Motor facilitation and sensory inhibition after spinal manipulation: a transcranial magnetic stimulation study

Abstract

J. Donald Dishman, DC, MSc, Kevin Ball, PhD, Seneca Falls, NY, USA; Patrick Zhu, MD, Syracuse, NY, USA; Jeanmarie Burke, PhD, Seneca Falls, NY, USAIntroduction: Despite the widespread use of spinal manipulative therapy (SMT) in the management of low back pain patients, the neurophysiologic mechanism in which SMT may reduce pain and muscular spasm has not been elucidated. One such mechanistic theory proposed is that SMT may intervene in the cycle of pain and spasm by affecting the resting excitability of the motoneuron pool (MNP) in the spinal cord. Previously reported data indicate that SMT leads to attenuation of the excitability of the MNP, when assessed by means of peripheral nerve Ia afferent stimulation using the Hoffmann reflex (H-reflex) [1]. The purpose of this study was to determine the effects of lumbar SMT on the excitability of the MNP, as assessed by means of transcranial magnetic stimulation (TMS) and the H-reflex. The TMS technique allows for assessment of the excitability of the MNP as a result of direct corticospinal activation, rather than through peripheral Ia fiber stimulation. Thus, a more direct assessment of MNP excitability can be obtained.Methods: Healthy young adult subjects were recruited for participation (n=12; 25.1±3.96 years; 177.5±8.11 cm; 79.6±14.09 kg). The local ethics committee approved all procedures. Subjects were placed supine on a treatment table. The right ankle was positioned at an angle of 90 degrees. Motor evoked potentials (MEP) were recorded subsequent to TMS. A 9-cm-diameter circular coil was centered over the vertex with a clockwise coil current. Stimulus intensity was set at 100% of the maximum stimulus output. MEP peak-to-peak amplitudes in the right gastrocnemius muscle (GM) were measured before and after a homolateral L5–S1 spinal manipulation. The amplitude of 10 MEP responses were measured at a rate of 0.05 Hz as prebaseline values. Immediately after the procedure, 10 MEP responses were measured at a rate of 0.05 Hz, and then at 5 and 10 minutes postprocedure. The subjects returned 48 hours later for a follow-up session in which tibial nerve H-reflexes were performed in the same pre-post SMT protocol as with the MEPs. The tibial nerve H-reflex as per the method of Hugon [2] was used. Separate, single-factor repeated measures analysis of variance models were used to determine the effects of a L5–S1 SM procedure on MEP amplitudes and H/Mmax ratios. The Dunnett's procedure for a priori contrasts was used to detect any differences between baseline values and postmanipulation time points for each evoked response, MEP amplitudes and H/Mmax ratios. An optical tracking system (system error <0.10 mm RMS) was used to monitor the three-dimensional position and orientation of the TMS coil, in real time, for each trial. Two clusters of four infrared LEDs were affixed to both the subject's face and to the TMS coil to provide these measurements.Results: There was a significant increase in MEP amplitudes from 20 to 60 seconds, after SMT (p<.05). There was a significant decrease in H/Mmax ratios from 10 to 40 seconds, after SMT (p<.05). The relationship between the prebaseline evoked responses, MEP amplitudes and H/Mmax ratios, was low (r=.14). Immediately after manipulation, the relationship between the amount of MEP facilitation and the amount of H/Mmax ratio inhibition was moderate (r=−.41). The optical monitoring precision results for coil placement revealed that there was no significant deviation of coil placement throughout the experiment.Conclusion: There was a different modulation of MEP amplitudes and H/Mmax ratios after a L5–S1 SM procedure. Physiologic differences between MEP amplitudes and H/Mmax ratios include activation patterns of spinal interneurons, the influence of presynaptic inhibition of Ia afferents and recruitment patterns among motoneurons. The increase in MEP amplitudes suggests that SMT may increase the ratio of EPSPs to IPSPs by altering the excitability of interneurons contacted by Ia and Ib afferents, as well as by cutaneous and joint afferents. Concurrently, SMT may increase presynaptic inhibition of Ia afferents, as evidenced by attenuation of H/Mmax ratios. Cortical excitability changes and the intrinsic susceptibility of different populations of motoneurons to EPSPs and IPSPs are two other potential mechanisms to explain the difference in the modulation of MEP amplitudes and H/Mmax ratios after a L5–S1 SMT procedure. Thus, SMT may involve two basic physiologic responses: a central motor facilitation and a peripheral sensory inhibition. These basic neurophysiological responses to SMT require further research to determine the possible role they may play in the effect of SMT on pain and spasm in the mechanical low back pain population.