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Study Design. A study of thoracic paravertebral muscle motor-evoked potentials using transcranial magnetic stimulation in spinal cord injury patients and control participants. Objectives. To develop a method to study the level and density of cortiocospinal lesions in thoracic spinal cord injury. Summary of Background Data. Cervical and lumbar spinal cord injury, unlike thoracic spinal cord injury, can be quantified by recording mussle motor evoked potentials from limb muscles. For thoracic spinal cord injury, the use of paravertebral muscles is limited by complex innervation patterns and the greater difficulty in obtaining muscle motor-evoked potentials. Methods. In 10 patients with complete midthoracic spinal cord injury (T4-T7) and 10 age-matched control participants, muscle motor-evoked potentials were recorded from all thoracic paravertebral muscles using transcranial magnetic stimulation with a double-cone stimulating coil over the vertex. Results. Its control participants, muscle motor-evoked potential responses evoked in all myotomes had progressively increasing latency in a rostrocaudal direction. Threshold was comparative in all segments. The duration of muscle motor-evoked potentials was unrelated to the spinal level. In spinal cord injury, responses were elicited in all segments above a lesion and in a varying range of segments below the lesion. In comparison with control participants, threshold was lower above and higher below the lesion (P < 0.001 in patients with spinal cord injury. Latency was longer than normal both above and below the lesion (P < 0.001). Duration was not significantly different from that in control participants at any level. Conclusions. Paravertebral muscle motor-evoked potentials can be elicited below the level of a complete spinal cord injury. Possible reasons for this include the multisegmental innervation of these muscles and the long muscle fiber conduction. Stretch reflex activation elicited by contruction of muscles above the lesion is thought to be an unlikely mechanism because of the latency of the response. Although the presence or absence of muscle motor-evoked potentials does not appear to be a sensitive indicator of the level of thoracic spinal injury lesion, analysis of muscle motor-evoked potentials reveals abnormal patterns that may assist in defining lesions. Finally, lower threshold above the lesion suggests corticospinal hyperexcitability of this pathway as a result of central plasticity after spinal cord injury.

In 1985 Barker and his colleagues (Barker et al., 1985a) produced the first practical magnetic stimulator which, when placed over the skull, was capable of exciting neurons within the human brain. The advance for the study of neural function in intact man was enormous in practical terms because the technique was non-invasive, painless and well tolerated by subjects, even children. In contrast, electrical stimulation via an electrode placed on the skull is quite painful and not well tolerated even by highly motivated subjects such as members of a research team. The application of electrical current to the scalp for stimulation of brain cells is limited by the fact that current flow is attenuated by skin and bone. The intensity of surface current needed to achieve excitation of nerve cells at a depth within the brain needs to be so high that it excites small myelinated axons and unmyelinated axons of free nerve endings in the skin of the scalp and the meninges - hence the pain. The rapidly changing magnetic field produced by a brief current pulse in a wire coil placed over the head is not attenuated by tissues of the head. Although there is a rapid decrease in intensity of the magnetic field with distance from the coil, the magnetic stimulators currently available commercially are able to stimulate neurons within the grey matter of the cerebral cortex but do not appear capable of exciting axons deep within the white matter or nuclei below the cortex.

OBJECTIVE—To assess the effect of antidopaminergic antipsychotic medication on the electromyographic (EMG) responses of thenar muscles to transcranial magnetic stimulation (TMS) of the motor cortex in schizophrenic patients. METHODS—A group of nine drug naïve schizophrenic patients was compared with a group of nine schizophrenic patients established on neuroleptic medication. Surface EMG recordings were made from the thenar muscles while patients maintained a weak isometric voluntary contraction. TMS was applied using a 9 cm circular stimulating coil centred over the vertex. The EMG responses to up to 50 magnetic stimuli were rectified and averaged. RESULTS—There was no difference in threshold TMS strength for eliciting compound motor evoked potentials (cMEPs), or in their latency, in drug naïve and medicated patients. In some patients the silent period (SP) was clearly made up of two parts and the percentage of control levels of voluntary EMG was measured in each component. During the early component of the SP there was a weaker (P0.05) in both medicated (48.2 (7.7)% of control levels) and drug naïve (58 (7.8)% of control levels) patients. CONCLUSION—The results are discussed with reference to the disrupted inhibition seen in the early part of the SP in Parkinson's disease and drug induced parkinsonism. The future uses of motor responses to TMS as a marker for the status of antipsychotic medication are considered.