Hearing Loss in the Unoperated Ear After High-Speed Drilling in Otologic and Skull Base Surgery.

OBJECTIVE: To evaluate if permanent hearing loss occurred in the unoperated ear of patients undergoing otologic and skull base surgery with high-speed otologic drilling. STUDY DESIGN: We retrospectively studied 250 patients (mean age 57.8 yr; 120 males, and 130 females) undergoing otologic or skull base surgery with high-speed drilling between 2013 and 2019. SETTING: The University of Pittsburgh Medical Center. PATIENTS: We evaluated preoperative and postoperative audiograms for patients undergoing surgery for cochlear implantation (95 patients, 38.0%), cholesteatoma or chronic ear disease (88 patients, 35.2%), repair of lateral skull base encephalocele (26 patients, 10.4%), resection of vestibular schwannoma or meningioma of the cerebellopontine angle (23 patients, 9.2%), lateral temporal bone resection (8 patients, 3.2%), microvascular decompression (7 patients, 2.8%), or other operations involving a high-speed otologic drill (3 patients, 1.2%). MAIN OUTCOME MEASURES: Hearing threshold shift, measured as the difference between postoperative threshold and preoperative threshold for each frequency. The association of age, gender, tested frequency, and surgery type with hearing threshold shift was investigated with analysis of covariance. RESULTS: A total of 102 patients (40.8%) had a 10-dB or greater worsening of their hearing in at least one frequency on their postoperative audiogram in the contralateral, unoperated ear. One hundred six subjects (42.4%) had no change in hearing of 10 dB or greater at any frequency. Among patients with longitudinal postoperative audiograms, accelerated age-related hearing loss was observed in low frequencies. CONCLUSIONS: A significant number of patients demonstrated poorer hearing thresholds in the contralateral, unoperated ear after otologic and skull base surgery.

Estimation of Intraoperative Stimulation Threshold of the Facial Nerve in Patients Undergoing Microvascular Decompression.

Introduction Facial weakness can result from surgical manipulation of the facial nerve. Intraoperative neuromonitoring reduces functional impairment but no clear guidelines exist regarding interpretation of intraoperative electrophysiological results. Most studies describe subjects with facial nerves encumbered by tumors or those with various grades of facial nerve weakness. We sought to obtain the neurophysiological parameters and stimulation threshold following intraoperative facial nerve triggered electromyography (t-EMG) stimulation during microvascular decompression for trigeminal neuralgia to characterize the response of normal facial nerves via t-EMG. Methods Facial nerve t-EMG stimulation was performed in seven patients undergoing microvascular decompression for trigeminal neuralgia. Using constant current stimulation, single stimulation pulses of 0.025 to 0.2 mA intensity were applied to the proximal facial nerve. Compound muscle action potentials, duration to onset, and termination of t-EMG responses were recorded for the orbicularis oculi and mentalis muscles. Patients were evaluated for facial weakness following the surgical procedure. Results Quantifiable t-EMG responses were generated in response to all tested stimulation currents of 0.025, 0.05, 0.1, and 0.2 mA in both muscles, indicating effective nerve conduction. No patients developed facial weakness postoperatively. Conclusions The presence of t-EMG amplitudes in response to 0.025 mA suggests that facial nerve conduction can take place at lower stimulation intensities than previously reported in patients with tumor burden. Proximal facial nerve stimulation that yields responses with thresholds less than 0.05 mA may be a preferred reference baseline for surgical procedures within the cerebellopontine angle to prevent iatrogenic injury.

Rationale and Design for the Remote Ischemic Preconditioning for Carotid Endarterectomy Trial.

