Abstract

Despite autonomic dysfunction after spinal cord injury (SCI) being the major cause of death and a top health priority, the clinical management options for these conditions are limited to drugs with delayed onset and nonpharmacological interventions with equivocal effectiveness. We tested the capacity of electrical stimulation, applied transcutaneously over the spinal cord, to manage autonomic dysfunction in the form of orthostatic hypotension after SCI. We assessed beat-by-beat blood pressure (BP), stroke volume, and cardiac contractility (dP/dt; Finometer), as well as cerebral blood flow (transcranial Doppler) in 5 individuals with motor-complete SCI (4 cervical, 1 thoracic) during an orthostatic challenge with and without transcutaneous electrical stimulation applied at the TVII level. During the orthostatic challenge, all individuals experienced hypotension characterized by a 37 ± 4 mm Hg decrease in systolic BP, a 52 ± 10% reduction in cardiac contractility, and a 23 ± 6% reduction in cerebral blood flow (all p < 0.05), along with severe self-reported symptoms. Electrical stimulation completely normalized BP, cardiac contractility, cerebral blood flow, and abrogated all symptoms. Noninvasive transcutaneous electrical spinal cord stimulation may be a viable therapy for restoring autonomic cardiovascular control after SCI.

Highlights

  • The recovery of walking has been the focus of the vast majority of research into electrical stimulation after spinal cord injury (SCI), the recovery of normal autonomic cardiovascular function is consistently reported to be more urgently desired by people living with SCI.[7]

  • Cardiovascular, cardiac, and cerebrovascular responses to orthostatic challenge were normalized with transcutaneous electrical spinal cord stimulation. (A) Blood pressure responses were normalized with stimulation. (B) Cerebral blood flow was normalized with stimulation. (C) systolic function in terms of contractility was normalized with stimulation, heart rate was still elevated and stroke volume was not restored. (D) Symptoms of orthostatic intolerance were almost completely abrogated with stimulation

  • All participants experienced clinically defined Orthostatic hypotension (OH), which was abrogated with stimulation at the TVII level (Figure 2); lower-limb skeletal muscle contraction did not occur, obviating the possibility that the pressor response was attributed to skeletal muscle pump action.[24]

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Summary

Introduction

Over the past 10 years, we have come to realize that electrical stimulation of the spinal cord caudal to the injury has the capacity to both directly excite spinal cord neurons and modulate spinal circuity.[1,2,3,4,5,6] the recovery of walking has been the focus of the vast majority of research into electrical stimulation after spinal cord injury (SCI), the recovery of normal autonomic cardiovascular function is consistently reported to be more urgently desired by people living with SCI.[7]. We reasoned that stimulation of the thoracic spinal cord, where sympathetic preganglionic neurons cell bodies are located, would elicit acute increases in BP, cerebral blood flow, and cardiac function when they were dangerously reduced because of orthostasis.

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