Triptan‐induced latent sensitization: A possible basis for medication overuse headache

Felice, Milena De; Ossipov, Michael H.; Wang, Ruizhong; Lai, Josephine; Chichorro, Juliana Geremias; Meng, Ian D.; Dodick, David W.; Vanderah, Todd W.; Dussor, Gregory; Porreca, Frank

doi:10.1002/ana.21897

Cited by 194 publications

(259 citation statements)

References 65 publications

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“…We do not know whether druginduced headache indicates a neuronal or vascular mechanism, a threshold or sensitivity effect, or even an allergic or immunological response. Recently, it has been shown that overuse of these medications could induce neural adaptations that result in a state of latent sensitization, which might increase sensitivity to migraine triggers [34]. The latent sensitization could provide a mechanistic basis for the transformation of migraine to medication overuse headache.…”

Section: Discussionmentioning

confidence: 99%

Triptans: over the migraine

et al. 2012

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Migraine is a chronic, recurrent, disabling condition that affects millions of people worldwide. Proper acute care treatment for migraineurs is based on triptans, a class of specific medications approved over 20 years ago. Triptans are serotonin (5-HT1B/1D) receptor agonists that are generally effective, well tolerated and safe. Seven triptans are available worldwide, although not all are available in every country, with multiple routes of administration, giving to doctors and patients a wide choice. Despite the similarities of the available triptans, pharmacological heterogeneity offers slightly different efficacy profiles. Triptans are not pain medications, they are abortive migraine medications which cannot prevent migraines. In addition to migraine attacks, triptans are also helpful for cluster headaches. If they are useful in other primary headaches rather than migraine and cluster headache it is yet to be addressed. In the literature there are only limited controlled clinical data to support a migraine-selective activity for triptans. Reports are available about efficacy of triptans to stop attacks of other types of primary headache, such as tension type headache, hypnic headache and other rare forms of primary headaches. On the other hand, sumatriptan failed to treat the indomethacin-responsive primary headache disorders like chronic paroxysmal hemicrania and hemicrania continua, nor was it effective in the myofascial temporal muscle pain or in atypical facial pain. Why triptans are effective in so different types of primary headaches remain unclear. Up to date, it is not clear whether the antimigrainous activity of the triptans involves an action only in the periphery or in the CNS as well. Probably we should consider triptans as "pain killers" and not only as "migraine killers". We clearly need additional studies on triptans as putative analgesics in well-accepted animal and clinical models of acute and chronic somatic pain.

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Section: Discussionmentioning

confidence: 99%

Triptans: over the migraine

et al. 2012

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“…Deafferentation is a well-recognized mechanism generating neuropathic pain. Changes in algogenic protein expression in trigeminal ganglia and latent sensitization have been demonstrated in rats chronically exposed to triptans [22]. A derangement of the central serotonin-dependent endogenous pain control system induced by chronic medication has been proposed [16].…”

Section: Discussionmentioning

confidence: 99%

Original article. Potential risk of dihydroergotamine causing medicationoveruse headache: preclinical evidence

Vibulyaseck

Bongsebandhu-phubhakdi

Grand

et al. 2014

Asian Biomedicine

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Background: Overuse of abortive medication is a common factor contributing to an increase in headache frequency in patients with migraine. Whether or not chronic exposure to dihydroergotamine (DHE) can lead to this transformation remains uncertain. Objective: To determine the effect of acute and chronic DHE exposure on development of cortical spreading depression (CSD) and trigeminal nociception. Methods: The study comprised two experiments, namely acute and chronic exposure. In the acute experiment, a single dose of DHE (100 μg/kg) was given to male Wistar rats after successful induction of CSD. In the chronic experiment, DHE was given daily for the period of 0, 7, 14, and 28 days. CSD was induced 30 minutes after the final injection and the cortical field potential was recorded. Expression of c-Fos in caudal brainstem was used as an indicator of trigeminal nociception. Results: Acute exposure to DHE attenuated the expression of c-Fos in the caudal brainstem without change in CSD response. By contrast, chronic exposure (14 and 28 days) to DHE increased the area under the curve of CSD waveforms. In parallel with the change in the CSD, there was significant increase of c-Fos expression within 14 days exposure to DHE and the expression remained significantly elevated for up to the 28 days examined. Conclusion: Our study demonstrated that chronic DHE administration can increase cortical excitability and increase c-Fos expression in caudal brainstem. Our preclinical evidence suggests the possible adverse effect of chronic DHE use in causing chronification of headache.

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“…Thus, CGRP is a key molecule in migraine pathogenesis. Interestingly, in MOH model animals, triptan increased CGRP levels [11]. In addition, exposure to µ opioids such as morphine also increased CGRP in cultured dorsal root ganglion cells [12,13].…”

Section: Introductionmentioning

confidence: 93%

Lack of association between CGRP-related gene polymorphisms and medication overuse headache in migraine patients

Ishii¹,

Katoh²,

Kurihara³

et al. 2015

Integr Mol Med

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We investigated whether calcitonin gene-related peptide (CGRP)-related gene polymorphisms are involved in the aggravation of migraines due to medication overuse. In total, 47 migraine patients (6 males and 41 females; 36.4 ± 10.3 years) and 22 medication overuse headache (MOH) patients (1 male and 21 females; 39.6 ± 9.9 years) who had migraine participated in this study. Calcitonin gene-related polypeptide-alpha (CALCA, α-CGRP, Insertion/Deletion rs1553005, rs145837941) and CGRP receptor (receptor activity-modifying protein 1: RAMP1, rs3754701, rs7590387) were analyzed by polymerase chain reaction (PCR) and PCR-restriction fragment length polymorphism (PCR-RFLP) methods. No significant differences were observed in the genotype distributions of CALCA and RAMP1 between migraine patients and MOH patients. The results of this study showed no association between CGRP-related gene polymorphisms and the complication of MOH in migraine patients.

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Triptan‐induced latent sensitization: A possible basis for medication overuse headache

Cited by 194 publications

References 65 publications

Triptans: over the migraine

Triptans: over the migraine

Original article. Potential risk of dihydroergotamine causing medicationoveruse headache: preclinical evidence

Lack of association between CGRP-related gene polymorphisms and medication overuse headache in migraine patients

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