: a critical analysis of its prognostic value. Acta Neurochir(Wien). 2001;143:365368.

    Kong DS, Park K, Shin BG, Lee JA, Eum DO. Prognostic value of the lateralspread response for intraoperative electromyography monitoring of the facialmusculature during microvascular decompression for hemifacial spasm.J Neurosurg. 2007;106:384387.

    Kuroki A, Itagaki S, Nagai O. Delayed facial palsy after microvascular decom-pression for hemifacial spasm. Facial Nerve Res. 1991;11:147150.

    Laskawi R. The use of botulinum toxin in head and face medicine: an interdis-ciplinary field. Head Face Med. 2008;4:18.

    Li CS. Varied patterns of postoperative course of disappearance of hemifacialspasm after microvascular decompression. Acta Neurochir (Wien). 2005;147:617620.

    Lovely TJ, Getch CC, Jannetta PJ. Delayed facial weakness after microvasculardecompression of cranial nerve VII. Surg Neurol. 1998;50:449452.

    Moller AR, Jannetta PJ. On the origin of synkinesis in hemifacial spasm: resultsof intracranial recordings. J Neurosurg. 1984;61:569576.

    Moller AR, Jannetta PJ. Hemifacial spasm: results of electrophysiologic recordingduring microvascular decompression operations. Neurology. 1985a;35:969974.

    Moller AR, Jannetta PJ. Microvascular decompression in hemifacial spasm:intraoperative electrophysiological observations. Neurosurgery. 1985b;16:612618.

    Moller AR, Jannetta PJ. Synkinesis in hemifacial spasm: results of recordingintracranially from the facial nerve. Experentia. 1985c;41:415 417.

    Moller AR, Jannetta PJ. Physiological abnormalities in hemifacial spasm studiedduring microvascular decompression operations. Exp Neurol. 1986;93:584600.

    Moller AR, Jannetta PJ. Monitoring facial EMG responses during microvasculardecompression operations for hemifacial spasm. J Neurosurg. 1987;66:681685.

    Nielsen VK. Pathophysiology of hemifacial spasm: I. Ephaptic transmission andectopic excitation. Neurology. 1984;34:418426.

    Nielsen VK. Electrophysiology of the facial nerve in hemifacial spasm: ectopic/ephaptic excitation. Muscle Nerve. 1985;8:545555.

    Poignonec S, Widaihet M, Lamas G, et al. Electrophysiological evidence forcentral hyperexcitability of facial motoneurons in hemifacial spasm. EurArch Otorhinolaryngol. 1994;S216S217.

    Ruby JR, Jannetta PJ. Hemifacial spasm: ultrastructural changes in the facialnerve induced by neurovascular compression. Surg Neurol. 1975;4:369 370.

    Sekula RF Jr, Bhatia S, Frederickson AM, et al. Utility of intraoperative electro-myography in Microvascular decompression for Hemifacial spasm: a meta-analysis. Neurosurg Focus. 2009;27:E10.

    Shin JC, Chung UH, Kim YC, Park CI. Prospective study of microvasculardecompression in hemifacial spasm. Neurosurgery. 1997;40:730735.

    Yamashita S, Kawaguchi T, Fukuda M, et al. Lateral spread response elicited bydouble stimulation in patients with hemifacial spasm. Muscle Nerve. 2002;25:845849.

    P. D. Thirumala et al. Journal of Clinical Neurophysiology Volume 28, Number 1, February 2011

    Copyright 2011 by the American Clinical Neurophysiology Society66