Repeated L5 Nerve Root Compromise Detected with Motor Evoked Potentials (MEP), but Not Electromyography (EMG): A Case Report.

We report a case where neuromonitoring, using motor evoked potentials (MEP), detected an intraoperative L5 nerve root deficit during a lumbosacral decompression and instrumented fusion procedure. Critically, the MEP changes were not preceded nor accompanied by any significant spontaneous electromyography (sEMG) activity. Presumptive L5 innervated muscles, including tibialis anterior (TA), extensor hallucis longus (EHL) and gluteus maximus, were targets for nerve root surveillance using combined MEP and sEMG techniques. During a high-grade spondylolisthesis correction procedure, attempts to align a left-sided rod resulted in repeated loss and recovery cycles of MEP from the TA and EHL. No accompanying EMG alerts were associated with any of the MEP changes nor were MEP variations seen from muscles innervated above and below L5. After several attempts, the rod alignment was achieved, but significant MEP signal decrement (72% decrease) remained from the EHL. Postoperatively, the patient experienced significant foot drop on the left side that recovered over a period of 3 months. This case contributes to a growing body of evidence that exclusive reliance on sEMG for spinal nerve root scrutiny can be unreliable and MEP may provide more dependable data on nerve root patency.

Identifying Suspected Volume Conduction Contamination of External Anal Sphincter Motor Evoked Potentials in Lumbosacral Spine Surgery.

PURPOSE: Iatrogenic injury to sacral nerve roots poses significant quality of life issues for patients. Motor evoked potential (MEP) monitoring can be used for intraoperative surveillance of these important structures. We hypothesized that volume conducted depolarizations from gluteus maximus (GM) may contaminate external anal sphincter (EAS) MEP results during lumbosacral spine surgery. METHODS: Motor evoked potential from the EAS and medial GM in 40 patients were prospectively assessed for inter-muscle volume conduction during lumbosacral spine surgeries. Peak latency matching between the EAS and GM MEP recordings conditionally identified volume conduction (VC+) or no volume conduction (VC-). Linear regression and power spectral density analysis of EAS and medial GM MEP amplitudes were performed from VC+ and VC- data pairs to confirm intermuscle electrical cross-talk. RESULTS: Motor evoked potential peak latency matching identified putative VC+ in 9 of 40 patients (22.5%). Mean regression coefficients (r2) from peak-to-peak EAS and medial GM MEP amplitude plots were 0.83 ± 0.04 for VC+ and 0.34 ± 0.06 for VC- MEP (P < 0.001). Power spectral density analysis identified the major frequency component in the MEP responses. The mean frequency difference between VC+ EAS and medial GM MEP responses were 0.4 ± 0.2 Hz compared with 3.5 ± 0.6 Hz for VC- MEP (P < 0.001). CONCLUSIONS: Our data support using peak latency matching between EAS and GM MEP to identify spurious MEP results because of intermuscle volume conduction. Neuromonitorists should be aware of this possible cross-muscle conflict to avoid interpretation errors during lumbosacral procedures using EAS MEP.

Cathodal Genesis of Ipsilateral Hand (Crossover) Motor Evoked Potentials: Evidence from a Patient with Previous Stroke.

A case is described where baseline transcranial electrical motor evoked potentials (TcMEP) and somatosensory evoked potentials (SSEP) results were unilaterally absent in a patient with previous hemispheric stroke undergoing a right-sided carotid endarterectomy. SSEP data confirmed right cortical pathology and excluded a technical rationale for absent motor evoked responses. Attempts at generating left-hand (contralateral) TcMEP from right cortical anodal stimulation failed despite high stimulus intensities. However, TcMEP responses from anodal stimulation of the right cortex were recorded from the right-hand (ipsilateral) which were attributed to "crossover." Ipsilateral TcMEP onset latencies derived from the stimulus-response data supports the idea that crossover is a product of cathodal stimulation initially acting on pericortical motor pathways.

