Spasticity has been traditionally defined as a velocity-dependent increase in muscle tone due to exaggeration of stretch reflex. In other words, if the clinician mobilizes quickly enough a patient's joint across its range, spastic muscles will react with involuntary, jerky muscle contraction.
In this perspective, spasticity is caused by a lesion disrupting descending pathways that regulates the stretch reflex. The imbalance between inhibitory and facilitatory pathways would determine spasticity.
However, this model does not explain why spasticity develops over weeks/months post- stroke, or why there is enduring abnormal EMG activity not only during the dynamic phase of a stretch, but also during the static phase (if the joint is kept extended).
To explain these issues there are two hidden phenomenon that should be considered, also because they could play a major contributions to muscle hypertonia and related functional limitations.
The first one is related to plastic changes in the spinal cord (progressive reduction in postactivation depression, see the article for further explanation) caused by protracted limb immobilization/non-use.
The second one is related to secondary soft tissue changes (fibrosis, contractures) caused again by prolonged immobilization.
Clinical implications
Because pathological neuroplastic and soft tissue changes are both caused by prolonged immobility, clinicians should prioritize active-assisted mobilization of the plegic limb, and discourage the adoption of 24h rest strategies (prolonged immobilization, casting). In particular, as opposed to what was previously believed, the provision of any form of assisted mobilization/stimulation/training (therapist, robotic, FES, somatosensory stimulation) is beneficial to improve functionality and prevent the development of spasticity.
Quick question: what is your therapeutic approach to manage/prevent spasticity? In your experience, how patients responded to treatment targeting hypertonia? Let me know in the comment section.
External links
PubMed must-read
This post is based on the article: Pathophysiology of spasticity: implications for neurorehabilitation
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