{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,2]],"date-time":"2026-06-02T08:45:59Z","timestamp":1780389959546,"version":"3.54.1"},"reference-count":47,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2019,7,18]],"date-time":"2019-07-18T00:00:00Z","timestamp":1563408000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["headachejournal.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Headache"],"published-print":{"date-parts":[[2019,9]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Premise<\/jats:title>\n                    <jats:p>The science of migraine pathophysiology has advanced significantly since the 1930\u2019s. Imaging techniques, neurochemical analysis, clinical trials, and the clinical experience of providers treating migraine patients have not only sharpened our understanding of the disease, but have also led to the development of novel neural\u2010based targets. Targeted therapies such as calcitonin gene\u2010related peptide (CGRP) antibodies and \u201cSecond Generation\u201d CGRP receptor antagonists (Gepants) have not only demonstrated efficacy, but have not resulted in any significant cardiovascular nor other serious adverse events. \u201cFirst Generation\u201d Gepants were associated with liver toxicity.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Problem<\/jats:title>\n                    <jats:p>Triptans and dihydroergotamine (DHE) are contraindicated in patients with hemiplegic and basilar migraine\u00a0based on theories of migraine pathophysiology from the 1930s. While our understanding of migraine has evolved substantially, perceived concerns of safety from almost a century ago continue to preclude their use in certain patient populations.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Potential solution<\/jats:title>\n                    <jats:p>While migraine aura was once thought to be primarily due to vasoconstriction, current evidence debunks this concept. For instance, hemiplegic migraine is the consequence of genetic mutations resulting in channelopathies without evidence of cerebral ischemia or infarction. Evidence of basilar artery constriction as postulated in basilar migraine is also lacking. This recognition has led the International Headache Society to rename basilar\u2010type migraine to migraine with brainstem aura.<\/jats:p>\n                    <jats:p>\n                      The following discussion reviews current literature with respect to migraine as a neuronal disorder, as well as the published data on the safety of triptans, DHE, Ditans (a novel class of 5\u2010HT\n                      <jats:sub>1f<\/jats:sub>\n                      receptor agonists), CGRP antibodies, and Gepants.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/head.13601","type":"journal-article","created":{"date-parts":[[2019,7,18]],"date-time":"2019-07-18T08:47:47Z","timestamp":1563439667000},"page":"1421-1426","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":34,"title":["Getting to the Heart of the Matter: Migraine, Triptans, DHE, Ditans, CGRP Antibodies, First\/Second\u2010Generation Gepants, and 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