What is the role of the central nervous system in the pathogenesis of autonomic dysreflexia?

Updated: Mar 02, 2020
  • Author: Ryan O Stephenson, DO; Chief Editor: Milton J Klein, DO, MBA  more...
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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. [4]  (However, a study by Solinsky et al of 78 male patients with SCI who had incidents of autonomic dysfunction found that out of 445 episodes, relative tachycardia occurred in 68.0%, far more frequently than relative bradycardia [0.3%]. [5] )

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