Naratriptan in the Preventive Treatment of Refractory Chronic Migraine: A Review of 27 Cases

Rapoport, Alan M.; Bigal, Marcelo E.; Volcy, Michel; Sheftell, Fred D.; Feleppa, Michele; Tepper, Stewart J.

doi:10.1046/j.1526-4610.2003.03094.x

Cited by 23 publications

(15 citation statements)

References 35 publications

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“…There are as yet no universally reliable prophylactic drugs for migraine. Drugs to treat acute attacks have already been developed, but they do not prevent attacks although naratriptan has been recommended for this purpose 223 . Of all of the classes of preventative drugs, few can be said to have been a great deal different from placebo.…”

Section: Preventing Migrainementioning

confidence: 99%

The Mode of Action of Migraine Triggers: A Hypothesis

Lambert

Zagami

2009

Headache

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Objectives.-To review conjectured modes of action of migraine triggers and to present a new hypothesis about them. Background.-Migraine attacks are initiated in many migraineurs by a variety of "triggers," although in some patients no external trigger can be identified. Many triggers provoke attacks with such a short latency that only some kind of neural mechanism can explain the triggering.Results.-We present here a hypothesis that the pain of migraine has its ultimate origin in the cortex, but that the immediate generator is in the brainstem. Our hypothesis is that most migraines have triggers that produce excitation of cortical neurons and that this directly causes withdrawal of descending sensory inhibition originating in the brainstem. A wide range of evidence from the literature that cortical activation induced by a number of different mechanisms often produces headache is presented to support this notion. Several nuclei in the brainstem appear to participate in the selective control of trigeminovascular sensation through descending inhibitory mechanisms that arise in the cortex. In this review we focus on 2 of them, the periaqueductal gray matter and nucleus raphe magnus. Our own past results and those of others show that this inhibition is specific for craniovascular sensation and involves the neurotransmitter 5-hydroxytryptamine. Finally, we summarize our own recent experiments, which show that cortical activation by migraine triggers (including cortical spreading depression) inhibits neuronal discharge in the brainstem and facilitates trigeminovascular sensation. Conclusion.-If the hypothesis can be proven and the neurotransmitters involved in the hypothetical trigger pathway can be identified, it may be possible to develop novel migraine preventative therapies.Key words: migraine, migraine trigger, cerebral cortex, brainstem, trigeminovascular sensory system Abbreviations: 5-HT 5-hydroxytryptamine, CGRP calcitonin gene-related peptide, CSD cortical spreading depression, DC direct current, ECT electroconvulsive therapy, LC locus coeruleus, NO nitric oxide, NRM nucleus raphe magnus, NTS nucleus tractus solitarius, PAG periaqueductal gray matter, PET positron emission tomography, SP substance P, TMS transcranial magnetic stimulation (Headache 2009;49:253-275) In this review, we present the hypothesis that most migraines have triggers that produce excitation of cortical neurons and that this excitation directly inhibits neurons in 2 brainstem nuclei: the periaqueductal gray matter (PAG) and the nucleus raphe magnus (NRM). These nuclei then release their ongoing descending control of dura mater sensation in the trigeminal nucleus and cause normal sensory traffic from the dura to be perceived as migraine pain.Migraine is one of our most common and debilitating organic diseases, yet bafflingly has no apparent pathology. It is a condition involving the "trigeminovascular system," in which the cranial vasculature, the trigeminal sensory system, and the central nervous system all play a part. Its cardinal fe...

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Section: Preventing Migrainementioning

confidence: 99%

The Mode of Action of Migraine Triggers: A Hypothesis

Lambert

Zagami

2009

Headache

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“…Furthermore, patients were not allowed to start new acute treatments during the study. So, although symptomatic treatment of headache pain may have prophylactic effects, 36 any such effect resulting from acute medication use would have already been present at the time of enrollment into the study. Furthermore, during the course of the study the use of acute medications decreased.…”

Section: Commentsmentioning

confidence: 99%

Botulinum Toxin Type A for the Prophylaxis of Chronic Daily Headache: Subgroup Analysis of Patients Not Receiving Other Prophylactic Medications: A Randomized Double‐Blind, Placebo‐Controlled Study

