Recovery of neuronal and network excitability after spinal cord injury and implications for spasticity

The state of areflexia and muscle weakness that immediately follows a spinal cord injury is gradually replaced by the recovery of neuronal and network excitability, leading to both improvements in residual motor function and the development of spasticity. In this review we summarize recent animal an...

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Main Authors: Jessica Maria D'Amico, Elizabeth G Condliffe, Karen J.B. Martins, David James Bennett, Monica Ann Gorassini
Format: Article
Language:English
Published: Frontiers Media S.A. 2014-05-01
Series:Frontiers in Integrative Neuroscience
Subjects:
Online Access:http://journal.frontiersin.org/Journal/10.3389/fnint.2014.00036/full
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spelling doaj-069fd4df10b947f8a1758672d43622d92020-11-24T22:32:48ZengFrontiers Media S.A.Frontiers in Integrative Neuroscience1662-51452014-05-01810.3389/fnint.2014.0003674376Recovery of neuronal and network excitability after spinal cord injury and implications for spasticityJessica Maria D'Amico0Elizabeth G Condliffe1Karen J.B. Martins2David James Bennett3Monica Ann Gorassini4Faculty of Medicine and Dentistry, University of AlbertaFaculty of Medicine and Dentistry, University of AlbertaUniversity of AlbertaFaculty of Rehabilitation Medicine, University of AlbertaFaculty of Medicine and Dentistry, University of AlbertaThe state of areflexia and muscle weakness that immediately follows a spinal cord injury is gradually replaced by the recovery of neuronal and network excitability, leading to both improvements in residual motor function and the development of spasticity. In this review we summarize recent animal and human studies that describe how motoneurons and their activation by sensory pathways become hyperexcitable to compensate for the reduction of descending and movement-induced sensory inputs and the eventual impact on the muscle. We discuss how replacing lost patterned activation of the spinal cord by activating synaptic inputs via assisted movements, pharmacology or electrical stimulation may help to recover lost spinal inhibition. This may lead to a reduction of uncontrolled activation of the spinal cord and thus, improve its controlled activation by synaptic inputs to ultimately normalize circuit function. Increasing the excitation of the spinal cord below an injury with spared descending and/or peripheral functional synaptic activation, instead of suppressing it pharmacologically, may provide the best avenue to improve residual motor function and manage spasticity after spinal cord injury.http://journal.frontiersin.org/Journal/10.3389/fnint.2014.00036/fullSerotoninSpinal Cord Injuriesmotoneuronnoradrenalinereflexespersistent inward currents
collection DOAJ
language English
format Article
sources DOAJ
author Jessica Maria D'Amico
Elizabeth G Condliffe
Karen J.B. Martins
David James Bennett
Monica Ann Gorassini
spellingShingle Jessica Maria D'Amico
Elizabeth G Condliffe
Karen J.B. Martins
David James Bennett
Monica Ann Gorassini
Recovery of neuronal and network excitability after spinal cord injury and implications for spasticity
Frontiers in Integrative Neuroscience
Serotonin
Spinal Cord Injuries
motoneuron
noradrenaline
reflexes
persistent inward currents
author_facet Jessica Maria D'Amico
Elizabeth G Condliffe
Karen J.B. Martins
David James Bennett
Monica Ann Gorassini
author_sort Jessica Maria D'Amico
title Recovery of neuronal and network excitability after spinal cord injury and implications for spasticity
title_short Recovery of neuronal and network excitability after spinal cord injury and implications for spasticity
title_full Recovery of neuronal and network excitability after spinal cord injury and implications for spasticity
title_fullStr Recovery of neuronal and network excitability after spinal cord injury and implications for spasticity
title_full_unstemmed Recovery of neuronal and network excitability after spinal cord injury and implications for spasticity
title_sort recovery of neuronal and network excitability after spinal cord injury and implications for spasticity
publisher Frontiers Media S.A.
series Frontiers in Integrative Neuroscience
issn 1662-5145
publishDate 2014-05-01
description The state of areflexia and muscle weakness that immediately follows a spinal cord injury is gradually replaced by the recovery of neuronal and network excitability, leading to both improvements in residual motor function and the development of spasticity. In this review we summarize recent animal and human studies that describe how motoneurons and their activation by sensory pathways become hyperexcitable to compensate for the reduction of descending and movement-induced sensory inputs and the eventual impact on the muscle. We discuss how replacing lost patterned activation of the spinal cord by activating synaptic inputs via assisted movements, pharmacology or electrical stimulation may help to recover lost spinal inhibition. This may lead to a reduction of uncontrolled activation of the spinal cord and thus, improve its controlled activation by synaptic inputs to ultimately normalize circuit function. Increasing the excitation of the spinal cord below an injury with spared descending and/or peripheral functional synaptic activation, instead of suppressing it pharmacologically, may provide the best avenue to improve residual motor function and manage spasticity after spinal cord injury.
topic Serotonin
Spinal Cord Injuries
motoneuron
noradrenaline
reflexes
persistent inward currents
url http://journal.frontiersin.org/Journal/10.3389/fnint.2014.00036/full
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