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MeSH Review

Migraine Disorders

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Disease relevance of Migraine Disorders


Psychiatry related information on Migraine Disorders


High impact information on Migraine Disorders

  • In particular, CGRP has potent activity in the cerebral circulation, which is possibly relevant to the pathology of migraine, whilst vascular sources of AM contribute to dysfunction in cardiovascular disease [11].
  • We studied the various clinical manifestations associated with mutations in CACNA1A in families with hemiplegic migraine with and without cerebellar signs [12].
  • Migraine provoked by aspartame [13].
  • Diltiazem prophylaxis in refractory migraine [14].
  • Nifedipine in the treatment of migraine in patients with Raynaud's phenomenon [15].

Chemical compound and disease context of Migraine Disorders


Biological context of Migraine Disorders

  • Serotonin-containing neurones in brain have been proposed to have a role in the control of physiological mechanisms such as sleep, thermoregulation, pain perception and endocrine secretions as well as in the physiopathology of migraine or depressive illness [23].
  • The abnormal release of substance P or as yet unidentified peptides or other transmitters from the fifth cranial nerve may explain both the hemicranial pain and the vasodilation which are characteristic of the headache of migraine [24].
  • In addition, we replicated previously reported typical-migraine susceptibility loci on chromosomes 6p12.2-p21.1 and 1q21-q23, the latter being within 3 cM of the rare autosomal dominant familial hemiplegic migraine gene (ATP1A2), a finding which potentially implicates ATP1A2 in familial typical migraine for the first time [25].
  • Stress response pathways will be important areas for elucidation of episodic disease genetics where stress is a common precipitant of many common disorders like epilepsy, migraine and cardiac arrhythmias [26].
  • We assessed the association of the MTHFR C677T variant with migraine and the mediating effect of cardiovascular risk factors and metabolic markers of genotype status [27].

Anatomical context of Migraine Disorders

  • These include increased Ca(v)2.1 current density in cerebellar neurons, enhanced neurotransmission at the neuromuscular junction, and, in the intact animal, a reduced threshold and increased velocity of cortical spreading depression (CSD; the likely mechanism for the migraine aura) [28].
  • The object of this study was to assess the vasoactive effects of the standard 6-mg subcutaneous dose of sumatriptan used in migraine on the systemic and pulmonary circulations and the coronary artery vasculature [29].
  • The different disorders probably arise from disruption of neurotransmission in specific brain regions: the cortex in the case of migraine, the thalamus in the case of absence epilepsy and the cerebellum in the case of ataxia [30].
  • Characterization of 5-hydroxytryptamine receptors in human temporal arteries: comparison between migraine suffers and nonsufferers [31].
  • Calcitonin gene-related peptide does not excite or sensitize meningeal nociceptors: implications for the pathophysiology of migraine [32].

Gene context of Migraine Disorders

  • A Cacna1a knockin migraine mouse model with increased susceptibility to cortical spreading depression [28].
  • OBJECTIVE: The current report concerns a genetic study to test the involvement of genes for dopamine (DA) receptors D2 (DRD2), D3 (DRD3), and D4 (DRD4) in migraine without aura, particularly in a subgroup with enhanced DA sensitivity [33].
  • RESULTS: No association was detected using the TDT between DRD3, DRD4, and migraine without aura either in the overall sample or in the subgroup [33].
  • Recent studies have shown that KCNQ openers have potential for the treatment of several CNS disorders characterized by neuronal hyperexcitability, such as migraine, epilepsy and neuropathic pain [34].
  • No mutations in CACNA1A and ATP1A2 in probands with common types of migraine [35].
  • Many novel ATP1A2 mutations were identified in patients with familial and sporadic hemiplegic migraine [36].

