From Wikipedia, the free encyclopedia - View original article

Jump to: navigation, search

Hyperreflexia (or hyper-reflexia) is defined as overactive or overresponsive reflexes. Examples of this can include twitching or spastic tendencies, which are indicative of upper motor neuron disease as well as the lessening or loss of control ordinarily exerted by higher brain centers of lower neural pathways (disinhibition). See Autonomic dysreflexia.


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.[1] Hyperreflexia, also known as autonomic dysreflexia is a state that is unique to patients after spinal cord injury at a T-5 level and above. Patients with a spinal cord injury at Thoracic 5 (T-5) level and above are very susceptible. Patients with spinal cord injuries at Thoracic 6 - Thoracic 10 (T6-T10) may be susceptible. Patients with Thoracic 10 (T-10) and below are usually not susceptible. Also, the older the injury the less likely the person will experience hyperreflexia.[2] Hyperreflexia can develop suddenly, and is a possible emergency situation. If not treated promptly and correctly, it may lead to seizures, stroke, and even death.[2] Hyperreflexia means an over-activity of the Autonomic Nervous System. It can occur when an irritating stimulus is introduced to the body below the level of spinal cord injury, such as an overfull bladder. The stimulus sends nerve impulses to the spinal cord, where they travel upward until they are blocked by the lesion at the level of injury. Since the impulses cannot reach the brain, a reflex is activated that increases activity of the sympathetic portion of autonomic nervous system. This results in spasms and a narrowing of the blood vessels, which causes a rise in the blood pressure. Nerve receptors in the heart and blood vessels detect this rise in blood pressure and send a message to the brain. The brain sends a message to the heart, causing the heartbeat to slow down and the blood vessels above the level of injury to dilate. However, the brain cannot send messages below the level of injury, due to the spinal cord lesion, and therefore the blood pressure cannot be regulated.[2]


There can be many stimuli that cause hyperreflexia. Anything that would have been painful, uncomfortable, or physically irritating before the injury may cause autonomic dysreflexia after the injury.[3] The most common cause of hyperreflexia is spinal cord injury. People with this condition have an excessive nervous system response to the types of stimulation that do not bother healthy people. Other causes include:

The following conditions share many symptoms with autonomic hyperreflexia, but have a different cause:

In 85% of cases hyperreflexia is related to either bladder distention or bowel impaction.[5] But hyperreflexia can be developed via many other causes, including medication and stimulant side effects, hyperthyroidism, electrolyte imbalance, serotonin syndrome, severe brain trauma, and Reye Syndrome.

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)
Skin-related Disorders
Sexual Activity


Hyperreflexia 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.[1]


Symptoms can include any of the following:

Sometimes there are no symptoms, even with a dangerous rise in blood pressure. Other symptoms may include:


Treatment of hyperreflexia must be initiated quickly to prevent complications.

After correcting an obvious problem, and if your catheter is not draining within 2–3 minutes, your catheter must be changed immediately. If you do not have a Foley or suprapubic catheter, perform a catheterization and empty your bladder. If your bladder has not triggered the episode of hyperreflexia, the cause may be your Bowel. Perform a digital stimulation and empty your bowel. If you are performing a digital stimulation when the symptoms first appear, stop the procedure and resume after the symptoms subside. If your bladder or bowel are not the cause, check to see if:

If you are unable to find the stimulus causing hyperreflexia, or your attempts to receive the stimulus fail, you need to obtain emergency medical treatment. Since not all physicians are familiar with hyperreflexia and its treatment, you should carry a card in your billfold that describes the condition and the treatment required. Treatment depends on diagnosing the specific pathology causing this symptom. Should it be caused by use of stimulants or other substances, then it may involve removing these drugs from use. http://calder.med.miami.edu/pointis/treatment.html


There have been reports of hyperreflexia 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 hyperreflexia. 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 hyperreflexia symptoms whilst using functional electrical stimulation. In some cases hyperreflexia 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 hyperreflexia to be relieved.


Prevention of hyperreflexia is very important. Following are precautions you can take which may prevent episodes: If you have an indwelling catheter:



Recovery of hyperreflexia can occur between several hours to several months after a spinal cord injury; however, the phase of recovery is likely to occur in stages rather than on a continuum.[8] The late stage can be defined as between two weeks and several months.[8] Individuals with a severe spinal cord injury (SCI) mainly present with a later stage of recovery because during the early stages they present with spinal shock.[8] Reflex and motor recovery can sometimes return simultaneously.[8]

See also[edit]

External links[edit]


  1. ^ a b "Autonomic Dysreflexia and Hyperreflexia". 
  2. ^ a b c "Automatic Dysreflexia (Hyperreflexia)". 
  3. ^ a b "Symptoms and Causes". 
  4. ^ "Autonomic hyperreflexia: MedlinePlus Medical Encyclopedia". U.S. National Library of Medicine. 
  5. ^ Teasell, Robert W.; J. Malcolm O. Arnold; Andrei Krassiouskov; Gail A. Delaney (2000). "Cardiovascular consequences of loss of supraspinal control of the sympathetic nervous system after spinal cord injury". Archives of Physical Medicine and Rehabilitation 81 (4): 506–516. doi:10.1053/mr.2000.3848. 
  6. ^ "Autonomic hyperreflexia: MedlinePlus Medical Encyclopedia". U.S National Library of Medicine. 
  7. ^ "PRevention". RehabTeamSite. Louis Calder Memorial Library of the University of Miami. 
  8. ^ a b c d Little, J., Ditunno, J. F., Stien, S., A., Harris, R. M. (1999). Incomplete spinal cord injury: Neuronal mechanisms of motor recovery and hyperreflexia. Arch Phys Med Rehabil 80(5): 587-599.