Relationships between stimulus intensity and peak latencies and amplitudes in posterior tibial nerve somatosensory evoked potential patterns were evaluated in ten healthy subjects. Eight intermediate latency peaks between 30 and 125 milliseconds (ms) after stimulus onset and seven amplitudes were analyzed. In general, there was a decrease in latency with each increase in stimulus intensity over a five step intensity range between 5 and 19 milliamps (mA) for most peaks. Similarly, increases in amplitudes generally occurred with increases in stimulus intensity for most peaks. Later peaks N105 and P115 as well as amplitudes P90-N105 and N105-P115 were least sensitive to stimulus intensity changes. The greatest changes in peak latency and amplitude occurred as stimulus intensity was increased from 7 to 11 mA. Beyond 11 mA relatively little change was observed in either peak latencies or amplitudes. Under anesthesia, by contrast, there was no stimulus intensity-peak latency interaction and beyond 11 mA there were decreases in amplitudes. Possible reasons for these findings are discussed.
The purpose of this study was to compare in normal and traumatic brain injury (TBI) subjects long latency cortical brain-evoked potential patterns obtained upon stimulation of the median nerves. Quantitative data were analysed involving nine peak latencies and eight amplitudes obtained simultaneously contralaterally and ipsilaterally. Left-right hemispheric differences were also analysed. The following was found: TBI latencies were significantly longer for five of nine peaks (N30, P40, N60, P185, P285). TBI amplitudes were significantly smaller for two of eight amplitudes (P185-N240 and N240-P285). A significant contralateral-ipsilateral latency difference occurred only at P40 where latencies in the contralateral hemisphere are shorter for both normals and TBIs. Significant contralateral-ipsilateral amplitude differences occurred in the four early amplitudes (N30-P40, P40-N60, N60-P105, P105-N140) with amplitudes being smaller on the ipsilateral side. A differential effect, however, was found for amplitudes N30-P40 and P40-N60 where the difference is significantly larger in the contralateral hemisphere for normals but not for TBIs. This suggests that contralateral-ipsilateral amplitude difference can be a marker of extent and severity of injury and may also be helpful in localizing site of injury, particularly interhemispheric or corpus callosal injury. The differential latency and amplitude responses for later peaks occurring in the P300 region suggest sensitivity to detecting impairments in pre-cognitive and early cognitive activities.
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