A 42-year-old woman with right-sided HFS underwent an MVD after serial botulinum toxin injections resulted in unsatisfactory results. During the operation, the AICA and PICA were noted to be tightly compressing the right facial nerve. During decompression of the PICA, the AMR resolved and could not be elicited (Fig. 26.4). The patient awoke from the operation with much reduced spasms, which gradually decreased and resolved entirely 4 months after the operation.

Team notes: Even after appropriate decompression of the facial nerve, as many as half of the patients have persistent spasms, which resolve over the course of a few weeks to 23 months [35]. Since the AMR often disappears when the offending vessel is lifted off of the facial nerve in a microvascular decompression procedure, its use has been suggested as an intraoperative guide to success [18, 40–43]. Because HFS disappears or gradually resolves over time in many patients in whom the AMR persists intraoperatively, many authors have questioned the utility of intraoperative EMG [44–47]. In a large study evaluating 300 patients, Kong et al. [43] found a statistical difference at 1-year follow-up in the outcomes between two groups based on whether the AMR resolved or persisted [43]. Their report is the only one to show a statistically different outcome in cases where the AMR did not resolve. A meta-analysis by Sekula et al. [35] of the data concerning the relationship between resolution or persistence of the AMR after MVD and the resolution or persistence of HFS showed that the chance of a cure if the AMR was abolished after MVD was 4.2 times greater than when the AMR persisted. Thirumala et al. [48], reporting on 259 patients undergoing MVD with intraoperative monitoring of the lateral spread response (LSR), found that abolishment of the LSR during surgery was associated with statistically significant rates of spasm relief immediately postoperatively and at discharge. This increased rate of spasm relief was not observed at later follow-up between the two groups [48]. Furthermore, reoperation for persistent symptoms and botulinum toxin treatments prior to surgery does not affect rates of intraoperative abolishment of the LSR [49, 50]. Based on these results, we support that AMR should be monitored routinely in the operating room, and surgical decision-making in the operating room should be guided by the absence or presence of the AMR.

The surgeon recommended observation and increasing use of the left shoulder for the first 6 weeks following the operation. During those 6 weeks, the patient’s shoulder pain increased to the point that she did not use the left shoulder and upper extremity and required assistance with dressing. The surgeon referred the patient for physical therapy, which was ineffective. The patient was then referred to an orthopedic surgeon who diagnosed her with a “frozen shoulder ” or adhesive capsulitis of the glenohumeral joint. MRI of the left shoulder confirmed adhesive capsulitis. The surgeon performed “manipulation” of the left shoulder under a general anesthetic in the operating room, and the patient awoke with reduced pain and improved range of motion. Over the next few weeks, the pain resolved entirely and range of motion was restored.

Team notes: The pathophysiology of adhesive capsulitis is elusive. Although this complication is rare with the contralateral decubitus position, it should be considered in the differential diagnosis of those patients complaining of pain and reduced range of motion of either shoulder. Additionally, extreme care should be taken when retracting the nondependent shoulder inferiorly due to the potential for stretching of the brachial plexus. This is true when shoulders are taped and pulled away from the operative field (see Fig. 26.2) whether in the supine (such as in an anterior cervical discectomy and fusion), prone (such as in a suboccipital decompression), or in lateral position, as in this case, a retromastoid approach for microvascular decompression .

A 35-year-old man with right-sided HFS was taken to the operating room for an MVD . After a retromastoid craniectomy was achieved, the dura was opened. The surgeon noted that the brain immediately “herniated through the dural opening.” After a dose of mannitol and 20 min of head elevation, the brain relaxed to the point that the dura could be closed. MVD was aborted, and the operation was rescheduled.

A 57-year-old woman with left-sided HFS underwent an MVD after serial botulinum toxin injections resulted in unsatisfactory results. During drilling of the retromastoid craniectomy, the neuromonitoring technician became concerned because of reduced amplitude and prolonged latency of the left ABR . After confirmation that the patient was hemodynamically stable, the neuromonitoring technician checked the left earpiece and noted that the earpiece had become dislodged. The earpiece was adjusted and the ABR returned to baseline.

