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Autonomic Dysreflexia Sections
- Autonomic Dysreflexia
- Mechanism of Autonomic Dysreflexia
- Causes of Autonomic Dysreflexia
- Functional Electrical Stimulation Headaches
- Autonomic Dysreflexia Wallet Card
Autonomic Dysreflexia, also known as Hyperreflexia, is a potentially life threatening condition which can be considered a medical emergency requiring immediate attention. It occurs where the blood pressure in a person with a spinal cord injury (SCI) above T5-6 becomes excessively high due to the over activity of the Autonomic Nervous System.
The most common symptoms of autonomic dysreflexia are sweating, pounding headache, tingling sensation on the face and neck, blotchy skin around the neck and goose bumps.
Not all the symptoms always appear at once, and their severity may vary. In untreated and extreme cases of autonomic dysreflexia, it can lead to a stroke and death.
Autonomic Dysreflexia is usually caused when a painful stimulus occurs below the level of spinal cord injury. The stimulus is then mediated through the Central Nervous System (CNS) and the Peripheral Nervous System (PNS).
The CNS is made up of the spinal cord and brain, which control voluntary acts and end organs via their respective nerves. The PNS is made up from 12 pairs of cranial nerves, spinal nerves and peripheral nerves. The PNS also is divided into the somatic nervous system and the autonomic nervous system. The autonomic nervous system is responsible for the signs and symptoms of autonomic dysreflexia. The autonomic nervous system normally maintains body homeostasis via its two branches, the parasympathetic autonomic nervous system (PANS) and the sympathetic autonomic nervous system (SANS). These branches have complementary roles through a negative-feedback system; that is, when one branch is stimulated, the other branch is suppressed.
The SANS is associated with the flight-or-fight response, causing dilation of the pupils, increased heart rate, vasoconstriction, decreased peristalsis and tone of the gut, release of epinephrine and norepinephrine, as well as other effects. The effects of PANS stimulation are the opposite of the SANS; for the most part, these are constriction of the pupil, decreased heart rate, as well as increased peristalsis and tone of the gut.
The PANS and SANS exit at different sites in the CNS. The PANS exits via the midbrain, pons, medulla (cranial nerves [CN] III, VII, IX, and X), and the sacral level of the spinal cord. The SANS exits via the thoracic and lumbar segments of the spinal cord. There is a major sympathetic output (called the splanchnic outflow) between T5 and L2.
In someone with a high-level spinal cord injury, intact lower motor neurons sense the painful stimuli below the level of injury and transmit the message up the spinal cord (see diagram). At the level of the spinal cord injury, the pain signal is interrupted and prevented from being transmitted to the cerebral cortex. The site of the spinal cord injury also interrupts the two branches of the autonomic nervous system and disconnects the feedback loop, causing the two branches to function independently.
The ascending information reaches the major splanchnic sympathetic outflow (T5-T6) and stimulates a sympathetic response. The sympathetic response causes vasoconstriction, resulting in hypertension, pounding headache, visual changes, anxiety, pallor, and goose bumps below the level of injury. This hypertension stimulates the baroreceptors in the carotid sinuses and aortic arch. The PANS is unable to counteract these effects through the injured spinal cord, however. Instead, the PANS attempts to maintain homeostasis by slowing down the heart rate. The brainstem stimulates the heart, through the vagus nerve, causing bradycardia and vasodilation above the level of injury. The PANS impulses are unable to descend past the lesion, and therefore no changes occur below the level of injury.
There can be many stimuli that cause autonomic dysreflexia. Anything that would have been painful, uncomfortable, or physically irritating before the injury may cause autonomic dysreflexia after the injury.
The most common cause seems to be overfilling of the bladder. This could be due to a blockage in the urinary drainage device, bladder infection (cystitis), inadequate bladder emptying, bladder spasms, or possibly stones in the bladder.
The second most common cause is a bowel that is full of stool or gas. Any stimulus to the rectum, such as digital stimulation, can trigger a reaction, leading to autonomic dysreflexia.
In 85% of cases autonomic dysreflexia is related to either bladder distention or bowel impaction (Teasell et al. 2000; Mathias & Frankel 2002).
Other causes include skin irritations, wounds, pressure sores, burns, broken bones, pregnancy, ingrown toenails, appendicitis, and other medical complications.
In general, noxious stimuli (irritants, things which would ordinarily cause pain) to areas of body below the level of spinal injury. Things to consider include:
Bladder (most common)
Overstretch or irritation of bladder wall
Urinary tract infection
Overfilled collection bag
Noncompliance with intermittent catheterisation program
Over distention or irritation
Constipation / impaction
Distention during bowel program (digital stimulation)
Haemorrhoids or anal fissures
Infection or irritation (eg. appendicitis)
Any direct irritant below the level of injury (eg. – prolonged pressure by object in shoe or wheelchair, cut, bruise, abrasion)
Pressure sores (decubitus ulcer)
Burns (eg. – sunburn, burns from using hot water)
Tight or restrictive clothing or pressure to skin from sitting on wrinkled clothing
Over stimulation during sexual activity [stimuli to the pelvic region which would ordinarily be painful if sensation were present] Menstrual cramps
Labour and delivery
Heterotopic ossification (“Myositis ossificans”, “Heterotopic bone”)
Acute abdominal conditions (gastric ulcer, colitis, peritonitis)