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

Spinal cord injury (SCI) with resultant quadriplegia or high paraplegia is associated with significant dysfunction of the sympathetic nervous system. This alteration of sympathetic nervous system activity occurs as a conseque nce of loss of supraspinal control of the sympathetic nervous system and is further complicated by at least three subsequent phenomena that occur belo w the level of SCI: reduced overall sympathetic activity, morphologic chang es in sympathetic preganglionic neurons, and peripheral alpha-adrenoceptor hyperresponsive ness. Reduced sympathetic activity below the level of SCI a ppears to result in orthostatic hypotension, low resting blood pressure, lo ss of diurnal fluctuation of blood pressure, reflex bradycardia, and, rarel y, cardiac arrest. peripheral alpha-adrenoceptor hyperresponsiveness likely accounts for some, if not the majority, of the excessive presser response in autonomic dysreflexia and may also contribute to decreased blood flow in the peripheral microcirculation, potentially increasing susceptibility to pressure sores. What has yet to be established is whether this alpha-adreno ceptor hyperresponsiveness is a consequence of receptor hypersensitivity or a failure of presynaptic reuptake of noradrenaline at the receptor level. Better understanding of the pathophysiology of sympathetic nervous system d ysfunction after high-level SCI should allow development of more effective measures to manage clinical complications.