The Journal of Pain
Volume 20, Issue 4, Supplement, April 2019, Page S69
K.Webe
Spinal manipulation (SM) is commonly used when managing patients with neck and back pain. The rationale regarding the use of SM has long been supported by the clinical opinion that a mechanical effect on the spine leads to therapeutic mechanical changes within the spine. However, a purely biomechanical mechanism remains controversial and speculative as studies have failed to link specific mechanical effects to meaningful subjective or objective improvement. SM’s therapeutic action may instead be mediated at the level of the central nervous system. Here, we use functional magnetic resonance imaging in 10 healthy volunteers (5 women, age=31.2±10.0 years) to study the effect of SM on pain-related activity within brain regions predictive of physical pain using the Neurologic Pain Signature (NPS). Functional imaging was performed with 5 minute runs of alternating 15 s blocks of noxious mechanical stimulation of the right index finger cuticle before and after thoracic SM. Evoked pain intensity (p<0.001) and NPS activation (p=0.020) significantly decreased following SM, and the changes in evoked pain and NPS activation were significantly correlated (r2=0.418, p=0.032). Within the different NPS sub-regions, activation within the dorsal anterior cingulate cortex (dACC, p=0.012) and right secondary somatosensory cortex (rS2, p=0.045) were significantly decreased following SM, and the changes in evoked pain intensity were significantly correlated to dACC activation (r2=0.477, p=0.019) and tended to be correlated to rS2 activation (r2=0.346, p=0.057). The findings suggest that SM may alter the processing of noxious sensory information from the periphery within pain-related brain regions, demonstrating that the change in NPS activation is associated with the change in perceived pain intensity. Informed randomized controlled trials involving patients with varying levels of spinal pain are necessary to determine whether this effect is specific to SM.
Research was supported by the following NIH grants: NIDA T32DA035165, NIDA K24 A029262, and NINDS K23NS10421.