Neurophysiologic effects of spinal manipulation in patients with chronic low back pain

Abstract

Background: While there is growing evidence for the efficacy of SM to treat LBP, little is known on the mechanisms and physiologic effects of these treatments. Accordingly, the purpose of this study was to determine whether SM alters the amplitude of the motor evoked potential (MEP) or the short-latency stretch reflex of the erector spinae muscles, and whether these physiologic responses depend on whether SM causes an audible joint sound.

Methods: We used transcranial magnetic stimulation to elicit MEPs and electromechanical tapping to elicit short-latency stretch reflexes in 10 patients with chronic LBP and 10 asymptomatic controls. Neurophysiologic outcomes were measured before and after SM. Changes in MEP and stretch reflex amplitude were examined based on patient grouping (LBP vs. controls), and whether SM caused an audible joint sound.

Results: SM did not alter the erector spinae MEP amplitude in patients with LBP (0.80±0.33 vs. 0.80±0.30 μV) or in asymptomatic controls (0.56±0.09 vs. 0.57±0.06 μV). Similarly, SM did not alter the erector spinae stretch reflex amplitude in patients with LBP (0.66±0.12 vs. 0.66±0.15 μV) or in asymptomatic controls (0.60±0.09 vs. 0.55±0.08 μV). Interestingly, study participants exhibiting an audible response exhibited a 20% decrease in the stretch reflex (p<0.05).

Conclusions: These findings suggest that a single SM treatment does not systematically alter corticospinal or stretch reflex excitability of the erector spinae muscles (when assessed~10-minutes following SM); however, they do indicate that the stretch reflex is attenuated when SM causes an audible response. This finding provides insight into the mechanisms of SM, and suggests that SM that produces an audible response may mechanistically act to decrease the sensitivity of the muscle spindles and/or the various segmental sites of the Ia reflex pathway.

Figure 1

The experimental setup for performing transcranial magnetic stimulation (TMS; left) to evoke motor evoked potentials (MEP; right) from the lumbar erector spinae muscles. SA=Stimulus artifact.

Figure 2

A. The experimental setup for evoking short-latency stretch reflexes from the lumbar paraspinal muscles. B. The tip of the electromechanical tapping apparatus was gradually pressed into the tissue to a pre-load of 30-Newtons was reached at which time the device delivered a rapid mechanical tap to the muscle with a net force of 90-Newtons. C. Representative examples of a short-latency stretch reflex recorded from the lumbar paraspinal muscles in response to a mechanical tap. SA= Stimulus artifact.

Figure 3

Schematic illustration of the high-velocity low-amplitude spinal manipulation technique.

Figure 4

Spinal manipulation did not alter the amplitude of the motor evoked potential (left) or short-latency stretch reflex (right) recorded from the erector spinae muscles in patients with chronic low back pain (LBP) or in asymptomatic controls.

Figure 5

Spinal manipulation did not alter the amplitude of the motor evoked potential (left) recorded from the erector spinae muscles in individuals who exhibited an audible response in response to spinal manipulation or in those who did not. Interestingly, spinal manipulation did reduce the amplitude of the short-latency stretch reflex in individuals who exhibited an audible response in response to spinal manipulation when compared to those who did not (*time × group interaction: p = 0.05; η² = 0.20).

Figure 6

A commonly proposed neural pathway suggested to form the basis of a pain-spasm-pain cycle. Specifically, it has been suggested that feedback of nociceptive afferents (N) on the gamma-motorneurons (γ) will increase the sensitivity of the muscle spindles (S) to stretch, which results in direct and indirect excitatory input (E) to the alpha-motorneurons (α) that will subsequently increase muscle activation. Reprinted from van Dieen et al., J Electromyogr Kineesiol. 13(4): 333-351, 2003.