eMedicine Specialties > Physical Medicine and Rehabilitation > Spinal Cord Injury

Autonomic Dysreflexia in Spinal Cord Injury

Denise I Campagnolo, MD, MS, Director of Multiple Sclerosis Clinical Research and Staff Physiatrist, Barrow Neurology Clinics, St Joseph's Hospital and Medical Center; Investigator for Barrow Neurology Clinics; Director, NARCOMS Project for Consortium of MS Centers

Updated: Jul 2, 2009

Introduction

Background

Autonomic dysreflexia (AD) is a syndrome of massive imbalanced reflex sympathetic discharge occurring in patients with spinal cord injury (SCI) above the splanchnic sympathetic outflow (T5-T6). Anthony Bowlby first recognized this syndrome in 1890 when he described profuse sweating and erythematous rash of the head and neck initiated by bladder catheterization in an 18-year-old patient with SCI. Guttmann and Whitteridge completed a full description of the syndrome in 1947. This condition represents a medical emergency, so recognizing and treating the earliest signs and symptoms efficiently can avoid dangerous sequelae of elevated blood pressure. SCI patients, caregivers, and medical professionals must be knowledgeable about this syndrome and its management. (See image below and Image 1.)

(A) A strong sensory input (not necessarily noxious) is carried into the spinal cord via intact peripheral nerves. The most common origins are bladder and bowel. (B) This strong sensory input travels up the spinal cord and evokes a massive reflex sympathetic surge from the thoracolumbar sympathetic nerves, causing widespread vasoconstriction, most significantly in the subdiaphragmatic (or splanchnic) vasculature. Thus, peripheral arterial hypertension occurs. (C) The brain detects this hypertensive crisis through intact baroreceptors in the neck delivered to the brain through cranial nerves IX and X (Vagus). (D) The brain attempts 2 maneuvers to halt the progression of this hypertensive crisis. First, the brain attempts to shut down the sympathetic surge by sending descending inhibitory impulses. These impulses do not get to most sympathetic outflow levels because of the spinal cord injury at T6 or above. Inhibitory impulses are blocked in the injured spinal cord. In the second maneuver, the brain attempts to bring down peripheral blood pressure by slowing the heart rate through an intact vagus (parasympathetic) nerve; however, this compensatory bradycardia is inadequate and hypertension continues. In summary, the sympathetics prevail below the level of neurologic injury, and the parasympathetic nerves prevail above the level of injury. Once the inciting stimulus is removed, reflex hypertension resolves.

Pathophysiology

This phenomenon occurs after the phase of spinal shock in which reflexes return. Individuals with injury above the major splanchnic outflow may develop autonomic dysreflexia (AD). Below the injury, intact peripheral sensory nerves transmit impulses that ascend in the spinothalamic and posterior columns to stimulate sympathetic neurons located in the intermediolateral gray matter of the spinal cord. The inhibitory outflow above the SCI from cerebral vasomotor centers is increased, but it is unable to pass below the block of the SCI. This large sympathetic outflow causes release of various neurotransmitters (norepinephrine, dopamine-b-hydroxylase, dopamine), causing piloerection, skin pallor, and severe vasoconstriction in arterial vasculature.¹ The result is sudden elevation in blood pressure and vasodilation above the level of injury. Patients commonly have a headache caused by vasodilation of pain sensitive intracranial vessels.

Vasomotor brainstem reflexes attempt to lower blood pressure by increasing parasympathetic stimulation to the heart through the vagus nerve to cause compensatory bradycardia. This reflex action cannot compensate for severe vasoconstriction, explained by the Poiseuille formula, where pressure in a tube is affected to the fourth power by change in radius (vasoconstriction) and only linearly by change in flow rate (bradycardia). Parasympathetic nerves prevail above the level of injury, which may be characterized by profuse sweating and vasodilation with skin flushing.