Team notes: Kinking of the ear insert tubing occurs infrequently and can be minimized by making sure the tubing is run away from the operative field. When the ABRs change without good reason, the insert and tubing should always be checked for proper delivery of the click stimulus (Fig. 26.5).

A 67-year-old woman with right-sided HFS underwent an MVD after serial botulinum toxin injections resulted in permanent facial weakness (House-Brackmann grade II/VI) [51]. After dural opening, a brain retractor was used to elevate the cerebellum away from the brainstem for exposure of the facial nerve. During this maneuver, the neuromonitoring technician advised the surgeon that waves III and V of the right ABRs had increased in latency by 0.8 ms. Within a few minutes, the neuromonitoring technician advised that the amplitude of the ABRs had decreased by 50 %.

After notification of a reduction in amplitude of the ABRs, the surgeon removed the retractor and stopped dissection. The anesthesiologist increased the mean arterial blood pressure 10 mmHg to a MAP of 80 mmHg. Within 2 min, the latency improved and the amplitude increased. Within 5 min, the ABRs had returned to baseline, and the surgeon resumed exposure of the facial nerve.

Team notes: Hearing loss remains a significant risk with MVD of the facial nerve for HFS, with partial hearing loss ranging from 0.5 to 9.5 % and complete hearing loss ranging from 0.7 to 7.6 % [2, 33, 52, 53]. Polo et al. [53] have provided data concerning a stepwise reduction in hearing with progressive latency increases of Peak V of the ABR during microvascular decompression. In their study of 84 consecutive patients undergoing MVD for HFS, they report that in the group with more than a 20-dB loss in pure tone audiogram, delays in the latency of Peak V were on average 1 ms. To this end, a recent study by our group showed that intraoperative loss of wave V resulted in significantly increased odds of hearing loss [38]. Recently, our group attempted to address this with avoidance of a fixed, self-retained cerebellar retractor in favor of dynamic retraction and subsequently demonstrated a reduction in ipsilateral high-frequency hearing loss (HFHL) from 50 to 7.4 % [36].

A 54-year-old woman with a 10-year history of right-sided HFS is brought to the operating room for MVD of the facial nerve. After positioning the patient in the contralateral decubitus position, the neuromonitoring technician reports an inability to obtain an AMR of the right facial nerve.

After confirming that the AMR was documented in the Cranial Nerve and Brainstem Disorders Clinic, discussion among the team revealed that a nondepolarizing muscle relaxant had been given during induction for intubation. The team waited 30 min before beginning the procedure, allowing the agent to wear off.

A 35-year-old woman with right-sided HFS underwent MVD of the right facial nerve. After exposing the facial nerve, the anterior inferior cerebellar arteries as well as multiple perforators of that vessel were noted to be tightly compressing the facial nerve. A preoperative MRI had revealed right-sided dolichoectasia of the vertebrobasilar system with clear compression of the right facial nerve. During the operation, the AICA with perforators and the vertebral artery were decompressed without incident. The AMR was abolished. SSEPs were not measured during the procedure.

Upon awakening, the patient was free of spasms, but, within an hour, she noted contralateral trunk and extremity hypalgesia and thermoanesthesia, ipsilateral Horner syndrome, ipsilateral hypohidrosis, and gait ataxia consistent with a Wallenberg syndrome [54, 55]. Stroke involving the PICA, vertebral artery, or their respective perforators was suspected [56], and a postoperative MRI of the brain confirmed a small infarct involving the lower lateral medulla and posterior cervical spinal cord. Because intraoperative videos did not indicate an avulsion of a perforator or major vessel during decompression of the vertebral and posterior inferior cerebellar arteries (including a complicated tangle of arterioles compressing the facial nerve likely representing PICA medullary perforators), occult compression or vasospasm of perforators was suspected. Although some authors have suggested the use of papaverine to prevent vasospasm-related ischemia [44], we do not routinely use papaverine during MVD due to concerns of vestibulocochlear toxicity [57]. The patient was discharged from acute rehabilitation on postoperative day 13 with improved and independent ambulation. At 10.3-month follow-up, ipsilateral hypohidrosis and gait ataxia had improved significantly with moderate improvement of contralateral extremity thermoanesthesia. The patient notes some incoordination with jogging and persistent difficulty with high humidity due to hypohidrosis.