Motor Control of Human Spinal Cord Disconnected from the Brain and Under External Movement

Adv Exp Med Biol. 2016:957:159-171. doi: 10.1007/978-3-319-47313-0_9.

Abstract

Motor control after spinal cord injury is strongly depending on residual ascending and descending pathways across the lesion. The individually altered neurophysiology is in general based on still intact sublesional control loops with afferent sensory inputs linked via interneuron networks to efferent motor outputs. Partial or total loss of translesional control inputs reduces and alters the ability to perform voluntary movements and results in motor incomplete (residual voluntary control of movement functions) or motor complete (no residual voluntary control) spinal cord injury classification. Of particular importance are intact functionally silent neural structures with residual brain influence but reduced state of excitability that inhibits execution of voluntary movements. The condition is described by the term discomplete spinal cord injury. There are strong evidences that artificial afferent input, e.g., by epidural or noninvasive electrical stimulation of the lumbar posterior roots, can elevate the state of excitability and thus re-enable or augment voluntary movement functions. This modality can serve as a powerful assessment technique for monitoring details of the residual function profile after spinal cord injury, as a therapeutic tool for support of restoration of movement programs and as a neuroprosthesis component augmenting and restoring movement functions, per se or in synergy with classical neuromuscular or muscular electrical stimulation.

Keywords: Discomplete; EMG; Functional electrical stimulation (FES); Injury; Motor unit; Neurorehabilitation; Spinal reflex; Sublesional control; Supraspinal control; Surface polielectromyography.

MeSH terms

  • Brain / physiopathology
  • Electric Stimulation
  • Electromyography
  • Humans
  • Movement / physiology*
  • Nerve Net / physiopathology
  • Spinal Cord / physiopathology*
  • Spinal Cord Injuries / physiopathology*