Role of gut microbiota dysbiosis on the functional outcomes in ischemic and haemorrhagic stroke patients: a systematic review

Background Stroke is a leading cause of death and long-term disability worldwide, yet the biological determinants of post-stroke recovery remain incompletely understood. Recent evidence implicates the gut microbiome as a key regulator of neuroinflammation, metabolic signalling, and immune response through microbiota-gut brain axis. However, the extent to which gut microbial dysbiosis influences neurological severity and functional recovery across ischemic and haemorrhagic stroke remains unclear. Methods This systematic review examined the relationship between gut dysbiosis and functional outcomes following stroke. A comprehensive search of PubMed, Scopus, Web of Science, ScienceDirect, and the Cochrane Library identified eligible studies published up to July 2025. Twenty-three clinical studies comprising 2,951 participants were included. Microbiome diversity indices, microbial taxa, and microbiota-derived metabolites were evaluated in relation to standardized stroke outcomes, including acute neurological severity (NIHSS) and functional outcomes (mRS, Barthel Index. The study quality was assessed using the Newcastle-Ottawa Scale and the Cochrane risk-of-bias framework. Results Across the included cohorts, stroke patients exhibited consistent alterations in gut microbial ecology compared with healthy controls. Alpha diversity analyses demonstrated a significant reduction in microbial richness and evenness in several cohorts, while beta diversity metrics revealed pronounced restructuring and clear separation between stroke and control microbiomes. Differential abundance analysis consistently identified depletion of short-chain fatty acid (SCFA)-producing commensals, including Roseburia, Faecalibacterium, and Coprococcus, alongside enrichment of opportunistic and pro-inflammatory taxa such as Enterobacteriaceae, Enterococcus, and Escherichia/Shigella. Metabolomic analysis further revealed a convergent disruption of key microbial metabolic pathways, including reduced SCFA production, increased endotoxin-associated signalling and trimethylamine-N-oxide (TMAO) metabolism. These microbial and metabolic perturbations were significantly associated with greater neurological severity, higher disability scores, increased infection risk, and poorer functional outcomes following stroke. Conclusion This systematic synthesis demonstrates that stroke is accompanied by a reproducible pattern of gut microbial dysbiosis characterized by ecological contraction, expansion of inflammatory pathobionts, and disruption of microbial metabolic signalling. These findings support the existence of a conserved gut-brain-metabolic axis influencing stroke severity and recovery trajectories. Integrating microbiome-derived biomarkers with clinical prognostic models may enable earlier risk stratification and the development of microbiota-targeted therapeutic strategies to improve post-stroke outcomes. Systematic review registration PROSPERO (Identifier: CRD420251106958).