Correlation between anxiety-depression disorders and brain structural connectivity abnormalities after subarachnoid hemorrhage

Figure 6 Temporal dynamic analysis and pathophysiological cascade process after subarachnoid hemorrhage. A: Time-course curves of various indicators after subarachnoid hemorrhage (SAH), showing that cellular edema appears earliest (1 hour), followed by elevation of inflammatory factors (6-12 hours), increased NOD-like receptor protein 3 expression (12-24 hours), decreased fractional anisotropy values (24-48 hours), and aggravated anxiety-depression behavior (24-72 hours); B: Proposed pathophysiological cascade model of “cellular edema → neuroinflammation → NOD-like receptor protein 3 activation → white matter fiber bundle damage → emotional disorders”, revealing the potential mechanistic link between early cellular changes and later behavioral manifestations after SAH. These temporal sequence characteristics provide important clues for understanding the mechanism of anxiety-depression disorders after SAH. SAH: Subarachnoid hemorrhage; ADC: Apparent diffusion coefficient; NLRP3: NOD-like receptor protein 3; IL-6: Interleukin-6; IL-1β: Interleukin-1β; FA: Fractional anisotropy.