• Pietro Cariga, Maria Catley, Alexander V Nowicky, Gordana Savic, Peter H Ellaway, and Nicholas J Davey.
• Department of Sensorimotor Systems, Faculty of Medicine, Imperial College School of Science, Technology and Medicine, Charing Cross Hospital, London, United Kingdom.
• Spine. 2002 Jul 1;27(13):1438-43.

Study DesignA study of thoracic paravertebral muscle motor-evoked potentials using transcranial magnetic stimulation in spinal cord injury patients and control participants.ObjectivesTo develop a method to study the level and density of corticospinal lesions in thoracic spinal cord injury.Summary Of Background DataCervical and lumbar spinal cord injury, unlike thoracic spinal cord injury, can be quantified by recording muscle 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.MethodsIn 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.ResultsIn control participants, muscle motor-evoked potential responses evoked in all myotomes had progressively increasing latency in a rostrocaudal direction. Threshold was comparable 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.ConclusionsParavertebral 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 contraction 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 cord 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.

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