Alleviating Autonomic Dysreflexia after Spinal Cord Injury
Technical Report,30 Sep 2015,29 Sep 2016
DREXEL UNIV PHILADELPHIA PA PHILADELPHIA United States
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Autonomic dysreflexia AD is a life-threatening dysfunction in which some stimulus below the level of SCI triggers extreme hypertension accompanied by bradycardia. It is thought to develop from 1 aberrant plasticity and 2 the loss of tonic input onto sympathetic preganglionic neurons SPN in the spinal cord that drive cardiovascular control. Both of these result in increased, unchecked activity of the SPN, leading to hypertension. This study aims to restore andor form circuitry to normalize SPN activity. One potential means to achieve this is to promote the regeneration of appropriate axons to restore more normal SPN innervation. We have previously shown that we are able to promote robust functional axonal regeneration using a combination of transplantation and inhibitory matrix modulation with chondroitinase. We have preliminary data indicating that modulation of microtubule dynamics with monastrol enhances this regeneration. We also have pilot data indicating the restoring innervation to the SPN diminishes AD. Another means to normalize SPN activity is pharmacologically. Pre-treatment with gabapentin GP has been shown to mitigate induced AD. However, whether post-treatment with GP effectively diminishes AD has not yet been demonstrated.