is also variable, although the chances of seizurefree outcome are improved if there is no evidence of persistent epileptiform activity following resection. A comprehensive discussion about the use of ECoG in the management of primary epilepsy remains beyond the scope of this chapter.

Somatosensory Evoked Potentials

Neurosurgical monitoring of sensory evoked potentials (SEPs) relies on the recognition of characteristic alterations in the excitable properties of compromised neurons. These alterations generally occur before the onset of irreversible damage and can thus theoretically guide or alter the subsequent surgical technique. Evoked potential recordings, in contrast to those obtained via EEG, can only be generated via the use of external stimuli of various means. In general, SEPs used in intraoperative monitoring are generated by applying a peripheral stimulus to the particular sensory modality that carries its signal through the neurological region at risk, with recordings being taken at standardized points along the afferent pathway that allow for the assessment of both amplitude and latency of the signal. These stimuli can take the form of peripheral nerve shocks for somatosensory evoked potentials (SSEPs), trains of auditory clicks for brainstem auditory evoked potentials (BAEPs), or flashes of light for visual evoked potentials (VEPs). Waveforms of the SEPs are amplified and undesirable background noise may be filtered out. Prolongation of signal latency or decreased amplitude suggests diminished function at some point along the sensory pathway.

For the interpretation of SSEP data, adequate analysis of the waveforms requires averaging of at least 100 responses to provide reliable and clear waveform morphology. The rate of stimulation is usually 4-5 Hz, which minimizes acquisition time without inducing attenuation of the cortical response. Therefore, feedback can be provided to the surgeon about every 30-60 seconds. It is optimal to perform bilateral recordings, which allows the contralateral hemisphere to serve as an internal control. Components of the evoked response recording are labeled as either positive or negative, relative to a reference electrode, followed numerically by their modal peak latency in milliseconds. As an example, characteristic median nerve SSEP waves should include N13, P14, N20, P20 and P25 peaks (Fig. 1.2). The clival area generates the N13 deflection and reflects activation of the caudal medial lemniscus. Thalamocortical afferent activity is represented by the P14 wave, and N20 is associated with activation of cortical neurons in the primary somatosensory cortex. The latency difference between N13 and N20 is referred to as the "central conduction time" (CCT).

There are several variables that must be taken into consideration when using SSEP during neurosurgical procedures. Factors that can alter SSEP performance intraoperatively include anesthetic depth and type, patient temperature, blood pressure, limb positioning, and specific placement of stimulator and recording electrodes. In general, anesthetics cause an attenuation of the cortical components of the SSEP, such as N20, while the subcortical components remain resistant. Wave amplitudes are reduced and latencies are prolonged in a dose-related manner, particularly with the halogenated agents. Several exceptions include etomidate and ketamine, which can enhance the amplitude of the cortical components. Baseline recordings are crucial for evaluating changes that occur as a result of the operative procedure; individuals with carotid stenosis often demonstrate prolonged baseline CCTs and decreased amplitudes of various cortical responses.

SSEP monitoring has been used as an indicator of cerebral ischemia in much the same way as EEG. However, SSEP has several advantages over EEG as an intraoperative monitoring technique, which include greater relative resistance to general anesthesia, fewer electrode sites, and comparative ease of recording and interpretation. Generally, reductions in SSEP amplitudes are initiated by decreased cerebral oxidative mechanisms rather than by permanent neuronal damage. Decreases in CBF leading to SSEP changes parallel those causing noticeable EEG changes. Fisher et al. summarized a series of seven studies that analyzed outcomes of CEA as a function of SSEP changes. Of the total of 3,028 patients in all studies, 5.6% demonstrated a significant decline of SSEP as a direct result of surgical manipulation. Among these individuals,

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