21.1 Key Learning Points

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  Somatosensory evoked potentials (SSEPs) and electroencephalography (EEG) recordings can be obtained continuously in real time during surgery.

  
  
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  SSEP and EEG are sensitive to changes in cerebral perfusion during surgery.

  
  
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  Significant changes in SSEPs, an increase in the latency and decrease in amplitude of the cortical responses, can be utilized as a criterion to warn the surgical team of impending neurological injury.

  
  
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  Significant decrease in the amplitude of the background EEG can serve as an indicator for cerebral perfusion and warn the surgical team.

  
  
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  SSEP and EEG can serve as a neurophysiological biomarker of cerebral perfusion and postoperative neurological deficits.

  
  
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  Motor evoked potential (MEP) and brainstem auditory evoked potential (BAEP) are especially useful in subcortical hypoperfusion related to perforator injury.

21.2 Introduction

Skull base surgery faces unique challenges including intimate relationships between tumors and cerebrovascular structures. Resection of tumors located along the path of the internal carotid artery (ICA) carries the risk of injuring the vessel and will be a significant concern. Another example of major arterial risk during skull base tumor resection is the basilar artery. Lesions involving the clivus and foramen magnum may also place the basilar artery, its tributaries, or its branches, at risk. In a similar way, lesions involving the anterior skull base can be intimately related to the anterior communicating artery complex vessels, including the anterior cerebral arteries, and frontopolar and fronto-orbital arteries. ¹

Vascular injury is one of the most feared complications due to its potential for significant morbidity. ^{2 ,​ 3 ,​ 4} Intraoperative neurophysiologic monitoring (IONM) with somatosensory evoked potentials (SSEPs), electroencephalography (EEG), and motor evoked potentials (MEPs) can detect significant cortical and subcortical cerebral hypoperfusion leading to potential corrective action. Real-time information about the functional status of the integrity of the nervous systems secondary to perfusion plays an essential role in the management of vascular complications guiding immediate corrective action before the onset of permanent neurological deficit. ^{2 ,​ 5 ,​ 6 ,​ 7 ,​ 8 ,​ 9}

In addition to direct vascular injury, which can usually be visually identified by the surgical team, other mechanisms can contribute to vascular complications such as cerebral hypoperfusion related to hypotension or hemodilution, and embolic phenomenon associated with vessel manipulation. ^{7 ,​ 10} In these cases, an ongoing injury can be overlooked unless continuous functional assessment is in progress.

21.3 Cerebral Perfusion Principles and Neurophysiologic Tools for Measurement

Normal cerebral blood flow (CBF) in awake adults is approximately 50 mL/100 g/minute, with cortical regions requiring higher levels compared with subcortical regions. Animal studies indicate that a decrease in CBF to 16 to 20 mL/100 g/minute results in reversible cellular dysfunction (ischemia) and a significant decrease in neurophysiological response amplitude. CBF below this level risks “electric failure” (functional threshold) and a loss of neurophysiological responses is an immediate precursor of “ion pump failure” and cellular death. The flow threshold for ion pump failure or infarction occurs at 10 to 12 mL/100 g/minute (lesion threshold). This means that there is a time window, as CBF decreases, wherein restoration of flow will avoid permanent injury. ^{6 ,​ 7 ,​ 8}

There is wide variability in the individual susceptibility to hemodynamic changes related to drop in systemic blood pressure, embolic events, direct vascular injury, or arterial cross-clamping. This susceptibility depends on self-regulatory mechanisms, including, but not limited to, the status of the circle of Willis, other collateral circulation, the presence of atherosclerosis, and autoregulation. Thus, during a vascular complication it is often necessary to determine intraoperatively if the hemodynamic situation during the complication is compatible with sufficient cerebral perfusion in each individual. ^{2 ,​ 11}

Numerous tools have been proposed that allow for intraoperative assessment of CBF such as Doppler, flow probes, which use ultrasonic measurements, stump pressure, EEG, and SSEPs, among others. ^{8 ,​ 11 ,​ 12} The distinct advantage of neurophysiological methods is the ability to evaluate the consequence of hemodynamic changes while Doppler, flow, and pressure provide local data without information on how it impacts the individual patient. ^{8 ,​ 11} Moreover, EEG and SSEP are noninvasive and technically easy to implement and record in the operating room (OR).

The SSEP evaluates the entire somatosensory neural axis which includes the peripheral nerve, spinal cord dorsal columns, the brainstem medial lemniscus pathways to the contralateral thalamus, and connections to the primary somatosensory cortex. These structures are represented by a sequence of scalp recorded SSEP components named according to the polarity (positive [P] or negative [N]) and peak latency. Thus, for the upper limb SSEPs, the N9, N13, and N20/P22 components of the SSEP are generated at the brachial plexus, cervicomedullary junction, and anterior parietal somatosensory cortex, respectively, while for lower limb SSEPs, the equivalent SSEP components are the N20, N30, and N37/P45 components, respectively. ^{7 ,​ 13}

Adequate CBF is necessary for the generation of SSEP responses by viable neurons. As stated earlier, decreases in CBF below 16 to 20 mL/100 g/minute causes a reversible decrease in the amplitude of cortical SSEP responses due to desynchronization of cortical neurons and a reduction in the number of functional neurons. ⁸ Cortical SSEP responses disappear with corresponding CBF values between 12 and 15 mL/100 g/minute as a result of the “electrical failure.” Considering that the flow threshold for ion pump failure or infarction occurs at 10 to 12 mL/100 g/minute, these changes in SSEPs can be a precursor of ion pump failure. ^{6 ,​ 7 ,​ 8 ,​ 14 ,​ 15 ,​ 16}

