Central Mechanisms of Controlled-Release Metoprolol in Migraine: A Double-Blind, Placebo-Controlled Study

Siniatchkin, Michael; Andrasik, Frank; Kropp, Peter; Niederberger, Uwe; Strenge, H; Averkina, N A; Lindner, V.; Stephani, Ulrich; Wd, Gerber

doi:10.1111/j.1468-2982.2007.01377.x

Cited by 48 publications

(41 citation statements)

References 29 publications

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“…35 The second study (smaller, underpowered; n ϭ 25) found cyclandelate significantly reduced the number of migraine days and duration (assessed using a contingent negative variation measure). 36 Conclusions. The efficacy of cyclandelate is unknown (conflicting Class II studies).…”

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confidence: 99%

Evidence-based guideline update: Pharmacologic treatment for episodic migraine prevention in adults

et al. 2012

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Objective: To provide updated evidence-based recommendations for the preventive treatment of migraine headache. The clinical question addressed was: What pharmacologic therapies are proven effective for migraine prevention? Methods:The authors analyzed published studies from June 1999 to May 2009 using a structured review process to classify the evidence relative to the efficacy of various medications available in the United States for migraine prevention. Results and Recommendations:The author panel reviewed 284 abstracts, which ultimately yielded 29 Class I or Class II articles that are reviewed herein. Divalproex sodium, sodium valproate, topiramate, metoprolol, propranolol, and timolol are effective for migraine prevention and should be offered to patients with migraine to reduce migraine attack frequency and severity (Level A). Frovatriptan is effective for prevention of menstrual migraine (Level A). Lamotrigine is ineffective for migraine prevention (Level A). Neurology Epidemiologic studies suggest approximately 38% of migraineurs need preventive therapy, but only 3%-13% currently use it.1 In 2000, the American Academy of Neurology (AAN) published guidelines for migraine prevention.2,3 Since then, new clinical studies have been published on the efficacy and safety of migraine preventive therapies. This guideline seeks to assess this new evidence to answer the following clinical question: For patients with migraine, which pharmacologic therapies are proven effective for prevention, as measured by reduced migraine attack frequency, reduced number of migraine days, or reduced attack severity? This article addresses the safety and efficacy of pharmacologic therapies for migraine prevention.Separate guidelines are available for botulinum toxin. 4 The 2008 guideline included a Level B recommendation that botulinum toxin was probably ineffective for treatment of episodic migraine. A new guideline is in development. An updated guideline on nonsteroidal anti-inflammatory drugs 5 and complementary alternative treatments has been approved for publication as a companion to this guideline. 5 DESCRIPTION OF THE ANALYTIC PROCESSThe AAN and the American Headache Society participated in the development process. An author panel of headache and methodologic experts was assembled to review the evidence. Computerized searches of the MEDLINE, PsycINFO, and CINAHL databases identified new studies (published in English). The search strategy used the MeSH term "headache" (exploded) and a published search strategy for identifying randomized controlled trials ( Appendices e-1-e-5, reference e1, and tables e-1 and e-2 are available on the Neurology Web site at www.neurology.org.

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confidence: 99%

Evidence-based guideline update: Pharmacologic treatment for episodic migraine prevention in adults

et al. 2012

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“…Reports are available regarding the lack of normalizing effect on CNV abnormal pattern with flunarizine Bussone et al, 1985], nifedipine [Diener et al, 1989], or riboflavin [Sndor et al, 2000]. Cyclandelate, a calcium antagonist with anti-5HT properties, reduced CNV amplitude in migraineurs, without recovery of normal habituation [Siniatchkin et al, 1998] (Table 1).…”

Section: Effects Of Preventive Agents On Interictal Neurophysiologic mentioning

confidence: 97%

Effects of antiepileptic drugs on neurophysiologic abnormalities subtending migraine

Tommaso

2007

Drug Development Research

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Recent theories about migraine pathogenesis have outlined migraine as a brain disorder. Migraine can be considered an aberrant physiological state with a low threshold for intermittent neuronal excitability. Neurophysiologic findings in migraine emphasized the presence of abnormal neuronal function during the asymptomatic phase, predisposing to attack occurrence, the main patterns being the loss of habituation of evoked and event related potentials and the hypersynchronization of electroencephalographic (EEG) activity. These studies confirmed the need of preventive agents able to act on neuronal excitability, with growing evidence in favor of the clinical efficacy of anti-epileptic drugs (AED), though electrophysiological evidence supporting migraine as a state of neuronal hypoexcitability rendered the rationale of their use and their fundamental action mechanism in preventing migraine rather questionable. In the last years, many studies reported the efficacy of other preventive agents than AED, such as -blockers, in reversing neurophysiologic abnormalities of migraine, while reducing headache frequency. Our recent results showed a normalizing effects of levetiracetam and topiramate vs. placebo on the dishabituation pattern of the contingent negative variation (CNV) and the efficacy of levetiracetam vs. both topiramate and placebo in reversing the hypersynchronization of alpha rhythm under flash stimulation. All these effects concurred with the clinical efficacy on migraine frequency, and confirmed the action of AED on the basal mechanisms of migraine. Considering our and previous results, migraine may be considered as a state of ''altered'' excitability, where the AED are modulating agents able to reverse the electrophysiological patterns predisposing to the attack occurrence. The challenge for the future may be the identification of subgroups of migraine patients with pronounced expression of some neurophysiologic indexes of migraine predisposition, e.g., hypersynchronization, which may optimize the choice of the preventive agent. Drug Dev Res 68: 369-375, 2007. r 2007

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“…Thus, there is evidence of cortical hyperexcitability and lack of habituation to repetitive stimuli in the migraine brain. Furthermore, this phenomenon can be normalised by treatment with beta-blockers, calcium channel blockers, aspirin and 5-HT 1 receptor agonists that show anti-migraine efficacy [174]. Similarly, hyperexcitability in the occipital cortex has also been demonstrated in migraine [10].…”

Section: Central Sensitizationmentioning

confidence: 99%

Neurobiology in primary headaches

Edvinsson

Uddman

2005

Brain Research Reviews

212

209

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Central Mechanisms of Controlled-Release Metoprolol in Migraine: A Double-Blind, Placebo-Controlled Study

Cited by 48 publications

References 29 publications

Evidence-based guideline update: Pharmacologic treatment for episodic migraine prevention in adults

Evidence-based guideline update: Pharmacologic treatment for episodic migraine prevention in adults

Effects of antiepileptic drugs on neurophysiologic abnormalities subtending migraine

Neurobiology in primary headaches

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