Southcoast Hospitals Physicians Believe, 'Autonomic Dysreflexia Does Not Exist -- and if it does, then it is only experienced by persons with Acute spinal cord injury...' They might want to do some fact checking.

Autonomic Dysreflexia in Spinal Cord Injury Author: Ryan O Stephenson, DO; Chief Editor: Robert H Meier, III, MD more... Updated: Jun 25, 2015 Overview Pathophysiology Causes of Autonomic Dysreflexia Prognosis Patient education Consultations Prevention Epidemiology History and Physical Examination Physical Therapy Occupational Therapy Recreational and Speech Therapies Treatment of Autonomic Dysreflexia Prevention of Autonomic Dysreflexia Show All Multimedia Library References 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.