Short Latency Somatosensory Evoked Potentials Following Sural Nerve Stimulation : Origin of the Potentials and Clinical Application

Cortical and subcortical somatosensory evoked potentials were elicited by stimulation of the right sural nerve in 36 normal adults and 10 patients with myelopathy. Recordings were done using reference electrodes placed on the skin over the C7 spinous process and Fpz (International 10-20system) and recording electrodes on Fs (2 cm behind Cz), CL, CR (left and right cortex 5 cm outer Fs) and L (L1 spinous process). Major positive wave, P42 and following N52 were identified at CL, Fs and CR referred to both Fpz and C7. : The early scalp potentials recorded using a C7 reference were P26, N27, P30 and N35. In most individuals the peaks of P42 and N35 were slightly delayed at the CL relative to CR Fs, and some cases showed reversed waves at CL. Since primary sensory area for the foot is located within the interhenispheric fissure, the initially positive primary cortical response would be seen principally by electrodes placed ipsilateral to the stimulated foot and the slight differences of the electrical dipole orientation may cause P42 or N35 inversion at the CL. The delay of the peak latency of P42 and N35 at CL may be due to summation of potentials generated by a different neuronal population, perhaps the result of intracortical spread to secondary cortical areas. N35 was not identified using Fpz reference, possibly because of inphase cancellation. I suppose that P42 is generated by primary sensory cortex and N35 represents complex summation of cortical and subcortical potentials and P33 may arise in thalamus or thalamocortical projection. Absolute mean latencies of N52, P42, N35, and L were significantly correlated with body height (R=0.44‐0.67, P<0.01) and these of P42, P30 and L were also correlated with age (Sepearman's test, R=0.36‐0.46, P<0.05‐0.01). But these correlations especially that with age were in my opinion not good enough to be applicable in clinical practice for correcting latency times because of relatively large variability. In the patients with myelopathy, early potentials were not detectable in 3 cases and the delayed latencies (slower than 2 SD) were obtained in other 4 cases. All potentials were delayed in 2 cases with thoracic lesion. Mean latencies of 7 cases were significantly delayed in all 6 potentials (t test, P<0.005). Because sites of lesions of these cases were ranged from C3 to Thll, the generator site of P26 is considered to be in the ascending sensory pathway in the upper cervical cord.