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Both traumatic and slow-onset disc herniation can directly compress and/or chemically irritate cervical nerve roots, and both types of root injury elicit pain in animal models of radiculopathy. This study investigated the relative contributions of mechanical compression and chemical irritation of the nerve root to spinal regulation of neuronal activity using several outcomes. Modifications of two proteins known to regulate neurotransmission in the spinal cord, the neuropeptide calcitonin gene-related peptide (CGRP) and glutamate transporter 1 (GLT-1), were assessed in a rat model after painful cervical nerve root injuries using a mechanical compression, chemical irritation or their combination of injury. Only injuries with compression induced sustained behavioral hypersensitivity (p≤0.05) for two weeks and significant decreases (p<0.037) in CGRP and GLT-1 immunoreactivity to nearly half that of sham levels in the superficial dorsal horn.

Cervical nerve roots are susceptible to compression injuries of various durations. The duration of an applied compression has been shown to contribute to both the onset of persistent pain and also the degree of spinal cellular and molecular responses related to nociception. This study investigated the relationship between peripherally evoked activity in spinal cord neurons during a root compression and the resulting development of axonal damage. Electrically evoked spikes were measured in the spinal cord as a function of time during and after (post-compression) a 15 minute compression of the C7 nerve root. Compression to the root significantly (p=0.035) reduced the number of spikes that were evoked over time relative to sham. The critical time for compression to maximally reduce evoked spikes was 6.6±3.0 minutes. A second study measured the post-compression evoked neuronal activity following compression applied for a shorter, sub-threshold time (three minutes).

Rapid neck motions can load cervical nerve roots and produce persistent pain. This study investigated the cellular basis of radicular pain and mechanical implications of tissue loading rate. A range of peak loads was applied in an in vivo rat model of dorsal root compression, and mechanical allodynia (i.e., pain) was measured. Axonal damage and nociceptive mediators were assessed in the axons and cell bodies of compressed dorsal roots in separate groups of rats at days 1 and 7 after injury. In the day 7 group, damage in the compressed axons, evaluated by decreased heavy chain neurofilament immunoreactivity, was increased for compressions above a load of 34.08 mN, which is similar to the load-threshold for producing persistent pain in that model.

While studies have demonstrated the cervical facet capsule is at risk for tensile injury during whiplash, the relationship between joint loading, changes in the capsule's structure, and pain is not yet fully characterized. Complementary approaches were employed to investigate the capsule's structure-function relationship in the context of painful joint loading. Isolated C6/C7 facet joints (n=8) underwent tensile mechanical loading, and measures of structural modification were compared for two distraction magnitudes: 300 µm (PV) and 700 µm (SV). In a matched in vivo study, C6/C7 facet joints (n=4) were harvested after the same SV distraction and the tissue was sectioned to analyze collagen fiber organization using polarized light microscopy. Laxity following SV distraction (7.30±3.01%) was significantly greater (p<0.001) than that produced following PV distraction (0.99±0.44%).

While extensive research points to mechanical injury of the cervical facet joint as a mechanism of whiplash injury, findings remain speculative regarding its potential for causing pain. The purpose of this study was to examine the relationship between facet joint distraction, capsular ligament strain, cellular nociceptive responses, and pain. A novel rat model of in vivo facet joint injury was used to impose C6/C7 joint distraction in separate studies of subcatastrophic and physiologic vertebral distraction, as well as sham procedures. A common clinical measure of behavioral hypersensitivity (allodynia) was measured for 14 days after injury, as quantification of resulting pain symptoms. Also, on day 14, spinal activation of microglia and astrocytes was quantified to examine the potential role of glial activation as a physiologic mechanism of facet-mediated painful injury. Vertebral distractions of 0.90±0.53 mm across the rat facet joint reliably produced symptoms of persistent pain.

Epidemiological and clinical studies have identified the cervical facet capsule as a potential site of whiplash injury and prerotation of the head and neck as a risk factor for whiplash injury. However, biomechanical data related to the cervical facet capsule and its role in whiplash injury remain limited in the literature. In this study, cervical spine motion segments were tested in a pure moment test frame and the full field strains were determined throughout the facet capsule. Motion segments were tested with and without a pretorque in pure bending. Bending tests were followed by isolated facet elongation tests to failure. Maximum principal strains during bending were compared to failure strains. Statistically significant increases in principal capsular strains were observed in the facet which was contralateral to the pretorque. In contrast, no significant differences were present in the ipsilateral facet when large flexion-extension moments were applied.

This study explores the dynamics of head and cervical spine impact with the specific goals of determining the effects of head inertia and impact surface on injury risk. Head impact experiments were performed using unembalmed head and neck specimens from 22 cadavers. These included impacts onto compliant and a rigid surfaces with the surface oriented to produce both flexion and extension attitudes. Tests were conducted using a drop track system to produce impact velocities on the order of 3.2 m/s. Multiaxis transduction recorded the head impact forces, head accelerations, and the reactions at T1. The tests were also imaged at 1000 frames/sec. Injuries occurred 2 to 30 msec following head impact and prior to significant head motion. Head motions were not found to correlate with injury classification. Decoupling was observed between the head and T1, resulting in a lag in the force histories.