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Autonomic Dysreflexia in Spinal Cord Injury

  • Author: Ryan O Stephenson, DO; Chief Editor: Robert H Meier, III, MD  more...
 
Updated: Jun 25, 2015
 

Overview

Autonomic dysreflexia is a potentially dangerous clinical syndrome that develops in individuals with spinal cord injury, resulting in acute, uncontrolled hypertension. All caregivers, practitioners, and therapists who interact with individuals with spinal cord injuries must be aware of this syndrome, recognize the symptoms, and understand the causes and treatment algorithm.[1]

Briefly, autonomic dysreflexia develops in individuals with a neurologic level of spinal cord injury at or above the sixth thoracic vertebral level (T6). Autonomic dysreflexia causes an imbalanced reflex sympathetic discharge, leading to potentially life-threatening hypertension. It is considered a medical emergency and must be recognized immediately. If left untreated, autonomic dysreflexia can cause seizures, retinal hemorrhage, pulmonary edema, renal insufficiency, myocardial infarction, cerebral hemorrhage, and death. Complications associated with autonomic dysreflexia result directly from sustained, severe peripheral hypertension. (See the image below.)

(A) A strong sensory input (not necessarily noxiou (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. (D) The brain attempts two 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 are unable to travel 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.
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Pathophysiology

The autonomic nervous system is the division of the peripheral nervous system that carries motor information to the visceral organs and glands. It is made up of the sympathetic and parasympathetic autonomic nervous systems. The sympathetic fibers are responsible for the fight-or-flight response and divert blood flow away from the gastrointestinal tract and skin through the process of vasoconstriction. As a result, blood flow to skeletal muscles and lungs is significantly enhanced (by as much as 1200% in the case of skeletal muscles).[2] This also causes bronchiolar dilatation of the lung, which allows for greater alveolar oxygen exchange and increases the heart rate and contractility of cardiac myocytes.

The parasympathetic fibers typically act in opposition of the sympathetic autonomic nervous system through negative feedback control. This action is a complementary response, causing a balance of sympathetic and parasympathetic responses. Overall, the parasympathetic outflow results in conservation and restoration of energy, reduction in heart rate and blood pressure, facilitation of digestion and absorption of nutrients, and excretion of waste products. This parasympathetic response is primarily mediated through cranial nerve X, the vagus nerve, and the S2, S3, and S4 spinal nerves.

In individuals with intact central and peripheral nervous systems, a noxious stimulus results initially in a sympathetic response, leading to elevation in heart rate and blood pressure primarily through spinal reflexes. This response is modulated by the central nervous system and peripheral baroreceptors through the parasympathetic nervous system; this results in heart rate and blood pressure control both through direct responses by the vagus nerve and through inhibitory spinal cord signals. An appropriate balance of sympathetic and parasympathetic outflow is attained and modulated by both the central and peripheral nervous systems.

In those with a spinal cord injury at the level of T6 and above, a noxious (or otherwise strong) stimulus below the level of injury results in an unbalanced physiologic response. The strong stimulus causes a peripheral sympathetic response through spinal reflexes, resulting in vasoconstriction below the level of injury. This reflex response ascends and descends the spinal cord and paraspinal sympathetic ganglia, causing both direct vasoconstriction through activation of perivascular receptors and systemic/indirect vasoconstriction through stimulation of the adrenal medulla, resulting in epinephrine and norepinephrine release into the systemic circulation. This therefore results in hypertension, primarily through splanchnic and peripheral vasoconstriction.

The baroreceptors in the carotid sinus and aortic arch convey appropriate responses to hypertension through the petrosal ganglion to the nucleus ambiguous and result in strong vagal (CN X) outflow, bradycardia, and vasodilatation above the level of injury. The central nervous system cannot directly detect the strong or noxious signal below the level of injury (owing to the lack continuity of the ascending sensory fibers from the underlying spinal cord injury), and, therefore, responds to hypertension by sending a strong inhibitory response through the spinal cord aimed at reducing the sympathetic response. However, because of the lack of spinal cord continuity, the descending inhibitory response only travels as far as the level of neurologic injury and does not cause the desired response in the sympathetic fibers below the injury; therefore, the hypertension remains uncontrolled.

As a result, there is flushing and sweating only above the level of injury, bradycardia, pupillary constriction, and nasal congestion (unopposed parasympathetic responses); and below the level of injury, there is pale, cool skin and piloerection due to sympathetic tone and lack of the descending inhibitory parasympathetic modulation.[3]

T6 is of particular importance in the pathogenesis of autonomic dysreflexia. The splanchnic vascular bed is one of the body’s largest reserves of circulatory volume and is controlled primarily by the greater splanchnic nerve. This important nerve derives its innervation from T5-T9. Lesions to the spinal cord at or above T6 allow the strong and uninhibited sympathetic tone to constrict the splanchnic vascular bed, causing systemic hypertension. Lesions below T6 generally allow enough descending inhibitory parasympathetic control to modulate the splanchnic tone and prevent hypertension.

