Sandra M. Garraway, Ph.D.
Assistant Professor of Physiology
Ph.D., University of Manitoba, 2000
Noxious information resulting from injury to the periphery is processed in the spinal cord dorsal horn before it is transmitted to the brain. Damage to the spinal cord produces several devastating effects including neuropathic pain. About 70% of spinal cord injury patients experience pain. Despite the prevalence of neuropathic pain after spinal cord injury, the neural mechanisms underlying its development are poorly understood. In addition, there are no clear factors that predict if and when neuropathic pain develops.
Our research focuses on identifying adaptive versus maladaptive cellular plasticity that influences functional recovery and the development of pain after spinal cord injury. Using rodent models of SCI (contusion injury and transection injury), our research combines behavioral, molecular and electrophysiological techniques to investigate:
(i) Development of segmental and below-level pain after SCI
(ii) Interactions between autonomic dysfunction and neuropathic pain
(iii) Neuronal/glial mechanisms influencing spinal nociceptive plasticity
(iv) Biological and/or experiential factors that predict the development of pain after SCI
(v) Roles of various neurotransmitters/modulators (BDNF, GABA, TNF alpha and other cytokines, PKC zeta)
Publications: PubMed search