Extraterritorial temperature pain threshold abnormalities in subjects with healed thermal injury

Abstract

Abstract-Approximately 1.25 million individuals sustain burn injuries annually in the United States. Pain is frequent in patients with burn injuries and is often refractory to pharmacotherapy. We report quantitative sensory data from five subjects who sustained external thermal injuries to their limb(s) 8 weeks to 11 years previously, demonstrating reduced thermal pain thresholds in regions outside the burn injury zone, including contralateral limbs. Warm and cold detection thresholds were not significantly different from controls. These results complement data from animal models that demonstrate that allodynia can develop contralateral to a focal burn injury as a result of changes within the spinal cord and suggest that systemic or central mechanisms contribute to pain after burn injury.

Dendritic spine dysgenesis in neuropathic pain

“…Nonetheless, in more common models of moderate burn injury (i.e., second degree, partial skin-thickness burns) there is an acute primary hyperalgesia, which presents rapidly within the cutaneous field of the burn injury site. This is followed by a progressive expansion of the secondary tactile allodynia response to the surrounding uninjured areas of the skin [2,21,86]. The inflammatory response within the skin, nerves, and spinal cord, e.g., microglia, MAPK activation has been shown to contribute to the burn injury-induced pain phenotype.…”

Dendritic Spine Dysgenesis in Neuropathic Pain

“…In humans and animal models with mild-moderate burn injury, primary hyperalgesia (which arises within the cutaneous area of the burn injury) is followed by a progressive expansion of secondary tactile allodynia to uninjured areas. 111,112 Inflammatory responses within the spinal cord and activation of p38 MAPK in spinal microglia have been implicated in the pathogenesis of burn-injury pain. 111,113,114 Pain after burn may also develop from abnormalities in newly regenerated nerve endings following damage and poor reinnervation of scar tissue.…”

Spinal cord motor neuron plasticity accompanies second‐degree burn injury and chronic pain

“…Globally, more than 11 million people a year suffer burn injuries severe enough to require medical treatment (Latarjet & Choinere, ; Peck, , ). Of these patients, many develop clinically intractable hyperexcitability disorders, for example, pain, long after healing of the initial injury is complete (Fischer and Waxman ). The failure to address burn injury‐associated complications is due in part to the lack of mechanistic insight into the development of changes within the central nervous system (CNS) (Guo et al, ).…”