# Early Use of Botulinum Toxin in Post-Stroke Spasticity Has the Potential to Prevent Post-Stroke Upper Limb Pain—A Secondary Analysis of the EUBoSS Randomised Controlled Trial

**Authors:** Cameron Lindsay, Fraser Philp, Anand D. Pandyan

PMC · DOI: 10.3390/toxins18030147 · Toxins · 2026-03-18

## TL;DR

Early use of botulinum toxin after a stroke may help prevent upper limb pain and reduce the need for painkillers.

## Contribution

This study suggests that early botulinum toxin treatment may prevent post-stroke upper limb pain.

## Key findings

- Pain prevalence increased from 29.0% to 63.4% at six months post-stroke.
- BoNTA treatment may prevent pain development at six months (OR = 0.42).
- BoNTA reduced analgesic use at six months (OR = 0.35).

## Abstract

Post-stroke upper limb pain is prevalent and challenging to manage once established. Early use of botulinum toxin can reduce spasticity and contracture development and has potential to prevent or reduce pain. A secondary analysis of the EUBoSS study was undertaken to report pain prevalence in people post-stroke with severe upper limb impairment and spasticity in a hyper/acute setting, identify if botulinum toxin Type-A (BoNTA) could prevent pain developing and reduce pain if already present and evaluate differences in analgesic use between BoNTA and placebo groups. Odds ratios (OR) with 95% confidence intervals (CI) were calculated. Ninety-three participants (48F:45M) were randomised at a median of 11 days post-stroke (IQR 8–19) and included in the intention-to-treat analysis. Pain prevalence increased from 29.0% (95% CI [20.1–37.9%]) to 63.4% (95% CI [54.0–72.9%]) at six months. BoNTA treatment may prevent the development of pain at six months (OR = 0.42, 95% CI [0.18 to 1.01]) but not at three months (OR = 0.57, 95% CI [0.25 to 1.32]). The odds ratio for being on at least one analgesic at six months in the BoNTA group was 0.35 ([95% 0.14 to 0.87]). This secondary analysis suggests that early treatment of spasticity with BoNTA may potentially help prevent post-stroke upper limb pain and reduce analgesic use but appears less effective once pain is established. Further prospective studies are required to verify the hypotheses generated from this secondary analysis.

## Full-text entities

- **Genes:** WDTC1 (WD and tetratricopeptide repeats 1) [NCBI Gene 23038] {aka ADP, DCAF9}
- **Diseases:** inflammatory (MESH:D007249), Spasticity (MESH:D009128), hypersensitivity (MESH:D004342), limb deformities (MESH:D017880), cognitive and communication difficulties (MESH:D003147), Shoulder pain (MESH:D020069), musculoskeletal conditions (MESH:D009140), subluxation (MESH:D004204), abnormal muscle (MESH:D009135), contracture (MESH:D003286), cognitive impairments (MESH:D003072), Upper Limb Impairment (MESH:D038062), Pain (MESH:D010146), aphasia (MESH:D001037), dystonia (MESH:D004421), falls (MESH:C537863), motor and sensory impairments (MESH:D015417), infection (MESH:D007239), neuropathic pain (MESH:D009437), injury to (MESH:D014947), Post (MESH:D000094025), Post-Stroke (MESH:D020521)
- **Chemicals:** sodium chloride (MESH:D012965), dydramol (-), paracetamol (MESH:D000082), co-codamol (MESH:C526278)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## References

39 references — full list in the complete paper: https://tomesphere.com/paper/PMC13029928/full.md

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Source: https://tomesphere.com/paper/PMC13029928