In both normal and SCI patients, noxious stimulation of peripheral sensory receptors (i.e., bladder distention) will activate afferent pathways to produce a sympathetic response. The sympathetic outflow stimulates peripheral vasoconstriction, thus elevating arterial blood pressure. Arterial vessel baroreceptors are then activated and signal brain-stem inhibitory pathways that descend the spinal cord to limit the sympathetic outflow and prevent excessive arterial vasoconstriction. The brain-stem inhibitory centers increase vagal stimulation to the heart, resulting in bradycardia. In SCI patients, vagal output to the heart still occurs; however, brain-stem inhibitory descending pathways that limit sympathetic outflow are blocked in the spinal cord at the level of the spinal cord lesion. This results in excessive vasoconstriction and markedly elevated blood pressure (Fig. 185.1).

The main clinical signs and symptoms of autonomic dysreflexia are related to both the excessive sympathetic output below the spinal cord level and from compensatory parasympathetic output originating from above the spinal cord level. Profound hypertension occurs because of excessive peripheral vasoconstriction, and the skin will appear cool and clammy below the spinal cord level. Above the spinal cord level, parasympathetic output may result in vasodilatation of blood vessels, resulting in a pounding headache, skin flushing, sweating, and nasal congestion. Other symptoms the patient may report include visual spots, blurry vision, and anxiety. The elevated blood pressure may lead to a host of clinical sequelae, including intracranial
hemorrhage, seizures, hypertensive encephalopathy, cerebral edema, atrial fibrillation, pulmonary edema, renal failure, coma, and death.