Association of Epidural Stimulation With Cardiovascular Function in an Individual With Spinal Cord Injury

Abstract

This study assesses the association between lumbosacral epidural stimulation to the lumbosacral spinal cord with cardiovascular function in an individual with a spinal cord injury.

Conflict of interest statement

Conflict of Interest Disclosures: None reported.

Figures

Figure 1.. Restoration of Integrated Cardiovascular Control in Response to Epidural Stimulation

A, Epidural spinal cord stimulation unit in combination with a 16-electrode array (red is cathode, blue is anode, white is inactive). B, Systolic blood pressure (SBP) responses during supine rest (minute 0) and 60° head-up tilt (minutes 1-5) with and without stimulation (data are presented as mean ± SEM across the 3 separate testing days); middle cerebral artery blood velocity (MCAv) response at rest and in response to 60° head-up tilt; and a raw steady state blood pressure (BP) tracing during 60° head-up tilt. The vertical dotted line indicates the start and end of stimulation. C, Changes in posterior cerebral artery velocity (PCAv) in response to cerebral activation (eyes open). D, End-diastolic volume (EDV), stroke volume (SV), cardiac output (CO), and heart rate (HR) responses during supine rest and 60° head-up tilt with and without stimulation. The gray arrowheads at the bottom of the panel indicate the direction and magnitude of the response. E, Trunk/lower-limb electromyography (EMG) recordings from the right/left rectus abdominis (RRA/LRA), right/left rectus femoris (RRF/LRF), and right/left soleus (RSOL/LSOL) during 60° head-up tilt with stimulation. RVLM indicates rostral ventrolateral medulla; Stim, stimulation.

Figure 2.. Theoretical Mechanisms by Which Epidural Stimulation Affects Cardiovascular Function

A, Descending sympathetic pathways from the rostral ventrolateral medulla (RVLM) in an intact spinal cord, leading to efficacious action potentials (ie, depolarization) in sympathetic circuitry, allow for supraspinal control over vascular tone (ie, vasoconstriction) and blood pressure. B, Interrupted descending sympathetic pathways due to an anatomically discomplete spinal cord injury (SCI), in which a few preserved descending sympathetic fibers crossing the site of injury are not capable of eliciting action potentials in sympathetic circuitry caudal to injury. C, Epidural spinal electrical stimulation (Stim) may increase the resting membrane potential of sympathetic circuitry caudal to the spinal cord injury, allowing for the previously nonefficacious preserved descending sympathetic fibers crossing the site of injury to actively regulate caudal sympathetic circuits and thereby restore control of vascular tone and blood pressure. D, Epidural electrical stimulation stimulates dorsal afferent relays, which likely affect the membrane potential of intersegmental and intrasegmental neurons that (1) receive direct input from descending sympathetic pathways and (2) directly and indirectly lead to depolarization of sympathetic preganglionic neurons, leading to regulation of vascular tone. The dotted lines indicate the depolarization threshold and the arrowheads indicate the response in the blood vessel (ie, when depolarization occurs then constriction of the artery occurs).