The underlying pathophysiological changes that occur in the spinal cord and in the periphery that cause autonomic dysreflexia have not been fully elucidated in a human model. It has been postulated that peripheral alpha-adrenergic receptors associated with blood vessels become hyperresponsive below the level of the spinal cord lesion. This hyperresponsiveness is secondary to a low resting catecholamine state associated with spinal cord injury. The orphaned receptors have a decreased threshold to react to adrenergic stimuli and react with an increased responsiveness.[4, 5, 6]

Another possible mechanism includes loss of supraspinal inhibitory control from the medulla oblongata–bulbospinal pathways; this loss of supraspinal control may cause a loss of the bulbospinal pathway’s inhibitory effect over serotonin in the intermediolateral nucleus of the spinal cord. The unabated serotonin then causes strong vasoconstriction.[7]

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Causes of Autonomic Dysreflexia

Episodes of autonomic dysreflexia can be triggered by many potential causes.[8] Essentially, any painful, irritating, or even strong stimulus below the level of the injury can cause an episode of autonomic dysreflexia. Bladder distension or irritation is responsible for 75-85% of the cases.[9] Bladder irritation is commonly caused by a blocked or kinked catheter or failure of a timely intermittent catheterization program. The second most common cause of autonomic dysreflexia is bowel distention, usually due to fecal impaction. This accounts for 13-19% of cases.[9] Although the list is not comprehensive, the following events or conditions all can cause episodes of autonomic dysreflexia:

  • Bladder distention
  • Urinary tract infection
  • Calculus
  • Cystoscopy/instrumentation
  • Urodynamic study [10]
  • Epididymitis or scrotal compression
  • Bowel distention
  • Bowel impaction
  • Bowel instrumentation/colonoscopy
  • Reflux or gastritis
  • Gallstones
  • Gastric ulcers
  • Invasive testing
  • Hemorrhoids
  • Gastrocolic irritation
  • Appendicitis or other intra-abdominal pathology/trauma
  • Anal fissure
  • 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 skeletal trauma
  • Surgical or diagnostic procedures

A literature review by Liu et al indicated that in patients with SCI, autonomic dysreflexia triggers from the lower urinary tract are often associated with clinical urologic procedures, suggesting that blood pressure monitoring should be routinely performed during such procedures. The study found, for example, that 36.7-77.8% of patients undergoing urodynamic testing experienced autonomic dysreflexia, with the problem also occurring in most patients when cystoscopy, transurethral litholapaxy, or extracorporeal shock-wave lithotripsy were performed without anesthesia. The investigators also found that autonomic dysreflexia occurred more often in patients with cervical SCI than in those with thoracic SCI.[11]

A study by Xiong et al of 89 patients indicated that in individuals with SCI who undergo cystolitholapaxy, autonomic dysreflexia is more likely to occur in those with larger or a greater number of bladder stones, an injury level above T6, a greater hydraulic irrigation height, and a longer surgical time.[12]

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Prognosis

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

In a literature review, Wan and Krassioukov identified the prevalence of various causes of life-threatening complications and death from autonomic dysreflexia in spinal cord injury, determining that central nervous system (CNS) – related causes were the most frequent. The investigators found that out of 32 patients identified as having either died or suffered life-threatening complications from autonomic dysreflexia, the prevalence of CNS-, cardiovascular-, and pulmonary-related causes were as follows[13] :

  • CNS: 23 patients (72%)
  • Cardiovascular: Seven patients (22%)
  • Pulmonary: Two patients (6%)

Seven patients in the study died directly owing to complications from an attack of autonomic dysreflexia.[13]

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Patient education

All medical professionals should educate the patient and family members or caregivers about this potentially life-threatening complication of spinal cord injury.[14] Such instruction should include prevention strategies, signs and symptoms of autonomic dysreflexia, and proper management of the condition. Patients should be encouraged to carry a wallet-sized card explaining symptoms and treatment for autonomic dysreflexia. Such cards can be found from multiple sources, including the following:

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Consultations

If the cause of the episode of autonomic dysreflexia is not found and blood pressure remains elevated, emergency department care is recommended for medication management, close monitoring, and further investigation of the possible cause. Consult an ICU specialist for ICU monitoring and treatment of the hypertension. Physicians specializing in physical medicine and rehabilitation are well-acquainted with the diagnosis and management of autonomic dysreflexia and can be of assistance in both acute management and prevention strategies of this syndrome.

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Prevention

Proper bladder and bowel care (ie, preventing fecal impaction, bladder distention) are mainstays in preventing episodes of autonomic dysreflexia. Regulation of the bladder routine via indwelling Foley catheter or intermittent catheterization and regular urologic follow-up is highly recommended for autonomic dysreflexia prevention. A regular bowel program to ensure appropriate fecal movement and prevent constipation is important. Autonomic dysreflexia caused by anorectal procedures, including the bowel program, or from intermittent bladder catheterization may be diminished with the use of prophylactic lidocaine or dibucaine.[8]

Patients with spinal cord injury should be educated to recognize the early symptoms of autonomic dysreflexia and understand the common causes and management. Those with recurrent symptoms should be educated on home blood pressure monitoring.

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Epidemiology

Reported prevalence rates vary for autonomic dysreflexia in the United States, but the generally accepted rate is 48-90% of all individuals who are injured at T6 and above. Patients who have a complete injury (no motor or sensation below the level of the spinal cord lesion) have a much higher incidence of autonomic dysreflexia (91% with complete injury vs 27% with incomplete injury 27%).[15]

The occurrence of autonomic dysreflexia increases as the patient evolves out of spinal shock. With the return of sacral reflexes, the possibility of autonomic dysreflexia increases.[14] Autonomic dysreflexia occurs during labor in approximately two thirds of pregnant women with spinal cord injury above the level of T6. Spinal epidural anesthesia can help reduce the risks of autonomic dysreflexia during pregnancy.

The male-to-female ratio for sustaining spinal cord injury is 4:1; however, autonomic dysreflexia has no sexual predilection.

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History and Physical Examination

History

The patient with autonomic dysreflexia generally gives a history of one or many of the following symptoms: Headaches, blurry vision, spots in the visual field, nasal congestion, blotchy skin above the level of injury, and a sense of anxiety or malaise. Feelings of apprehension or anxiety over an impending physical problem commonly are exhibited.

Physical examination

A patient with autonomic dysreflexia may have one or more of the following findings on physical examination:

  • Significant rise in systolic and diastolic blood pressure greater than 20 mm Hg systolic or 10 mm Hg diastolic above baseline (The sudden rise in blood pressure in autonomic dysreflexia is usually associated with bradycardia. Normal systolic blood pressure for an individual with spinal cord injury above T6 is 90-110 mm Hg; blood pressure of 20-40 mm Hg above the reference range for such patients may be a sign of autonomic dysreflexia. However, patients with autonomic dysreflexia may display no symptoms, despite elevated blood pressure.)
  • Profuse sweating above the level of lesion - Especially in the face, neck, and shoulders; rarely occurs below the level of the lesion because of sympathetic activity
  • Goose bumps below the level of the lesion
  • Flushing of the skin above the level of the lesion - Especially in the face, neck, and shoulders; this is a frequent symptom
  • Blurred vision
  • Nasal congestion – A common symptom
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Physical Therapy

Physical therapists who treat patients with SCI need to have a good understanding of autonomic dysreflexia and be familiar with the signs and symptoms of this potentially life-threatening condition.[14] Throughout the physical therapy sessions, the therapist needs to monitor the urinary catheter for any blockage or twisting.

If the patient becomes hypertensive during therapy and autonomic dysreflexia is the suspected cause, the therapist should place the patient in an upright position immediately. This takes advantage of an orthostatic response and helps with the pooling of blood in the lower extremities. The therapist needs to complete careful inspection to identify the source of painful stimuli (eg, catheter, restrictive clothing, leg bag straps, abdominal supports, orthoses).[8] A less common cause of autonomic dysreflexia during physical therapy sessions may originate with muscle stretching, either from range-of-motion or passive stretching.

If the patient develops autonomic dysreflexia, the physical therapist needs to treat it as a medical emergency and be familiar with established protocols for medical management within his or her particular setting. The individual therapy session then must be discontinued to allow the patient to stabilize and recover. Please refer to Guidelines of the Consortium for Spinal Cord Medicine for the management of autonomic dysreflexia if no guidelines are available at your facility.

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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 and be able to respond quickly if the condition develops during a therapy session.[14]

Occupational therapists perform extensive training in the performance of activities of daily living with patients who have sustained SCI. Such activities include proper bowel and bladder management, which can help to prevent to the occurrence of autonomic dysreflexia. The occupational therapist may be involved in establishing a regular bowel program and may complete patient and family/caregiver education on this aspect of care.

Both occupational and physical therapists should educate the patient and family members about autonomic dysreflexia and ensure that they are familiar with prevention strategies, signs and symptoms, and proper management of the condition.

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Recreational and Speech Therapies

Recreational therapy

Recreational therapists also are important members of the rehabilitation team, as they help patients with SCI to become involved in recreational, community, 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.[14]

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 treatment of individuals with SCI, speech therapists must be familiar with the manifestations of this potentially life-threatening condition.[14]

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Treatment of Autonomic Dysreflexia

Check the patient's blood pressure. If the blood pressure is elevated, have the person sit up immediately and loosen any clothing or constrictive devices. Sitting allows some gravitational pooling of blood in the lower extremities and reduces blood pressure. Survey the person for instigating causes, beginning with the urinary system, the most common cause of autonomic dysreflexia.[10, 16]

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.

