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Botulinum toxin type A improves passive stretch-evoked activity and CMAP in post-stroke spasticityBotulinum toxin helps muscle control after a stroke

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Key Takeaway
Note that Botulinum toxin type A improves passive stretch-evoked activity and CMAP in post-stroke spasticity.

This meta-analysis evaluates the neurophysiological mechanisms underlying Botulinum toxin type A treatment in 760 patients with post-stroke spasticity. The analysis focuses on several secondary outcomes, including passive stretch-evoked activity, voluntary activation, and compound muscle action potential (CMAP) amplitude.

Key findings include a large pooled effect for passive stretch-evoked activity (Hedges' g = 0.80; 95% CI 0.35-1.24) and a significant change in CMAP amplitude (Hedges' g = 0.69; 95% CI 0.23-1.14). Improvements in reciprocal motor control were also noted (Hedges' g = 0.52; 95% CI 0.23-0.81). However, results for voluntary activation (Hedges' g = 0.31; 95% CI -0.38 to 1.00) and normalized Hmax/Mmax (Hedges' g = 0.22; 95% CI -0.74 to 1.17) were smaller and more heterogeneous.

The authors note low to very low certainty of evidence and significant methodological heterogeneity, particularly regarding supraspinal outcomes. These findings suggest that Botulinum toxin type A may provide a rationale for individualized, mechanism-based rehabilitation during the post-injection therapeutic window. Clinical application should be tempered by the preliminary nature of the supraspinal data.

How this fits prior evidence

This meta-analysis addresses a gap in the understanding of the neurophysiological mechanisms of Botulinum toxin type A for post-stroke spasticity. It complements previous findings where acupuncture was reviewed for post-stroke spasticity, though that evidence also required careful interpretation due to certainty levels. While this study confirms the efficacy of Botulinum toxin type A in improving muscle activity and CMAP, it provides a more specific physiological focus than previous reports on Botulinum toxin type A for tremor, sialorrhea, or scar appearance.

Living with muscle stiffness, known as spasticity, after a stroke can make daily movements difficult and painful. A large review of 760 patients looked at how botulinum toxin type A (a common injectable treatment) affects the underlying ways muscles and nerves work together. The goal was to see how the treatment changes the physical signals in the body.

The study found that the injection significantly increased certain muscle activities and improved reciprocal motor control, which is how muscles work in pairs. While some improvements in muscle activation were less consistent across the board, the results suggest that the treatment does change how muscles respond to stretching. Because the evidence for some specific brain-related outcomes was less certain, the findings are still early.

These results help doctors understand exactly what happens when a patient gets an injection. By knowing which muscle signals change the most, doctors can better tailor physical therapy to the specific needs of each patient. This helps create a more personalized plan during the time right after the treatment is given.

What this means for you:
Botulinum toxin injections can improve muscle activity and coordination for people with post-stroke stiffness.

Common questions

How does botulinum toxin help with muscle stiffness?

The treatment impacts the neurophysiological mechanisms of the muscle. Specifically, it was shown to increase passive stretch-evoked activity and improve reciprocal motor control. These changes help the muscles function better after a stroke. Because the evidence for some specific outcomes is low to very low certainty, talk to your doctor about how it applies to your specific case.

What specific muscle changes were found?

The study of 760 patients showed a significant change in compound muscle action potential (CMAP) amplitude and an increase in stretch-evoked activity. While some measures like voluntary activation and Hmax/Mmax were more varied and showed smaller effects, the overall data provides a clearer picture of how the injection affects muscle signals.

How does this help with rehabilitation?

By identifying which muscle mechanisms change after an injection, doctors can provide more individualized, mechanism-based rehabilitation. This helps them target the right movements during the specific window of time after the botulinum toxin is administered to help you regain better control.

Study Details

Study typeMeta analysis
Sample sizen = 760
EvidenceLevel 1
PublishedSep 2026
View Original Abstract ↓
BACKGROUND: Botulinum toxin type A (BoNT-A) is globally recognized as a standard treatment for post-stroke spasticity (PSS), although its secondary mechanisms remain underinvestigated. The objective of this study was to investigate the neurophysiological mechanisms underlying BoNT-A treatment in PSS and explore their implications for mechanism-based rehabilitation. METHODS: A systematic review and meta-analysis (PROSPERO registration number ID: CRD420261352230) of 39 studies involving 760 patients was conducted on 18 August 2026, following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. PubMed, Web of Science, Scopus, and Embase were systematically searched using the PICO framework. Where possible, quantitative data were pooled according to predefined neurophysiological constructs, including passive stretch-evoked activity, voluntary activation of the injected muscle, compound muscle action potential (CMAP), reciprocal motor control, normalized Hmax/Mmax, and specific spinal inhibitory mechanisms. RESULTS: Quantitative synthesis demonstrated construct-specific neurophysiological changes following BoNT-A treatment. Passive stretch-evoked activity showed the largest pooled effect (Hedges' = 0.80, 95% CI 0.35-1.24), followed by CMAP amplitude ( = 0.69, 95% CI 0.23-1.14) and reciprocal motor control ( = 0.52, 95% CI 0.23-0.81). Effects on voluntary activation of the injected muscle ( = 0.31, 95% CI -0.38 to 1.00) and normalized Hmax/Mmax ( = 0.22, 95% CI -0.74 to 1.17) were smaller and more heterogeneous. Reciprocal and recurrent inhibition were each represented by single-study estimates, while supraspinal outcomes were synthesized narratively due to methodological heterogeneity. CONCLUSIONS: The findings support a predominantly peripheral mechanism of BoNT-A while suggesting possible secondary changes within spinal and supraspinal motor control pathways. However, the certainty of evidence was low to very low. These neurophysiological effects provide a rationale for individualized, mechanism-based rehabilitation during the post-injection therapeutic window, although higher-quality evidence is required to confirm this framework.
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