Neurophysiologic monitoring is used during surgery to evaluate functional integrity of the central and peripheral nervous system in real-time. The goal of neurophysiologic monitoring is to identify potential neurologic deficits and alert the neurophysiologist, surgeon, and anesthesiologist of an impending injury and allow modifications in surgical interventions to prevent permanent damage and improve patient outcome. Commonly used intraoperative neurophysiologic monitoring includes electroencephalogram (EEG), somatosensory evoked potentials (SSEP), brainstem auditory evoked potentials (BAEP), motor evoked potentials (MEP), and electroneuromyography (EMG). The combination of these techniques can overcome the limitations of each individual method and increase the sensitivity to identifying an insult. It is imperative that the anesthesiologist becomes familiar with these monitoring techniques because several anesthetic drugs can affect the neurophysiological data.
The EEG is a noninvasive test that uses electrodes placed on the scalp to measure the electrical activity of the neurons in the cerebral cortex. Less frequently, a more invasive derivative technique may also be applied, with the disposition of the electrodes directly in the surgical field, which is called electrocorticography (ECoG). The data obtained from the EEG provide relevant information during surgery as ensuring electric silence during hypothermic arrest, the depth of anesthesia, and adequate cerebral blood flow. Thus, EEG monitoring has a role in cardiovascular procedures (eg, carotid endarterectomy, aneurysmal clipping), warning for signs of ischemia that are expressed by focal abnormalities in the EEG. Several other factors can affect the EEG waveforms intraoperatively such as medications, hypoglycemia, hypoxia, hypercarbia, hypothermia, and seizures (Table 28-1).
TABLE 28-1Effects of Several Factors on the EEG ||Download (.pdf) TABLE 28-1 Effects of Several Factors on the EEG
|Factors ||Effects on EEG |
|Volatile agents ||Progressive depression at higher doses; Burst suppression at approximately 1.5 MAC. |
|IV anesthetics (eg, propofol, barbiturates, etomidate, benzodiazepines) ||At higher doses, produce the typical EEG anesthetic depression pattern described with volatile agents. |
|Nitrous oxide and Ketamine ||N2O produces fast oscillatory EEG activity. Ketamine increases theta frequencies. They do not produce burst suppression. |
|Opioids ||Loss of beta waves, slow alpha waves, and increase in delta waves activity. Usually, do not produce burst suppression in clinical doses. |
|Dexmedetomidine ||Produces an EEG similar to slow-wave sleep. It does not produce burst suppression. |
|Hypoglycemia ||Increased activity in the delta and theta frequencies. |
|CBF ||Rapid and progressive changes: loss of high-frequency activity, loss of power, and EEG silence. |
The EEG data may be presented in the form of unprocessed tracings (“raw” EEG) or displayed after a computerized processing for a more manageable reading in the operating room. The analysis of the unprocessed EEG involves two main factors: frequency and amplitude. The frequency corresponds to the number of oscillations per second and is thought to have correlation with the rhythmic activity from connections between the brainstem and thalamus. There are five widely recognized ranges of frequency: Delta ...