Abstract
The state of areflexia and muscle weakness that immediately follows a spinal cord injury (SCI) 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 functional activation of the spinal cord and the eventual impact on the muscle. Specifically, decreases in the inhibitory control of sensory transmission and increases in intrinsic motoneuron excitability are described. We present the idea that 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 with spared descending and/or peripheral inputs by facilitating movement, instead of suppressing it pharmacologically, may provide the best avenue to improve residual motor function and manage spasticity after SCI.
Highlights
In the months following a spinal cord injury (SCI), 70–80% of individuals develop spasticity (Maynard et al, 1990; Skold et al, 1999), which is characterized by involuntary muscle activity such as spasms, hyperreflexia, clonus and co-contraction (Pandyan et al, 2005; Nielsen et al, 2007)
We compare evidence from both animal and human studies to discuss how muscle and non-muscle tissues respond to the different phases of SCI and how neurons and neuronal circuits increase their excitability and decrease their inhibitory capacity to compensate for the loss of descending and movement-related sensory inputs, leading to the development of spasticity
In addition to being voltage-sensitive, persistent inward currents (PICs) require the concomitant activation of serotonergic (5-HT) or noradrenergic (NA) receptors located on the motoneurons
Summary
We present the idea that 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 improve its controlled activation by synaptic inputs to normalize circuit function. Increasing the excitation of the spinal cord with spared descending and/or peripheral inputs by facilitating movement, instead of suppressing it pharmacologically, may provide the best avenue to improve residual motor function and manage spasticity after SCI
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