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ORIGIN OF COMPONENT N16 IN SHORT LATENCY SOMATOSENSORY EVOKED POTENTIALS (SSEP) TO MEDIAN NERVE STIMULATION:CORRELATION BETWEEN COMPONENT N16 AND THALAMUS Ei-ichirou Urasaki 1 , Yasuhiko Matsukado 1 , Shin-ichi Wada 1 , Shinji Nagahiro 1 , Chikahide Yadomi 1 , Akinobu Fukumura 2 1Department of Neurosurgery, Kumamoto University Medical School 2Neurosurgical Section, Shimonoseki Kosei Hospital pp.393-402
Published Date 1985/4/1
DOI https://doi.org/10.11477/mf.1406205500
  • Abstract
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Short latency somatosensory evoked potentials (SSEP) to median nerve stimulation consists of four main subcortical components, namely P 9, P 11, P 13 and N 16 which appears before cortial N 18. However, the origin of component N 16 is a subject of controversy.

In an attempt to learn about the generator source (s) of component N 16, SSEP was recorded from 25 patients with various focal lesions of the brain stem and/or thalamus, and abnormalities of the each potential was correlated to the clinically and radiologically defined site of the lesions. Furthermore, the effects of the different frequency in stimulation were also investigated in 6 normal subjects, because latency changes of each compo-nent might contribute to the understanding of the generation.

Recordings were obtained from 13 patients with brain stem lesion which included 3 cases with pontine hemorrhage, 3 cases with pontine tumor, 3 cases with cerebello-pontine angle tumor, one case of pontine angioma, one case of chordoma, one case of tentorial tumor and one case of MLFsyndrome. SSEP changes in these cases were clas-sified into four types as follows : type 1 ; no re-sponse over the base line was recorded, type 2 ; some responses over the base line were recorded but N 16 was uncertain, type 3 ; component N 16 was cleary identified but its latency was signifi-cantly prolonged, type 4 ; component N 16 was divided into two peaks. Bilateral abnormality on SSEP with splitted combination of these four types in various degree was obseved. Furthermore, these SSEP abnormalities were seen even in the some cases without sensory disturbance.

On the other hand, component N 16 was clearly identified in all 12 patients with thalamic lesion which included 11 cases with thalamic hemorrhage and one case with thalamic tumor on the effected side. Comparison of latency and amplitude bet-ween normal side and affected side statistically showed no laterality of components P 9, P 11 and P 13, but a tendency of delay in latency of com-ponent N 16 on the affected side.

Different stimulus repetition rate revealed some other characteristics of each component. Electrical stimuli to median nerve at the wrist were deli-vered at rates of 3, 6, 9, 12, 15, 18, 21, 24 and 27 Hz. Latencies of components P 9, P 11, P 13, N 16 in Fro.-Cv 7 lead and component N 18 in Par.-Erb lead were measured and all latency changes werecaluculated relative to the 3 Hz stimulation. P 9 and P 11 showed continually stable in latency through 3 to 27 Hz, while P 13, N 16 and N 18 were prolonged in latency with increasing rate. Especially, N 18 could not be obtained in 2 sub-jects when the rate of stimulation was up to 9 or 12 Hz. Comparison between the latency changes of P 9 and those of following components under the same stimulus rate was carried out statistically. The test showed no significant difference at all stimulus rates between P 9 and P 11, however, P 13 was significantly prolonged than P 9 at 24 Hz stimulation and N 16 and N 18 were also signifi-cantly prolonged than P 9 when the stimulation was up to 12 Hz.

The suggestion was made that P 9 and P 11 were generated by the first order neurons and P 13 was a potential interposed by the synaptic event, while N 16 and N 18 were potentials inter-posed by two or more synaptic events.

In conclusion, the result of this study indicated that component N 16 mainly reflected the activi-ties of the subthalamic source (s), especially, it was strongly suggested collateral branch from the me-dial lemniscal pathway in the brain stem region was important for the generation of component N 16.


Copyright © 1985, Igaku-Shoin Ltd. All rights reserved.

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電子版ISSN 2185-405X 印刷版ISSN 0006-8969 医学書院

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