Cameron and colleagues have found that site-directed genetic manipulation of fiber sprouting in the spinal dorsal horns in a cord compression rat model could alter the extent of hyperreflexia after bowel distention, indicating that endogenous spinal cord circuitry/neural sprouting plays a role in the pathophysiology of AD.²

Frequency

United States

Reported prevalence rates vary, but the generally accepted rate is 48-90% of all individuals who are injured at T6 and above. Some incidence has been reported in SCI as low as T10. Autonomic dysreflexia (AD) occurs during labor in approximately two thirds of pregnant women with SCI above the level of T6. The occurrence of AD increases as the patient evolves out of spinal shock. With the return of sacral reflexes, the possibility of AD increases.³

Mortality/Morbidity

Sex

The male-to-female ratio for sustaining SCI is 4:1; therefore, autonomic dysreflexia is primarily a male phenomenon.

Age

No specific relationship has been documented between autonomic dysreflexia and age.

Clinical

History

The patient with autonomic dysreflexia generally gives a history of blurry vision, headaches, and a sense of anxiety. Feelings of apprehension or anxiety over an impending physical problem commonly are exhibited.

Physical

A patient with autonomic dysreflexia (AD) may have 1 or more of the following findings on physical examination:

• A sudden significant rise in systolic and diastolic blood pressures, usually associated with bradycardia, can appear. The normal systolic blood pressure for SCI above T6 is 90-110 mm Hg. Blood pressure 20-40 mm Hg above the reference range for such patients may be a sign of AD.
• Profuse sweating above the level of lesion, especially in the face, neck, and shoulders, may be noted, but it rarely occurs below the level of the lesion because of sympathetic cholinergic activity.
• Goose bumps above, or possibly below, the level of the lesion may be observed.
• Flushing of the skin above the level of the lesion, especially in the face, neck, and shoulders, frequently is noted.
• The patient may report blurred vision.
• Spots may appear in the patient's visual fields.
• Nasal congestion is common.
• No symptoms may be observed, despite elevated blood pressure.

Causes

Episodes of autonomic dysreflexia (AD) can be triggered by many potential causes.⁴ Essentially any painful, irritating, or even strong stimulus below the level of the injury can cause an episode of AD. Although the list is not comprehensive, the following events or conditions all can cause episodes of AD:

• Bladder distension
• Urinary tract infection
• Cystoscopy
• Urodynamics
• Detrusor-sphincter dyssynergia⁵
• Epididymitis or scrotal compression
• Bowel distension
• Bowel impaction
• Gallstones
• Gastric ulcers or gastritis
• Invasive testing
• Hemorrhoids
• Gastrocolic irritation
• Appendicitis or other abdominal pathology trauma
• Menstruation
• Pregnancy, especially labor and delivery
• Vaginitis
• Sexual intercourse
• Ejaculation
• Deep vein thrombosis
• Pulmonary emboli
• Pressure ulcers
• Ingrown toenail
• Burns or sunburn
• Blisters
• Insect bites
• Contact with hard or sharp objects
• Temperature fluctuations
• Constrictive clothing, shoes, or appliances
• Heterotopic bone
• Fractures or other trauma
• Surgical or diagnostic procedures
• Pain

Differential Diagnoses

Other Problems to Be Considered

Essential hypertension
Pheochromocytoma

Treatment

Rehabilitation Program

Physical Therapy

Physical therapists who treat SCI patients need to have a good understanding of autonomic dysreflexia (AD) and be familiar with the signs and symptoms of this potentially life-threatening condition.³ When completing physical therapy sessions, the therapist needs to monitor the urinary catheter for any blockage or twisting. If the patient becomes hypertensive during therapy, he/she should be placed in an upright position immediately, rather than remain in a supine or reclining position. The therapist needs to complete careful inspection to identify the source of painful stimuli (eg, catheter, restrictive clothing, leg bag straps, abdominal supports, orthoses).⁴

A less common cause of AD during physical therapy sessions may originate with muscle stretching, either from range of motion or passive stretching. If the patient develops AD, the physical therapist needs to treat it as a medical emergency and be familiar with established protocols for medical management within his/her particular setting. The individual therapy session then must be discontinued to allow the patient to stabilize and recover.

