Autonomic Dysreflexia and Hyperreflexia
- Description and Symptoms
- Immediate Treatment
- Mechanism of Autonomic Dysreflexia
- Causes and Triggers of AD
- Functional Electrical Stimulation Headaches
- Autonomic Dysreflexia Wallet Card
Description and Symptoms
Autonomic dysreflexia, also known as hyperreflexia is a potentially life threatening condition which is considered a medical emergency requiring immediate attention. This condition occurs due to an exaggerated autonomic response to pain below the level of spinal cord injury resulting in the blood pressure becoming excessively high.
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 it can lead to a stroke and death.
Immediate steps to reduce high blood pressure due to autonomic dysreflexia include:
- Relieving pain stimulus below spinal cord injury level.
- Sitting patient in an upright position to use gravity to reduce intra cranial blood pressure
- In severe cases of autonomic dysreflexia a blood pressure lowering drug should be administered such as: phentolamine 5-10mg intravenously, gylceryl trinitrate 300 micro-grams sub-lingually or nifedipine 5-10mg sub-lingually.
Mechanism of Autonomic Dysreflexia
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). See the autonomic dysreflexia image for additional help.
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 mid brain, 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 brain stem 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.
Causes and Triggers of AD
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 is the 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 the formation of 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 this condition 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.
Bladder (most common)
- Overstretch or irritation of bladder wall
- Urinary tract infection
- Urinary retention
- Blocked catheter
- Overfilled collection bag
- Bladder stones
- Noncompliance with intermittent catheterisation program
- Over distention or irritation
- Constipation / impaction
- Distention during bowel program (digital stimulation)
- Hemorrhoids 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)
- Ingrown toenails
- 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)
- Skeletal fractures
Functional Electrical Stimulation (FES)
There have been reports of autonomic dysreflexia resulting in headaches in individuals undertaking functional electrical stimulation. Caution should be exercised in the use of functional electrical stimulation by people with a spinal cord injury with lesion levels above the major splanchnic outflow (T6).
If an autonomic headache is experienced whilst undertaking functional electrical stimulation, the program should be halted, which in most cases will result in the cessation of symptoms. If a muscle tear or fracture has occurred, then the headaches may continue after stimulation has ceased. Generally, individuals with osteoporosis, severe spasticity, contractures and pressure sores may experience symptoms whilst using functional electrical stimulation. In some cases autonomic dysreflexia is causes by the electrical current passing through, and activating the muscles.
If any of the above sources of pain are found, they must be addressed in order for autonomic dysreflexia to be relieved.
The above information has been written with reference from the following sources:
Curt, A. (1997)Assessment of autonomic dysreflexia in patients with spinal cord injury. Journal of Neurology, Neurosurgery and Psychiatry 62: 5, 473-477.
Gatehouse, M. (1998)Moving Forward: A guide to living with spinal cord injury (2nd edn). London: Spinal Injuries Association and MBA Group.
Grundy, D., Swain, A. (1996)ABC of Spinal Cord Injury (3rd edn). London: BMJ Publishing Group.
Lightner, D. (1998)Contemporary urologic management of patients with spinal cord injury. Mayo Clinic Proceedings 73: 5, 434-438. http://www.spinalcord.org/resource-center/askus/index.php?pg=kb.page&id=1395