We have examined input-output patterns in the corticospinal system after incomplete spinal cord injury. The amplitude of the motor evoked potential (MEP) to transcranial magnetic stimulation (TMS) was used to study the patterns of recruitment, with increasing stimulus intensity, and facilitation, with increasing voluntary contraction, in thenar muscles of 12 patients with incomplete spinal cord injuries and 13 control subjects. The patients had all suffered spinal cord injury at a segmental level rostral to C8 and T1, the segments supplying innervation of thenar muscles. The patients showed a less pronounced increase in MEP amplitude with increasing strength of TMS compared with the controls. Specifically, at a stimulus strength of 120% threshold and above, the patients showed significantly smaller MEPs relative to the maximum ulnar nerve M-wave response than the controls. The patients also showed a less steep pattern of facilitation with voluntary drive. The MEP continued to increase up to 50% maximum voluntary contraction (MVC) whereas the controls reached a plateau around 10% MVC. The results indicate that the patients show modified corticospinal recruitment and facilitation of the motoneurone pool. We speculate that the function of the adapted corticospinal system after spinal cord injury might be to regulate and modulate drive to motoneurones originating from segmental and other descending inputs. We discuss how such a modified corticospinal system might be of functional benefit to the patients.

Objective-To investigate changes in electromyographic (EMG) responses to transcranial magnetic stimulation (TMS) of the motor cortex after incomplete spinal cord injury in humans. Methods-A group of 10 patients with incomplete spinal cord injury (motor level C3-C8) was compared with a group of 10 healthy control subjects. Surface EMG recordings were made from the thenar muscles. TMS was applied with a 9 cm circular stimulating coil centred over the vertex. The EMG responses to up to 50 magnetic stimuli were rectified and averaged. (J Neurol Neurosurg Psychiatry 1998;65:80-87) Results-Thresholds

Twenty-one patients (ages 18 ± 72 years) with iSCI (level C2 ± C7, ASIA impairment grades C ± D) and 10 healthy control subjects (ages 27 ± 57 years) were studied. Electrophysiological tests of corticospinal function were carried out using transcranial magnetic stimulation (TMS) of the motor cortex and electromyographic (EMG) recordings from thenar muscles. Both tests were performed on a number of occasions, beginning 19 ± 384 days and ending 124 ± 1109 days post-injury, and the group data were pooled into time epochs of 50 or 100 days post-injury for analysis. Seven of the patients were studied on seven or more occasions and were also assessed individually. Results: Individual and pooled data indicated that neurological scores improved progressively and tended to stabilise by around 300 days post-injury. When the patients were ®rst assessed, the mean latency for motor evoked potentials (MEPs) and inhibition of voluntary EMG were signi®cantly dierent from control values. There was no signi®cant change in latency on subsequent sessions for either the grouped or individual patient data. There was no correlation between clinical assessment and electrophysiological data. Conclusion: We conclude that the weakened inhibition seen following iSCI is established within a few days of the time of spinal cord trauma. We argue that reduced corticospinal inhibition may be a prerequisite for the recovery of useful motor function. Sponsorship: The work was supported by a project grant from The Wellcome Trust. Spinal Cord (2000) 38, 292 ± 300

Objectives-(1) A biochemical investigation of the motor cortex in patients with incomplete spinal cord injury and normal control subjects using proton magnetic resonance spectroscopy (MRS). (2) To relate any altered biochemistry with the physiological changes in corticospinal function seen after spinal cord injury. Methods-a group of six patients with incomplete spinal cord injury who showed good recovery of motor function were selected. The patients were compared with five healthy control subjects. Electromyographic (EMG) responses of thenar muscles to transcranial magnetic stimulation (TMS) of the motor cortex showed that inhibition of cortical output was weaker in the patients than the controls. Proton MRS data were collected from a plane at the level of the centrum semiovale. Two 4.5 cm 3 voxels in the motor cortex and a third voxel in the ipsilateral occipital cortex were examined in the patients and control subjects. Results-The mean level of N-acetylaspartate (NAA), expressed relative to the creatine (Cr) peak (NAA/Cr), was significantly increased in the motor cortex of the patients compared with their ipsilateral occipital cortex or either cortical area in the controls. No diVerences between patients and controls were seen for any of the other metabolite peaks (choline (Cho), glutamate/glutamine (Glx) or the aspartate component of NAA (Asp NAA )) relative to Cr. Choline relative to Cr (Cho/Cr) was higher in the motor cortex of the control subjects than in their ipsilateral occipital cortex. This diVerence was not present in the patients. Conclusions-Raised NAA/Cr in the motor cortex of the patients probably results from increased NAA rather than a decrease in the more stable Cr. The possible relevance of a raised NAA/Cr ratio is discussed, particularly with regard to the changed corticospinal physiology and the functional recovery seen in the patients. (J Neurol Neurosurg Psychiatry 1998;65:748-754)