Dr. Christopher West School of Kinesiology, UBC
Abstract: Damage to the central nervous system, as in the case of spinal cord injury (SCI), results in disrupted supraspinal sympathetic influence and subsequent cardiovascular control impairments. Consequently, people with SCI suffer from disordered basal haemodynamics and devastating fluctuations in blood pressure, as in the case of autonomic dysreflexia (AD), which likely contribute to this population’s leading cause of mortality: cardiovascular disease (CVD). The development of AD is related, at least in part, to neuroanatomical changes that include disrupted descending supraspinal sympathetic control, changes in propriospinal circuitry, and inappropriate afferent sprouting in the dorsal horn. These anatomical mechanisms may thus be targeted by neural regenerative and protective therapies to improve cardiovascular control and reduce AD. Here, we discuss the relationship between abnormal cardiovascular control and its underlying neuroanatomy. We then review current studies investigating biochemical strategies to reduce the severity of AD through 1) reducing aberrant calcitonin gene-related peptide immunoreactive (CGRP+) afferent sprouting, 2) inhibiting inflammatory processes, and 3) reestablishing descending supraspinal sympathetic control. Finally, we discuss why additional biochemical agents and combinational approaches may be needed to completely ameliorate this condition.
Squair, J., West, C., and Krassioukov, A. (published online ahead of print January 2015). Neuroprotection, plasticity manipulation, and regenerative strategies to improve cardiovascular function following spinal cord injury. Journal of Neurotrauma. doi:http://online.liebertpub.com/doi/pdfplus/10.1089/neu.2014.3743
