This clinical syndrome occurs in patients who have had a spinal cord injury at, or above T6 spinal level.

Briefly, afferent signals, most commonly triggered by faecal impaction or urinary retention (but many other triggers have been reported) cause a sympathetic spinal reflex via thoracolumbar outflow. The usual, centrally mediated, parasympathetic response however is prevented by the cord lesion = different responses above and below the level of the injury

• PSN response above the level of the injury
  • Dilatation of blood vessels in the face (flushing)
  • headache (relaxed blood vessels in the head)
  • Sweating
• SNS response below the level of the injury

The result is an unbalanced physiological response, characterised by extreme hypertension, flushing and sweating above the level of the cord lesion, agitation, and in untreated cases severe consequences of extreme hypertension have been reported, e.g. haemorrhagic stroke.

Management of autonomic dysreflexia involves removal/control of the stimulus and treatment of any life-threatening hypertension and/or bradycardia.