Patients with a spinal cord injury at T7 or higher are at risk for autonomic hyperreflexia. Normally, the reflexic response to cutaneous, visceral (bladder), and proprioceptive stimuli are to some extent attenuated by descending, inhibitory impulses. However, in patients with SCI, these impulses may be curtailed, leading to uninhibited spinal cord reflexes and consequent vascular instability – initially a substanial increase BP above the level of the lesion, followed by an overzealous vagal response, with bradycardia, heart block, vasodilation, and flushing all possible.
Autonomic Hyperreflexia
- Anatomy: Spinal cord injury T7 or above
- Stimulus: Cutaneous, visceral (bladder), proprioceptive, below the level of the lesion
- Etiology: Spinal reflex which is normally inhibited by descending feedback
- Result: hypertension followed by overzealous vagal response (brady, heart block, vasodilation)
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