Mechanisms underlying reversal of motor unit activation order in electrically evoked contractions after spinal cord injury.

Published

Journal Article

Extracellular stimulation normally activates larger-diameter axons, innervating motor units producing higher force, at lower stimulation intensities than required to activate small-diameter axons innervating motor units producing low force. However, activation of weaker thenar motor units at lower stimulation intensities than required to activate strong motor units has been reported during extracellular stimulation of the median nerve in persons with chronic cervical spinal cord injury. We used a computational model that reproduced this experiment to identify the potential mechanisms for the observed reversal of the inverse recruitment order, including preferential death of large motoneurons, demyelination and remyelination, and denervation and reinnervation of muscle fibers. Five sets of simulations assessed these mechanisms with seven simulated subjects. Preferential reinnervation, with small-diameter axons reinnervating more abandoned muscle fibers than larger-diameter axons, accounted for the apparent reversal of the inverse recruitment order observed previously. Preferential death of larger axons enhanced the reversal, but alone could not account for the observed reversal. Further, demyelination and remyelination, even in an extreme case and when combined with preferential death of large motoneurons, could not reproduce the reversal of inverse recruitment order. Thus, the apparent reversal of the inverse recruitment order was not a reversal of activation order across different diameter nerve fibers, but rather was a consequence of the redistributed force-generating capacity of the motor units resulting from denervation and reinnervation.

Full Text

Duke Authors

Cited Authors

  • Kayagil, TA; Grimes, JP; Grill, WM

Published Date

  • February 2008

Published In

Volume / Issue

  • 37 / 2

Start / End Page

  • 210 - 218

PubMed ID

  • 17990292

Pubmed Central ID

  • 17990292

Electronic International Standard Serial Number (EISSN)

  • 1097-4598

International Standard Serial Number (ISSN)

  • 0148-639X

Digital Object Identifier (DOI)

  • 10.1002/mus.20914

Language

  • eng