The Winnipeg Intraspinal Pressure Monitoring Study (WISP): A protocol for validation of fiberoptic pressure monitoring for acute traumatic spinal cord injury.

BACKGROUND: Research efforts have been focused on limiting secondary injury after traumatic spinal cord injury by performing spinal decompression and early optimization of spinal cord perfusion. The Winnipeg Intraspinal Pressure Monitoring Study (WISP) was designed to validate the technique of intraspinal pressure monitoring at the site of injury using a fiberoptic pressure monitor placed at the site of injury. OBJECTIVES: To describe the design of the WISP study. STUDY DESIGN: Descriptive. METHODS: We explain the current limitations in the available scientific literature around the topic of blood pressure management for acute traumatic spinal cord injury and rational for the WISP study. Then, we describe the design of WISP including the patient selection criteria, study interventions, follow up schedules and outcome measurements. A multitude of future research avenues are also discussed. RESULTS: The WISP study is a single center pilot study designed to validate the technique of intraspinal pressure monitoring following acute traumatic spinal cord injury. The study involves the measurement of intraspinal pressure from within the subarachnoid space at the site of injury to derive a number of physiological parameters including spinal cord perfusion pressure, spinal cord blood volume, measures of spinal cord compliance and vascular reactivity indices. Twenty eligible patients will be recruited and followed for a period of 12 months with visits scheduled for the first 5 days and 1, 3, 6, and 12 months following surgical intervention. CONCLUSIONS: The WISP study will provide the first attempt in North America at validation of intraspinal pressure monitoring with a fiberoptic pressure monitor at the site of injury. Successful validation will lead to future studies to define optimal spinal cord perfusion pressure, relationships of neural injury biomarkers and outcomes as well as epigenetic studies. TRIAL REGISTRATION: This study has been registered at clinicaltrials.gov (registration# NCT04550117).

A novel method for quantitative evaluation of motor evoked potential monitoring during cerebrovascular surgeries.

Transcranial motor evoked potential (MEP) monitoring, intended to assess cerebral cortical ischemia, may produce false negative results when the stimulation inadvertently activates the deep, subcortical motor pathways. This study examined hand MEP onset latency as a potential means to differentiate superficial versus deep stimulus penetration in surgical patients monitored for cerebral ischemia. Intraoperative MEP data were prospectively collected from 40 patients treated for intracranial aneurysm or carotid stenosis. Onset latencies of hand MEP responses were measured over a range of stimulation intensities from both the contralateral and ipsilateral hand (crossover responses). At the threshold for superficial, cortical stimulation of the contralateral hand, the MEP latency was 26.9 ± 0.4 ms. MEP onset latencies measurements became shorter as stimulation intensities were increased. At the maximum intensity (when crossover response was usually generated), the contralateral hand MEP latency of 22.5 ± 0.3 ms was significantly shorter than at threshold stimulation (p < 0.001). Latency-stimulus intensity plots best fit a 3 parameter hyperbolic decay function (r2 = 0.85 ± 0.02) and revealed a narrow window of acceptable MEP stimuli to obtain superficial cortical activation. Our analysis refutes the utility of the crossover response in reliably gauging depth of activation. Additionally, we found that differentiation between long and short MEP onset latency times may serve as a dependable marker for depth of stimulation. Attention to hand MEP onset latency may reduce inadvertent stimulation of the deep corticospinal tract pathways and avoid false negative MEP recordings during cerebrovascular surgeries.

Peripheral leg ischemia detected via intraoperative neurophysiological monitoring during a multilevel complex anterior and posterior operation.

Intraoperative neurophysiologic monitoring is a technique utilized during spinal operations to minimize sensory and motor function morbidity. We herein report a case of a 73-year-old female with renal cell carcinoma and metastatic involvement of the cervical and thoracic spine, who underwent a multilevel complex anterior and posterior operation. Neurophysiological monitoring was able to localize the lower limb ischemia utilizing somatosensory evoked potentials. This prompted intraoperative investigation of the peripheral ischemia, and the patient was found to have an Angio-Seal device embolus in the right popliteal artery that dislodged from the right femoral artery.

