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Background/Objectives: In the past few years increasing attention has been given to the application of dry needling (DN) for spasticity in stroke survivors. Nevertheless, the underlying mechanisms of this technique have not yet been confirmed. The aim of this systematic review was to distinguish the effects of DN in post-stroke spasticity on both structural–mechanical muscle properties (SMMPs) and neurophysiological properties to address these mechanisms. Methods: A literature search was performed in Web of Science, PubMed, Scopus and Embase following PRISMA guidelines (PROSPERO ID: 1163064). Randomized controlled trials and case–control studies involving adults with post-stroke spasticity treated with DN were included. Outcomes were categorized as SMMPs (e.g., muscle architecture, passive stiffness, PROM) or neurophysiological measures (e.g., H-reflex, H/M ratio). Standardized effect sizes (Hedges’ g) were calculated when possible; however, heterogeneity in outcomes and incomplete variance reporting precluded meta-analysis. Results: Twelve studies met the inclusion criteria. Most of these studies assessed passive range of motion, reporting a significant increase following the intervention. Only two of the included studies examined structural characteristics, and five studies included neurophysiological outcomes. Correlations between mechanistic outcomes and clinical spasticity grading (MAS/MMAS) were weak. Emerging evidence suggests DN may additionally modulate local inflammatory mediators, indicating a potential neuroimmune contribution to its effects. Conclusions: DN appears to improve structural–mechanical muscle properties and produce moderate reductions in reflex excitability in individuals with post-stroke spasticity. Mechanical adaptations are more consistently demonstrated than neural changes, and neither domain is proportionally reflected in clinical spasticity scales. Evidence remains limited by small samples, methodological variability, and incomplete reporting. Further mechanistic research is needed to clarify how DN influences the complex pathophysiology of post-stroke spasticity.
Eeckhaut et al. (Sat,) studied this question.