# Elucidating spinal sensorimotor network components that underlie recovery of motor functions via lumbosacral epidural electrical stimulation in humans with spinal cord injury

> **NIH NIH R01** · MAYO CLINIC ROCHESTER · 2020 · $538,730

## Abstract

PROJECT SUMMARY / ABSTRACT
Trauma to the spinal cord disrupts neural pathways that convey signals between the brain and spinal
sensorimotor networks (SSN) that reside below the injury site, resulting in chronic paralysis. There is currently
no cure for spinal cord injury (SCI); however, recent studies involving a small number of humans with SCI have
shown that paralyzed functions can be restored by electrically stimulating the dorsal surface of the lumbosacral
spinal cord. Last year, our team reported the use of lumbosacral epidural stimulation (ES) with intense
rehabilitation enabled recovery of independent standing and stepping by a man with complete paralysis due to
a mid-thoracic SCI that occurred several years prior. The stimulation systems that are implanted in humans with
SCI were originally developed, and subsequently approved by the U.S. Food and Drug Administration, for use
in humans to treat intractable neuropathic pain. The mechanism of action through which ES alleviates pain is
thought to involve inhibition of pathologic signals transmitted through the dorsal sensory roots and ascending
dorsal columns of the spinal cord. Contrary to pain treatment, computational modeling and electrophysiological
studies indicate ES enables motor functions after SCI via excitation of dorsal root signaling to downstream SSNs.
Assuming appropriate parameters of ES (e.g., pulse frequency, pulse width, pulse amplitude, location on the
dura mater) are applied, SSNs are capable of producing robust motor outputs that result in functions such as
weight bearing standing and/or walking. However, currently available scientific evidence does not explain how
ES interacts with nearby spinal structures to produce functional gains in humans with chronic paralysis. To
address this gap in knowledge, we will temporarily implant spinal electrodes in 32 humans with lower extremity
paralysis to stimulate the dorsal sensory roots and/or dorsal surface of the spinal cord during 10 days of
rehabilitation. Dorsal root stimulation (DRS) and ES waveforms will be independently-controlled to inhibit and/or
activate nearby structures. Each stimulus pulse will be synchronized to electrophysiologic recordings of
downstream neuromuscular activity in order to characterize SSN activity in response to DRS and/or ES
stimulation. We hypothesize unilateral DRS during motor-enabling ES will result in ipsilateral suppression of SSN
outputs. We further hypothesize that bilateral DRS alone will enable motor functions that are similar to those
generated by ES. To investigate the role of rehabilitation during stimulation-enabled motor recovery, we
hypothesize that stimulation-enabled motor performance will improve significantly across 10 motor rehabilitation
sessions with DRS/ES. Completion of this work will generate new information on the interactions that occur
during SSN facilitation via spinal stimulation. This information will be used to develop algorithms that correlate
stimulation waveform...

## Key facts

- **NIH application ID:** 9943433
- **Project number:** 1R01NS115877-01
- **Recipient organization:** MAYO CLINIC ROCHESTER
- **Principal Investigator:** Peter Jonas Grahn
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $538,730
- **Award type:** 1
- **Project period:** 2020-08-15 → 2025-07-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9943433

## Citation

> US National Institutes of Health, RePORTER application 9943433, Elucidating spinal sensorimotor network components that underlie recovery of motor functions via lumbosacral epidural electrical stimulation in humans with spinal cord injury (1R01NS115877-01). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/9943433. Licensed CC0.

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