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Episodic to Chronic Migraine: The Basis for the Transformation

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52:902

<AAN-East Asian Neurology Forum-JSN Joint Symposium (2)―2―3>

Solving the enigma of migraine

Episodic to Chronic Migraine: The Basis for the Transformation

David W. Dodick, M.D.

(臨床神経 2012;52:902)

CM is currently defined as headache on"15 days!month for"3 months with "8 days!month fulfilling criteria for mi-graine and!or respond to a triptan or ergot. The estimated prevalence of CM worldwide is 1% to 3%, and every year, between 2.5 and 4.6% of people with episodic migraine ex-perience progression to chronic migraine. Long-term follow up over 3 years indicates that only 26% experience remis-sion of chronic migraine (defined as <15 headache days per month). Compared with EM, CM is associated with greater headache-related disability, reduced health-related quality of life, higher direct and indirect healthcare costs, and higher rates of medical and psychiatric comorbidities. The preva-lence, disability, progression, and treatment needs associated with CM has created an urgent need for epidemiologic, clini-cal, and basic research to help better understand the clinical course of this disorder and to facilitate development of effec-tive therapies.

A number of risk factors for the transformation from EM to CM have been identified, including acute headache medi-cation overuse, high frequency of headache (10-14 days per month), obesity, snoring, allodynia, depression, anxiety, caf-feine, head injury, stressful life events, and low education !so-cioeconomic status. Predictors of remission included a lower baseline headache fre-quency (15-19 versus 25-31 headache days!month), and the absence of allodynia.

Recent research suggests that CM is associated with func-tional and structural brain abnormalities. Activity-indepen-dent sensitization of central trigeminothalamic pathways is considered to be a possible cause of the development of chronic migraine. Such sensitization might occur during re-peated migraine attacks through impaired descending inhibi-tion and!or enhanced descending facilitainhibi-tion of trigeminal nociception. Enhanced cortical processing involving sensory,

visual, auditory, and affective networks that exceed that seen in patients with episodic migraine or migraine-free con-trols, has also been demonstrated in individuals with chronic migraine. Whether this finding is due to intrinsically in-creased excitability or impaired intra-cortical inhibitory mechanisms is unclear.

The overuse of acute pain medications has plays a role in some patients with chronic migraine who overuse (>10 days per month) acute headache pain medications. Experiments in animal models have revealed persistent pronociceptive adap-tations following exposure to opioids and triptans, resulting in enhanced sensitivity to stimuli that trigger migraine in hu-mans. These findings could provide insight into the adaptive changes that occur in patients who have chronic migraine as-sociated with medication overuse and thus further elucidate the pathophysi-ology of chronic migraine.

※Author s disclosure of potential Conflicts of Interest (COI). David W. Dodick: Remuneration, Allergan, Aider, Pfizer, Merck, Coherex, Ferring, Neurocore, Neuralieve, NeurAxon, NuPathe Inc., MAP, SmithKline Beecham, Boston Scientific, Medtronic Inc., Nautilus, Eli Lilly & Company, Novartis, ColuCid, GlaxsoS-mithKline, Autonomic Technologies, MAP Pharmaceuticals, Inc., Zogenix, Inc. , Impax Laboratories, Inc. , Bristol-Myers Squibb, Nevro Corporation, Atlas and Arteaus; Research fee, Advanced Neurostimulation Systems, Boston Scientific, St Jude Medical, Inc., and Medtronic; Trabel and Gifts, Allergan, Aider, Pfizer, Merck, Coherex, Ferring, Neurocore, Neuralieve, NeurAxon, NuPathe Inc., MAP, SmithKline Beecham, Boston Scientific, Medtronic Inc., Nautilus, Eli Lilly & Company, Novartis, ColuCid, GlaxsoS-mithKline, Autonomic Technologies, MAP Pharmaceuticals, Inc., Zogenix, Inc. , Impax Laboratories, Inc. , Bristol-Myers Squibb, Nevro Corporation, Atlas and Arteaus.

Mayo Clinic

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