Occupational Therapy

Occupational therapy is another discipline involved extensively in the rehabilitation of individuals with SCI. The occupational therapist also must be familiar with the signs and symptoms of autonomic dysreflexia (AD) and be able to respond quickly if the condition develops during a therapy session.³ The occupational therapist performs extensive training in the performance of activities of daily living with patients who have sustained SCI. Activities of daily living include proper bowel and bladder management, which can help prevent the occurrence of AD. The occupational therapist may be involved in establishing a regular bowel program and also may complete patient and family/caregiver education on this aspect of care. The occupational and physical therapists should educate the patient and family members about AD and ensure that they are familiar with prevention strategies, signs and symptoms, and proper management of the condition.

Speech Therapy

Generally, the treatment provided by the speech therapist is not associated with any painful stimuli below the lesion that may precipitate an autonomic dysreflexia response; however, as health care providers involved in the care of individuals with SCI, the speech therapist must be familiar with the manifestations of this potential life-threatening complication.³

Recreational Therapy

Recreational therapists also are important members of the rehabilitation team, as they help patients with SCI to become involved in recreational and social activities. As members of the SCI team, they also must be knowledgeable about autonomic dysreflexia and know how to respond appropriately if the patient develops symptoms during a recreational therapy session.³

Medical Issues/Complications

Complications associated with autonomic dysreflexia result directly from sustained, severe peripheral hypertension and include retinal/cerebral hemorrhage, myocardial infarction, and seizures.

Consultations

If the cause of the autonomic dysreflexia episode is not found and blood pressure remains elevated, recommend that the patient go to the nearest emergency department for close monitoring and further investigation of the possible cause. Consult an intensive care specialist for ICU monitoring and treatment of the hypertension.

Medication

Check the patient's blood pressure. If blood pressure is elevated and the person is supine, have the person sit up immediately and loosen any clothing or constrictive devices. Sitting leads to pooling of blood in the lower extremities and may reduce blood pressure. Monitor blood pressure and pulse every 2-5 minutes until they have stabilized; blood pressures can fluctuate quickly during an AD episode from impaired autonomic regulation. Survey the person for instigating causes, beginning with the urinary system, the most common cause of autonomic dysreflexia (AD).⁶

• If an indwelling urinary catheter is not in place, catheterize the patient.
• If the individual has an indwelling urinary catheter, check the system along its entire length for kinks, folds, constrictions, or obstructions and for correct placement of the indwelling catheter.
• If the catheter appears to be blocked, gently irrigate the bladder with a small amount of fluid, such as normal saline at body temperature. Avoid manually compressing or tapping on the bladder.
• If the catheter is draining and blood pressure remains elevated, suspect fecal impaction, the second most common cause of AD, and check the rectum for stool using lidocaine jelly as lubricant.
• Use an antihypertensive agent with rapid onset and short duration while the causes of AD are being investigated.
• The most commonly used agents are nifedipine and nitrates (eg, nitroglycerine paste). Nifedipine should be in the immediate release form; bite-and-swallow is the preferred method of administration, not sublingual. Other agents used are mecamylamine, diazoxide, and phenoxybenzamine.
• Use antihypertensives with extreme caution in older persons or people with coronary artery disease.
• Monitor the individual's symptoms and blood pressure for at least 2 hours after resolution of the AD episode to ensure that elevation of blood pressure does not recur. AD may resolve because of medication, not because of resolution of the underlying cause.
• If there is poor response to treatment and/or if the cause of the AD has not been identified, send the patient to ER for monitoring, maintenance of pharmacologic control of blood pressure, and investigation of other possible causes of the AD.
• Document the episode.

A Taiwanese study indicated that in patients with SCI who have detrusor sphincter dyssynergia, using a combination of fluoroscopy and electromyography to localize the external urethral sphincter, with a Foley catheter employed to visualize vesicourethral anatomy, makes transperineal injection of botulinum toxin type A into the external urethral sphincter safe, accurate, and easy to perform.⁵ Such injections have been shown to reduce the occurrence and degree of autonomic dysreflexia, as well as of vesicoureteral reflux, hydronephrosis, and urinary tract infection.

