Intractable Eye Pain: Indication for Triptans

May, Arne; Gamulescu, Maria-Andreea; Bogdahn, Ulrich; Lohmann, CP

doi:10.1046/j.1468-2982.2002.00342.x

Cited by 12 publications

(6 citation statements)

References 8 publications

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“…157 Work from our laboratories was the first to show that anti-migraine drugs with agonist activity at 5-HT receptors might act at this synapse; 107 our later work demonstrated that this site of action was relatively specific for processing of sensory information from the dura mater and involved the 5-HT1D receptor subtype. 156 A similar mechanism may occur in the cornea because triptans have been reported to ease pain following keratotomy, 158 an effect that may also be mediated via 5-HT1D receptors. 159 Serotonin infusions themselves also suppress discharges of these first-order sensory neurons in cats.…”

Section: Cerebral Cortexmentioning

confidence: 96%

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: Cerebral Cortexmentioning

confidence: 96%

The Mode of Action of Migraine Triggers: A Hypothesis

Lambert

Zagami

2009

Headache

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“…115 Another attempt to control the pain level after surface ablation combines the use of triptanes, known from migraine therapy, with classic analgesic agents. 116,117 This strategy seems valuable as analgesic agents are known to have a poor effect on pain mediated by the trigeminal nerve. We have seen impressive results with rizatriptan 10 mg in some of our patients with disabling pain despite our routine prescription of oral acetaminophen (Paracetamol) and metamizole (Novaminsulfon).…”

Section: Complicationsmentioning

confidence: 99%

Surface ablation techniques

Taneri

Weisberg

Azar

2011

Journal of Cataract and Refractive Surgery

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The ongoing quest for a safe, simple, effective, minimally invasive, and stable refractive surgical procedure to correct refractive errors has stimulated the development of surface ablation techniques and laser in situ keratomileusis. In this review, we describe the history, patient assessment, techniques, outcomes, and complications of surface ablation (photorefractive keratectomy, laser-assisted sub-epithelial keratectomy, epithelial laser-assisted in situ keratomileusis) and compare the results of various surface techniques. Surface ablation procedures will continue to evolve, with potential improvements in outcomes accompanying future sophisticated ablation profiles and laser technology.

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“…Migraine produces a pain in the dura and there are no reports of it producing pain centered on other “nociceptor‐only” trigeminal receptive fields such as the cornea or the teeth. The action of the triptans, for instance, is likewise confined to dural pain; there appears to be only one report of their use in eye pain 106 and apparently none at all of their successful use against toothache. The is one report on the action of sumatriptan as an analgesic in intestinal tract inflammation, 107 but the authors were unable to decide between a peripheral and a central action.…”

Section: A Pain In the Duramentioning

confidence: 99%

The Lack of Peripheral Pathology in Migraine Headache

Lambert

2010

Headache

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This article reviews the baffling problem of the pathophysiology behind a peripheral genesis of migraine pain--or more particularly the baffling problem of its absence. I examine a number of pathophysiological states and the effector mechanisms for these states and find most of them very plausible and that they are all supported by abundant evidence. However, this evidence is mostly indirect; to date the occurrence of any of the presumed pathological states has not been convincingly demonstrated. Furthermore, there is little evidence of increased trigeminal sensory traffic into the central nervous system during a migraine attack. The article also examines a number of observations and experimental programs used to bolster a theory of peripheral pathology and suggests reasons why they may in fact not bolster it. I suggest that a pathology, if one exists, may be in the brain and even that it may not be a pathology at all. Migraine headache might just happen because of random noise in an exquisitely sensitive and complex network. The article suggests an experimental program to resolve these issues.

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Intractable Eye Pain: Indication for Triptans

Cited by 12 publications

References 8 publications

The Mode of Action of Migraine Triggers: A Hypothesis

The Mode of Action of Migraine Triggers: A Hypothesis

Surface ablation techniques

The Lack of Peripheral Pathology in Migraine Headache

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