Intraspinal Plasticity Associated With the Development of Autonomic Dysreflexia After Complete Spinal Cord Injury

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11 Scopus citations


Traumatic spinal cord injury (SCI) leads to disruption of sensory, motor and autonomic function, and triggers structural, physiological and biochemical changes that cause reorganization of existing circuits that affect functional recovery. Propriospinal neurons (PN) appear to be very plastic within the inhibitory microenvironment of the injured spinal cord by forming compensatory circuits that aid in relaying information across the lesion site and, thus, are being investigated for their potential to promote locomotor recovery after experimental SCI. Yet the role of PN plasticity in autonomic dysfunction is not well characterized, notably, the disruption of supraspinal modulatory signals to spinal sympathetic neurons after SCI at the sixth thoracic spinal segment or above resulting in autonomic dysreflexia (AD). This condition is characterized by unmodulated sympathetic reflexes triggering sporadic hypertension associated with baroreflex mediated bradycardia in response to noxious yet unperceived stimuli below the injury to reduce blood pressure. AD is frequently triggered by pelvic visceral distension (bowel and bladder), and there are documented structural relationships between injury-induced sprouting of pelvic visceral afferent C-fibers. Their excitation of lumbosacral PN, in turn, sprout and relay noxious visceral sensory stimuli to rostral disinhibited thoracic sympathetic preganglionic neurons (SPN) that manifest hypertension. Herein, we review evidence for maladaptive plasticity of PN in neural circuits mediating heightened sympathetic reflexes after complete high thoracic SCI that manifest cardiovascular dysfunction, as well as contemporary research methodologies being employed to unveil the precise contribution of PN plasticity to the pathophysiology underlying AD development.

Original languageEnglish
Article number505
JournalFrontiers in Cellular Neuroscience
StatePublished - Nov 8 2019

Bibliographical note

Funding Information:
We greatly thank Matt Hazzard and Tom Dolan for their artistic renditions, University of Kentucky, College of Medicine. Funding. We gratefully acknowledge the support of an endowment from the University of Kentucky, Spinal Cord and Brain Injury Research Center (AGR).

Publisher Copyright:
© Copyright © 2019 Michael, Patel and Rabchevsky.


  • cardiovascular dysfunction
  • hypertension
  • interneuron
  • propriospinal
  • sympathetic preganglionic neurons

ASJC Scopus subject areas

  • Cellular and Molecular Neuroscience


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