American Pain Society's 27th Annual Scientific Meeting (May 8 – 10, 2008): Acute neck trauma in rats produces diffuse and chronic changes in nociceptive responding

8145 Acute neck trauma in rats produces diffuse and chronic changes in nociceptive responding

May 9, 2008: May 9, 2008
East Hall (Tampa Convention Center)
S.E. Harte , Department of Internal Medicine/Rheumatology, University of Michigan Health System, Ann Arbor, MI
J. Meyers , Department of Neurology, University of Michigan Health System, Ann Arbor, MI
D.J. Clauw , Department of Internal Medicine/Rheumatology, University of Michigan Health System, Ann Arbor, MI
T.J. Morrow , Neurology Service, VA Ann Arbor Healthcare System, Ann Arbor, MI
Acute musculoskeletal injuries sometimes lead to chronic regional or widespread pain, as well as diffuse hyperalgesia/allodynia. Animal models of post-traumatic pain would be useful to study the neurobiology of this phenomenon. In one such model, unilateral injections of acidic saline into the rodent hindlimb produce bilateral, mechanical hyperalgesia in the hindpaws that persists for approximately 30 days (Sluka et al., Muscle & Nerve, 2001). However, human studies suggest that proximal musculoskeletal trauma is more closely linked to chronic pain than distal trauma. Also, the contralateral limb to an initial injury could develop nociceptive changes because of segmental rather than central mechanisms. Therefore, we modified this model and injected acidic saline into the neck, and measured the subsequent nociceptive response in the hindpaws, as a measure of the “extra-segmental” response to this initial injury. Male, Sprague-Dawley rats were injected with 200 μl of sterile acidic saline (pH 4.0) on Days 0 and 5 into the deep muscles of the neck. Nociceptive responses were measured by evaluating withdrawal responses in both hindpaws to mechanical cutaneous stimulation. Preliminary results showed that neck injections of acidic saline produced mechanical hyper-responsiveness in both hindpaws. In contrast to the pain produced by acid injections into the hindlimb, the development of mechanical hyper-responsiveness following neck injections was delayed for 19-26 days after the first acid injection and it persisted for more than 60 days. Histological analysis of postmortem neck tissue revealed no persistent inflammatory response or muscle pathology in the area of acid injection. Control rats that underwent identical injections with physiologically neutral saline had no changes in nociceptive responding. These preliminary findings suggest that trauma to the neck can lead to chronic and diffuse changes in nociceptive processing, even after the acute injury has healed, as has been noted in conditions such as fibromyalgia.
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