Suppression of motor neuron firing by transcranial magnetic stimulation in a patient with multiple sclerosis.
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Biofeedback, Psychology↗
Biomedical subjects
S J Boniface
Publications and source records attributed to S J Boniface.
Responses of single spinal motoneurons to magnetic brain stimulation in healthy subjects and patients with multiple sclerosis.
Magnetic stimuli delivered over the scalp can cause single motor units to discharge in intrinsic hand muscles. The discharge characteristics of 26 tonically active, low threshold single motor units in the first dorsal interosseous muscle of 13 healthy subjects and of 21 motor units in 9 patients with multiple sclerosis (MS) were studied. Up to 500 transcranial magnetic stimuli were delivered at the vertex and were given randomly with respect to, or at a fixed delay after, the previous voluntary discharge. Peristimulus time histograms (PSTHs) of motor unit discharges were constructed. In healthy subjects, two periods of increased firing probability were seen at onset latencies of 20-31 ms and 56-90 ms after the stimulus. These periods have been termed the primary peak and the secondary peak. The primary peak had a mean duration of 4.6 ms and was found to be multimodal in 17 motor units. Subpeaks had intermodal intervals of between 0.6 and 2.4 ms. Subpeaks probably result from a sequence of excitatory postsynaptic potentials (EPSPs) induced at the motoneuron by corticospinal impulses. In patients with MS, the primary peak could be absent, delayed in onset, of increased duration without discernible subpeaks, or showing increased intermodal intervals between subpeaks. In 3 motor units from patients with MS, PSTHs with normal features were found. It is postulated from this study of the corticospinal inputs to single motoneurons that motor impairment in MS can be due to a number of mechanisms including slowed conduction in corticospinal fibres, dispersion of arrival times of corticospinal impulses at spinal motoneurons and conduction block in corticospinal fibres, which may be frequency dependent.
Adult↗
Origin of the secondary increase in firing probability of human motor neurons following transcranial magnetic stimulation. Studies in healthy subjects, type I hereditary motor and sensory neuropathy and multiple sclerosis.
In tonically active human motor neurons serving upper limb muscles there is a late rise in firing probability following transcranial magnetic stimulation termed the secondary peak (SP). The aim was to study the mechanism of SP and the pathway that mediates it. For this purpose, the response to transcranial magnetic stimulation of 62 repetitively firing low threshold single motor units from upper limb muscles was studied with peri-stimulus time histograms in 8 healthy subjects and in 13 patients with either Type I hereditary motor and sensory neuropathy (HMSN) or multiple sclerosis (MS). Separate peri-stimulus time histograms, constructed for trials in which the motor unit fired in the primary peak (PP) and those in which it fired in SP, showed that SP was not caused by a resumption of firing after the preceding PP. In the first dorsal interosseous muscle, the observed increase in the interval between PP and SP in patients with either HMSN or MS, when compared with healthy subjects, suggested that the pathway mediating SP had both peripheral and central components. Evidence for a peripheral component was substantiated by the observed slope of the line relating the latency of SP in different upper limb muscles to peripheral conduction distance, which was more than 3 times greater than that for PP, and by comparisons in the same motor unit made between the latency of responses to finger taps and to transcranial magnetic stimulation. Evidence for the origin of SP was consistent with a long loop reflex, or with collateral activation of gamma motor neurons and subsequent motor neuron firing from muscle afferent inputs. SP discharges were found to occur earlier than expected on the basis of the spontaneous motor unit firing rate, suggesting that SP was caused by the rising phase of an excitatory post-synaptic potential, rather than by the decay of an inhibitory postsynaptic potential.
Action Potentials↗
The firing probability of single motor units following transcranial magnetic stimulation in healthy subjects and patients with neurological disease.
Magnetic stimuli applied to the scalp can cause single motor units (MUs) to discharge in intrinsic hand or more proximal arm muscles. MUs are much more likely to be fired by stimuli if they are being activated voluntarily at the same time. The changes in firing probability induced by magnetic stimuli in such tonically active MUs have been studied in healthy subjects and patients using peri-stimulus time histograms (PeSTHs). The mean firing level in the 250 msec before the stimulus, was used to define 2 peaks of increased firing after the stimulus. The first, termed the primary peak (PP), was always present, had an onset latency in first dorsal interosseous (FDI) muscle of 20-31 msec and was short in duration (mean 4.9 msec). A second increase in firing probability, the secondary peak (SP), was present in about half the FDI MUs studied, had a mean peak latency of 81.5 msec and had a duration up to about 40 msec. PP often consisted of a number of sub-peaks with intermodal intervals of around 1.5 msec. It is believed that PP is the result of activation of corticospinal (CS) fibres making monosynaptic connections and that sub-peaks within PP are due to the arrival at the motoneuron of successive CS impulses produced by the stimulus. SP is probably due to operation of other excitatory inputs to the motoneuron. In patients, a number of different abnormalities have been identified. PP has been found to be normal, absent, delayed and dispersed or having abnormally separated sub-peaks. Clearly the technique is a powerful tool for dissecting abnormalities in CS projections at the synaptic level.
Action Potentials↗
[Changes in the responses of motor units to transcranial magnetic stimulation in patients with multiple sclerosis and stroke].
In multiple sclerosis and stroke the muscle responses to transcranial magnetic stimulation are frequently delayed, reduced in amplitude or absent. To investigate the underlying pathophysiological mechanisms, responses of single motor units to transcranial magnetic stimulation were analysed using peri-stimulus time histograms. The following response patterns were detected: 1. prolongation of latency and duration of the primary peak which occurs in healthy controls 17 to 30 ms after the stimulus and has a duration of 2 to 8 ms, 2. lack of an excitatory response, 3. prolongation of the interval between sub-peaks within the primary peak and 4. multimodal responses. Possible mechanisms for these changes are: reduction and dispersion of conduction velocities in corticospinal axons associated with impaired summation of excitatory post-synaptic potentials at the spinal motoneurone, frequency-dependent or complete conduction block in corticospinal neurones and compensatory activation of other descending motor pathways.
Adult↗