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Curr Opin Genet Dev 1999

Distinct mechanisms can be discerned within the pathophysiology of EBI, encompassing cerebral metabolic distress (nitric oxide uncoupling, oxidative stress, and adenosine triphosphate (ATP) depletion), cortical spreading depolarization, neuro-inflammation (microglial activation, release of cytokines and chemokines, and adhesion molecule expression), microvascular dysfunction, activation of the coagulation system (platelet activation and aggregation, microthrombi formation), and cellular phenomena such as endothelial cell apoptosis, autophagy, neuronal swelling and cell death (5, 911, 21, 22)

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Despite advances in antifungal monotherapy and combination strategies, critical challenges remain, such as overcoming the escalating drug resistance, optimizing individualized therapeutic regimens tailored to diverse patient populations, and improving long-term treatment efficacy to reduce recurrence and disease progression