Marshall F. Wilkinson

Facial Motor Neuron Excitability in Hemifacial Spasm: A Facial MEP Study.

INTRODUCTION Hemifacial spasm (HFS) may be due to peripheral axon ephapsis or central motor neuron hyperexcitability. Low facial motor evoked potential (MEP) thresholds or MEP responses to single pulse stimulation (normally multipulse stimulation is needed) may support the central hypothesis. METHODS We retrospectively compared response thresholds for facial MEPs in 65 patients undergoing surgical microvascular decompression (MVD) for HFS and 29 patients undergoing surgery for skull base tumors. RESULTS Single pulse stimulation elicited facial Mep in up to 87% of HFS patients whereas only 10% of tumor patients responded to single pulse stimulation. When comparing facial MEP thresholds using multi-pulse stimulus trains the voltage required in the HFS group were significantly lower then in skull base tumor patients (p < 0.001). the MEP latencies and amplitudes at threshold stimulation were similar between the two groups. CONCLUSIONS these results suggest the facial corticobulbar pathway demonstrates enhanced excitability in HFS.

Is hemifacial spasm a phenomenon of the central nervous system? – The role of desflurane on the lateral spread response

OBJECTIVE A signature EMG feature of hemifacial spasm (HFS) is the lateral spread response (LSR). Desflurane is a common anesthetic with potent effects on synaptic transmission. We tested the hypothesis that the LSR is mediated by corticobulbar components by comparing the LSR during total intravenous anesthesia (TIVA) or TIVA plus desflurane during microvascular decompression (MVD) surgery. METHODS 22 HFS patients undergoing MVD surgery participated in this prospective study. The LSR data was recorded from the o. oculi, o. oris and mentalis muscles prior to opening dura. LSR onset latencies and amplitudes were determined under TIVA and TIVA/desflurane (0.5 and 1MAC). Facial muscle LSRs and EEG were analyzed. RESULTS Desflurane (1MAC) significantly decreased the LSR amplitude in all 3 facial muscles (p<0.01). Pooled LSR data from all facial muscles showed desflurane inhibited the LSR amplitude by 43% compared to TIVA (p<0.001). No effects on the latency of the LSR or on EEG state were observed. CONCLUSIONS LSR inhibition by desflurane suggests a central mechanism involvement in the genesis of this signature HFS response. SIGNIFICANCE This study demonstrates that facial nerve vascular compression and plastic changes within the CNS are part of the pathophysiology of HFS.

Analysis of facial motor evoked potentials for assessing a central mechanism in hemifacial spasm

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 ).

Hemodynamic Perturbations in Deep Brain Stimulation Surgery: First Detailed Description

Background: Hemodynamic perturbations can be anticipated in deep brain stimulation (DBS) surgery and may be attributed to multiple factors. Acute changes in hemodynamics may produce rare but severe complications such as intracranial bleeding, transient ischemic stroke and myocardium infarction. Therefore, this retrospective study attempts to determine the incidence of hemodynamic perturbances (rate) and related risk factors in patients undergoing DBS surgery. Materials and Methods: After institutional approval, all patients undergoing DBS surgery for the past 10 years were recruited for this study. Demographic characteristics, procedural characteristics and intraoperative hemodynamic changes were noted. Event rate was calculated and the effect of all the variables on hemodynamic perturbations was analyzed by regression model. Results: Total hemodynamic adverse events during DBS surgery was 10.8 (0–42) and treated in 57% of cases. Conclusion: Among all the perioperative variables, the baseline blood pressure including systolic, diastolic, and mean arterial pressure was found to have highly significant effect on these intraoperative hemodynamic perturbations.