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Autonomic dysreflexia: a cardiovascular disorder following spinal cord injury
Journal article   Open access   Peer reviewed

Autonomic dysreflexia: a cardiovascular disorder following spinal cord injury

Hisham Sharif and Shaoping Hou
Neural regeneration research, v 12(9), pp 1390-1400
01 Sep 2017
PMID: 29089975
url
https://doi.org/10.4103/1673-5374.215241View
Published, Version of Record (VoR)CC BY-NC-SA V4.0 Open

Abstract

Cell Biology Life Sciences & Biomedicine Neurosciences Neurosciences & Neurology Science & Technology
Autonomic dysreflexia (AD) is a serious cardiovascular disorder in patients with spinal cord injury (SCI). The primary underlying cause of AD is loss of supraspinal control over sympathetic preganglionic neurons (SPNs) caudal to the injury, which renders the SPNs hyper-responsive to stimulation. Central maladaptive plasticity, including C-fiber sprouting and propriospinal fiber proliferation exaggerates noxious afferent transmission to the SPNs, causing them to release massive sympathetic discharges that result in severe hypertensive episodes. In parallel, upregulated peripheral vascular sensitivity following SCI exacerbates the hypertensive response by augmenting gastric and pelvic vasoconstriction. Currently, the majority of clinically employed treatments for AD involve anti-hypertensive medications and Botox injections to the bladder. Although these approaches mitigate the severity of AD, they only yield transient effects and target the effector organs, rather than addressing the primary issue of central sympathetic dysregulation. As such, strategies that aim to restore supraspinal reinnervation of SPNs to improve cardiovascular sympathetic regulation are likely more effective for AD. Recent pre-clinical investigations show that cell transplantation therapy is efficacious in reestablishing spinal sympathetic connections and improving hemodynamic performance, which holds promise as a potential therapeutic approach.

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Cell Biology
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