Sensory stimulation prior to spinal cord injury induces post-injury dysesthesia in mice.

Chronic pain and dysesthesias are debilitating conditions that can arise following spinal cord injury (SCI). Research studies frequently employ rodent models of SCI to better understand the underlying mechanisms and develop better treatments for these phenomena. While evoked withdrawal tests can assess hypersensitivity in these SCI models, there is little consensus over how to evaluate spontaneous sensory abnormalities that are seen in clinical SCI subjects. Overgrooming (OG) and biting after peripheral nerve injury or spinal cord excitotoxic lesions are thought to be one behavioral demonstration of spontaneous neuropathic pain or dysesthesia. However, reports of OG after contusion SCI are largely anecdotal and conditions causing this response are poorly understood. The present study investigated whether repeated application of sensory stimuli to the trunk prior to mid-thoracic contusion SCI would induce OG after SCI in mice. One week prior to SCI or laminectomy, mice were subjected either to nociceptive and mechanical stimulation, mechanical stimulation only, the testing situation without stimulation, or no treatment. They were then examined for 14 days after surgery and the sizes and locations of OG sites were recorded on anatomical maps. Mice subjected to either stimulus paradigm showed increased OG compared with unstimulated or uninjured mice. Histological analysis showed no difference in spinal cord lesion size due to sensory stimulation, or between mice that overgroomed or did not overgroom. The relationship between prior stimulation and contusion injury in mice that display OG indicates a critical interaction that may underlie one facet of spontaneous neuropathic symptoms after SCI.