Autonomic Dysreflexia in Spinal Cord Injury: Mechanisms and Prospective Therapeutic Targets

High-level spinal cord injury (SCI) often leads to cardiovascular dysfunction, particularly autonomic dysreflexia, characterized by hypertension and bradycardia triggered by stimuli below the injury level. This dysautonomia arises from the loss of supraspinal control over sympathetic neurons, maladaptive plasticity in sensory inputs, and excessive sympathetic preganglionic neuron discharge after SCI. While neural control is disrupted, the renin-angiotensin system (RAS), which uses hormones to control blood pressure, is upregulated, though its role in autonomic dysreflexia remains debated.

• 1
  Transplantation of embryonic presympathetic neurons into the injured spinal cord can reestablish supraspinal regulation of sympathetic activity, reducing autonomic dysreflexia in rodent SCI models.
• 2
  Cell transplantation combined with selected RAS inhibition may improve neuroendocrine homeostasis and enhance cardiovascular recovery after SCI.
• 3
  The study highlights the potential of targeting the RAS system, alongside cell transplantation, as a therapeutic strategy for autonomic dysreflexia.