Orthostatic hypotension following spinal cord injury: understanding clinical pathophysiology

• Published in: Spinal cord 2006-06, Vol.44 (6), p.341-351
• Main Authors: Claydon, V E, Steeves, J D, Krassioukov, A
• Format: Article
• Language: English
• Subjects: Anatomy; Baroreflex; Biological and medical sciences; Biomedical and Life Sciences; Biomedicine; Blood Pressure; Cerebrospinal fluid. Meninges. Spinal cord; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases; Heart - physiopathology; Human Physiology; Humans; Hypotension, Orthostatic - diagnosis; Hypotension, Orthostatic - etiology; Hypotension, Orthostatic - physiopathology; Hypotension, Orthostatic - therapy; Injuries of the nervous system and the skull. Diseases due to physical agents; Medical sciences; Nervous system (semeiology, syndromes); Neurochemistry; Neurology; Neuropsychology; Neurosciences; review; Spinal Cord - physiopathology; Spinal Cord Injuries - complications; Spinal Cord Injuries - diagnosis; Spinal Cord Injuries - physiopathology; Spinal Cord Injuries - therapy; Traumas. Diseases due to physical agents
• ISSN: 1362-4393; 1476-5624
• DOI: 10.1038/sj.sc.3101855

Motor and sensory deficits are well-known consequences of spinal cord injury (SCI). During the last decade, a significant number of experimental and clinical studies have focused on the investigation of autonomic dysfunction and cardiovascular control following SCI. Numerous clinical reports have suggested that unstable blood pressure control in individuals with SCI could be responsible for their increased cardiovascular mortality. The aim of this review is to outline the incidence and pathophysiological mechanisms underlying the orthostatic hypotension that commonly occurs following SCI. We describe the clinical abnormalities of blood pressure control following SCI, with particular emphasis upon orthostatic hypotension. Possible mechanisms underlying orthostatic hypotension in SCI, such as changes in sympathetic activity, altered baroreflex function, the lack of skeletal muscle pumping activity, cardiovascular deconditioning and altered salt and water balance will be discussed. Possible alterations in cerebral autoregulation following SCI, and the impact of these changes upon cerebral perfusion are also examined. Finally, the management of orthostatic hypotension will be considered.