Periods of Cluster Headache Induced by Nitrate Therapy and Spontaneous Remission of Angina Pectoris During Active Clusters

Ekbom, Karl; Sjöstrand, Christina; Svensson, DA; Waldenlind, Elisabet

doi:10.1111/j.1468-2982.2004.00634.x

Cited by 13 publications

(13 citation statements)

References 34 publications

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“…Clinically, the attacks were identical to the spontaneous attacks of the patients. In one case series, long-acting nitrates, such as isosorbide mononitrate, were even able to convert cluster patients from out of bout to in bout [16]. Neuroimaging studies in GTN-induced cluster headache attacks were able to reveal activations in central nervous system areas (hypothalamus), pointing to a relevant structure in the genesis of cluster headache [17].…”

Section: Selected So-called ‘Secondary Headaches’mentioning

confidence: 99%

Secondary headaches: secondary or still primary?

Schankin¹,

Straube²

2012

J Headache Pain

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The second edition of the International Classification of Headache Disorders makes a distinction between primary and secondary headaches. The diagnosis of a secondary headache is made if the underlying disease is thought to cause headache or if a close temporal relationship is present together with the occurrence of the headache. At first glance, this may allow clearly secondary headaches to be distinguished from primary headaches. However, by reviewing the available literature concerning several selected secondary headaches, we will discuss the hypothesis that some secondary headaches can also be understood as a variation of primary headaches in the sense that the underlying cause (e.g. infusion of glyceryl trinitrate [ICHD-II 8.1.1], epilepsy [7.6.2], brain tumours [7.4], craniotomy [5.7], etc.) triggers the same neurophysiologic mechanisms that are responsible for the pain in primary headache attacks.

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Section: Selected So-called ‘Secondary Headaches’mentioning

confidence: 99%

Secondary headaches: secondary or still primary?

Schankin¹,

Straube²

2012

J Headache Pain

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“…Cluster headache attacks typically occur in series (cluster periods) lasting for weeks or months and interrupted by remission periods usually lasting months or years (Headache Classification Committee of the International Headache Society, 2004). Although it is a rare type of headache, it is important to include it in this review because nitrate therapy may induce or exacerbate cluster attacks (Ekbom et al. , 2004).…”

Section: Headaches Are Not Uniformmentioning

confidence: 99%

Headache‐type adverse effects of NO donors: vasodilation and beyond

Bagdy

Riba

Kecskeméti

et al. 2010

British J Pharmacology

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Although nitrate therapy, used in the treatment of cardiovascular disorders, is frequently associated with side-effects, mainly headaches, the summaries of product characteristics of nitrate-containing medicines do not report detailed description of headaches and even do not highlight the possibility of nitrate-induced migraine. Two different types of nitrate-induced headaches have been described: (i) immediate headaches that develop within the first hour of the application, are mild or medium severity without characteristic symptoms for migraine, and ease spontaneously; and (ii) delayed, moderate or severe migraine-type headaches (occurring mainly in subjects with personal or family history of migraine), that develop 3-6 h after the intake of nitrates, with debilitating, long-lasting symptoms including nausea, vomiting, photo-and/or phono-phobia. These two types of headaches are remarkably different, not only in their timing and symptoms, but also in the persons who are at risk. Recent studies provide evidence that the two headache types are caused by different mechanisms: immediate headaches are connected to vasodilation caused by nitric oxide (NO) release, while migraines are triggered by other actions such as the release of calcitonin gene-related peptide or glutamate, or changes in ion channel function mediated by cyclic guanosine monophosphate or S-nitrosylation. Migraines usually need anti-attack medication, such as triptans, but these drugs are contraindicated in most medical conditions that are treated using nitrates. In conclusion, these data recommend the correction of summaries of nitrate product characteristics, and also suggest a need to develop new types of anti-migraine drugs, effective in migraine attacks, that could be used in patients with risk for angina pectoris.

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“…A few weeks of therapeutic administration of long-acting organic nitrate for the treatment of angina may induce a cluster period in patients who had not had a cluster period for many years. 56 Christiansen et al 57 explored the possibility that long-term exposure to a long-acting nitrate (ISMN) could be a treatment of the cluster headache. Patients received 30 mg ISMN 3 times daily for 4 weeks in a double-blind, placebo-controlled, crossover design.…”

Section: Cluster Headachementioning

confidence: 99%

Nitric Oxide-Related Drug Targets in Headache

Olesen

2010

Neurotherapeutics

104

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Summary: Nitric oxide (NO) is a very important molecule in the regulation of cerebral and extra cerebral cranial blood flow and arterial diameters. It is also involved in nociceptive processing. Glyceryl trinitrate (GTN), a pro-drug for NO, causes headache in normal volunteers and a so-called delayed headache that fulfils criteria for migraine without aura in migraine sufferers. Blockade of nitric oxide synthases (NOS) by L-nitromonomethylarginine effectively treats attacks of migraine without aura. Similar results have been obtained for chronic the tension-type headache and cluster headache. Inhibition of the breakdown of cyclic guanylate phosphate (cGMP) also provokes migraine in sufferers, indicating that cGMP is the effector of NO-induced migraine.Similar evidence suggests an important role of NO in the tension-type headache and cluster headache.These very strong data from human experimentation make it highly likely that antagonizing NO effects will be effective in the treatment of primary headaches. Nonselective NOS inhibitors are likely to have side effects whereas selective compounds are now in early clinical trials. Antagonizing the rate limiting cofactor tetrahydrobiopterin seems another very likely new treatment. It is more unlikely that antagonism of cGMP or its formation will be feasible, but augmenting its breakdown via phosphodiesterase activation is a possibility, as well as other ways of inhibiting the NO-cGMP pathway.

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Periods of Cluster Headache Induced by Nitrate Therapy and Spontaneous Remission of Angina Pectoris During Active Clusters

Cited by 13 publications

References 34 publications

Secondary headaches: secondary or still primary?

Secondary headaches: secondary or still primary?

Headache‐type adverse effects of NO donors: vasodilation and beyond

Nitric Oxide-Related Drug Targets in Headache

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