Using strength-duration analysis to identify the afferent limb of the lateral spread response in hemifacial spasm patients during microvascular decompression surgery.

Strength-duration analysis has been used to identify excitability differences between motor and sensory axons in human peripheral mixed nerves. The trigeminal and facial nerves have both been suggested to play a role in mediating the lateral spread response (LSR) in patients with hemifacial spasm (HFS). We sought to investigate this hypothesis by analyzing strength-duration properties of spasm side mentalis M wave and o. oculi LSR in 22 patients undergoing microvascular decompression surgery for HFS. Simultaneous recordings of mentalis M wave and o. oculi LSR prior to dural opening were collected following marginal mandibular facial nerve branch stimulation. Threshold responses were observed at stimulus pulse widths from 0.05 to 1.0 ms and the chronaxie and rheobase calculated from charge versus stimulus pulse width plots. The mean chronaxie (±SEM) of mentalis M wave was 0.34 ± 0.03 ms and 0.33 ± 0.04 ms for the LSR (p = 0.42, one-tailed t-test). The rheobase for the M wave (8.0 ± 1.0 mA) was found to be significantly different than the LSR rheobase (5.7 ± 0.7 mA; p = 0.03, one-tailed t-test) likely due to differences in the threshold amplitudes of the M wave versus the LSR. These results are highly suggestive of the facial nerve and not the trigeminal nerve in mediating the LSR.

Correction to: Is the new ASNM intraoperative neuromonitoring supervision "guideline" a trustworthy guideline? A commentary.

The article Is the new ASNM intraoperative neuromonitoring supervision "guideline" a trustworthy guideline? A commentary, written by Stanley A. Skinner, Elif Ilgaz Aydinlar, Lawrence F. Borges, Bob S. Carter, Bradford L. Currier, Vedran Deletis, Charles Dong, John Paul Dormans, Gea Drost, Isabel Fernandez­Conejero, E. Matthew Hoffman, Robert N. Holdefer, Paulo Andre Teixeira Kimaid, Antoun Koht, Karl F. Kothbauer, David B. MacDonald, John J. McAuliffe III, David E. Morledge, Susan H. Morris, Jonathan Norton, Klaus Novak, Kyung Seok Park, Joseph H. Perra, Julian Prell, David M. Rippe, Francesco Sala, Daniel M. Schwartz, Martín J. Segura, Kathleen Seidel, Christoph Seubert, Mirela V. Simon, Francisco Soto, Jeffrey A. Strommen, Andrea Szelenyi, Armando Tello, Sedat Ulkatan, Javier Urriza and Marshall Wilkinson, was originally published electronically on the publisher's internet portal (currently SpringerLink) on 05 January 2019 without open access. With the author(s)' decision to opt for Open Choice the copyright of the article changed on 30 January 2019 to © The Author(s) 2019 and the article is forthwith distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits use, duplication, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license and indicate if changes were made. The original article has been corrected.

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.

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 ).

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.

Controversies in the anesthetic management of intraoperative rupture of intracranial aneurysm.

Despite great advancements in the management of aneurysmal subarachnoid hemorrhage (SAH), outcomes following SAH rupture have remained relatively unchanged. In addition, little data exists to guide the anesthetic management of intraoperative aneurysm rupture (IAR), though intraoperative management may have a significant effect on overall neurological outcomes. This review highlights the various controversies related to different anesthetic management related to aneurysm rupture. The first controversy relates to management of preexisting factors that affect risk of IAR. The second controversy relates to diagnostic techniques, particularly neurophysiological monitoring. The third controversy pertains to hemodynamic goals. The neuroprotective effects of various factors, including hypothermia, various anesthetic/pharmacologic agents, and burst suppression, remain poorly understood and have yet to be further elucidated. Different management strategies for IAR during aneurysmal clipping versus coiling also need further attention.

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.