The mechanism of electroacupuncture treatment for post-stroke spasticity: A systematic review and Meta-analysis

This study assesses whether electroacupuncture (EA) is an effective treatment for post-stroke spasticity (PSS) and examines the mechanisms by which it modulates PSS. Clinical and mechanistic evidence are analyzed to clarify its therapeutic value and biological basis.

A literature search was conducted in databases including PubMed, Web of Science (WOS), Embase，Medline and SinoMed. The quality was evaluated by the Systematic Review Centre for Laboratory Animal Experimentation (SYRCLE) bias risk assessment tool and Collaborative Approach to Meta-analysis and Review of Animal Data from Experimental Studies (CAMARADES) checklist. Meta-analyses were performed using Stata 15.0 and Rstudio software.

Twenty studies involving 388 animals were included, with quality scores ranging from 4 to 8 (mean: 6.1). Zea Longa and Modified Ashworth Scale (MAS) were selected as primary outcomes, while secondary outcomes included Bederson score, electrophysiological tracing, balance beam walking, cerebral water content, cerebral infarction degree, Interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), malondialdehyde (MDA), gamma-aminobutyric acid (GABA), glutamate (Glu), gamma-aminobutyric acid transaminase (GABA-T), glutamate decarboxylase 67 (GAD67), brain-derived neurotrophic factor (BDNF), tropomyosin receptor kinase B (TrkB), BDNF messenger RNA (BDNF mRNA), TrkB messenger RNA (TrkB mRNA), glutathione (GSH), solute carrier family 7 member 11 (SLC7A11), glutathione peroxidase 4 (GPX4), SLC7A11 messenger RNA (SLC7A11 mRNA), and GPX4 messenger RNA (GPX4 mRNA).Meta-analysis demonstrated significant improvements in primary outcomes: Zea Longa score [MD = -1.05, 95 % CI (-1.30, -0.80), P < 0.001]，MAS score: [MD = -1.06, 95 % CI (-1.43, -0.69), P < 0.001]. EA therapy demonstrated significant efficacy in enhancing neurological recovery, alleviating limb spasticity, and improving postural balance. Furthermore, it effectively reduced cerebral infarct volume, mitigated cerebral edema severity, and modulated biochemical markers by decreasing serum levels of IL-6, TNF-α, MDA, Glu, and GABA-T (P < 0.05). Concurrently, therapeutic intervention upregulated multiple neuroprotective indicators including GSH, GABA, SLC7A11 mRNA, GPX4 (with its mRNA expression), GAD67, BDNF, TrkB (and its mRNA), along with enhancing GPX4 activity (P < 0.05). Heterogeneity analysis revealed publication bias in MAS assessments, while heterogeneity in intervention protocols (waveform parameters, acupoint selection, or treatment duration) potentially contributed to elevated heterogeneity across other outcome measures.

EA modulates neurotransmitter levels and associated enzymatic, while concurrently suppressing microglia-mediated neuroinflammatory responses. This intervention mitigates oxidative stress byproducts, maintains tissue redox homeostasis, and enhances synaptic plasticity while promoting neuronal development. Collectively, our findings underscore EA's therapeutic potential in PSS management, necessitating further mechanistic investigations and optimization of clinical protocols.