AD. This condition may arise when spinal shock starts to resolve and reflexes return. A stimulus (typically a noxious one) activates the spinal reflex mechanism, causing vasoconstriction below the injury level, which in turn causes BP to rise. Injuries at the T6 level and higher involve the splanchnic vascular bed, resulting in a “visceral squeeze,” which further increases BP and boosts venous return to the heart. Baroreceptors in the carotid arteries and aortic arch detect the critical rise in BP and send signals to the brainstem, which responds by sending messages via the parasympathetic nervous system to induce vasodilation and slow the heart rate. Unfortunately, those messages can’t descend below the injury level to disrupt vasoconstriction. As a result, pallor develops below the injury level while flushing, sweating, and pounding headache occur above it.