In summary, this study has revealed that corticospinal excitability, driving ES muscles close to the site of pain, is lowered in patients with chronic low back pain.

Trunk muscles receive corticospinal innervation ipsilaterally and contralaterally and here we investigate the degree of ipsilateral innervation and any cortical asymmetry in pairs of trunk muscles and proximal and distal limb muscles. Transcranial magnetic stimulation (TMS) was applied to left and right motor cortices in turn and bilateral electromyographic (EMG) recordings were made from internal oblique (IO; lower abdominal), deltoid (D; shoulder) and first dorsal interosseus (1DI; hand) muscles during voluntary contraction in ten healthy subjects. We used a 7-cm figure-of-eight stimulating coil located 2 cm lateral and 2 cm anterior to the vertex over either cortex. Incidence of ipsilateral motor evoked potentials (MEPs) was 85% in IO, 40% in D and 35% in 1DI. Mean (+/- S.E.M.) ipsilateral MEP latencies were longer ( P<0.05; paired t-test) than contralateral MEP latencies (contralateral vs. ipsilateral; IO: 16.1+/-0.4 ms vs. 19.0+/-0.5 ms; D: 9.7+/-0.3 ms vs. 15.1+/-1.9 ms; 1DI: 18.3+/-0.6 ms vs. 23.3+/-1.4 ms), suggesting that ipsilateral MEPs were not a result of interhemispheric current spread. Where data were available, we calculated a ratio (ipsilateral MEP areas/contralateral MEP areas) for a given muscle (IO: n=16; D: n=8; 1DI: n=7 ratios). Mean values for these ratios were 0.70+/-0.20 (IO), 0.14+/-0.05 (D) and 0.08+/-0.02 (1DI), revealing stronger ipsilateral drive to IO. Comparisons of the sizes of these ratios revealed a bias towards one cortex or the other (four subjects right; three subjects left). The predominant cortex showed a mean ratio of 1.21+/-0.38 compared with 0.26+/-0.06 in the other cortex ( P<0.05). It appears that the corticospinal control of IO has a strong ipsilateral component relative to the limb muscles and also shows hemispheric asymmetry.

Clinical practice and scientific research may soon lead to treatments designed to repair spinal cord injury. Repair is likely to be partial in the first trials, extending only one or two segments below the original injury. Furthermore, treatments that are becoming available are likely to be applied to the thoracic spinal cord to minimise loss of function resulting from damage to surviving connections. These provisos have prompted research into the improvement of clinical and physiological tests designed (1) to determine the level and density of a spinal cord injury, (2) to provide reliable monitoring of recovery over one or two spinal cord segments, and (3) to provide indices of function provided by thoracic spinal root innervation, presently largely ignored in assessment of spinal cord injury. This article reviews progress of the Clinical Initiative, sponsored by the International Spinal Research Trust, to advance the clinical and physiological tests of sensory, motor and autonomic function needed to achieve these aims.

Objective: The clinical and functional assessment of back muscles in human spinal cord injury (SCI) has received little attention. The aim of this study was to develop a method to assess the level of a thoracic spinal cord lesion based on the reflex activation of back muscles. Methods: In 11 control subjects and in 12 subjects with clinically complete thoracic SCI (T2-T12), either a spinous process or an erector spinae muscle was prodded to elicit short latency reflexes recorded electromyographically at the spinal level of stimulation. An electromagnetic servo, attached to a blunt probe, applied stimuli at a frequency of 1 Hz and amplitude of 3 mm. Two trials of 50 mechanical prods were conducted at each site. Results: Reflexes were evoked in control subjects in 82% of trials when the spinous process was prodded, and in 80% of trials when the muscle was prodded. In contrast, reflexes in SCI subjects could be elicited in 90-100% of trials two segments either above or below the lesion. Reflex responses in control subjects had a mean (SEM) latency of 5.72 (0.53) ms when the spinous process was prodded, and 5.42 (0.42) ms when the muscle was prodded. In the SCI subjects, responses had slightly (but insignificantly) longer latencies both above and below the lesion to either stimulus. The amplitude of reflex responses, expressed as a percentage of the background EMG, was on average 2-3 times larger at the three vertebral levels spanning the lesion in SCI subjects than at sites above or below the lesion or at any level in control subjects. Conclusion: We propose that the size of these mechanically evoked reflexes may be useful in determining the level of thoracic SCI. Furthermore, the reflexes might provide a valuable tool with which to monitor recovery after an intervention to repair or improve function of a damaged spinal cord.