Naratriptan in the Prophylaxis of Transformed Migraine

Sheftell, Fred D.; Rapoport, Alan M.; Coddon, David R.

doi:10.1046/j.1526-4610.1999.3907506.x

Cited by 26 publications

(22 citation statements)

References 12 publications

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“…That is, putatively low baseline levels of serotonin production might be normalized and stressors might no longer be as readily able to elicit attacks. In at least one study, naratriptan, used daily, has been found to reduce the frequency and severity of daily headache (58). However, chronic sumatriptan use can also worsen headaches (53), and it is not excluded that this effect might be due to increased 5‐HT neurotransmission.…”

Section: Discussionmentioning

confidence: 99%

Effects of Acute or Chronic Administration of Anti-Migraine Drugs Sumatriptan and Zolmitriptan on Serotonin Synthesis in the Rat Brain

et al. 2004

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Triptans are 5-HT1 receptor agonists used as anti-migraine drugs. They act primarily on meningeal blood vessels and on trigeminovascular afferents, but they may also exert central effects. We studied the regional effects of acute and chronic treatment with sumatriptan or zolmitriptan on the rate of serotonin (5-HT) synthesis in the rat brain, using the alpha-14C-methyl-L-tryptophan quantitative autoradiographic method. Sumatriptan at low (300 microg/kg, s.c.) and high (1 mg/kg) doses, as well as zolmitriptan (100 microg/kg), acutely decreased (15-40%, P < 0.05-0.001) 5-HT synthetic rate in many brain regions, including the dorsal raphe nucleus. Chronically, sumatriptan (21 days, approximately 300 microg/kg per day via osmotic minipumps) induced significant increases in the 5-HT synthesis rate in many projection areas but had no effect in the dorsal raphe nucleus. The acute effects on 5-HT synthesis rate would be compatible with activation of 5-HT1 autoreceptors that inhibit serotonin release. In contrast, the increased 5-HT synthesis rate observed after chronic sumatriptan might possibly result from a down-regulation/desensitization of 5-HT1 receptors and/or unmasking of excitatory triptan-sensitive 5-HT receptors. Overall, the present findings indicate that not only zolmitriptan but also sumatriptan affect brain serotonergic neurotransmission.

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Section: Discussionmentioning

confidence: 99%

Effects of Acute or Chronic Administration of Anti-Migraine Drugs Sumatriptan and Zolmitriptan on Serotonin Synthesis in the Rat Brain

et al. 2004

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“…The decision to use naratriptan in the patients presented was based on their refractoriness to other preventive therapies (alone and in combinations), as well as on the good results obtained in three previous patients followed in the same headache center (not included in this study) 20 . Patients were enrolled in this study no less than 6 months after they had tried and failed a headache management program.…”

Section: Methodsmentioning

confidence: 99%

“…Naratriptan was the third selective 5‐HT 1B/1D agonist to be introduced in the United States for the acute treatment of migraine. In a previous study by Sheftell et al, three patients with CM previously refractory to a wide variety of traditional preventive pharmacologic and nonpharmacologic interventions experienced a remarkable reduction in the frequency and intensity of daily headache while receiving preventive treatment with daily naratriptan 20 . Subjective improvement in quality of life and restoration of normal functioning (including a decrease in missed workdays) also was reported by those patients.…”

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confidence: 99%

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

et al. 2003

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“…It is now generally accepted that the triptans achieve their effect at a neurological, rather than vascular, site of action. Preventative drugs do not seem to work the same way, and acute treatment drugs have usually proved to be ineffective as preventatives, although there is some evidence supporting a preventative effect for naratriptan on the basis of its CNS-penetrating ability [Newman et al, 2001;Sheftell et al, 1999]. Prophylactic drugs work only in some patients.…”

Section: Drug-based Migraine Preventionmentioning

confidence: 99%

Looking in the wrong place? The search for an ideal migraine preventative

Lambert¹

2007

Drug Development Research

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The cause of migraine headache is still unknown, although triggers for it are often apparent. There are, in consequence, no reliable migraine headache preventative drugs that act through an influence on known causal pathways. This review discusses the pathophysiology of migraine, the link between migraine triggers and the consequent headache and the putative mode of action of different classes of migraine drugs in the light of a number of pathophysiological models. It advances the idea that migraine triggers produce headache because they increase cortical excitability and discharge, which in turn reduces the inhibitory drive of the descending pain control system, selectively for trigeminovascular sensation. Supporting evidence for such a mechanism is presented and suggestions made as to the modes and sites of action of future improved migraine preventative agents. Drug Dev Res 68: 376-388, 2007.

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Naratriptan in the Prophylaxis of Transformed Migraine

Cited by 26 publications

References 12 publications

Effects of Acute or Chronic Administration of Anti-Migraine Drugs Sumatriptan and Zolmitriptan on Serotonin Synthesis in the Rat Brain

Effects of Acute or Chronic Administration of Anti-Migraine Drugs Sumatriptan and Zolmitriptan on Serotonin Synthesis in the Rat Brain

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

Looking in the wrong place? The search for an ideal migraine preventative

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