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Accepted (AM)Open Access (License Unspecified), Open
Journal article
Autonomic Dysreflexia in Spinal Cord Injury: Mechanisms and Prospective Therapeutic Targets
The Neuroscientist (Baltimore, Md.), pp 10738584231217455-10738584231217455
12 Dec 2023
PMID: 38084412
Featured in Collection : UN Sustainable Development Goals @ Drexel
Abstract
High-level spinal cord injury (SCI) often results in cardiovascular dysfunction, especially the development of autonomic dysreflexia. This disorder, characterized as an episode of hypertension accompanied by bradycardia in response to visceral or somatic stimuli, causes substantial discomfort and potentially life-threatening symptoms. The neural mechanisms underlying this dysautonomia include a loss of supraspinal control to spinal sympathetic neurons, maladaptive plasticity of sensory inputs and propriospinal interneurons, and excessive discharge of sympathetic preganglionic neurons. While neural control of cardiovascular function is largely disrupted after SCI, the renin-angiotensin system (RAS), which mediates blood pressure through hormonal mechanisms, is up-regulated after injury. Whether the RAS engages in autonomic dysreflexia, however, is still controversial. Regarding therapeutics, transplantation of embryonic presympathetic neurons, collected from the brainstem or more specific raphe regions, into the injured spinal cord may reestablish supraspinal regulation of sympathetic activity for cardiovascular improvement. This treatment reduces the occurrence of spontaneous autonomic dysreflexia and the severity of artificially triggered dysreflexic responses in rodent SCI models. Though transplanting early-stage neurons improves neural regulation of blood pressure, hormonal regulation remains high and baroreflex dysfunction persists. Therefore, cell transplantation combined with selected RAS inhibition may enhance neuroendocrine homeostasis for cardiovascular recovery after SCI.
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Details
- Title
- Autonomic Dysreflexia in Spinal Cord Injury: Mechanisms and Prospective Therapeutic Targets
- Creators
- Cameron T. Trueblood - Drexel UniversityAnurag Singh - Drexel Univ, Coll Med, Mar Murray Spinal Cord Res Ctr, Dept Neurobiol & Anat, 2900 Queen Lane, Philadelphia, PA 19129 USAMarissa A. Cusimano - Drexel UniversityShaoping Hou - Drexel University
- Publication Details
- The Neuroscientist (Baltimore, Md.), pp 10738584231217455-10738584231217455
- Publisher
- Sage
- Number of pages
- 15
- Grant note
- SAP 4100083087 / Pennsylvania Commonwealth Universal Research Enhancement R01 NS121336; NS099076; F31NS122245 / National Institute of Neurological Disorders and Stroke (National Institutes of Health); United States Department of Health & Human Services; National Institutes of Health (NIH) - USA; NIH National Institute of Neurological Disorders & Stroke (NINDS)
- Resource Type
- Journal article
- Language
- English
- Academic Unit
- Neurobiology and Anatomy; Pharmacology and Physiology
- Web of Science ID
- WOS:001126505900001
- Scopus ID
- 2-s2.0-85179934399
- Other Identifier
- 991021811619904721
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InCites Highlights
Data related to this publication, from InCites Benchmarking & Analytics tool:
- Web of Science research areas
- Clinical Neurology
- Neurosciences