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SCI Health Issues
Autonomic Dysreflexia & Hyperreflexia
Autonomic Dysreflexia Sections
Autonomic Dysreflexia, also known as Hyperreflexia is a potentially life threatening condition which is considered a medical emergency requiring immediate attention. The condition of autonomic dysreflexia 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 of autonomic dysreflexia, it can lead to a stroke and death.
Immediate steps to reduce high blood pressure due to autonomic dysreflexia include:
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:
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 autonomic dysreflexia. 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 autonomic dysreflexia 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.
Autonomic Dysreflexia Sections
The above information has been written with reference from the following sources: