Abstract
Due to their traumatic etiology, spinal cord injury patients present with injuries to other parts of the body. These associated injuries can be a source of pain input through the damaged spinal cord. Animal research has shown that activating nociceptive fibers soon after injury induces maladaptive plasticity (Grau et al., 2004). In those studies, male rats received six minutes of variable electrical stimulation to the tail at an intensity that engaged C-fibers. Acutely, shocked animals show increases in pro-inflammatory cytokines and cell death (Turtle et at., 2017). Chronically, a single exposure caused the lesion to expand, locomotor deficits, and increased mortality (Grau et al., 2004). Recent work suggests that the loss of tissue at the site of injury is related to a breakdown in the blood spinal cord barrier (BSCB) and infiltration of blood (hemorrhage) at the site of injury. The present study explored the generality of these effects by examining whether chemically activating unmyelinated C fibers, by applying the irritant capsaicin to one hind paw, would have the same effect. Male rats underwent a contusion injury at T12. Twenty-four hours later, subjects received an intradermal injection of capsaicin (3%) or vehicle to one hind paw. Tissue was collected at three and 24 hours after injection and assessed for hemorrhage. Capsaicin treatment induced an acute disruption in locomotor performance. Cellular assays showed that pain input increased the infiltration of blood into the area of injury. We next examined whether these effects generalize to female rats. Here too capsaicin induced an acute disruption in locomotor performance and increased hemorrhage. Further, capsaicin treatment disrupted long-term locomotor recovery in male rats. These findings extend the generality of our results and suggest that pain input (polytrauma) after SCI impairs recovery because it expands the region of secondary injury through a breakdown of the BSCB.
Published Version
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