Orthostatic hypotension following spinal cord injury: understanding clinical pathophysiology

Abstract

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.

Orthostatic hypotension in the first month following acute spinal cord injury

“…8 Clinical observations strongly suggest that the extent over which prolonged and severe hypotension occurs, requiring vasopressor therapy, is associated with the grade of the SCI, and can last up to 5 weeks after injury. 1,8 We evaluated the influence of age, gender, level and grade of injury on the development of OH after SCI, and found that the level and grade of SCI were the two major contributing factors. These findings were consistent with observations in previous studies 4, [13][14][15] Illman et al 4 reported that OH was most likely to develop in quadriplegic rather than in paraplegic individuals regardless of grade of injury.…”

“…However, insufficient sympathetic control resulting in lack of reflex vasoconstriction is considered to be among the major causes of initial hypotension and persistent OH in individuals with SCI. 1,8,10 Low sympathetic tone following SCI is a result of interruption of descending axons within the spinal cord, traveling from the brainstem to the sympathetic preganglionic neurons localized within the lateral horns of the thoracic and upper lumbar segments of the spinal cord. Previous animal experimental data and clinical observation suggest that the grade of injury to the descending spinal pathways may influence the severity of cardiovascular dysfunction following SCI.…”

“…1 During the initial few hours after SCI, particularly following a cervical injury, severe hypotension and persistent bradycardia may be observed as the hallmarks of neurogenic shock. 2 As spinal reflexes reappear and spinal shock subsides, cardiovascular control may continue to be severely disrupted as a result of an imbalance between the sympathetic and parasympathetic nervous systems.…”

Assessing the capacity of the sympathetic nervous system to respond to a cardiovascular challenge in human spinal cord injury

“…In able-bodied individuals, the same postural change causes an increase in BP with virtually no change in heart rate (HR). 9 We know that in the able-bodied during an inspiratorycapacity apnoea with the glottis closed and the inspiratory muscles relaxed, there is a reflex increase in muscle sympathetic nerve activity (MSNA) that is sustained for the period of the apnoea. 10 Cutaneous sympathetic nerve activity increases transiently at the onset and offset of the inflation, but not throughout the entire apnoea.…”

Orthostatic responses to anticholinesterase inhibition in spinal cord injury

“…[1][2][3][4] Although many individuals with tetraplegia remain asymptomatic during periods of significant hypotension, associations between persistent and episodic asymptomatic hypotension and cognitive dysfunction [5][6][7] and mood disorders 8,9 is reported in the general medical literature. Moreover, our group recently reported reduced memory and marginally impaired attention processing in hypotensive individuals with spinal cord injury (SCI) compared to a normotensive SCI cohort.…”