Autonomic dysreflexia is a sudden overreaction of the autonomic nervous system, primarily affecting individuals with a spinal cord injury. This syndrome is a medical emergency because the uncontrolled response can lead to dangerously high blood pressure. The condition results from a breakdown in communication between the brain and the body below the injury site. This disruption prevents the regulation of involuntary functions and causes an imbalanced sympathetic reflex.
The Autonomic Nervous System and Spinal Cord Injury
The autonomic nervous system controls involuntary actions like heart rate and blood pressure. It has two main divisions: the sympathetic nervous system, which prepares the body for the “fight or flight” response, and the parasympathetic nervous system, which handles “rest and digest” functions. These two systems work in a coordinated manner to maintain a stable internal environment, with the brain sending signals down the spinal cord to modulate their activity. A spinal cord injury can sever this communication pathway.
An injury at or above the sixth thoracic vertebra (T6) is a high-risk factor for autonomic dysreflexia. This level is above the major outflow of sympathetic nerves controlling blood vessels in the abdominal organs and lower body. An injury here means the brain cannot send calming parasympathetic signals below the lesion, leaving the sympathetic nervous system unregulated.
Initiation by a Noxious Stimulus
An episode of autonomic dysreflexia is triggered by a painful or irritating event, known as a noxious stimulus, below the level of the spinal cord injury. The person may not consciously feel the discomfort, but their body still reacts. Sensory nerves detect the problem and transmit signals up the spinal cord, but these signals are blocked when they reach the lesion, preventing them from reaching the brain. The most frequent cause is bladder-related issues, such as a distended bladder from a blocked catheter, accounting for 75-85% of cases. The second most prevalent cause is bowel distention from fecal impaction, responsible for 13-19% of episodes.
Other stimuli can also initiate the reflex, including:
- Pressure sores
- Ingrown toenails
- Skin infections
- Restrictive clothing
The Uncontrolled Sympathetic Response
When the ascending sensory signals are halted at the injury site, the spinal cord below the lesion initiates a reflex action on its own. This results in a massive and unregulated discharge from the sympathetic nervous system throughout the parts of the body below the injury. This sympathetic surge causes widespread vasoconstriction, the narrowing of blood vessels, in the abdominal organs and the lower extremities.
This extensive vasoconstriction forces blood through narrower vessels, leading to a rapid and severe increase in blood pressure, known as hypertension. This spike in blood pressure is the primary sign of autonomic dysreflexia, with systolic readings often rising 20 to 40 mmHg or more above the individual’s baseline.
The response is so extreme because the brain’s moderating signals cannot travel down the spinal cord past the injury. The sympathetic activity continues unchecked, driven by the local reflex arc. This leads to the release of hormones like norepinephrine and epinephrine, which further intensifies the vasoconstriction and hypertension.
The Body’s Compensatory Reaction
The body attempts to counteract the sudden rise in blood pressure. Specialized pressure sensors called baroreceptors, located in the major arteries of the chest and neck, detect the severe hypertension and send signals to the brain. In response, the brain initiates compensatory measures to bring the pressure down.
The brain’s primary response is twofold. First, it increases parasympathetic output through the vagus nerve, a large nerve that influences heart function. This action is intended to slow down the heart rate, a condition called bradycardia, to reduce the amount of blood being pumped. The brain also attempts to trigger widespread vasodilation, or the widening of blood vessels, to lower the overall resistance in the circulatory system.
However, the effectiveness of these compensatory signals is severely limited by the spinal cord injury. The brain’s commands to cause vasodilation and calm the sympathetic system can only travel down the spinal cord to the parts of the body above the level of the lesion. This results in a distinctive set of symptoms. Above the injury, vasodilation causes flushing, a pounding headache, and profuse sweating, while below the injury, the uncontrolled sympathetic response continues, causing pale, cool skin due to persistent vasoconstriction. This clear dividing line on the body illustrates the communication failure that defines the condition.