Suppression and long latency excitation of single spinal motoneurons by transcranial magnetic stimulation in health, multiple sclerosis, and stroke.
Whether or not suppression at the level of the spinal motoneuron plays a role in motor deficits such as central paresis is unknown. In this study suppression in the firing of tonically active low threshold single motoneurons following low intensity transcranial magnetic stimulation is described in health and disease. Changes in firing probability in the absence of an early excitatory response were studied in a total of 14 motor units from 4 healthy subjects, 5 patients with multiple sclerosis, and 1 patient with stroke. Firing probability began to fall 18-59 ms after the stimulus and remained low for a period of 27-133 ms. There were no obvious differences between the three subject groups. The change in firing probability was not associated with specific physical signs. Late rises in firing probability were seen in 7 of the 14 motor units at latencies that were similar to the secondary peak which is known to occur with higher stimulus intensities. It is argued that the mechanism of partial suppression is not dependent on the full integrity of the pyramidal tract and is likely to involve a transient withdrawal of descending excitatory drive rather than an inhibitory postsynaptic potential at the spinal motoneuron.
Boniface
S J
SJ
University Department of Clinical Neurology, Oxford, United Kingdom.
Schubert
M
M
Mills
K R
KR
D000328:Adult; D001921:Brain / Q000473:pathology / Q000503:physiopathology*; D002561:Cerebrovascular Disorders / Q000473:pathology / Q000503:physiopathology*; D004558:Electric Stimulation; D004594:Electrophysiology; D006801:Humans; D008875:Middle Aged; D009046:Motor Neurons / Q000502:physiology*; D009103:Multiple Sclerosis / Q000473:pathology / Q000503:physiopathology*; D011930:Reaction Time; D012016:Reference Values; D013116:Spinal Cord / Q000473:pathology / Q000503:physiopathology*; D050781:Transcranial Magnetic Stimulation