• Nanna B Finnerup, Louise H Pedersen, Astrid J Terkelsen, Inger L Johannesen, and Troels S Jensen.
• Danish Pain Research Center and Department of Neurology, Aarhus University Hospital, Norrebrogade 44, DK-8000 Aarhus, Denmark. finnerup@ki.au.dk <finnerup@ki.au.dk>
• Exp. Neurol. 2007 May 1;205(1):190-200.

AbstractCentral neuropathic pain is a debilitating and frequent complication to spinal cord injury (SCI). Excitatory input from hyperexcitable cells around the injured grey matter zone is suggested to play a role for central neuropathic pain felt below the level of a spinal cord injury. Direct evidence for this hypothesis is difficult to obtain. Capsaicin, activating TRPV1 receptors on small sensory afferents, induces enhanced cellular activity in dorsal horn neurons and produces a central mediated area of secondary hyperalgesia. We hypothesized that sensory stimuli and capsaicin applied at and just above the level of a spinal cord injury which already is hyperexcitable, would cause enhanced responses in patients with central pain at the level of injury compared to patients without neuropathic pain and healthy controls. Touch, punctuate stimuli, cold stimuli and topical capsaicin was applied above, at, and below injury level in 10 SCI patients with central pain below a thoracic injury, in 10 SCI patients with a thoracic injury but without neuropathic pain, and in corresponding areas in 10 healthy control subjects. The study found increased responses to touch at injury level compared to controls (p=0.033) and repetitive punctuate stimuli above and at injury level compared to controls and pain-free SCI patients (p<0.04) but not an increased response to capsaicin in patients with central pain. These results suggest that SCI patients with below-level pain have increased responses to some but not all sensory input at the level of injury.

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