Boniface, Simon John; (1991) Response of single spinal motoneurones to transcranial magnetic simulation in healthy subjects and patients with upper motor neurone disorders. Doctoral thesis (M.D), UCL (University College London).

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Abstract

The problem addressed by this study was: How does the human corticospinal tract influence the discharge of spinal motoneurones and what are the effects of neurological disease? The method employed was to study the firing probability of 78 tonically active single motor units of the upper limb following transcranial magnetic stimulation. This was performed in healthy subjects and in a group of patients with different upper motor neurone (UMN) disorders. The inducing current flowed in an anticlockwise direction through a circular coil which was positioned tangentially at the vertex. Two peaks were produced in the peri-stimulus time histogram. The primary peak (PP) had an onset latency in healthy subjects ranging from 13 ms (deltoid and biceps) to 31 ms (first dorsal interosseous muscle) (FDI) and had a short duration of 4.6 ±1.7 ms (mean ± SD). PP frequently consisted of 1-3 sub-peaks, with a mean intermodal interval of 1.4 ms for FDI and 2.9 ms for forearm and upper arm muscles. This interval probably reflects the maximal rise time of one in a sequence of excitatory postsynaptic potentials (EPSPs) at the motoneurone. An increase either in the interval between the stimulus and the preceding voluntary discharge, or in the intensity of stimulation, raised the probability of discharges occurring within PP and influenced their latency. The secondary peak (SP) had an onset latency in FDI ranging from 56-90 ms and a long duration of 20.9 ±12.0 ms. Evidence suggests that SP was caused by the rising phase of a late EPSP mediated via a pathway which included a peripheral afferent component. When compared with healthy subjects, PP in UMN patients was found to be either normal, absent, delayed and dispersed (by up to 28 ms and 21 ms, respectively) or found to consist of sub-peaks with abnormally long inter- modal intervals. These findings suggest specific mechanisms including cortical inexcitability, variable degrees of slowing in the velocity of propagation in descending fibres, frequency dependent conduction block, delay between EPSPs caused by the operation of more than one pathway and ineffective spatial or temporal summation at the spinal motoneurone.

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