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Drug\u2010induced aseptic meningitis (<jats:styled-content style=\"fixed-case\">DIAM<\/jats:styled-content>) may be due to two mechanisms: (i) a direct meningeal irritation caused by the intrathecal administration of drugs and (ii) an immunologic hypersensitivity reaction to a systemic administration. If the direct meningeal irritation allows a rather easy recognition, the immunologic hypersensitivity reaction is a source of challenging diagnostics. <jats:styled-content style=\"fixed-case\">DIAM<\/jats:styled-content> linked to a systemic treatment exerts typically an early onset, usually within a week. This period can be shortened to a few hours in case of drug rechallenge. The fast and spontaneous regression of clinical symptoms is usual after stopping the suspected drug. Apart from these chronological aspects, no specific clinical or biological parameters are pathognomonic. <jats:styled-content style=\"fixed-case\">CSF<\/jats:styled-content> analysis usually shows pleiocytosis. The proteinorachia is increased while glycorachia remains normal. Underlying pathologies can stimulate the occurrence of <jats:styled-content style=\"fixed-case\">DIAM<\/jats:styled-content>. Thus, systemic lupus erythematosus appears to promote <jats:styled-content style=\"fixed-case\">DIAM<\/jats:styled-content> during <jats:styled-content style=\"fixed-case\">NSAID<\/jats:styled-content> therapy, especially ibuprofen\u2010based one. Similarly, some patients with chronic migraine are prone to intravenous immunoglobulin\u2010induced aseptic meningitis. <jats:styled-content style=\"fixed-case\">DIAM<\/jats:styled-content> will be mainly evoked on chronological criteria such as rapid occurrence after initiation, rapid regression after discontinuation, and recurrence after rechallenge of the suspected drug. When occurring, positive rechallenge may be very useful in the absence of initial diagnosis. Finally, <jats:styled-content style=\"fixed-case\">DIAM<\/jats:styled-content> remains a diagnosis of elimination. 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