Antihypertensives

Antihypertensive agents with rapid onset and short duration are administered while the causes of autonomic dysreflexia (AD) are investigated if BP is at or above 150 mm Hg systolic. Patients who have experienced episodes of AD are treated with antihypertensives prior to procedures known to cause their AD episodes.

Nifedipine (Procardia)

Calcium ion influx inhibitor (slow-channel blocker or calcium ion antagonist); inhibits transmembrane influx of calcium ions into cardiac and smooth muscle. Reduces arterial pressure at rest and at a given level of exercise by dilating peripheral arterioles and reducing the total peripheral resistance (afterload).

Dosing

Adult

10 mg cap PO initially; bite and swallow

Pediatric

Not recommended

Interactions

Concomitant administration with beta-blocking agents usually well tolerated; may increase likelihood of congestive heart failure, severe hypotension, or exacerbation of angina; concomitant administration with nitrates safe, but no controlled studies evaluate antianginal effectiveness
Isolated reports of patients with elevated digoxin levels; possible interaction between digoxin and nifedipine; monitor digoxin levels when initiating, adjusting, and discontinuing
Rare reports of interaction between quinidine and nifedipine with a decreased plasma level of quinidine
Rare reports of increased prothrombin time in patients taking Coumadin anticoagulants and nifedipine; relationship uncertain
Significant increase in peak plasma levels (80%) and area-under-the-curve (74%) after 1 week of cimetidine at 1000 mg/d and nifedipine at 40 mg/d
Smaller nonsignificant increases with ranitidine; effect possibly mediated by known inhibition of cimetidine on hepatic cytochrome P-450, enzyme system probably responsible for first-pass metabolism
Cautious titration advised if nifedipine therapy initiated in patient receiving cimetidine

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Decreases peripheral vascular resistance; careful monitoring of BP advised during initial administration and titration
Mild-to-moderate peripheral edema seen in 1/10 patients, associated with arterial vasodilation, not from left ventricular dysfunction
Occasional significant elevations of enzymes (eg, alkaline phosphatase, CPK, LDH, SGOT, SGPT); rarely associated with clinical symptoms; cholestasis with or without jaundice reported; allergic hepatitis; decreases platelet aggregation in vitro; moderate but statistically significant decrease in platelet aggregation and increase in bleeding time in some patients; probably function of inhibition of calcium transport across platelet membrane; no clinical significance demonstrated for these findings; positive direct Coombs test with or without hemolytic anemia reported but causal relationship not determined

Nitroglycerine (Depo-Nit, Nitrostat, Nitrol, Nitro-Bid)

Principal pharmacologic action of nitroglycerin is relaxation of vascular smooth muscle, producing vasodilator effect on both peripheral arteries and veins with more prominent effects on the latter. Dilation of postcapillary vessels, including large veins, promotes peripheral pooling of blood and decreases venous return to the heart, thereby reducing left ventricular end-diastolic pressure (preload). Arteriolar relaxation reduces systemic vascular resistance and arterial pressure (after-load).

Dosing

Adult

0.4 mg per metered spray for SL use or 2% nitroglycerine ointment
Start with 0.5-in strip to chest wall and titrate as necessary; alternatively, 0.15-0.6 mg tab SL or 5 mcg/min IV

Pediatric

Not established

Interactions

Alcohol may enhance sensitivity to hypotensive effects of nitrates (acts directly on vascular muscle); other agents that depend on vascular smooth muscle as final common path may have decreased or increased effect depending upon agent; symptomatic orthostatic hypotension reported when calcium channel blockers and oral controlled-release nitroglycerin concomitantly administered; dose adjustments sometimes necessary

Contraindications

Documented hypersensitivity; concurrent use of sildenafil (Viagra)

