Autonomic Dysreflexia (AD) is a potentially life-threatening medical emergency characterized by an abrupt and severe elevation in blood pressure. It is most frequently observed in individuals with a spinal cord injury (SCI). The sudden, dangerously high rise in systemic blood pressure poses a significant risk for complications like stroke or seizure. Understanding the underlying mechanisms is necessary to address this unique physiological response.
The Necessary Anatomical Prerequisite
The development of Autonomic Dysreflexia is strictly dependent on the location of the spinal cord injury. Individuals must have a lesion situated at or above the sixth thoracic vertebra (T6) to be susceptible. This anatomical cutoff is significant because it separates the central nervous system’s ability to regulate lower body functions from the brain’s major blood pressure control centers.
The sympathetic nervous system (SNS) controls the constriction and dilation of blood vessels, managing overall blood pressure. A major portion of the sympathetic outflow controlling the large abdominal blood vessels (splanchnic circulation) originates below the T6 level. When an injury occurs at or above T6, the spinal cord below the injury becomes functionally isolated from the brain’s regulatory centers.
The connection between the brainstem and the sympathetic ganglia below the lesion is severed. Consequently, the brain can no longer send signals to inhibit or moderate the activity of these lower spinal segments. This anatomical separation primes the lower body’s sympathetic system to react in an exaggerated, unregulated manner to stimuli. The spinal cord segment below the injury acts as an independent reflex center, ready to trigger a massive response without higher brain control.
Ascending Signals and Sympathetic Overdrive
Autonomic Dysreflexia is initiated by a noxious or irritating stimulus originating below the level of the spinal cord injury. Common triggers are typically related to visceral functions, such as an overly full bladder or blocked urinary catheter tubing. Bowel impaction, hemorrhoids, tight clothing, or pressure sores can also serve as initiating factors.
Sensory receptors detect this irritation and transmit the signal along afferent nerves toward the spinal cord. These signals travel upward until they reach the level of the injury, where they cannot ascend past the lesion to the brain. Instead of continuing for conscious perception, the signals activate local reflex arcs within the spinal cord segments below the injury.
This intense, uninhibited afferent input triggers a massive, widespread discharge of the sympathetic nervous system below the lesion. Since the brain cannot modulate this response, sympathetic neurons fire excessively, releasing large amounts of norepinephrine. This sudden surge of neurotransmitters causes severe, generalized vasoconstriction (the narrowing of blood vessels) in the abdomen and lower extremities.
The resulting constriction dramatically increases resistance to blood flow in the lower half of the body. This rapid increase in peripheral vascular resistance is the direct cause of the sudden, severe spike in systemic blood pressure.
The Failure of Descending Inhibitory Control
The sudden rise in blood pressure immediately activates the body’s natural regulatory mechanisms. Specialized sensory receptors called baroreceptors, located primarily within the carotid arteries and the aortic arch, sense this dangerously high pressure. These receptors immediately transmit signals to the brainstem’s cardiovascular control centers.
In response to the detected hypertension, the brain initiates powerful corrective measures aimed at lowering systemic pressure. The primary mechanism is to increase parasympathetic activity and send descending inhibitory signals to the sympathetic outflow tracts. This parasympathetic response, carried primarily by the vagus nerve, successfully acts on the heart, causing a compensatory slowing of the heart rate (bradycardia).
However, the attempt to inhibit the massive sympathetic firing and cause vasodilation below the injury is completely thwarted. The inhibitory signals generated in the brainstem must travel down the spinal cord to reach the sympathetic ganglia located below T6. The spinal cord lesion acts as an insurmountable physical barrier, blocking these descending regulatory commands from reaching their targets.
Because the sympathetic neurons below the lesion remain disconnected, they continue to fire uncontrollably, sustaining severe vasoconstriction in the lower body. The brain’s attempts to lower blood pressure are only partially effective, limited to slowing the heart rate and causing vasodilation above the injury. This failure of descending inhibitory control is the precise reason the hypertensive crisis persists.
Distinct Physiological Manifestations
The clinical presentation of Autonomic Dysreflexia is a unique combination of symptoms reflecting the differential nervous system activity above and below the spinal cord injury. Above the lesion, the brain’s corrective parasympathetic response is fully effective because the neural pathways involved remain intact.
This localized parasympathetic dominance causes vasodilation in the head, neck, and upper chest, leading to profuse sweating and visible skin flushing. Nasal congestion is also a common manifestation, resulting from the vasodilation of mucosal blood vessels. Simultaneously, vagus nerve activity causes a significant, though often insufficient, slowing of the heart rate (bradycardia).
In stark contrast, body regions below the injury exhibit the effects of uncontrolled sympathetic overdrive. The intense, sustained vasoconstriction results in the skin appearing pale, cool, and clammy. The difference in skin appearance above and below the SCI is a hallmark sign of the episode.
The rapid and severe rise in systemic blood pressure causes a sudden increase in intracranial pressure. This mechanical pressure on the blood vessels of the brain is the direct cause of the characteristic, pounding headache reported during an AD episode. These distinct, dual manifestations provide clear evidence of the physiological disconnect between the brain’s control centers and the isolated spinal cord segments.