Factors affecting SSEP
Last updated: 06/03/2016
Recordings for SSEPs (somatosensory evoked potentials) are generated at a peripheral nerve, and recorded at the cortical or subcortical level. The signal travels via a peripheral nerve to the appropriate dorsal root ganglion, into the posterior spinal column, the medial lemniscus to the thalamus, and then to the sensory cortex.
The signal is broken down into two readings: amplitude, and latency. Amplitude is the voltage difference from the signal origin to what is recorded. A change in amplitude is more sensitive of neurologic damage than are changes in latency. Latency is the time from stimulation to the time of response. An increase in time by 50% from the baseline is considered significant.
Anesthetics have an impact on the readings:
- Volatile agents: Increase latency and decrease amplitude; predominantly by attenuating transmission at synapses. Up to 1 MAC, however, is generally well tolerated.
- Nitrous: No change in latency, but there is a greater decrease in amplitude than volatiles at equipotent MAC.
- Propofol: induction doses typically have minimal effect. Initiation of TIVA with propofol and opioids may cause a temporary increase in latency and decrease in amplitude that may resolve in approximately 30 minutes.
- Etomidate: Increases amplitude by 4 times for cortical readings.
- Ketamine: Increases cortical amplitude readings; but no change in subcortical readings.
- Opioids, benzodiazepines, and dexmedetomidine: Minimal effect
- Paralytics: No effect.
- Regional anesthesia: decreases or completely blocks recordings.
- Hypotension: Decreases amplitude; no change in latency
- Hypothermia: Increases latency; SSEPs may be unchanged
- Hypocarbia: Decreases latency; no change with amplitude
- Hypercarbia: Has no effect if mild
- Hypoxia: no effect until ~PaO2 of 50mmHg; after which there is an increase in latency and decrease in amplitude
- Hemodilution: Amplitude increases with a Hct between 16-20% and decreases if falls below 16%.
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