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| Funder | Veterans Affairs |
|---|---|
| Recipient Organization | James J Peters Va Medical Center |
| Country | United States |
| Start Date | Apr 01, 2023 |
| End Date | Mar 31, 2025 |
| Duration | 730 days |
| Number of Grantees | 1 |
| Roles | Principal Investigator |
| Data Source | NIH (US) |
| Grant ID | 10692551 |
Most individuals with spinal cord injury (SCI) retain spared neural activity at and below the site of injury, activating these neural circuits may enhance neural plasticity to promote recovery of motor, sensory, and autonomic function. Individuals with SCI struggle with life-long autonomic nervous system (ANS) dysfunction with serious adverse consequences. The dynamic balance between the
sympathetic and parasympathetic branches of the ANS is impaired in individuals with SCI at or above T6, which negatively impacts internal homeostasis during daily activities such as transferring from the supine to the seated position, regulating core body temperature (Tcore), and exercise performance.
For the estimated millions of people living with SCI globally, impaired ANS regulation is common, and has been implicated in widespread cardiovascular complications, which are a leading cause of morbidity and mortality in this population. One of the most prominent consequences of cardiovascular ANS impairment is blood pressure (BP) instability, which includes hypotension, orthostatic
hypotension (OH), and autonomic dysreflexia (AD). These BP impairments lead to an absence or reversal of the nocturnal BP dip, and increased daytime sleepiness, which detract from wellbeing, independence, social engagement and quality of life. Further, ANS cardiovascular impairment in athletes with SCI limits the heart rate (HR) response during competition, lowers BP,
and increases fatigue, thereby compromising endurance and sports performance. In fact, some athletes with SCI enhance their performance in competition by self-inducing AD, a practice known as “boosting,” to increase BP and create a generalized efferent sympathetic response. In addition to cardiovascular complications, ANS deficits post-SCI also contribute to abnormal
sudomotor function and dysregulation of Tcore. With climate change becoming increasingly apparent, the effects of wide variation in environmental conditions are anticipated to be more severe and more devastating to overall health, independence, and quality of life in individuals with SCI who lack adequate ANS thermoregulatory control. For these reasons, individuals with
SCI prioritize restoration of ANS functions higher than regaining the ability to walk; however, there are no clinical interventions proven to be safe and effective for managing widespread ANS dysfunction following SCI. This project will focus on using non-invasive, transcutaneous spinal cord stimulation
(TSCS) to restore intrinsic ANS control of BP and determine the effects on exercise endurance and Tcore. A recent report found that the use of TSCS in 6 individuals with cervical SCI (C3-C5) improved ANS regulation of HR, sudomotor, thermoregulation, and bladder control and a separate team found that TSCS restored ANS control of orthostatic BP, cardiac contractility, and cerebral blood
flow velocity in 5 individuals with chronic motor-complete SCI (C5-T2). Most recently, the safety and efficacy of TSCS was reported during digital anal rectal stimulation (DARS), a known trigger of AD, in one individual with chronic, motor-complete SCI (C4). The results indicate that TSCS parameters
targeted for BP control restored baseline BP after AD was induced during DARS, and prevented the BP rise when TSCS was administered before DARS onset. Thus, TSCS does not merely increase BP, rather targeted stimulation parameters appear to restore intrinsic ANS regulation of BP. Herein, we propose to test TSCS parameters targeted for BP control (active TSCS) on exercise endurance,
HR recovery from exercise, Tcore responses and subjective reporting of thermal comport during exposure to a cool ambient environment, in a cohort of participants with chronic SCI, during well controlled trials compared to a sham TSCS stimulation paradigm.
James J Peters Va Medical Center
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