Autonomic dysreflexia after spinal cord injury: Systemic pathophysiology and methods of management

Khalid C. Eldahan, Alexander G. Rabchevsky

Research output: Contribution to journalReview articlepeer-review

150 Scopus citations


Traumatic spinal cord injury (SCI) has widespread physiological effects beyond the disruption of sensory and motor function, notably the loss of normal autonomic and cardiovascular control. Injury at or above the sixth thoracic spinal cord segment segregates critical spinal sympathetic neurons from supraspinal modulation which can result in a syndrome known as autonomic dysreflexia (AD). AD is defined as episodic hypertension and concomitant baroreflex-mediated bradycardia initiated by unmodulated sympathetic reflexes in the decentralized cord. This condition is often triggered by noxious yet unperceived visceral or somatic stimuli below the injury level and if severe enough can require immediate medical attention. Herein, we review the pathophysiological mechanisms germane to the development of AD, including maladaptive plasticity of neural circuits mediating abnormal sympathetic reflexes and hypersensitization of peripheral vasculature that collectively contribute to abnormal hemodynamics after SCI. Further, we discuss the systemic effects of recurrent AD and pharmacological treatments used to manage such episodes. Contemporary research avenues are then presented to better understand the relative contributions of underlying mechanisms and to elucidate the effects of recurring AD on cardiovascular and immune functions for developing more targeted and effective treatments to attenuate the development of this insidious syndrome following high-level SCI.

Original languageEnglish
Pages (from-to)59-70
Number of pages12
JournalAutonomic Neuroscience: Basic and Clinical
StatePublished - Jan 2018

Bibliographical note

Publisher Copyright:
© 2017 Elsevier B.V.


  • Hypertension
  • Maladaptive plasticity
  • Primary afferent
  • Propriospinal
  • Sprouting
  • Sympathetic

ASJC Scopus subject areas

  • Endocrine and Autonomic Systems
  • Clinical Neurology
  • Cellular and Molecular Neuroscience


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