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SSEP and anesthetics




General anesthesia has an inhibitory effect on neurotransmission and, therefore, on the EP. The effect of anesthetics is greater on synaptic transmission than on axonal conduction. For this reason, responses recorded from polysynaptic pathways (e.g., cortical recordings) are affected by anesthesia to a much greater extent than those recorded from oligosynaptic pathways (e.g., spinal cord and subcortical recordings).”

All volatile anesthetics produce a dose-dependent increase in SSEP latency and a decrease amplitude. All volatile anesthetics, even at concentrations above 1.0 MAC, only minimally affect the sub-cortical waveform, resulting in high recordability and reliability.

The effect of volatile anesthetics on cortical SSEP amplitude is compounded by nitrous oxide.

Intravenous anesthetics generally affect SSEPs less than inhaled anesthetics do.

Etomidate and ketamine increase SSEP amplitude.

Propofol, midazolam, and barbiturates have a moderate depressant effect on SSEP amplitude.

In a normothermic individual, SSEP monitoring can detect cerebral ischemia during barbiturate anesthesia at doses that induce burst suppression.

Most authors report minimal to no effect of opioids on SSEP amplitude.

Dexmedetomidine affects SSEP amplitude minimally at sedative doses. During isoflurane anesthesia, dexmedetomidine blunts the effect of isoflurane on SSEP amplitude

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