Latency and duration of the muscle silent period following transcranial magnetic stimulation in multiple sclerosis, cerebral ischemia, and other upper motoneuron lesions.
In muscles with sustained voluntary contraction, EMG activity is transiently inhibited after transcranial magnetic stimulation. We recorded this postexcitatory silent period (SP) at 1.5 times individual stimulus threshold level from the first dorsal interosseus muscle in 65 neurologic patients aged 11 to 80 years. When compared with 20 healthy volunteers and a subgroup of patients with peripheral neurologic conditions not affecting the tested pathways, the SP was significantly longer on the paretic side in cerebral ischemia (p < 0.001) and chronic inflammatory CNS diseases, such as multiple sclerosis or neurosarcoidosis (p < 0.01). There was a similar tendency in pyramidal tract lesions due to CNS tumors and spinal cord trauma. In lesser degrees of paresis, SP duration is more sensitive than central motor conduction time (CMCT), but its specificity awaits further evaluation. SP is dependent on the integration of motor excitatory and inhibitory pathways and, possibly, sensorimotor reflex systems. In contrast to SP duration, which proved to be an independent variable giving supplementary information over the usual CMCT measurement, SP onset latency correlates well with CMCT and peripheral nerve conduction slowing, as in polyradiculoneuritis.[1]References
- Latency and duration of the muscle silent period following transcranial magnetic stimulation in multiple sclerosis, cerebral ischemia, and other upper motoneuron lesions. Haug, B.A., Kukowski, B. Neurology (1994) [Pubmed]
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