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. 2018 Apr 12;14:1744806918767697. doi: 10.1177/1744806918767697

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© The Author(s) 2018

Creative Commons Non Commercial CC BY-NC: This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (http://www.creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage).

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Figure 1. — The proposed pathophysiological process of chronic migraine (CM). Both recurring headache attacks and other risk factors for migraine transformation (medication-overuse, anxiety, and depression) promote the derangement of top-down pain modulation and also atypical release of nociceptive molecules, which aggravates trigeminal sensitization induced by repeated nociceptive inputs. With this hypersensitive state, the episodic migraine finally progresses to a “never-ending” condition, namely, CM. To be noted, the neural plasticity induced by the risk factors of CM may influences themselves in turn. ACC: anterior cingulate cortex; PAG: periaqueductal gray; CGRP: calcitonin gene-related peptide; 5-HT: serotonin; PACAP: pituitary adenylate cyclase activating polypeptide.