Autonomic dysreflexia

Published on 07/02/2015 by admin

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Last modified 07/02/2015

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Autonomic dysreflexia

Michael E. Johnson, MD, PhD

Autonomic dysreflexia (AD, also referred to as autonomic hyperreflexia) is a potentially life-threatening emergency. It occurs in at least two thirds of patients with a spinal cord injury at T6 or above and is characterized by acute hypertension, usually accompanied by bradycardia, in response to a noxious stimulus below the level of the spinal cord lesion. Distention of the bladder or bowel is a frequent cause of AD.

Pathophysiology

AD results from unopposed sympathetic efferent outflow in response to noxious afferent input below the level of the spinal cord injury, with reflex activation of parasympathetic outflow above the T6 dermatomal level. The pathways involved are summarized in Figure 178-1.

Figure 178-1 Diagram illustrating how autonomic dysreflexia occurs in a person with a spinal cord injury. The afferent stimulus—in this case, a distended bladder—triggers a peripheral sympathetic response, which results in vasoconstriction and hypertension. Descending inhibitory signals, which would normally counteract the rise in blood pressure, are blocked at the level of the spinal cord injury. The roman numerals (IX, X) refer to the cranial nerves. (Reprinted, with permission, from Blackmer J. Rehabilitation medicine: 1. Autonomic dysreflexia. Can Med Assoc J. 2003;169:931-935.)

Afferent stimuli from an insult below the level of the spinal cord injury can ascend via spinothalamic and posterior columns to activate sympathetic neurons up to the level of the cord injury, discharging these neurons as an independent reflex at the level of the cord. Ordinarily this would elicit compensatory bulbospinal sympathetic inhibition via descending spinal pathways, but these pathways are now blocked by the spinal cord injury, resulting in unopposed vasoconstriction below the injury. With a spinal cord injury at T6 or higher, noxious stimuli result in intense constriction of splanchnic vascular beds and the vasculature in the lower extremities, leading to an exaggerated hypertensive response. Cord injury below T10 does not cause AD, whereas patients with injuries at the T6 to T10 levels may have a mild blood pressure elevation without full-blown AD. AD can occur in patients with incomplete spinal cord injuries, but the AD is more severe in those with a complete injury.

Baroreceptors in the aortic arch and carotid sinus respond to hypertension by activating brainstem vasomotor reflexes, resulting in increased parasympathetic activation via the intact cranial nerve X effector pathway, which is unaffected by the spinal cord injury, usually resulting in bradycardia. Tachycardia is also possible but occurs less frequently, presumably depending on the balance between catecholamines that diffuse into the bloodstream after sympathetic neuron activation below the spinal cord lesion and vagal outflow. Parasympathetic activation also causes vasodilation above the level of the cord injury.

Although AD has been reported to occur in the acute phase of a spinal cord injury, it generally becomes evident 1 to 6 months after the initial injury. This delayed occurrence is attributed to injury-induced changes in the structure and electrophysiology of both primary afferents and spinal neurons, as well as increased sensitivity of the peripheral vasculature to α-adrenergic stimulation, which heightens the exaggerated sympathetic response to noxious stimuli.

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