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in severe hypotension, particularly with upright posture, possible; use with caution in subjects with volume depletion from diuretic therapy or with low systolic blood pressure; paradoxic bradycardia and increased angina pectoris from nitroglycerin-induced hypotension; may aggravate angina caused by hypertrophic cardiomyopathy; tolerance and cross-tolerance to other nitrates possible; tolerance to vascular and antianginal effects of nitrates demonstrated in clinical trials, occupational exposure, and tissue experiments in laboratory; tolerance in industrial workers demonstrated; physical dependence occurs since chest pain, acute myocardial infarction, and sudden death occur in industrial workers during withdrawal

Phenoxybenzamine hydrochloride (Dibenzyline)

Long-acting, adrenergic, alpha-receptor blocking agent that can produce and maintain chemical sympathectomy by oral administration; increases blood flow to skin, mucosae, and abdominal viscera and lowers supine and erect blood pressures.
No effect on parasympathetic system.

Dosing

Adult

Adjust dose to fit needs of each patient
Slowly increase dose until desired effect obtained or side effects from blockade problematic
Observe patient on each level before instituting increase
Dosage should provide symptomatic relief and/or objective improvement, but not to where side effects from blockage are troublesome
Initially, administer 10 mg of Dibenzyline (phenoxybenzamine hydrochloride) PO bid; increase dose qod, usually to 20-40 mg 2 or 3 times/d, until an optimal dosage is obtained, as judged by blood pressure control

Pediatric

Not established

Interactions

Alpha-adrenergic blockade leaves beta-adrenergic receptors unopposed; compounds stimulating both types of receptors associated with exaggerated hypotensive response and tachycardia; caution in patients with marked cerebral or coronary arteriosclerosis or renal damage; may aggravate symptoms of respiratory infections; may interact with compounds that stimulate alpha-adrenergic and beta-adrenergic receptors (eg, epinephrine) to produce exaggerated hypotensive response and tachycardia; blocks hyperthermia production by levarterenol and hypothermia production by reserpine

Contraindications

Documented hypersensitivity; those to whom a fall in blood pressure would be undesirable

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in cerebral or coronary arteriosclerosis and renal impairment; can worsen symptoms of respiratory tract infections
Adverse effects include postural hypotension, tachycardia, inhibition of ejaculation, nasal congestion, miosis, gastrointestinal irritation, drowsiness, fatigue

Mecamylamine (Inversine)

Potent oral secondary amine, antihypertensive agent, and ganglion blocker.
Produces smooth and predictable reduction of blood pressure with small oral dose.
Antihypertensive effect predominantly orthostatic, but supine blood pressure also significantly reduced.
Used for management of moderately severe-to-severe essential hypertension and in uncomplicated cases of malignant hypertension.

Dosing

Adult

2.5 mg PO prn

Pediatric

Not established

Interactions

Antibiotics and sulfonamides; may be potentiated by anesthesia, other antihypertensive drugs, and alcohol

Contraindications

Documented hypersensitivity; coronary insufficiency, pyloric stenosis, glaucoma, uremia, recent myocardial infarction, unreliable/uncooperative patients

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in impaired renal function, previous CNS abnormalities, prostatic hypertrophy, bladder obstruction, patients receiving sulfonamides or antibiotics that cause neuromuscular blockade; adverse effects include dizziness, lightheadedness (getting up slowly is advised)
Interstitial pulmonary edema and fibrosis, urinary retention, impotence, decreased libido, weakness, fatigue, sedation, marked cerebral and coronary arteriosclerosis, recent cerebral accident may occur
No restriction of sodium intake necessary, but adjustment of dosage of ganglion blocker if necessary
Caution in prostatic hypertrophy, bladder neck obstruction, and urethral stricture
Frequent loose bowel movements with abdominal distention and decreased borborygmi are first signs of paralytic ileus (discontinue immediately and take remedial steps)

Diazoxide (Hyperstat)

Nondiuretic benzothiadiazine antihypertensive agent; achieves prompt reduction of blood pressure by relaxing smooth muscle in peripheral arterioles; cardiac output increases as blood pressure is reduced.

