B Autonomic hyperreflexia and dysautonomia
Definition
Autonomic dysreflexia (or autonomic hyperreflexia) is a disorder that appears after resolution of spinal shock.
Incidence and prevalence
The incidence and prevalence depend on the level of spinal cord transection. About 85% of patients with spinal cord transection above T5 may exhibit this syndrome. Autonomic dysreflexia is unlikely to be associated with spinal cord transection below T10. The stimulation of a surgical procedure, however, is a potent trigger of autonomic dysreflexia even in patients with no previous history of this response.
Pathophysiology
Autonomic dysreflexia can be initiated by cutaneous or visceral stimulation below the level of spinal cord transection. Distention of a hollow viscus (bladder or rectum) is a common stimulus. This stimulus initiates afferent impulses that enter the spinal cord below that level. These impulses elicit reflex sympathetic activity over the splanchnic outflow tract. This outflow is isolated from inhibitory impulses such that generalized vasoconstriction persists below the level of injury. Vasoconstriction results in increased blood pressure, which is then transmitted by the carotid sinus. Subsequent activation of the carotid sinus results in decreased efferent outflow from the sympathetic nervous system. Activity from the central nervous system (CNS) is manifested as a predominance of parasympathetic nervous system activity at the heart and peripheral vasculature. This predominance cannot be produced below the level of spinal cord transection (this part of the body remains neurologically isolated). Therefore, vasoconstriction persists below the level of spinal cord transection. If spinal cord transection is above the level of splanchnic outflow (T4–T6), vasodilation in the neurologically intact portion of the body is insufficient to offset the effects of vasoconstriction (reflected by persistent hypertension).
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