This preliminary study has examined motor evoked potentials (MEPs) and inhibition of voluntary contraction induced by transcranial magnetic stimulation (TMS) of the motor cortex in the ankle flexor and extensor muscles in patients suffering from unilateral sciatica and in control subjects.

With local ethical approval and informed consent nine sciatica patients were recruited from the orthopaedic and fracture clinic at Charing Cross Hospital and compared with seven control subjects. The patients were on the waiting list for surgery or caudal epidural drug injections to alleviate the symptoms. Electromyographic (EMG) recordings were made bilaterally from tibialis anterior (TA) and lateral gastrocnemius (LGN) muscles using self-adhesive surface electrodes. TMS was delivered using a MagStim 200 stimulator connected to an angled double-cone coil, which was positioned with its cross-over located over the vertex, and the induced current in the brain in a posterior to anterior direction. The threshold (expressed as percentage of maximum stimulator output, %MSO) for inducing MEPs in relaxed muscles was assessed. TMS was delivered in steps equivalent to 0.1 X threshold starting at 1.2 X threshold and working downwards. Sets of a minimum of six stimuli were delivered both when the subject was relaxed and while making a 20 % maximum voluntary contraction (MVC) of both muscles in turn. The duration and latency of the MEPs were measured and, in experiments involving contracted muscles, duration and extent (percentage of voluntary EMG remaining) of inhibition were measured. Statistical comparisons were made within patients between the affected leg and the unaffected leg using Student’s paired t test and between patients and control subjects using Student’s unpaired t test. Statistical significance was taken when P < 0.05.

At 1.2 X threshold stimulus intensity and with subjects relaxed or contracting to 20 % MVC, there was no difference in latency or duration of the MEPs between legs in the patients or controls; the data for both the legs were therefore pooled and there were no differences between the patients and the control subjects. The duration and extent of inhibition over a range of stimulus strengths were not different between legs in the patients or between the patients and the control subjects. There were no significant differences in the thresholds for MEPs or inhibition between legs in the patients or in the controls. However, the mean (± S.E.M.) thresholds for eliciting MEPs and inhibition in TA muscles were higher in the patients (MEPs: 50.11 ± 2.40 % MSO; inhibition: 28.25 ± 1.64 % MSO) than in the control subjects (MEPs: 42.86 ± 2.59 % MSO; inhibition: 21.5 ± 1.25 % MSO). Mean thresholds in LGN were raised in the patients (MEPs: 52.00 ± 1.36 % MSO; inhibition: 25.97 ± 1.63 % MSO) compared with controls (MEPs: 46.14 ± 2.86 % MSO; inhibition: 22.43 ± 1.30 % MSO) but the differences did not reach significance.

Although the patients showed no corticospinal abnormality in their affected leg, they did exhibit a general increase in threshold for both MEPs and inhibition compared with the controls. It is possible that the chronic pain experienced by the patients has led to plasticity resulting in reduction of corticospinal drive to the legs. These changes might well help to invoke a protective stability in the legs. Investigation of these patients following remedial treatment will allow us to establish if the changes are transient in nature.

This work was supported by the Arthritis Research Campaign.