Takumi Emori

The effect of stimulus rate upon common peroneal, posterior tibial, and sural nerve somatosensory evoked potentials

We examined the effect of stimulus rate on somatosensory evoked potentials (SEPs) following stimulation of the common peroneal nerve (CPN) at the knee, and the posterior tibial nerve (PTN) and sural nerve (SN) at the ankle. We measured the amplitude of P40-N50 and N50-P60 in the PTN-SEP and corresponding amplitude of CPN-SEP and SN-SEP at the rate of 2.3, 3.4, 4.1, and 5.1 Hz. When the stimulation rate was increased from 2.3 to 5.1 Hz, the P40-N50 amplitude decreased by 50% for the CPN-SEP and 20% for the PTN-SEP. Also, the N50–P60 amplitude was reduced by 30% in the CPN-SEP and 20% in the PTN-SEP. In contrast, this change in stimulus rate produced no significant amplitude decline in the SN-SEP. Blocking the peroneal nerve with lidocaine just distal to the stimulating electrodes eliminated the descending peroneal nerve volley and abolished the amplitude attenuation observed with the faster stimulus rate. The findings suggest that at higher rates of stimulation, the afferent volleys induced by the movements that follow mixed nerve stimulation interfere with the SEP produced by electrical activation of the sensory afferents. The interference is greater when the more proximal site of the mixed nerve is stimulated.

Presence of two subcomponents in P9 far-field potential following stimulation of the median nerve

Close scrutiny of scalp recorded P9 far-field potentials following stimulation of the median nerve often revealed dilobed wave forms. We observed that the P9 became 2 distinct peaks (P9a and P9b) when the arm was flexed 90 degrees forward at the shoulder and that it became a pointed single peak with 90-170 degrees lateral abduction of the arm. A simultaneously recorded stationary negative peak (N9), registered over the stimulated arm with the use of a distant reference, also showed similar changes, a dilobed configuration (N9a and N9b) with forward flexion and a single peak with lateral abduction. The latencies of the scalp recorded P9a and P9b and arm recorded N9a and N9b were close but not exactly the same. Nevertheless, the latencies of the scalp-positive and arm-negative peaks shifted in nearly a parallel fashion by changing the arm positions. These findings suggest that the change of axial orientation of the propagating nerve impulse plays an important role for the rise of P9a and that the change of volume geometry surrounding the nerve contributes to the P9b generation. Also, the scalp recorded P9 and arm recorded N9 are one and the same, and oriented with dipole fields extending from the arm, body and to the scalp.