Medication Overuse Headache and Applicability of the ICHD-II Diagnostic Criteria: 1-Year Follow-Up Study (CARE I Protocol)

Ghiotto, Natascia; Sances, Grazia; Galli, Federica; Tassorelli, Cristina; Guaschino, Elena; Sandrini, Giorgio; Nappi, Giuseppe

doi:10.1111/j.1468-2982.2008.01712.x

Cited by 48 publications

(61 citation statements)

References 33 publications

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“…An important clinical concern is that triptan overuse can lead to medication-overuse headache (MOH). 16,17 Consequently, it is recommended that acute treatments not be used more than twice per week, thus rendering these drugs inappropriate as preventive treatments. 18 Opioids in combination with NSAIDs or acetaminophen, and barbiturates are also used, principally in the United States.…”

Section: Acute Migrainementioning

confidence: 99%

Targeting TRP Channels For Novel Migraine Therapeutics

Dussor

Yan

Xie

et al. 2014

ACS Chem. Neurosci.

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Migraine is increasingly understood to be a disorder of the brain. In susceptible individuals, a variety of “triggers” may influence altered central excitability, resulting in the activation and sensitization of trigeminal nociceptive afferents surrounding blood vessels (i.e., the trigeminovascular system), leading to migraine pain. Transient receptor potential (TRP) channels are expressed in a subset of dural afferents, including those containing calcitonin gene related peptide (CGRP). Activation of TRP channels promotes excitation of nociceptive afferent fibers and potentially lead to pain. In addition to pain, allodynia to mechanical and cold stimuli can result from sensitization of both peripheral afferents and of central pain pathways. TRP channels respond to a variety of endogenous conditions including chemical mediators and low pH. These channels can be activated by exogenous stimuli including a wide range of chemical and environmental irritants, some of which have been demonstrated to trigger migraine in humans. Activation of TRP channels can elicit CGRP release, and blocking the effects of CGRP through receptor antagonism or antibody strategies has been demonstrated to be effective in the treatment of migraine. Identification of approaches that can prevent activation of TRP channels provides an additional novel strategy for discovery of migraine therapeutics.

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Section: Acute Migrainementioning

confidence: 99%

Targeting TRP Channels For Novel Migraine Therapeutics

Dussor

Yan

Xie

et al. 2014

ACS Chem. Neurosci.

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“…Only few relapse after 12 months 159–166. There are conflicting results regarding at what time during the first year patients relapse, with some suggesting that most patients relapse within the first 6 months and others suggesting between 6 and 12 months 160–162,166,167. The literature is not clear regarding to what degree the pre-existent headache type or type of overused medication predicts successful withdrawal or relapse 59,159–166.…”

Section: Long-term Outcome and Relapse Ratementioning

confidence: 99%

Medication-overuse headache: a review

Kristoffersen

Lundqvist²

2014

JPR

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Medication-overuse headache (MOH) is a worldwide health problem with a prevalence of 1%–2%. It is a severe form of headache where the patients often have a long history of headache and of unsuccessful treatments. MOH is characterized by chronic headache and overuse of different headache medications. Through the years, withdrawal of the overused medication has been recognized as the treatment of choice. However, currently, there is no clear consensus regarding the optimal strategy for management of MOH. Treatment approaches are based on expert opinion rather than scientific evidence. This review focuses on aspects of epidemiology, diagnosis, pathogenesis, prevention, and treatment of MOH. We suggest that information and education about the risk of MOH is important since the condition is preventable. Most patients experience reduction of headache days and intensity after successful treatment. The first step in the treatment of MOH should be carried out in primary care and focus primarily on withdrawal, leaving prophylactic medication to those who do not manage primary detoxification. For most patients, a general practitioner can perform the follow-up after detoxification. More complicated cases should be referred to neurologists and headache clinics. Patients suffering with MOH have much to gain by an earlier treatment-focused approach, since the condition is both preventable and treatable.

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“…One limitation in their clinical use is that they can contribute to migraine chronification and more frequent episodes of headache, a condition referred to as medication overuse headache (MOH), recently characterized as a global epidemic [9; 11; 27; 28; 38; 41; 45; 77]. The triptan receptors are both Gi-protein coupled, which they share with other classes of analgesics, including those that act at mu-opioid or CB cannabinoid receptors [67; 74].…”

Section: Discussionmentioning

confidence: 99%

“…Thus, opioids, which are used clinically to treat moderate-to-severe pain, especially agonists at the mu-opioid receptor (MOR), may come to exacerbate or actually produce pain during their chronic administration, a phenomenon referred to as opioid-induced hyperalgesia (OIH) [6; 60; 63]. Similarly, the triptan class of drugs, used to treat migraine [25; 35; 76], also facilitates pain chronification and/or contributes to migraine chronification, a condition referred to as medication overuse headache (MOH; [9; 11; 26; 28; 38; 41; 45; 77]). The target for the therapeutic effect of triptans is thought to be 5-HT 1B and 5-HT 1D receptors that, like MOR are inhibitory G-protein coupled receptors (Gi-GPCRs) [37; 42; 64; 86; 95; 96].…”

Section: Introductionmentioning

confidence: 99%

Gi-protein–coupled 5-HT1B/D receptor agonist sumatriptan induces type I hyperalgesic priming

Araldi

Ferrari

Levine

2016

Pain

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We have recently described a novel form of hyperalgesic priming (type II) induced by agonists at two clinically important Gi-protein coupled receptors (Gi-GPCRs), mu-opioid and A1-adenosine. Like mu-opioids, the anti-migraine triptans, which act at 5-HT1B/D Gi-GPCRs have been implicated in pain chronification. We determined if sumatriptan, a prototypical 5-HT1B/D agonist produces type II priming. Characteristic of hyperalgesic priming, intradermal injection of sumatriptan (10 ng) induced a change in nociceptor function such that a subsequent injection of prostaglandin-E2 (PGE2) induces prolonged mechanical hyperalgesia. However, onset to priming was delayed 3 days, characteristic of type I priming. Also characteristic of type I priming, a protein kinase Cε (PKCε), but not a PKA inhibitor attenuated the prolongation phase of PGE2 hyperalgesia. The prolongation of PGE2 hyperalgesia was also permanently reversed by intradermal injection of cordycepin, a protein translation inhibitor. Also, hyperalgesic priming did not occur in animals pre-treated with pertussis toxin or IB4-positive nociceptor toxin, IB4-saporin. Finally, as observed for other agonists that induce type I priming, sumatriptan did not induce priming in female rats. The prolongation of PGE2 hyperalgesia induced by sumatriptan was partially prevented by co-injection of antagonists for the 5-HT1B and 5-HT1D, but not 5-HT7, serotonin receptors, and completely prevented by co-administration of a combination of the 5-HT1B and 5-HT1D antagonists. Moreover, the injection of selective agonists, for 5-HT1B and 5-HT1D receptors, also induced hyperalgesic priming. Our results suggest that sumatriptan, which signals via Gi-GPCRs, induces type I hyperalgesic priming, unlike agonists at other Gi-GPCRs, which induce type II priming.

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Medication Overuse Headache and Applicability of the ICHD-II Diagnostic Criteria: 1-Year Follow-Up Study (CARE I Protocol)

Cited by 48 publications

References 33 publications

Targeting TRP Channels For Novel Migraine Therapeutics

Targeting TRP Channels For Novel Migraine Therapeutics

Medication-overuse headache: a review

Gi-protein–coupled 5-HT1B/D receptor agonist sumatriptan induces type I hyperalgesic priming

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