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. Also, the neuropeptide substance P and glial cell line-derived neurotrophic factor and its receptor significantly decreased (p<l0.02) with increasing load in the small nociceptive neurons of the dorsal root ganglion, suggesting that axonal damage may also decrease neurotrophic support in injured nociceptive afferent fibers. In a separate study, roots were compressed at 2 mm/s, and held, to develop a quasi-linear viscoelastic model that was validated through comparisons to quasistatic loading. The model demonstrated that nearly 23% less displacement was required to reach the axonal injury load threshold during dynamic loading than for quasistatic rates. Together, these studies demonstrate that nerve root compressions that produce pain symptoms are sufficient to mediate nociceptive cellular changes, and that thresholds for pain and nociceptive pathophysiology may be lower for dynamic loading scenarios.