{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,9]],"date-time":"2026-06-09T14:06:01Z","timestamp":1781013961540,"version":"3.54.1"},"reference-count":67,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2013,10,3]],"date-time":"2013-10-03T00:00:00Z","timestamp":1380758400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Headache"],"published-print":{"date-parts":[[2014,1]]},"abstract":"<jats:p>\n                    The pathogenesis of medication overuse headache is unclear. Clinical and preclinical studies have consistently demonstrated increased excitability of neurons in the cerebral cortex and trigeminal system after medication overuse. Cortical hyperexcitability may facilitate the development of cortical spreading depression, while increased excitability of trigeminal neurons may facilitate the process of peripheral and central sensitization. These changes may be secondary to the derangement of central, probably serotonin (5\u2010\n                    <jats:styled-content style=\"fixed-case\">HT<\/jats:styled-content>\n                    )\u2010, and perhaps endocannabinoid\u2010dependent or other, modulating systems. Increased expression of excitatory cortical 5\u2010\n                    <jats:styled-content style=\"fixed-case\">HT<\/jats:styled-content>\n                    <jats:sub>2A<\/jats:sub>\n                    receptors may increase the susceptibility to developing cortical spreading depression, an analog of migraine aura. A reduction of diffuse noxious inhibitory controls may facilitate the process of central sensitization, activate the nociceptive facilitating system, or promote similar molecular mechanisms to those involved in kindling. Low 5\u2010\n                    <jats:styled-content style=\"fixed-case\">HT<\/jats:styled-content>\n                    levels also increase the expression and release of calcitonin gene\u2010related peptide from the trigeminal ganglion and sensitize trigeminal nociceptors. Thus, derangement of central modulation of the trigeminal system as a result of chronic medication use may increase sensitivity to pain perception and foster or reinforce medication overuse headache.\n                  <\/jats:p>","DOI":"10.1111\/head.12224","type":"journal-article","created":{"date-parts":[[2013,10,11]],"date-time":"2013-10-11T22:15:12Z","timestamp":1381529712000},"page":"204-210","source":"Crossref","is-referenced-by-count":56,"title":["Pathophysiology of Medication Overuse Headache\u2014An Update"],"prefix":"10.1111","volume":"54","author":[{"given":"Anan","family":"Srikiatkhachorn","sequence":"first","affiliation":[{"name":"Department of Physiology Faculty of Medicine Chulalongkorn University  Bangkok Thailand"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Supang Maneesri","family":"le Grand","sequence":"additional","affiliation":[{"name":"Department of Pathology Faculty of Medicine Chulalongkorn University  Bangkok 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