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Methods to Quantify Pharmacologically Induced Alterations in Motor Function in Human Incomplete SCI
Published on: April 18, 2011
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Enhanced Reticulospinal Output in Subacute Spinal Cord Injury Patients with Spasticity
Dalia De Santis1, Monica A Perez2,3,4
1Shirley Ryan AbilityLab, Chicago, Illinois 60611.
Summary
Spinal cord injury (SCI) spasticity is linked to increased reticulospinal tract activity in the subacute phase, persisting long-term. This heightened reticulospinal drive, not corticospinal changes, appears crucial for spasticity development after SCI.
Area of Science:
- Neuroscience
- Neurology
- Rehabilitation Medicine
Background:
- Spasticity is a common and debilitating complication following spinal cord injury (SCI).
- The precise mechanisms underlying spasticity development, particularly in the early phases post-injury, remain incompletely understood.
- Damage to descending motor tracts, including the corticospinal and reticulospinal tracts, is implicated in SCI-related spasticity.
Purpose of the Study:
- To investigate the role of motor pathway reorganization in the subacute phase of SCI.
- To determine the association between spasticity and reticulospinal tract function using the StartReact response.
- To examine changes in corticospinal excitability and voluntary motor output in relation to spasticity.
Main Methods:
- Assessed the StartReact response (reaction time to startling stimuli) in individuals with subacute incomplete SCI (with and without spasticity) and controls.
- Measured motor evoked potentials (MEPs) via transcranial magnetic stimulation and maximal voluntary contractions (MVCs) of the quadriceps femoris.
- Utilized clinical and kinematic assessments to evaluate spasticity.
- Conducted follow-up measurements one year post-injury in a subset of participants.
Main Results:
- Individuals with spasticity exhibited significantly shorter reaction times to startling cues, indicating heightened reticulospinal influences.
- MEP size and MVCs were similarly reduced in both SCI groups compared to controls, suggesting widespread corticospinal impairment.
- Follow-up data confirmed persistent exaggerated StartReact responses and reduced MEP amplitudes in individuals with spasticity.
Conclusions:
- Spasticity in subacute SCI is associated with an early upregulation of reticulospinal pathways.
- This enhanced reticulospinal drive appears to be a critical factor in the pathogenesis of spasticity.
- Corticospinal tract function is reduced post-SCI irrespective of spasticity, while reticulospinal alterations are specific to spasticity development.
