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

Frontiers in Integrative Neuroscience, 2014 · DOI: 10.3389/fnint.2014.00036 · Published: May 12, 2014

Spinal Cord Injury Neurology Rehabilitation

Simple Explanation

After a spinal cord injury (SCI), the initial muscle weakness transitions to a phase where neurons become more excitable. This can lead to improved motor function but also to spasticity. This review discusses how motoneurons and sensory pathways become hyperexcitable to compensate for reduced spinal cord activation, affecting muscles. The authors suggest activating synaptic inputs through movement or stimulation to recover lost spinal inhibition, potentially reducing uncontrolled spinal cord activation and improving circuit function.

Study Duration

Not specified

Participants

Animal and human studies

Evidence Level

Review Article

Key Findings

1
Motoneuron Persistent Inward Currents (PICs) are reduced in spinal shock but re-emerge in the weeks following SCI, contributing to both motor recovery and spasticity.
2
In chronic SCI, 5-HT2 and NAα1 receptors on motoneurons become constitutively active, contributing to the recovery of PICs and increased excitability, even with reduced monoamine levels.
3
Sensory transmission to motoneurons is altered after SCI, including loss of IPSPs and emergence of long-duration EPSPs, which can trigger PICs and involuntary muscle spasms.

Research Summary

Following SCI, the spinal cord adapts to reduced synaptic excitation by increasing motoneuron excitability. This is done via mechanisms like increased constitutive monoamine receptors and downregulated KCC2. Current pharmacological treatments suppress spinal cord or muscle activity, often causing side effects like drowsiness and weakness. Physical treatments, like stretching and treadmill training, can reduce spasticity and improve motor function. An alternative approach involves enhancing functional synaptic activation of the spinal cord to strengthen purposeful muscle activation and reduce involuntary activation.

Practical Implications

Pharmacological Targets

Developing more specific inverse agonists to 5-HT2/NAα1 receptors with fewer side effects than cyproheptadine may lead to better oral control of involuntary muscle spasms and clonus in SCI.

Physical Therapy Strategies

Active physical treatments that provide functional, patterned synaptic activation of the spinal cord may enhance activation of spinal inhibitory circuitry by strengthened descending motor pathways and decrease sensory transmission.

Combined Therapies

Combining excitatory pharmacological and physical treatments may increase spinal cord excitability and promote motor recovery by increasing control over excitatory circuits and enhancing intrinsic inhibitory mechanisms.

Study Limitations

1
Current pharmacological treatments often produce generalized CNS depression.
2
Long-term intrathecal baclofen delivery has a high rate of complications.
3
More research is needed to determine the best long-term approach for treating and managing spasticity after SCI.

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