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M Shahani

Publications and source records attributed to M Shahani.

8 recordsLinked to original sources

Long-latency spinal reflexes in humans.

Stretching human muscles with a mechanical device gave rise to multiple peaks in the rectified and averaged electromyogram. In the first dorsal interosseous the latency of the first peak (M1) was 32.4 +/- 2.4 ms (SD) and the latency of the second peak (M2) was 55.1 +/- 11.3 ms, in both cases measured from the time of the stimulus to the take-off point of the peak. Often a third peak (M3) was seen, having a considerably longer latency. The origin of peak M1 was considered to be in the stretch reflex arc because of its latency and its invariable association with muscle movement. Peak M2 was due to stimulation of afferent terminals in the skin and/or subcutaneous tissues by the mechanical device producing the muscle stretch. The conduction velocity of the pathway involved in the generation of the M1 component is the same as that for M2. This implies that central processing in the spinal cord delays the M2 response. The M2 mechanism does not involve a transcortical (long-loop) pathway because in foot muscles the M1-M2 delay remains the same as is found for hand muscles, although M1 latency is prolonged (to 39.4 +/- 6.2 ms for extensor digitorum longus). This indicates that there is not time for M2 impulses to traverse a pathway any longer than that passing to and from the spinal cord.

Afferent Pathways

Neuropathy in tetanus.

Thirty-four cases of severe tetanus were studied. On clinical examination weakness and sensory loss compatible with peripheral neuropathy was found in 27. The pattern was usually asymmetrical, the commonest nerves affected being ulnar, median and lateral popliteal, although occasionally circumflex, musculocutaneous, femoral and facial nerves were also involved. Electrophysiological studies showed spontaneous activity resembling denervation potentials, diphasic and positive sharp waves. In some muscles there was also activity resembling spontaneous firing of motor units. Motor and sensory conduction velocities in the affected nerves were moderately reduced and the amplitude of sensory potentials was also reduced. No conduction was found in 11 nerves in 8 patients on initial studies, but 4 out of 7 nerves that could be studied showed rapid recovery. Although most of the nerves in the rest of the patients showed clinical recovery, conduction velocities showed improvement most often when examined about 10 weeks after the onset of trismus. The clinical and electrophysiological evidence suggests the involvement of peripheral nerves in severe tetanus. Serum neuritis, hypersensitivity reaction to tetanus toxoid or drug-induced neuropathy have been ruled out.

Adolescent