What is the physiologic basis of somatosensory evoked potentials (SEPs)?

Updated: Oct 25, 2019
  • Author: Andrew B Evans, MD; Chief Editor: Selim R Benbadis, MD  more...
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Large-diameter group Ia fibers and group II cutaneous afferents are primarily responsible for SEPs. Because of the ease of delivery and quantification, electrical stimulation is typically used, though other types of sensory stimuli have been tried with success. When a mixed nerve is stimulated, Ia muscle afferents are activated. In the spinal cord, the dorsal columns are mainly responsible for conduction of the activity that generates the SEP. In the brain, the lemniscal and thalamocortical pathways are involved. Extralemniscal pathways also may play a role.

Drews et al, in a study investigating the contribution of group I muscle afferent activation to the production of H reflexes and SEP in humans, found that in most subjects, H reflex was correlated with SEP size. [39] If 2 identical stimuli were applied to the posterior tibial nerve with an interval of 1 sec, the second H reflex was 30% smaller than the first one. The corresponding SEPs were reduced only slightly. Postactivation depression presumably results from intrinsic properties of synapses of group I muscle afferents.

In this study, electrical stimuli were applied to the tibial nerve in the popliteal fossa to study how the information is transferred from group I muscle afferents to motor neurons and to the somatosensory cortex. [39] For control purposes, identical stimuli were applied to the skin. The SEP evoked by skin stimulation alone had a peak latency that was 5 msec longer than the SEP to transcutaneous nerve stimulation. The threshold intensity to evoke an H reflex was at least twice as high as the threshold for an SEP.

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