Whole body vibration has been postulated to contribute to the onset of back pain. However, little is known about the relationship between vibration exposure, the biomechanical response, and the physiological responses of the seated human. The aim of this study was to measure the frequency and corresponding muscle responses of seated male volunteers during whole body vibration exposures along the vertical and anteroposterior directions to define the transmissibility and associated muscle activation responses for relevant whole body vibration exposures. Seated human male volunteers underwent separate whole body vibration exposures in the vertical (Z-direction) and anteroposterior (X-direction) directions using sinusoidal sweeps ranging from 2 to 18 Hz, with a constant amplitude of 0.4 g. For each vibration exposure, the accelerations and displacements of the seat and lumbar and thoracic spines were recorded. In addition, muscle activity in the lumbar and thoracic spines was recorded using electromyography (EMG) and surface electrodes in the lumbar and thoracic region. Transmissibility was determined, and peak transmissibility, displacement, and muscle activity were compared in each of the lumbar and thoracic regions. The peak transmissibility for vertical vibrations occurred at 4 Hz for both the lumbar (1.55 ± 0.34) and thoracic (1.49 ± 0.21) regions. For X-directed seat vibrations, the transmissibility ratio in both spinal regions was highest at 2 Hz but never exceeded a value of 1. The peak muscle response in both spinal regions occurred at frequencies corresponding to the peak transmissibility, regardless of the direction of imposed seat vibration: 4 Hz for the Z-direction and 2-3 Hz for the X-direction. In both vibration directions, spinal displacements occurred primarily in the direction of seat vibration, with little off-axis motion. The occurrence of peak muscle responses at frequencies of peak transmissibility suggests that such frequencies may induce greater muscle activity, leading to muscle fatigue, which could be a contributing mechanism of back pain.

STRUCTURED ABSTRACT Study Design Immunohistochemistry labeled pre- and post-synaptic structural markers to quantify excitatory and inhibitory synapses in the spinal superficial dorsal horn at 14 days after painful facet joint injury in the rat. Objective The objective of this study was to investigate the relationship between pain and synapse density in the spinal cord after facet injury. Summary of Background Data Neck pain is a major contributor to disability and often becomes chronic. The cervical facet joints are susceptible to loading-induced painful injury, initiating spinal central sensitization responses. Although excitatory synapse plasticity has been reported in the superficial dorsal horn early after painful facet injury, whether excitatory and/or inhibitory synapse density is altered at a time when pain is maintained is unknown. Methods Rats underwent either a painful C6/C7 facet joint distraction or sham surgery. Mechanical hyperalgesia was measured and immunohistochemistry techniques for synapse quantification were used to quantify excitatory and inhibitory synapse densities in the superficial dorsal horn at day 14. Logarithmic correlation analyses evaluated whether the severity of facet injury correlated with either behavioral or synaptic outcomes. Results Facet joint injury induces pain that is sustained until day 14 (p<0.001) and both significantly greater excitatory synapse density (p=0.042) and lower inhibitory synapse density (p=0.0029) in the superficial dorsal horn at day 14. Injury severity is significantly correlated with pain at days 1 (p=0.0011) and 14 (p=0.0002), but only with inhibitory, not excitatory, synapse density (p=0.0025) at day 14. Conclusions This study demonstrates a role for structural plasticity in both excitatory and inhibitory synapses in the maintenance of facet-mediated joint pain, and that altered inhibitory, but not excitatory, synapse density correlates to the severity of painful joint injury. Understanding the functional consequences of this spinal structural plasticity is critical to elucidate mechanisms of chronic joint pain.

These findings suggest that nonpainful insults to the facet joint, when combined, can generate painful outcomes, possibly mediated by upregulation of MMP-3 and mature NGF.

Repeated loading of ligamentous tissues during repetitive occupational and physical tasks even within physiological ranges of motion has been implicated in the development of pain and joint instability. The pathophysiological mechanisms of pain after repetitive joint loading are not understood. Within the cervical spine, excessive stretch of the facet joint and its capsular ligament has been implicated in the development of pain. Although a single facet joint distraction (FJD) at magnitudes simulating physiologic strains is insufficient to induce pain, it is unknown whether repeated stretching of the facet joint and ligament may produce pain. This study evaluated if repeated loading of the facet at physiologic nonpainful strains alters the capsular ligament's mechanical response and induces pain. Male rats underwent either two subthreshold facet joint distractions (STFJDs) or sham surgeries each separated by 2 days. Pain was measured before the procedure and for 7 days; capsular mechanics were measured during each distraction and under tension at tissue failure. Spinal glial activation was also assessed to probe potential pathophysiologic mechanisms responsible for pain. Capsular displacement significantly increased (p = 0.019) and capsular stiffness decreased (p = 0.008) during the second distraction compared to the first. Pain was also induced after the second distraction and was sustained at day 7 (p < 0.048). Repeated loading weakened the capsular ligament with lower vertebral displacement (p = 0.041) and peak force (p = 0.014) at tissue rupture. Spinal glial activation was also induced after repeated loading. Together, these mechanical, physiological, and neurological findings demonstrate that repeated loading of the facet joint even within physiologic ranges of motion can be sufficient to induce pain, spinal inflammation, and alter capsular mechanics similar to a more injurious loading exposure.