BACKGROUND: While the perioperative stroke rate after carotid endarterectomy (CEA) is low, "silent" microinfarctions identified by magnetic resonance imaging (MRI) are common and have been correlated with postoperative neurocognitive decline. Our study will investigate the role of remote ischemic preconditioning (RIPC) as a potential neuroprotective mechanism. RIPC is a well-tolerated stimulus that, through neuronal and humoral pathways, generates a systemic environment of greater resistance to subsequent ischemic insults. We hypothesized that patients undergoing RIPC before CEA will have improved postoperative neurocognitive scores compared with those of patients undergoing standard care. METHODS: Patients undergoing CEA will be randomized 1:1 to RIPC or standard clinical care. Those randomized to RIPC will undergo a standard protocol of 4 cycles of RIPC. Each RIPC cycle will involve 5 min of forearm ischemia with 5 min of reperfusion. Forearm ischemia will be induced by a blood pressure cuff inflated to 200 mm Hg or at least 15 mm Hg higher than the systolic pressure if it is >185 mm Hg. This will occur after anesthesia induction and during incision/dissection but before manipulation or clamping of the carotid; thus, patients will be blinded to their assignment. Before carotid endarterectomy, all patients will undergo baseline neurocognitive testing in the form of a Montreal Cognitive Assessment (MoCA) and National Institutes of Health (NIH) Toolbox. MoCA testing only will be conducted on postoperative day 1 in the hospital. The full neurocognitive testing battery will again be conducted at 1-month follow-up in the office. Changes from baseline will be compared between arms at the follow-up time points. Assuming no drop-ins or dropouts and a 10% loss to follow-up, we would need a sample size of 43 patients for 80% power per treatment arm. The primary endpoint, change in MoCA scores, will be analyzed using a random effects model, and secondary outcomes will be analyzed using either linear or logistic regression where appropriate. CONCLUSIONS: RIPC, if shown to be effective in protecting patients from neurocognitive decline after CEA, represents a safe, inexpensive, and easily implementable method of neuroprotection.

Otoprotective Effects of Stephania tetrandra S. Moore Herb Isolate against Acoustic Trauma.

Noise is the most common occupational and environmental hazard, and noise-induced hearing loss (NIHL) is the second most common form of sensorineural hearing deficit. Although therapeutics that target the free-radical pathway have shown promise, none of these compounds is currently approved against NIHL by the United States Food and Drug Administration. The present study has demonstrated that tetrandrine (TET), a traditional Chinese medicinal alkaloid and the main chemical isolate of the Stephania tetrandra S. Moore herb, significantly attenuated NIHL in CBA/CaJ mice. TET is known to exert antihypertensive and antiarrhythmic effects through the blocking of calcium channels. Whole-cell patch-clamp recording from adult spiral ganglion neurons showed that TET blocked the transient Ca2+ current in a dose-dependent manner and the half-blocking concentration was 0.6 + 0.1 µM. Consistent with previous findings that modulations of calcium-based signaling pathways have both prophylactic and therapeutic effects against neural trauma, NIHL was significantly diminished by TET administration. Importantly, TET has a long-lasting protective effect after noise exposure (48 weeks) in comparison to 2 weeks after noise exposure. The otoprotective effects of TET were achieved mainly by preventing outer hair cell damage and synapse loss between inner hair cells and spiral ganglion neurons. Thus, our data indicate that TET has great potential in the prevention and treatment of NIHL.

Predictors of cross-clamp-induced intraoperative monitoring changes during carotid endarterectomy using both electroencephalography and somatosensory evoked potentials.

OBJECTIVE: The efficacy of selective shunting during carotid endarterectomy (CEA) using intraoperative monitoring (IOM) for detection of cerebral ischemia is well established. There is mounting evidence that monitoring of both electroencephalography (EEG) and somatosensory evoked potentials (SSEPs) increases the sensitivity of cerebral ischemia detection. Predictors of cerebral ischemia requiring selective shunt placement using IOM of both EEG and SSEPs have not been previously identified. METHODS: Consecutive patients who underwent CEA between January 1, 2000, and December 31, 2010, were retrospectively analyzed. Primary end points were IOM changes at any time during the operation or IOM changes with carotid cross-clamping. Risk factors assessed included demographics; baseline comorbidities; severity of ipsilateral and contralateral disease; symptomatic status; and use of statin, antiplatelet, and beta-blocker medications. Univariate and multivariate logistic regression was used for analysis. RESULTS: During the 11-year study period, a total of 758 patients underwent 804 CEAs (mean age, 70.6 ± 9.5 years; 59.8% male; 39.2% symptomatic) using IOM of both SSEPs and EEG for selective shunting guidance. Postoperative stroke rate was 1.37%; 27.1% of patients had significant SSEP or EEG changes, and 49.1% of these were clamp induced (within 5 minutes of cross-clamping). Of these patients, 83.2% received a shunt (11.4% overall). The most common reason that a shunt was not placed after cross-clamp-induced changes was that the changes resolved with further blood pressure elevation (8 of 17 patients). Clamp-induced IOM changes were predictive of postoperative stroke (odds ratio [OR], 5.5; P = .005). Risk factors for clamp-induced IOM changes were contralateral carotid occlusion (OR, 2.5; P = .01), symptomatic stenosis (OR, 1.8; P = .006), and diabetes (OR, 1.6; P = .03), whereas there was a trend toward increased risk with female sex (OR, 1.5; P = .08). Risk factors for any IOM change (clamp and nonclamp induced) were symptomatic carotid stenosis (OR, 1.8; P < .001), use of beta blockers (OR, 1.5; P = .03), and female sex (OR, 1.5; P = .02). CONCLUSIONS: Whereas some patients can be expected to experience IOM changes by monitoring of SSEPs and EEG, a much smaller percentage will receive a shunt. Contralateral carotid occlusion, symptomatic stenosis, diabetes, and female sex increase the risk of clamp-induced IOM changes and should be anticipated to need a shunt. Patients receiving beta blockers are likely to experience IOM changes during the operation that are not associated with clamping.

