Several nonphysiological processes may contribute to changes in ABRs during IOM [14]. Inherent to any IOM, ABRs are susceptible to mechanical failure and operative errors such as malfunctioning equipment, accidental removal of the stimulating earpiece, or an obstruction in the tubing connected to the earpiece. These conditions may artificially produce increases in latency, decreases in amplitude, or even an entire loss of signal recordings. Other possible nonphysiological processes that can affect ABR signal recording include artifact created by electrocautery or ultrasonic aspirating devices. In the present case, all the data collection and recording equipment was inspected and determined to be working properly. The use of electrocautery was infrequent and no cavitational ultrasonic surgical aspirator devices were being utilized. We therefore determined that changes in ABR recordings were not caused by a nonphysiological etiology.

Short-latency ABR recordings are relatively resistant to the effects of intravenous and volatile anesthetic agents even at levels of anesthesia that attenuate or abolish other forms of IOM (EEG, SSEP, etc.). However, ABRs become more susceptible to anesthetic agent levels when the patient is hypothermic or hypotensive. While reversible prolongation of peak latencies have been observed in patients undergoing induced hypothermia during cardiac procedures [15], unintended mild hypothermia during a prolonged surgical case or even localized hypothermia due to room temperature irrigation baths may produce some degree of latency change in ABR wave peaks. In our case, the patient’s core temperature had not changed and only warm saline was used as irrigation for the operative site. Therefore, it was unlikely that the changes in ABR latency observed in our patient were due to hypothermia. Invasive blood pressure monitoring ruled out any contribution of hypotension to the ABR changes as the patient’s mean arterial pressure was not significantly lower than baseline measures. In examination of the changes seen in Fig. 27.1, the waveforms in the figure are clearly present and few, if any, changes are seen in the amplitude of the evoked responses. However, a gradual increase in latencies is seen in all wave peaks and between peaks. This observation would argue against the direct mechanical manipulation or dissection of the auditory nerve since such an injury would elicit an abrupt change in the ABR waveform and, when severe, is often accompanied by loss of wave peaks. Additionally, ischemia to the cochlea via damage to the anterior inferior cerebellar artery or the internal auditory artery would also cause an abrupt change to the responses and potential loss of wave peaks. Alternatively, stretch or excessive retraction of the auditory nerve would cause a gradual increase in wave latencies consistent with the finding in our case. Finally, ischemia or injury to the brainstem may also cause changes in ABR recording, and often these changes are bilateral. However, ABRs may not show any changes during ongoing brainstem or cerebral ischemia if there is sparing of the auditory region. In our case, the lack of baseline changes in concomitant SSEP and EEG recordings indicated that a more pronounced ischemic event was not occurring.

The surgeon was notified that the ABR changes were most consistent with stretch or retraction of the acoustic nerve. At that point, the surgeon temporarily removed the retractors and then reapplied the retraction intermittently throughout the remainder of the case. As seen in Fig. 27.1, the latency of the ABRs improved and approached baseline measurements by the end of the case. Additionally, EMG activity of the facial nerve gradually resolved. The patient was extubated in the operating room and transported to the neurosurgical intensive care unit. Postoperative evaluation revealed no new neurological deficits.

A 67-year-old man with coronary artery disease, diabetes, and hypothyroidism presented with diplopia and was diagnosed with a right-sided sphenoid wing meningioma . He was scheduled for a frontal temporal craniotomy after undergoing preoperative embolization of the tumor a day prior to surgery. Preoperative examination revealed a normal neurological evaluation except for mild diplopia with lateral gaze. The patient was anesthetized with induction boluses of lidocaine, propofol, rocuronium, and fentanyl. The patient was intubated and maintenance of anesthesia was provided by intravenous infusions of propofol, lidocaine, and remifentanil. Additional monitoring included left radial arterial line and a urinary catheter with temperature probe. IOM was established with EMG recordings of cranial nerves III, IV, VI, and VII along with four-limb SSEP. The patient was placed in supine position with slight rotation of the torso. His head was secured with Mayfield pins. A warm-air temperature regulation blanket was placed on the patient. After the surgical area was prepped and draped, baseline EMG and SSEP recordings were normal. The craniotomy proceeded uneventfully with nominal blood loss. As the tumor was being resected, a marked decline in amplitude of the right upper extremity SSEP recordings was noted. Cranial nerve recordings were unchanged from baseline (Fig. 27.2).