What mechanisms are associated with the pathogenesis of autonomic dysreflexia with spinal cord injury?

Updated: Mar 02, 2020
  • Author: Ryan O Stephenson, DO; Chief Editor: Milton J Klein, DO, MBA  more...
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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. [6, 7, 8]

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. [9]

A study by Phillips et al suggested that the brain may buffer moderate instances of autonomic dysreflexia. During spontaneous episodes of autonomic dysreflexia in four patients with motor-complete cervical SCI, the report found that although the mean arterial blood pressure rose from 66 to 83 mm Hg, the cerebral blood flow and end-tidal partial pressure of carbon dioxide remained approximately the same. [10]

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