Figure 1 Inflammatory pathways in post-stroke fatigue. This figure illustrates the interactive network between PSF and inflammatory responses, along with related mechanisms. Key elements include the following: after an ischemic stroke, activated microglia and astrocytes release pro-inflammatory cytokines, triggering systemic and chronic inflammation accompanied by elevated hs-CRP. These inflammatory factors can cross the blood–brain barrier and affect the basal ganglia and hypothalamus, leading to neuroendocrine changes, disruption of the sleep–wake cycle, and abnormal neurotransmitter release, particularly within dopaminergic and serotonergic systems. Additionally, inflammation impairs synaptic plasticity. The interplay of these factors contributes to the onset and persistence of PSF. hs-CRP – high-sensitivity C-reactive protein; IL – interleukin; PSF – post-stroke fatigue; TNF – tumor necrosis factor.