to the sympathetic preganglionic neurons that control the critical splanchnic bed resulting in neurogenic shock during the early stages of SCI and long-lasting resting hypotension post injury. 5 Loss of supraspinal tonic inhibitory input to the sympathetic preganglionic neurons provides an environment in which sensory-evoked reflexes can cause unopposed below-lesion sympathetic activation, leading to profound vasoconstriction and consequent episodes of hypertension. This condition, termed autonomic dysreflexia (AD), affects up to 90% of individuals with motor complete cervical SCI 6 and can lead to a sequelae of cardiovascular effects, such as myocardial infarction, 7 intracranial hemorrhage, 8
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