Dosing

Adult

1-3 mg/kg IV to maximum dose of 150 mg in single injection; repeat at 5-15 min intervals until reduction of BP is satisfactory (eg, diastolic pressure <100 mm Hg)

Pediatric

Administer as in adults

Interactions

Highly bound to serum protein, can be expected to displace other substances also bound to protein (eg, bilirubin or coumarin and derivatives, resulting in higher blood levels of these substances)
Hypotension may result when administered to patients who have received other antihypertensive medication within 6 h
Excessive hypotension in 1 patient after concomitant administration with hydralazine and methyldopa may occur
Maternal hypotension and fetal bradycardia occurred in patient in labor who received reserpine and hydralazine prior to administration
Neonatal hyperglycemia following intrapartum administration after injection also reported; should not be administered IV within 6 h of administration of hydralazine, reserpine, alphaprodine, methyldopa, beta-blockers, prazosin, minoxidil, nitrites
Concomitant administration with thiazides or other commonly used diuretics may potentiate hyperuricemic and antihypertensive effects
Hyperglycemic and hyperuricemic effects of diazoxide preclude proper assessment of metabolic states
Increased renin secretion, IgG concentrations, decreased cortisol secretion noted
Inhibits glucagon-stimulated insulin release and causes false-negative insulin response to glucagon
Increased serum free fatty acids and decreased plasma insulin levels in rat, dog, monkey

Contraindications

Documented hypersensitivity; aortic coarctation, pheochromocytoma, arteriovenous shunts, and aortic aneurysm; compensatory hypertension (eg, that associated with aortic coarctation or arteriovenous shunt)

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Transient hyperglycemia in most patients usually requires treatment only in patients with diabetes mellitus; responds to usual management measures, including insulin
Monitor blood glucose levels, especially in patients with diabetes and in those requiring multiple injections
Cataracts observed in animals receiving repeated daily doses of intravenous diazoxide
May precipitate edema and congestive heart failure if injected frequently
Increased volume of extracellular fluid may cause treatment failure in nonresponsive patients because of increased extracellular fluid
Increase in fluid volume responds to diuretics if renal function adequate
Concurrent administration of thiazide diuretics may potentiate antihypertensive and hyperuricemic actions of diazoxide (see Interactions above)
Should be administered only into peripheral vein
Alkalinity of solution irritates tissue, so avoid extravascular injection or leakage
SC administration produces inflammation and pain without subsequent necrosis; if leakage into subcutaneous tissue occurs, area should be treated with warm compresses and rest

Follow-up

Deterrence

Good bladder and bowel care (ie, preventing fecal impaction, bladder distention) are mainstays in preventing episodes of autonomic dysreflexia.

Patient Education

All medical professionals should educate the patient and family members or caregivers about this potentially life-threatening complication of SCI.³

Miscellaneous

Medicolegal Pitfalls

Failure to have a high index of suspicion and recognize autonomic dysreflexia quickly could present medical and legal problems for the physician. For example, a physician who assumes that headache and anxiety in a person with complete C6 tetraplegia is a manifestation of depression, without checking vital signs, is at medical/legal risk.

Multimedia

Media file 1: (A) A strong sensory input (not necessarily noxious) is carried into the spinal cord via intact peripheral nerves. The most common origins are bladder and bowel. (B) This strong sensory input travels up the spinal cord and evokes a massive reflex sympathetic surge from the thoracolumbar sympathetic nerves, causing widespread vasoconstriction, most significantly in the subdiaphragmatic (or splanchnic) vasculature. Thus, peripheral arterial hypertension occurs. (C) The brain detects this hypertensive crisis through intact baroreceptors in the neck delivered to the brain through cranial nerves IX and X (Vagus). (D) The brain attempts 2 maneuvers to halt the progression of this hypertensive crisis. First, the brain attempts to shut down the sympathetic surge by sending descending inhibitory impulses. These impulses do not get to most sympathetic outflow levels because of the spinal cord injury at T6 or above. Inhibitory impulses are blocked in the injured spinal cord. In the second maneuver, the brain attempts to bring down peripheral blood pressure by slowing the heart rate through an intact vagus (parasympathetic) nerve; however, this compensatory bradycardia is inadequate and hypertension continues. In summary, the sympathetics prevail below the level of neurologic injury, and the parasympathetic nerves prevail above the level of injury. Once the inciting stimulus is removed, reflex hypertension resolves.

