Pain affects as many as 50 million Americans, with annual costs estimated as high as $90 billion. Unfortunately, the mechanism of injuries leading to persistent pain syndromes remain largely uncharacterized. A common painful injury results due from mechanical loading of nerve roots, which can occur for spinal injuries in both the low back and neck. Relationships have been demonstrated between tissue compression and behavioral hypersensitivity responses in animal models, with differential patterns of sensitivity depending on the nature of the mechanical insult (Colburn et al., 1999). Mechanical allodynia (MA) is an increased behavioral sensitivity to a non-noxious stimulus and is observed in the dermatome of the injured tissue. It can be measured by the frequency of paw withdrawals elicited by stimulation with normally non-noxious von Frey filaments. Allodynia is a clinical measure of sensitivity and, therefore, provides a useful gauge of nociceptive responses. Animal studies have shown that compression of neural structures initiates a variety of physiologic responses, including decreased electrical activity, increased edema formation, and increased endoneurial pressure in the region of compression (Lundborg et al., 1983; Olmarker et al., 1989, 1990; Pedowitz et al., 1992). While these studies document physiologic changes immediately following injury, they do not describe the temporal nature of these changes following tissue loading as they relate to pain behaviors. Moreover, despite this evidence of edema formation and increased endoneurial pressure locally in the nerve roots, no study has simultaneously documented local changes in nerve root geometry following compressive injury and how these changes may be linked to the onset and/or maintenance of pain-associated behaviors. Therefore, this study examines injury biomechanics for pain-behaviors in a radiculopathy (nerve root injury) model and temporally characterizes the local geometric changes in the nerve root for a series of postsurgical time points following compressive injury. While these results indicate that compression magnitude clearly modulates pain responses, the local nerve root swelling does not appear to directly drive behavioral changes. This suggests a complicated physiology for injury which likely contributes to the manifestation of pain. Findings are also presented for preliminary investigations into tissue rebound/recovery responses for varied mechanical insult magnitudes to begin to understand potential injury mechanisms leading to pain.

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