Serotonin Depletion, Cortical Spreading Depression, and Trigeminal Nociception

Supornsilpchai, Weera; Sanguanrangsirikul, Sompol; Maneesri, Supang; Srikiatkhachorn, Anan

doi:10.1111/j.1526-4610.2006.00310.x

Cited by 88 publications

(75 citation statements)

References 14 publications

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“…There are at least 7 classes and 14 subtypes of 5-HT receptors, with varying biological effects. In general, the 5-HT 1 receptors mediate inhibitory neurotransmission, while the 5-HT [2][3][4][5][6][7] receptors mediate excitatory neurotransmission [4•]. In the brain, 5-HT is stored within synaptic vesicles, where it is protected from enzymatic degradation.…”

Section: The Serotonergic System and Cluster Headachementioning

confidence: 99%

“…Several studies conducted on the relation between migraine and serotonin metabolism [5] show low available levels of serotonin in the migrainous brain and a dysfunction of the brainstem serotonergic neurotransmission, which could act as a pain-triggering mechanism along the trigeminovascular pathway [6]. By contrast, only a few studies have been published on serotonin metabolism in patients with CH.…”

Section: The Serotonergic System and Cluster Headachementioning

confidence: 99%

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Serotonergic Agents in the Management of Cluster Headache

Lambru

Matharu

2011

Curr Pain Headache Rep

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Cluster headache is a highly disabling primary headache disorder, characterized by unilateral headache attacks occurring in association with cranial autonomic symptoms. Serotonergic agents, such as the ergot alkaloids, have traditionally been used for the acute and preventive treatment of cluster headache and other primary headaches. Although it initially was thought that their efficacy was due solely to the vasoconstriction of extracranial cerebral vessels, new mechanisms of action of these drugs have been ascertained as a consequence of advances in elucidation of the pathogenesis of primary headaches and the development of triptans. This article reviews the current knowledge about serotonergic agonists and antagonists used in the management of cluster headache, focusing on their mechanisms of action and on the possible role of serotonin system dysfunction in this complex disorder.

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Section: The Serotonergic System and Cluster Headachementioning

confidence: 99%

Section: The Serotonergic System and Cluster Headachementioning

confidence: 99%

Serotonergic Agents in the Management of Cluster Headache

Lambru

Matharu

2011

Curr Pain Headache Rep

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“…First, pharmacological agents interacting with serotonin (5-HT) and/or its receptors are highly Neuropsychiatric Genetics effective in acute and prophylactic migraine treatment [The Subcutaneous Sumatriptan International Study Group, 1991;Hargreaves, 2007]. In addition, drugs known to facilitate 5-HT release are able to induce migraine attacks [Panconesi and Sicuteri, 1997] and low 5-HT blood levels predispose to cortical spreading depression (CSD) in rats [Supornsilpchai et al, 2006], the suggested upstream event of a migraine attack, particularly in MA [Moskowitz, 2007]. Although there is controversy, most studies point toward altered 5-HT levels in migraine patients both during attacks and interictally [Ferrari and Saxena, 1993;Hamel, 2007] and suggest that reduced 5-HT availability could be a fundamental event in migraine pathophysiology.…”

Section: Introductionmentioning

confidence: 99%

Association study of the serotoninergic system in migraine in the spanish population

Corominas

Sobrido

Ribasés

et al. 2009

American J of Med Genetics Pt B

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In order to evaluate the contribution of 19 serotonin-related genes to the susceptibility to migraine in a Spanish population we performed a case-control association study of 122 single nucleotide polymorphisms (SNPs), selected according to genetic coverage parameters, in 528 migraine patients -308 with migraine without aura (MO) and 220 with migraine with aura (MA)- and 528 sex-matched migraine-free controls. The single-marker analysis identified nominal associations with the migraine phenotype or with the MO or MA subtypes. The multiple-marker analysis revealed risk haplotypes in three genes that remained significantly associated with migraine after correction by permutations. Two-marker risk haplotypes were identified in the HTR2B (rs16827801T-rs10194776G) and MAOA (rs3027400G-rs2072743C) genes conferring susceptibility to MO, and a four-marker haplotype in DDC was specific of MA (rs2329340A-rs11974297C-rs2044859T-rs11761683G). The present study supports the involvement of HTR2B and MAOA genes in the genetic predisposition to MO, while DDC might confer susceptibility to MA. These results suggest a differential involvement of serotonin-related genes in the genetic background of MO and MA.

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“…We hypothesize that the migraine patients with paradoxical aggravation after the introduction of a new prophylactic drug had a paradoxical decrease in the CSD induction threshold. Mechanisms of such a decrease are unknown and are probably multifactorial, but it has been experimentally demonstrated that changes in serotonin neurotransmission modify cortical excitability and favour CSD [12]. …”

Section: Discussionmentioning

confidence: 99%

Possible Precipitation of Migraine Attacks with Prophylactic Treatment

Donnet

Diego²,

Lantéri-Minet³

2008

Eur Neurol

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The initiation of a prophylactic treatment in a migraine sufferer depends upon the stratification of the patient’s frequency of attacks and the disability they cause, as well as the patient’s acute consumption and comorbid diseases. We report on 14 patients who were among a group of 618 migraine sufferers who received a new preventative treatment. These 14 patients developed an increase in the frequency of their migraine attacks that was possibly induced by this new prophylactic treatment. The clinical description of the migraine attacks remained the same but the frequency of the attacks of migraine without aura was dramatically increased. This is, to our knowledge, the first description of a possible precipitation of attacks of migraine without aura with a prophylactic treatment. There is no link with a specific class of prophylactic treatment. We hypothesize that the migraine sufferers who experienced aggravation after the new prophylactic drug had been introduced had a paradoxical decrease in the induction threshold for cortical spreading depression (CSD). Mechanisms of such a decrease are unknown and are probably multifactorial, but changes in serotonin neurotransmission have been experimentally demonstrated to modify cortical excitability and favour CSD. The aggravation was described only for attacks without aura. However, with only 14 patients, it is not possible to predict whether suffering from that the type of migraine is a factor that predisposes a patient to aggravation. While additional cases are necessary, physicians should be aware of the possibility that prophylactic treatment may exacerbate migraine attacks.

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Serotonin Depletion, Cortical Spreading Depression, and Trigeminal Nociception

Cited by 88 publications

References 14 publications

Serotonergic Agents in the Management of Cluster Headache

Serotonergic Agents in the Management of Cluster Headache

Association study of the serotoninergic system in migraine in the spanish population

Possible Precipitation of Migraine Attacks with Prophylactic Treatment

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