• Mohammed F Shamji.
• Neurosurgery. 2015 Aug 1;62 Suppl 1:206-7.

IntroductionWhile acute disc herniation-induced radiculopathy most frequently resolves without clinical sequelae, a fraction of patients experience long-term sensory dysfunction. This study examined chronic sensitivity of the rodent hind paw following resolution of acute inflammatory neuropathy.MethodsC57BL/6 mice underwent mid-thigh sciatic nerve dissection, with either exposure only (control) or placement of nucleus pulposus (NP). Animals were evaluated throughout 1, 3, and 5 weeks for mechanical allodynia, thermal hyperalgesia, cold allodynia, and gait stability. At each time point, animals received intraplantar injection of capsaicin (0.1 μg) or vehicle alone, thereafter the same behavioral testing. Immunohistochemistry was performed of sciatic nerve, dorsal root ganglion (DRG), and spinal cord for inflammatory activation as well as TRPV1 receptor expression. Ex vivo DRG explants were assessed for capsaicin sensitivity to TRPV1 activation (cobalt staining).ResultsUpon resolution of acute inflammatory pain, mice at 3 and 5 weeks (but not 1 week) demonstrated profound mechanical allodynia to subthreshold capsaicin compared with sham-operated controls or NP-stimulation animals delivered vehicle only. Conversely, perineural lymphocyte and intraneural macrophage infiltration was only observed at 1 week. Heightened spinal cord dorsal horn and DRG TRPV1 expression were seen, and DRG explants derived from NP-treated animals exhibited greater cobalt staining upon capsaicin stimulation compared with controls.ConclusionNoncompressive disc herniation sensitizes the sciatic nerve distribution in this animal model, despite resolution of acute intraneural macrophage migration. The demonstrated role of TRPV1 may explain how acute inflammatory pain transforms into chronic neuropathic pain. Decreasing TRPV1 expression may prevent the development of the long-term painful phenotype.

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