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ObjectivePrevious studies have shown that cortical-evoked potentials on magnetic stimulation of muscles are influenced by muscle contraction, vibration, and muscle spasm. This study was carried out to determine whether these potentials correlate with palpatory muscle spasm, patient symptoms, and disability in patients with low back pain.MethodsA prospective observational study was performed on 13 subjects with a history of low back pain visiting an orthopedic hospital-based clinic. Patients were screened for serious pathologic conditions by an orthopedic surgeon. The patients were then evaluated for the presence of muscle spasm by one of the investigators who was blinded to the results of the evoked potential studies. Patients were asked to complete a low back pain visual analogue scale (VAS) and a Roland-Morris Activity Scale (RMAS). Cortical-evoked potentials were recorded with a magnetic stimulator placed over the lumbar paraspinal muscles with the patient in the prone position. The palpatory examination, VAS, RMAS, and the cortical potentials were repeated after 2 weeks of therapy commonly used to reduce muscle spasm.ResultsThe patients demonstrated a significant decrease in low back pain VAS and RMAS scores after treatment compared with before treatment. There was a reduction in the amount of palpatory muscle spasm in 11 of 13 cases. The cortical potentials before treatment were attenuated compared with previously reported controls and showed a significant increase before and after treatment in the amplitude of these potentials with multivariate analysis of variance. There was significant correlation between the changes in cortical potentials after treatment and the changes noted in paraspinal muscle spasm and VAS and RMAS scores.ConclusionsThis study confirms the previous report that the amplitude of cerebral-evoked potentials on magnetic stimulation of paraspinal muscles is depressed in the presence of palpable muscle spasm. The close correlation among these potentials, paraspinal muscle spasm, and clinical symptoms suggests that the measurement of muscle activity may be more important in the assessment of low back pain than is commonly accepted.

H-reflexes in normals were elicited by percutaneous electrical and magnetic stimulation of proximal nerve roots at the cauda equina. H-M interval to S1 nerve root stimulation at the level of the S1 foramen was 6.8 +/- 0.33 ms, with side to side difference of 0.16 +/- 0.13 ms. Compression/ischemia of the sciatic nerve in the mid-thigh abolished the H-reflex to stimulation of the tibial nerve at the popliteal fossa when the H-reflex to S1 nerve root stimulation was preserved. The length of the S1 nerve root in human cadavers was measured to be 17.5 +/- 03 cm, providing an estimated dorsal root conduction velocity of 67.3 m/s and a ventral root conduction velocity of 54 m/s. We conclude that the H-M interval to S1 root stimulation can provide reliable measures of conduction within the spinal canal including proximal afferents, anterior horn cells and ventral roots.

We tested the hypothesis that magnetic stimulation of muscle evokes cerebral potentials by causing a muscle contraction that then activates muscle receptors. We measured cerebral evoked potentials accompanying magnetic stimulation of muscle in 3 patients during surgery both before and after muscle paralysis with succinylcholine, a depolarizing agent. The magnetic stimulation was at low intensity (30%) and at a 2/s rate. The administration of succinylcholine sufficient to produce muscle paralysis did not alter cerebral potentials evoked by either low-intensity magnetic stimulation of muscle (gastrocnemius/soleus) or electrical stimulation of peripheral nerve (tibial nerve). In 1 normal subject, the S1 nerve root action potentials conducting at rapid velocity (> 60 m/s) were detected at the S1 foramen with a needle electrode using electrical stimulation of the tibial nerve. However, no S1 nerve root potentials could be identified to magnetic stimulation of muscle that evoked a cerebral potential. We conclude that magnetic stimulation of muscle activates terminal afferents in the muscle to provide the afferent drive for the cerebral potentials independent of muscle contraction. The failure to detect the afferent volley in S1 nerve root to magnetic stimulation suggests that only a few afferents are activated or that the activation of afferents is temporally dispersed.

Cerebral somatosensory evoked potentials (SEPs) were elicited by magnetic stimulation of paraspinal muscles unilaterally at the L2 and L5 levels in 20 healthy subjects and 16 patients with low back pain and unilateral muscle spasm. A magnetic coil with a mean diameter of 4.7 cm was placed tangentially to the skin. The stimulus strength was sufficient to induce a visible muscle twitch without producing muscle contraction in the legs. The potentials recorded over the scalp consisted of several components (P30, N40, P55, N70, and P90) and were elicited in all subjects. In both healthy and patient subjects, paraspinal muscle evoked potentials were readily elicited. Vibration applied to paraspinal muscles, as well as voluntary contraction of paraspinal muscles, was associated with attenuation of the evoked potentials. This finding suggests that muscle spindle receptors provide the afferent input responsible for the early components of the magnetically evoked cerebral potentials. In patients with unilateral muscle spasm, the amplitudes of P30-N40, N40-P50, and P50-N70 were decreased significantly on the affected side when compared with values on stimulation of the unaffected side, as well as those obtained from control subjects. The cerebral evoked potentials returned to normal amplitude when the muscle spasm subsided following a period of time and after the application of spinal manipulative therapy. The technique has potential for quantitative evaluation of muscle spasm in low back pain.

We elicited H-reflexes by magnetic and electrical stimulation of several different nerves in 10 healthy subjects and two patients with S-1 radiculopathy. The posterior tibial nerve at the popliteal fossa and the femoral nerve at the inguinal ligament were tested with both electrical and magnetic stimulation; the proximal sciatic nerve was tested only with magnetic stimulation. Muscle activity was recorded from the soleus muscle for posterior tibial and sciatic nerve stimulation and from the vastus medialis muscle for femoral nerve stimulation. No significant difference was found between the latency of H-reflexes evoked by magnetic or electrical stimulation. With magnetic stimulation, the mean (+/- SD) Ia sensory fiber conduction velocity in the proximal segment of the sciatic nerve was 72.4 +/- 3.3 m/s, while the motor nerve fiber conduction velocity in the same portion of the nerve was significantly slower, at 60.6 +/- 2.0 m/s. In two patients with unilateral S-1 radiculopathy, the latency of the H-reflex from the soleus muscle to both magnetic and electrical stimulation of the posterior tibial nerve was absent or prolonged on the affected side. Magnetic stimulation can be used to study the H-reflex and Ia fiber conduction velocity and is particularly advantageous when testing deeply located nerve trunks.