The spinal cord is essential for normal autonomic nervous system regulation of the cardiovascular system as the preganglionic neurons controlling the heart and blood vessels originate in the thoracolumbar spinal segments. The site and extent of a spinal cord injury determine the degree of autonomic involvement in cardiovascular dysfunction after the injury. After complete cervical cord lesions the entire sympathetic outflow is separated from cerebral control; this may cause orthostatic hypotension. Commonly after traumatic injuries to the spinal cord, one or more segments are totally destroyed. However, the distal portion of the spinal cord often retains function and activation of spinal cord reflexes working independently of the brain can result in paroxysmal hypertension. This chapter will focus on orthostatic hypotension and paroxysmal hypertension in cord-injured people with lesions affecting the cervical and upper thoracic spinal cord. Conditions promoting these abnormalities in blood pressure will be elaborated. Possible mechanisms for the hypo- and hypertension will be discussed, as will strategies for managing these problems.
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http://dx.doi.org/10.1016/S0079-6123(05)52015-6 | DOI Listing |
Orthop Surg
January 2025
Department of Orthopedics, Tianjin Medical University General Hospital, International Science and Technology Cooperation Base of Spinal Cord Injury, Tianjin Key Laboratory of Spine and Spinal Cord, Tianjin, China.
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Pride Veterinary Referrals, IVC Evidensia Group, Derby, United Kingdom.
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View Article and Find Full Text PDFTrauma Surg Acute Care Open
January 2025
Department of Emergency and Critical Care Medicine, Nippon Medical School, Bunkyo-ku, Tokyo 1138603, Japan.
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University Hospitals Birmingham NHS Foundation Trust, Edgbaston, Birmingham B15 2GW, UK.
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December 2024
Department of Chemical and Biological Engineering, Hanbat National University, Daejeon 34158, Korea.
Maintenance of neural progenitors requires Notch signaling in vertebrate development. Previous study has shown that Jagged2-mediated Notch signaling maintains proliferating neural progenitors in the ventral spinal cord. However, components for Jagged-mediated signaling remain poorly defined during late neurogenesis.
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