The EEG is a graphical representation of global neuronal electrical activity within the entire cerebral cortex. Physiologically reversible EEG changes such as a decrease in amplitude and frequency alterations also occur with decrease in CBF. For example, decrease in α (8–13 Hz)/β (≥14 Hz) frequencies and increase in θ (5–7 Hz)/δ (0.5–4 Hz) frequencies occur when CBF decreases to ≤22 mL/100 g/minute, while isoelectric (i.e., flat) EEG (absence of cerebral activity of over 2 microvolts [μV]) can be observed following more significant reductions in CBF (7–15 mL/100 mg/minute). ^{8 ,​ 11 ,​ 17} To facilitate interpretation and comparison of EEG activity across different time-points during surgery, processed spectral EEG activity can also be used, which use fast Fourier transformation of the raw EEG data. ¹²

Other neurophysiologic modalities that may be useful during vascular procedures that pose a risk for vessel injury include brainstem auditory evoked potential (BAEP) and transcranial motor evoked potentials (TcMEPs). BAEPs are generated in response to independent auditory stimulation delivered to the ear and consist of a sequence of deflections called Jewitt Waves I, II, III, IV, and V which originate from the distal cochlear nerve, cochlear nucleus, superior olivary complex, lateral lemniscus (LL), and inferior colliculus (IC), respectively. Thus, the BAEP can assess the integrity of the cochlear nerve and the auditory structures of the brainstem from the pontomedullary junction to the lower midbrain. ^{6 ,​ 13 ,​ 18} Primate studies on the effect of focal brainstem ischemia on BAEPs demonstrate that ischemia increases the latency and reduces the amplitude of BAEP waveforms. The gradient of sensitivity to ischemia where the latency of BAEP responses from the LL was increased at CBF was 12 to 15 mL/100 g/minute, and the CBF was above 20 mL/100 g/minute for inferior colliculus. ⁶

TcMEPs assess the integrity of the descending corticospinal tract (CST) from the primary cortex of the frontal, precentral cortex to the skeletal muscles, traversing through the corona radiata, the posterior limb of the internal capsule, the medullary pyramid, the anterior and lateral tracts of the spinal cord, the alpha motor neuron, and the neuromuscular junction. The subcortical CST pathway can be selectively affected by perforating artery injuries which may be undetected as they can occur while other neurophysiologic modalities such as SSEPs and the EEG remain unchanged. ^{2 ,​ 22} For example, during clipping of a cerebral aneurysm in the anterior and middle cerebral arteries, inadvertent occlusion of the perforating arteries (e.g., anterior choroidal artery) can lead to change in TcMEPs without significant change in SSEPs and EMPs.

Electromyography (EMG) is another neurophysiological modality which is often used during skull base surgeries for monitoring the motor branches of certain cranial nerves. However, EMG monitoring has no direct role in the management of vascular injury during skull base procedures. For this reason, cranial nerve EMG monitoring is not discussed in this chapter.

Each IONM modality has its strengths and limitations; thus, multimodality monitoring is essential in identifying ischemia during skull base procedures. The selection of IONM modalities should be guided considering the risks of the surgical procedure for each patient and the location of the pathology (▶ Table 21.1).

21.4 IONM Modalities: Technical Considerations

21.5 Anesthetic Considerations

Effects of anesthesia on IONM modalities are well documented in the literature. ^{13 ,​ 16 ,​ 24 ,​ 25 ,​ 26} Theoretically, any drug has some potential to compromise IONM while IONM may be realized under any anesthetic regimen. It depends on the dose used, the stability of the infusion, and the neurophysiologic modalities being used. Therefore, proper interaction between the anesthesiology and neurophysiology teams is crucial.

In general, cortical, polysynaptically generated responses are more affected than subcortical or peripheral responses. Anesthetic changes typically result in a symmetric decrease in the amplitude as well as a prolongation of latency of responses. It is possible, however, for previously damaged pathways to display more pronounced paradoxical, unilateral changes which can be misleading during interpretation of systemic effects of various anesthetic agents.

MEPs are particularly adversely affected by volatile anesthetic agents, while BAEP are least susceptible and SSEPs have intermediate vulnerability. TcMEPs are readily abolished with the use of pharmacological paralytic agents, inhalational agents, barbiturates, and benzodiazepines. Thus, total intravenous anesthesia (TIVA) with steady infusion rates of opioid and propofol are recommended when multimodality monitoring will be used as the TIVA technique has the least deleterious effect on MEP and SSEP recordings. Conversely, some drugs can actually enhance the evoked potential responses. These include ketamine, etomidate, or even neuromuscular blocking agents which can improve EEG, SSEP, and BAEP responses by optimizing the signal-to-noise rate due to the reduction of muscle activity. ^{26 ,​ 27}

Regarding EEG, at lower anesthetic levels, fast frequencies are common with induction agents, followed by a dose-dependent reduction in frequency and amplitude. The anesthetic-induced fast frequencies are the first to be eliminated during ischemia, which may aid in identification of perfusion asymmetries. Further increase in anesthetic concentrations results in a burst suppressed pattern of EEG and even complete cessation of all EEG activities which precludes accurate analysis of cerebral perfusion.

Of course, not all anesthetic agents follow these general principles. However, details about the effect of specific agents are beyond the scope of this chapter. For further information, targeted literature is recommended. ^{12 ,​ 24 ,​ 25 ,​ 26 ,​ 27}