title: Early autonomic dysreflexia.
abstract: BACKGROUND
  During the stage of spinal shock the conventional view is that autonomic activity is abolished. Here, evidence is presented that autonomic activity is still present.
  
  
  METHODS
  Four patients with acute cord transactions are presented: one new case and three from the literature.
  
  
  BACKGROUND
  The definitions of spinal shock and autonomic dysreflexia are given.
  
  
  METHODS
  All four cases showed acute autonomic dysreflexia between 7 and 31 days after acute cord transection at a stage when the tendon reflexes were abolished.
  
  
  RESULTS
  Two cases showed a severe rise in blood pressure; the two earlier cases, before blood pressure was routinely recorded, profuse sweating. In two cases autonomic dysreflexia was obtained when the bladder was overdistended with 1000 ml and 1600 ml. In the other two cases it occurred in response to traumatic catheterisation. This was found when supramaximal stimuli were applied. It has not been recorded routinely as, with modern management, the bladder does not get overdistended or traumatised.
  
  
  CONCLUSIONS
  Other evidence, the blood pressure, and urethral tone is presented to show that sympathetic reflex activity of the cord is not abolished during spinal shock.
  
  
  CONCLUSIONS
  The clinical importance of this is that autonomic dysreflexia can be seen at an early stage and it should be considered in the differential diagnosis of a sick patient immediately after spinal injury.
authors.affiliation: The Chiltern Hospital, Great Missenden, Bucks, UK.
authors.forename: J R
authors.initials: JR
authors.lastname: Silver
mesh_terms: D020211:Autonomic Dysreflexia / Q000175:diagnosis* / Q000209:etiology / Q000503:physiopathology*; D001341:Autonomic Nervous System / Q000503:physiopathology*; D001794:Blood Pressure; D003937:Diagnosis, Differential; D006339:Heart Rate; D006801:Humans; D008297:Male; D012021:Reflex, Abnormal; D013119:Spinal Cord Injuries / Q000150:complications*; D013546:Sweating; D001750:Urinary Bladder, Neurogenic / Q000209:etiology / Q000503:physiopathology