References

1. Brown R, Burton A, Macefield VG. Input-output relationships of a somatosympathetic reflex in human spinal injury. Clin Auton Res. Apr 18 2009;[Medline].

2. Cameron AA, Smith GM, Randall DC, et al. Genetic manipulation of intraspinal plasticity after spinal cord injury alters the severity of autonomic dysreflexia. J Neurosci. Mar 15 2006;26(11):2923-32. [Medline]. [Full Text].

3. Schottler J, Vogel L, Chafetz R, et al. Patient and caregiver knowledge of autonomic dysreflexia among youth with spinal cord injury. Spinal Cord. Mar 10 2009;[Medline].

4. Krassioukov A, Warburton DE, Teasell R, et al. A systematic review of the management of autonomic dysreflexia after spinal cord injury. Arch Phys Med Rehabil. Apr 2009;90(4):682-95. [Medline].

5. Tsai SJ, Ying TH, Huang YH, et al. Transperineal injection of botulinum toxin A for treatment of detrusor sphincter dyssynergia: localization with combined fluoroscopic and electromyographic guidance. Arch Phys Med Rehabil. May 2009;90(5):832-6. [Medline].

6. McMahon D, Tutt M, Cook AM. Pharmacological management of hemodynamic complications following spinal cord injury. Orthopedics. May 2009;32(5):331. [Medline].

7. Chen D, Apple DF Jr, Hudson LM, Bode R. Medical complications during acute rehabilitation following spinal cord injury--current experience of the Model Systems. Arch Phys Med Rehabil. Nov 1999;80(11):1397-401. [Medline].

8. Claydon VE, Elliott SL, Sheel AW, et al. Cardiovascular responses to vibrostimulation for sperm retrieval in men with spinal cord injury. J Spinal Cord Med. 2006;29(3):207-16. [Medline]. [Full Text].

9. Eltorai IM, Wong DH, Lacerna M, et al. Surgical aspects of autonomic dysreflexia. J Spinal Cord Med. Jul 1997;20(3):361-4. [Medline].

10. Giannantoni A, Di Stasi SM, Scivoletto G, et al. Autonomic dysreflexia during urodynamics. Spinal Cord. Nov 1998;36(11):756-60. [Medline].

11. Gondim FA, Lopes AC Jr, Cruz PR, et al. On the complex autonomic changes involved in the inhibition of gastrointestinal motility after spinal cord injury (SCI). Dig Dis Sci. Jun 2006;51(6):1136. [Medline].

12. Hambly PR, Martin B. Anaesthesia for chronic spinal cord lesions. Anaesthesia. Mar 1998;53(3):273-89. [Medline].

13. Karlsson AK. Autonomic dysreflexia. Spinal Cord. Jun 1999;37(6):383-91. [Medline].

14. Landrum LM, Thompson GM, Blair RW. Does postsynaptic alpha 1-adrenergic receptor supersensitivity contribute to autonomic dysreflexia?. Am J Physiol. Apr 1998;274(4 Pt 2):H1090-8. [Medline]. [Full Text].

15. Naftchi NE, Richardson JS. Autonomic dysreflexia: pharmacological management of hypertensive crises in spinal cord injured patients. J Spinal Cord Med. Jul 1997;20(3):355-60. [Medline].

16. Pasquina PF, Houston RM, Belandres PV. Beta blockade in the treatment of autonomic dysreflexia: a case report and review. Arch Phys Med Rehabil. May 1998;79(5):582-4. [Medline].

17. Teasell RW, Arnold JM, Krassioukov A, Delaney GA. Cardiovascular consequences of loss of supraspinal control of the sympathetic nervous system after spinal cord injury. Arch Phys Med Rehabil. Apr 2000;81(4):506-16. [Medline].

