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As PPRs are activated by molecules resembling microbes, that is, pathogen-associated molecular patterns or damage-associated molecular patterns that can be of nonmicrobial origin, exposure to pathogen-associated molecular patterns and damage-associated molecular patterns may promote an excessive inflammatory response, promoting excessive cell death and tissue remodeling. We present a narrative review describing the role of PPRs, pathogen-associated molecular patterns, and damage-associated molecular patterns in the formation, progression, and eventual rupture of intracranial aneurysms, as well as in the neuronal damage caused by aneurysmal subarachnoid hemorrhage. 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