Somatosensory Evoked Potentials and Electroencephalography during Carotid Endarterectomy Predict Late Stroke but not Death.

BACKGROND: Late stroke and death rates are anticipated to be higher in patients undergoing carotid endarterectomy (CEA) compared with healthy counterparts. However, little is known regarding predictors other than the baseline comorbidities. We have recently shown that dual intraoperative somatosensory evoked potentials (SSEPs) and electroencephalography (EEG) monitoring improves the ability to predict perioperative strokes. We seek to determine if dual intraoperative monitoring (IOM) can further predict long-term strokes and death. METHODS: Consecutive patients who underwent CEA under dual SSEP and EEG IOM between January 1, 2000 and December 31, 2010 were analyzed. Patients were divided in 2 groups, those with and those without IOM changes. IOM changes were classified as either occurring during carotid cross-clamp placement or at any time during the operation. End points were time to stroke and death. Log-rank tests and Cox regression analysis were used to identify predictors of postoperative stroke and death. RESULTS: A total of 853 CEAs (mean age 70.6 ± 9.5 years, 58.7% male, 38.9% symptomatic) were performed during the study period with a mean clinical follow-up of 48 ± 38 months. One hundred seven patients (13.6%) had significant SSEP or EEG changes at the time of clamping, while considerably more patients (217, 25.4%) had SSEP and/or EEG changes recorded at any point during the procedure, including clamping. Baseline characteristics including rates of bilateral disease, statin use, and antiplatelet use were similar between groups. Female gender, symptomatic disease, and significant contralateral carotid stenosis were more frequent in the group with IOM changes. The overall stroke-free survival rate at 5 years was significantly higher in patients without IOM changes (94.7% vs. 88.2%, P < 0.05) and at 10 years (86.1% vs. 78.0%, P < 0.05). Despite differences in stroke-free survival, overall survival at 10 years was not different between groups (44.0% in patients with IOM changes vs. 42.8% in patients without, P = 0.7). Renal insufficiency (hazards ratio [HR] 2.13, P = 0.03), diabetes (HR 1.84, P = 005), and age > 80 at the time of operation (HR 3.24, P = 0.001) were significant predictors of late stroke, while statins were significantly protective (HR 0.55, P = 0.05). Controlling for these factors, IOM changes (HR 2.5, P = 0.004) were a strong predictor of long-term risk of stroke after CEA. CONCLUSION: Intraoperative SSEP and/or EEG changes are predictive of late stroke but not death following CEA indicating a need for further elucidation and management of the underlying risk factors driving the elevated stroke risk in this subset of CEA patients.

American Clinical Neurophysiology Society Guideline 2: Guidelines for Standard Electrode Position Nomenclature.

This revision to the EEG Guidelines is an update incorporating current electroencephalography technology and practice and was previously published as Guideline 5. While the 10-10 system of electrode position nomenclature has been accepted internationally for almost two decades, it has not been used universally. The reasons for this and clinical scenarios when the 10-10 system provides additional localizing information are discussed in this revision. In addition, situations in which AF1/2, AF5/6, PO1/2 and PO5/6 electrode positions may be utilized for EEG recording are discussed.

American Clinical Neurophysiology Society Guideline 3: A Proposal for Standard Montages to Be Used in Clinical EEG.

This revision to the EEG Guidelines is an update incorporating current electroencephalography technology and practice and was previously published as Guideline 6. A discussion of methodology for the appropriate selection of reference electrodes is added. In addition, montages are added to assist with localization of abnormal activity in mesial frontal and anterior temporal regions.