Cardiovascular consequences of loss of supraspinal control of the sympathetic nervous system after spinal cord injury

Teasell, Robert; Arnold, J. Malcolm O.; Krassioukov, Andrei V.; Delaney, Gail A.

doi:10.1053/mr.2000.3848

Cited by 510 publications

(411 citation statements)

References 97 publications

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“…The division of the groups into upper and lower thoracic was based on previous clinical observations of cardiovascular disturbances in this population. [8][9][10] The patients were further divided on the basis of SCI grade into two subgroups: motor complete (ASIA A and B) and motor incomplete (ASIA C and D). Neurological recovery was defined on the basis of improvement in ASIA impairment scale.…”

Section: Study Groupsmentioning

confidence: 99%

Orthostatic hypotension in the first month following acute spinal cord injury

et al. 2007

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Study Design: Retrospective data analysis. Objectives: To determine prevalence of orthostatic hypotension (OH) in patients with spinal cord injury (SCI) during the acute rehabilitation period. Setting: Quaternary care spinal unit, Vancouver General Hospital, British Columbia, Canada Methods: Eighty-nine patients with acute SCI stratified by neurological level (cervical, 55 (62%); upper thoracic, 12 (13%); lower thoracic, 22 (25%)), and graded by American Spinal Injury Association standards. Non-invasive measurement of systolic and diastolic blood pressure and heart rate were made at baseline and 3 min following an orthostatic challenge test administered during the first month after SCI. Results: Patients with cervical or upper thoracic motor complete SCI more frequently experienced OH (Po0.01). OH persisted during the first month following SCI in 74% of cervical and only 20% of upper thoracic motor complete SCI patients. Conclusion: Patients with cervical and upper thoracic motor complete SCI are more likely to experience persistent OH than those with lower level or motor incomplete SCI during the first month of rehabilitation.

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Section: Study Groupsmentioning

confidence: 99%

Orthostatic hypotension in the first month following acute spinal cord injury

et al. 2007

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“…The increased responsiveness to pressors seen in spinal injured patients may be due to increased reactivity of resistance vessels or decreased neuronal reuptake from the synaptic cleft. 5 Charcot's spine, ®rst described by Kronig in 1884 in patients with tabes dorsalis has since been reported by various authors as occurring in traumatic paraplegia. 6 ± 8 There is a predilection for Charcot changes to occur in the lumbar spine thought to be related to the absence of rib support and increased weight bearing function of this area of the spine.…”

Section: Introductionmentioning

confidence: 99%

Neuropathic lumbar spondylolisthesis – a rare trigger for posture induced autonomic dysreflexia

Thumbikat

Ravichandran

2001

Spinal Cord

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Study design: Case report. Objectives: Description of a rare trigger for autonomic dysre¯exia. Setting: Princess Royal Spinal Injuries Unit, She eld. Methods and Results: A case of Charcot's spine (neuropathic spinal arthropathy) in a woman with a traumatic T5 paraplegia is described. She developed symptoms of autonomic dysre¯exia, brought on by changes in posture. The postural variation was attributable to a freely mobile neuropathic spondylolisthesis at the L4/5 level. A laminectomy performed for the implantation of a sacral anterior root stimulator was identi®ed as a causative factor in the development of the neuropathic joint. Surgical stabilisation and fusion resulted in amelioration of her symptoms. Conclusion: Neuropathic spine is a rare cause of autonomic dysre¯exia that should be considered when other more common factors have been excluded. The development of Charcot's spine in the spinal cord injured population is facilitated by surgical procedures involving the vertebrae. Spinal Cord (2001) 39, 564 ± 567

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“…3 This results in a variety of cardiovascular abnormalities that have been well documented in human studies, as well as in animal models. [4][5][6][7][8] However, the recognition and management of cardiovascular dysfunctions following SCI represent challenging clinical issues.…”

Section: Introductionmentioning

confidence: 99%

Orthostatic hypotension following spinal cord injury: understanding clinical pathophysiology

2005

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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.

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Cardiovascular consequences of loss of supraspinal control of the sympathetic nervous system after spinal cord injury

Cited by 510 publications

References 97 publications

Orthostatic hypotension in the first month following acute spinal cord injury

Orthostatic hypotension in the first month following acute spinal cord injury

Neuropathic lumbar spondylolisthesis – a rare trigger for posture induced autonomic dysreflexia

Orthostatic hypotension following spinal cord injury: understanding clinical pathophysiology

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