18. Teichman JM, Barber DB, Rogenes VJ, Harris JM. Malone antegrade continence enemas for autonomic dysreflexia secondary to neurogenic bowel. J Spinal Cord Med. Jul 1998;21(3):245-7. [Medline].

19. Vaidyanathan S, Soni BM, Sett P, et al. Pathophysiology of autonomic dysreflexia: long-term treatment with terazosin in adult and paediatric spinal cord injury patients manifesting recurrent dysreflexic episodes. Spinal Cord. Nov 1998;36(11):761-70. [Medline].

Keywords

autonomic dysreflexia, dysreflexia, hyperreflexia, spinal cord injury, SCI, autonomic nervous system, sympathetic nervous system, parasympathetic nervous system, parasympathetic, spinal cord injuries, autonomic disorders, autonomic hyperreflexia, paroxysmal hypertension, hypertensive autonomic crisis, visceroautonomic stress syndrome, autonomic spasticity, sympathetic hyperreflexia, mass reflex

Contributor Information and Disclosures

Author

Denise I Campagnolo, MD, MS, Director of Multiple Sclerosis Clinical Research and Staff Physiatrist, Barrow Neurology Clinics, St Joseph's Hospital and Medical Center; Investigator for Barrow Neurology Clinics; Director, NARCOMS Project for Consortium of MS Centers
Denise I Campagnolo, MD, MS is a member of the following medical societies: Alpha Omega Alpha, American Association of Neuromuscular and Electrodiagnostic Medicine, American Paraplegia Society, Association of Academic Physiatrists, and Consortium of Multiple Sclerosis Centers
Disclosure: Teva Neuroscience Honoraria Speaking and teaching; Serono-Pfizer Honoraria Speaking and teaching

Medical Editor

Milton J Klein, DO, MBA, Consulting Physiatrist, Heritage Valley Health System-Sewickley Hospital, Allegheny General Hospital, and Ohio Valley General Hospital.
Milton J Klein, DO, MBA is a member of the following medical societies: American Academy of Disability Evaluating Physicians, American Academy of Medical Acupuncture, American Academy of Osteopathy, American Academy of Physical Medicine and Rehabilitation, American Medical Association, American Osteopathic Association, American Osteopathic College of Physical Medicine and Rehabilitation, American Pain Society, and Pennsylvania Medical Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Kat Kolaski, MD, Assistant Professor, Departments of Orthopedic Surgery and Pediatrics, Wake Forest University School of Medicine
Kat Kolaski, MD is a member of the following medical societies: American Academy for Cerebral Palsy and Developmental Medicine and American Academy of Physical Medicine and Rehabilitation
Disclosure: Nothing to disclose.

CME Editor

Kelly L Allen, MD, Regional Medical Director, IMX-Medical Management Services
Disclosure: Nothing to disclose.

Chief Editor

Robert H Meier III, MD, Director, Amputee Services of America; Active Medical Staff, Presbyterian/St Luke's Hospital, Spalding Rehabilitation Hospital, Select Specialty Hospital; Consulting Staff, Kindred Hospital
Robert H Meier III, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation and Association of Academic Physiatrists
Disclosure: Nothing to disclose.

Related eMedicine topics:
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Cardiovascular Concerns in Spinal Cord Injury
Neurogenic Bladder
Post Head Injury Autonomic Complications
Posttraumatic Syringomyelia
Spinal Cord Trauma and Related Diseases

Clinical guidelines:
Acute management of autonomic dysreflexia: individuals with spinal cord injury presenting to health-care facilities. Consortium for Spinal Cord Medicine - Private Nonprofit Organization
Paralyzed Veterans of America - Private Nonprofit Organization.  1997 Feb (updated 2001 Jul; reviewed 2006).  29 pages.  NGC:002190

Clinical trials:
Prazosin Vibrostimulation Autonomic Dysreflexia and Spinal Cord Injury Study

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