From Neurophysiological Mechanisms to Rehabilitation After Botulinum Toxin Type A in Post-Stroke Spasticity.

Toxins (Basel)Sep 20, 2026 (epub)

Bart Eeckhaut, Steven Truijen, Parham Haghshenas et al.

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In 30 seconds

This systematic review and meta-analysis examined the neurophysiological mechanisms of botulinum toxin type A (BoNT-A) in treating post-stroke spasticity (PSS) across 39 studies with 760 patients. The analysis revealed significant changes in passive stretch-evoked activity (Hedges' g = 0.80), CMAP amplitude (g = 0.69), and reciprocal motor control (g = 0.52), supporting a peripheral mechanism of action.

Key findings

  • Passive stretch-evoked activity showed the largest pooled effect (Hedges' g = 0.80).
  • CMAP amplitude demonstrated a significant effect (g = 0.69).
  • Reciprocal motor control had a pooled effect size of g = 0.52.
  • Effects on voluntary activation and normalized Hmax/Mmax were smaller and more heterogeneous.

Why it matters

Understanding the neurophysiological mechanisms of BoNT-A can enhance rehabilitation strategies for post-stroke spasticity, allowing for more tailored and effective treatment approaches during recovery.

What to keep in mind

The certainty of evidence was low to very low, indicating a need for higher-quality studies.

Source

Published in Toxins (Basel). This summary was written by xxcode from the publication's abstract and metadata. It is not peer reviewed and is not a substitute for the original article. For clinical decisions, review the original publication.

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AI-generated summaries may contain errors or omissions. Verify clinically important information with the original publication.

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