Intensity of subarachnoid space inflammation corresponds to the evolution of vessel wall remodeling during the acute and chronic phases of bacterial meningitis

Cerebrovascular alterations in acute bacterial meningitis significantly contribute to adverse patient outcomes, with reported complication rates ranging from 10% to 29%. Focal alterations in arterial lumens, leading to vasoconstriction, are common in cerebral ischemic and inflammatory conditions, such as bacterial meningitis, presenting neurological complications, such as seizures, brain swelling, hydrocephalus, hearing loss and ischemic or hemorrhagic brain damage. The observed arterial narrowing during meningitis is attributed to diverse factors, including direct encroachment by inflammatory exudate, vascular wall edema, vasospasm, and vasculitis due to cellular infiltration and vessel remodeling. Early‐stage constriction might result from a watery exudate's encroachment, whereas persistent inflammation leads to thicker exudates, attracting inflammatory cells and inducing arteriopathic growth factor synthesis. This process promotes structural modifications in the vessel wall, progressing from subintimal infiltration to organic intimal thickening, culminating in vasculitis and the risk of cerebral ischemia. Accordingly, this review seeks to more clearly delineate the intricate relationship between subarachnoid space inflammation and acute and chronic vessel wall remodeling during bacterial meningitis. Conceivably, understanding this pathological process holds promise in unveiling potential treatment avenues to improve patient outcomes, and reduced morbidity and mortality associated with cerebrovascular complications during bacterial meningitis.