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The prevailing theory posits that CSD triggers the release of pronociceptive mediators, leading to the dilation of meningeal arteries and activation of perivascular primary afferents, thereby causing headache [4, 5]

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The inflammatory markers monocyte chemoattractant protein-1 (MCP-1) and tumor necrosis factor (TNF- ), were reduced by treatment with exendin-4 in response to lipopolysaccharide in cultured peritoneal macrophages harvested from mice [65]