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 autonomic dysreflexia, and check the rectum for stool, using lidocaine jelly as lubricant. If impacted, gentle manual evacuation is recommended.

Monitor blood pressure and pulse every 2-5 minutes until the patient has stabilized; impaired autonomic regulation can cause blood pressure to fluctuate quickly during an episode of autonomic dysreflexia.

Use of an antihypertensive agent is recommended when the systolic blood pressure is at or above 150 mm Hg. Once the offending agent is identified and corrected, the autonomic dysreflexia subsides and blood pressure returns to normal (systolic, 90-110 mm Hg). For this reason, medicating with a short-acting antihypertensive is of utmost importance.

The most commonly used agents are nifedipine and nitrates (eg, nitroglycerine paste or sublingual nitroglycerine). Nifedipine should be in the immediate-release form; bite and swallow is the preferred method of administering the drug, not sublingual administration. Other agents used are prazosin, captopril, terazosin, mecamylamine, diazoxide, and phenoxybenzamine. Use antihypertensives with extreme caution in older persons or in people with coronary artery disease. Note that men with spinal cord injury often use cGMP-specific phosphodiesterase type 5 (PDE5) inhibitors (eg, sildenafil, vardenafil, tadalafil.) for sexual dysfunction. Use of nitrates is contraindicated in this situation.

If there is poor response to treatment and/or if the cause of the autonomic dysreflexia has not been identified, the patient should be seen in an emergency department for monitoring and pharmacologic control of blood pressure. The emergency department has better access to the necessary tests to investigate the possible etiology of the autonomic dysreflexia.

Monitor the individual's symptoms and blood pressure for at least 2 hours after resolution of the autonomic dysreflexia episode to ensure that elevation of blood pressure does not recur. Autonomic dysreflexia may resolve because of medication, not because of resolution of the underlying cause. Unless the underlying cause is identified and addressed, recurrence should be expected.

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Prevention of Autonomic Dysreflexia

Patients who have previously experienced autonomic dysreflexia may be able to prevent the reoccurrence by using simple prevention strategies. The prevention strategies may mitigate further episodes of autonomic dysreflexia.

Common triggers are as follows:

  • Bladder: Intermittent catheterization should be regular and timely; only clean catheters should be used. Indwelling catheters should be changed routinely and regularly checked for blockage or kinking. Detrusor sphincter dyssynergia causing autonomic dysreflexia may be treated with intravesicular onabotulinumtoxinA or intravesicular capsaicin. [17] Other successful methods trialed to help prevent autonomic dysreflexia are sacral denervation and sphincterotomy.
  • Bowels: A regular bowel program is essential for the prevention of constipation, impaction, and ileus. Prior to a bowel procedure, an anal block helps prevent autonomic dysreflexia. [18] Topical lidocaine may be of help.
  • Labor and delivery: Spinal anesthesia can help to prevent autonomic dysreflexia.
  • Pressure ulcers: Routine weight shifts and skin checks are necessary to prevent ulceration. Any skin breakdown should be addressed early by a knowledgeable wound care team or physician.
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Contributor Information and Disclosures
Author

Ryan O Stephenson, DO Assistant Professor, Department of Physical Medicine and Rehabilitation, University of Colorado Health Science Center; Physiatrist, Medical Director of PM&R Inpatient Consultation Service, Medical Director of Polytrauma and Brain Injury, Medical Director of Regional Amputee Center, Department of Physical Medicine and Rehabilitation, Eastern Colorado Veterans Affairs Medical Center

Ryan O Stephenson, DO is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

Jeffrey Berliner, DO Clinical Director, Spinal Cord Injury Medicine, The Institute for Rehabilitation and Research, Memorial Hermann Hospital; Assistant Professor, University of Texas Medical School at Houston

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

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, American Academy of Physical Medicine and Rehabilitation

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, Association of Academic Physiatrists

Disclosure: Nothing to disclose.

Additional Contributors

Milton J Klein, DO, MBA Consulting Physiatrist, Heritage Valley Health System-Sewickley 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, Pennsylvania Medical Society

Disclosure: Nothing to disclose.

Acknowledgements

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; Genzyme Corporation Grant/research funds investigator; Biogen Idec Grant/research funds investigator; Genentech, Inc Grant/research funds investigator; Eli Lilly & Company Grant/research funds investigator; Novartis investigator; MSDx LLC Grant/research funds investigator; BioMS Technology Corp Grant/research funds investigator; Avanir Pharmaceuticals Grant/research funds investigator

References
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(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. (D) The brain attempts two 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 are unable to travel 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.
 
 
 
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