Dodick¹,

Mauskop²,

Elkind³

et al. 2005

Headache

196

146

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Objective.-To assess the efficacy and safety of botulinum toxin type A (BoNT-A; BOTOX ® , Allergan, Inc., Irvine, CA) for the prophylaxis of headaches in patients with chronic daily headache (CDH) without the confounding factor of concurrent prophylactic medications.Background.-Several open-label studies and an 11-month, randomized, double-blind, placebo-controlled study suggest that BoNT-A may be an effective therapy for the prophylaxis of headaches in patients with CDH.Design and Methods.-This was a subgroup analysis of an 11-month, randomized double-blind, placebocontrolled study of BoNT-A for the treatment of adult patients with 16 or more headache days per 30-day periods conducted at 13 North American study centers. All patients had a history of migraine or probable migraine. This analysis involved data for patients who were not receiving concomitant prophylactic headache medication and who constituted 64% of the full study population. Following a 30-day screening period and a 30-day single-blind, placebo injection, eligible patients were injected with BoNT-A or placebo and assessed every 30 days for 9 months The following efficacy measures were analyzed per 30-day periods: change from baseline in number of headache-free days; change from baseline in headache frequency; proportion of patients with at least 30% or at least 50% decrease from baseline in headache frequency; and change from baseline in mean headache severity. Acute medication use was assessed, and adverse events were recorded at each study visit.Results.-Of the 355 patients randomized in the study, 228 (64%) were not taking prophylactic medication and were included in this analysis (117 received BoNT-A, 111 received placebo injections). Mean age was 42.4 ± 10.90 years; the mean frequency of headaches per 30 days at baseline was 14.1 for the BoNT-A group and 12.9 for the placebo group (P = .205). After two injection sessions, the maximum change in the mean frequency of headaches per 30 days was −7.8 in the BoNT-A group compared with only −4.5 in the placebo group (P = .032), a statistically significant between-group difference of 3.3 headaches. The between-group difference favoring BoNT-A treatment continued to improve to 4.2 headaches after a third injection session (P = .023). In addition, BoNT-A treatment at least halved the frequency of baseline headaches in over 50% of patients after three injection sessions compared to baseline. Statistically significant differences between BoNT-A and placebo were evident for the change from baseline in headache frequency and headache severity for most time points from day 180 through day 270. Only 5 patients (4 patients receiving BoNT-A treatment; 1 patient receiving placebo) discontinued the study due to adverse events and most treatment-related events were transient and mild to moderate in severity.Conclusions.-BoNT-A is an effective and well-tolerated prophylactic treatment in migraine patients with CDH who are not using other prophylactic medications.

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“…24 A retrospective study found a reduction of 36.5% in headache frequency at 2 months in patients using daily naratriptan. 26 We found that levetiracetam may be an effective drug in the prevention of TM. For the ITT population, headache frequency decreased 34.9%, the number of days with moderate or severe headache pain decreased by 42.2%, and disability scores decreased significantly (both, P _< 0.01).…”

Section: Discussionmentioning

confidence: 84%

Levetiracetam in the preventive treatmentof transformed migraine: A prospective, open-label, pilot study

RAPOPORT¹,

SHEFTELL²,

TEPPER³

et al. 2005

Current Therapeutic Research

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Background: Most preventive agents used for transformed migraine (TM) have not been studied specifically for the treatment of this syndrome. Openlabel trials have demonstrated the effectiveness of levetiracetam in the treatment of refractory headaches.Objective: The aim of this study was to assess the effectiveness and tolerability of levetiracetam in the preventive treatment of refractory TM. Methods:This prospective, open-label, pilot study was conducted at The New England Center for Headache, Stamford, Connecticut. We included patients aged ~18 years with refractory TM according to the criteria proposed by Silberstein et al. All participants had failed on at least 1 but not more than 3 preventive drugs. Other preventive drugs were allowed if they had been received at a stable dose for >30 days. The dosage of the levetiracetam tablets ranged from 1000 to 3000 mg/d in 2 divided doses. The treatment phase lasted 3 months. The primary end point was headache frequency (expressed as the number of headache days per month), and the secondary end point was the frequency of moderate or severe headache (d/mo). Other end points were headache score, Migraine Disability Assessment (MIDAS) Questionnaire score, and Headache Impact Test (HIT-6) score. Statistical analyses were performed in the intent-totreat (ITT) population (patients who received at least 1 dose of study medication) using data subjected to the last-observation-carried-forward algorithm. We also conducted per-protocol (PP) analyses in patients who completed the study. Results:The ITT population consisted of 36 patients (26 women, 10 men; A.M. Rapoport et aLvs baseline). At baseline, the mean number of moderate or severe headache days was 16.8 d/mo compared with 13.2, 11.9, and 9.7 d/mo at 1, 2, and 3 months, respectively (P = NS, <0.01, and <0.01, respectively). The mean MIDAS score was significantly reduced at 3 months compared with baseline (40.8 vs 62.8 d/mo; P = 0.01). The mean HIT-6 score was 59.4 at 3 months versus 63.4 at baseline (P < 0.01). In the PP population, the mean (SD) headache frequency was reduced from 26.1 (4.1) d/mo at baseline to 14.3 (4.8) d/mo at the end of the study (P < 0.001). The mean (SD) headache score was reduced from 51.3 (17.1) at baseline to 34.0 (22.0) at 3 months (P < 0.016). Conclusion:The results of this study in patients with TM support the role of levetiracetam in the preventive treatment of refractory TM. (Curr Ther Res Clin Exp. 2005;66:212-221)

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Naratriptan in the Preventive Treatment of Refractory Chronic Migraine: A Review of 27 Cases

Abstract: Naratriptan may have a role in the preventive treatment of intractable chronic migraine. Prospective, controlled studies should be considered.

Cited by 23 publications

References 35 publications

The Mode of Action of Migraine Triggers: A Hypothesis

The Mode of Action of Migraine Triggers: A Hypothesis

Botulinum Toxin Type A for the Prophylaxis of Chronic Daily Headache: Subgroup Analysis of Patients Not Receiving Other Prophylactic Medications: A Randomized Double‐Blind, Placebo‐Controlled Study

Levetiracetam in the preventive treatmentof transformed migraine: A prospective, open-label, pilot study

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