eMedicine Specialties > Physical Medicine and Rehabilitation > Spinal Cord Injury

Autonomic Dysreflexia in Spinal Cord Injury

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
Contributor Information and Disclosures

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 noxio...

(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.

(A) A strong sensory input (not necessarily noxio...

(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

Morbidity related to autonomic dysreflexia is associated with hypertension, which can cause retinal/cerebral hemorrhage, myocardial infarction, or seizures. Mortality is rare.

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

More on Autonomic Dysreflexia in Spinal Cord Injury

Overview: Autonomic Dysreflexia in Spinal Cord Injury
Differential Diagnoses & Workup: Autonomic Dysreflexia in Spinal Cord Injury
Treatment & Medication: Autonomic Dysreflexia in Spinal Cord Injury
Follow-up: Autonomic Dysreflexia in Spinal Cord Injury
Multimedia: Autonomic Dysreflexia in Spinal Cord Injury
References
Further Reading

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].

Further Reading

Related eMedicine topics:
Athletes With Disabilities
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

Keywords

autonomic dysreflexia, dysreflexia, hyperreflexia, spinal cord injury, SCI, autonomic nervous system, sympathetic nervous systemparasympathetic 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.

 
 
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