Analytical, diagnostic and therapeutic context of Migraine Disorders


  1. Migraine is a food-allergic disease. Monro, J., Carini, C., Brostoff, J. Lancet (1984) [Pubmed]
  2. Effect on migraine of closure of cardiac right-to-left shunts to prevent recurrence of decompression illness or stroke or for haemodynamic reasons. Wilmshurst, P.T., Nightingale, S., Walsh, K.P., Morrison, W.L. Lancet (2000) [Pubmed]
  3. Risk of cardiac events in atypical transient ischaemic attack or minor stroke. The Dutch TIA Study Group. Koudstaal, P.J., Algra, A., Pop, G.A., Kappelle, L.J., van Latum, J.C., van Gijn, J. Lancet (1992) [Pubmed]
  4. Nitric oxide is a key molecule in migraine and other vascular headaches. Olesen, J., Thomsen, L.L., Iversen, H. Trends Pharmacol. Sci. (1994) [Pubmed]
  5. Behavioural pharmacology of 5-HT3 receptor antagonists: a critical update on therapeutic potential. Greenshaw, A.J. Trends Pharmacol. Sci. (1993) [Pubmed]
  6. Drug targets in stress-related disorders. Covelli, V., Passeri, M.E., Leogrande, D., Jirillo, E., Amati, L. Current medicinal chemistry. (2005) [Pubmed]
  7. Serotonin1B receptors: from protein to physiological function and behavior. Sari, Y. Neuroscience and biobehavioral reviews. (2004) [Pubmed]
  8. Comorbidity of migraine. Scher, A.I., Bigal, M.E., Lipton, R.B. Curr. Opin. Neurol. (2005) [Pubmed]
  9. Dopamine interacts directly with its D3 and D2 receptors on normal human T cells, and activates beta1 integrin function. Levite, M., Chowers, Y., Ganor, Y., Besser, M., Hershkovits, R., Cahalon, L. Eur. J. Immunol. (2001) [Pubmed]
  10. Teratogenic effects mediated by inhibition of histone deacetylases: evidence from quantitative structure activity relationships of 20 valproic acid derivatives. Eikel, D., Lampen, A., Nau, H. Chem. Res. Toxicol. (2006) [Pubmed]
  11. Vascular actions of calcitonin gene-related peptide and adrenomedullin. Brain, S.D., Grant, A.D. Physiol. Rev. (2004) [Pubmed]
  12. The clinical spectrum of familial hemiplegic migraine associated with mutations in a neuronal calcium channel. Ducros, A., Denier, C., Joutel, A., Cecillon, M., Lescoat, C., Vahedi, K., Darcel, F., Vicaut, E., Bousser, M.G., Tournier-Lasserve, E. N. Engl. J. Med. (2001) [Pubmed]
  13. Migraine provoked by aspartame. Johns, D.R. N. Engl. J. Med. (1986) [Pubmed]
  14. Diltiazem prophylaxis in refractory migraine. Smith, R., Schwartz, A. N. Engl. J. Med. (1984) [Pubmed]
  15. Nifedipine in the treatment of migraine in patients with Raynaud's phenomenon. Kahan, A., Weber, S., Amor, B., Guerin, F., Degeorges, M. N. Engl. J. Med. (1983) [Pubmed]
  16. Treatment of migraine with metoprolol. Ljung, O. N. Engl. J. Med. (1980) [Pubmed]
  17. Chenodeoxycholic acid in the prevention of migraine. Lévy, V.G., Nusinovici, V., Rosner, D., Darnis, F. N. Engl. J. Med. (1978) [Pubmed]
  18. Vitamin C and migraine: a case report. Bali, L., Callaway, E. N. Engl. J. Med. (1978) [Pubmed]
  19. Central serotonergic nerves project to the pial vessels of the brain. Edvinsson, L., Degueurce, A., Duverger, D., MacKenzie, E.T., Scatton, B. Nature (1983) [Pubmed]
  20. Letter: Chocolate, beta-phenethylamine and migraine re-examined. Schweitzer, J.W., Friedhoff, A.J., Schwartz, R. Nature (1975) [Pubmed]
  21. The role of nitric oxide (NO) in migraine, tension-type headache and cluster headache. Olesen, J. Pharmacol. Ther. (2008) [Pubmed]
  22. The effects of vitamin supplementation and MTHFR (C677T) genotype on homocysteine-lowering and migraine disability. Lea, R., Colson, N., Quinlan, S., Macmillan, J., Griffiths, L. Pharmacogenet. Genomics (2009) [Pubmed]
  23. Glycogenolysis induced by serotonin in brain: identification of a new class of receptor. Quach, T.T., Rose, C., Duchemin, A.M., Schwartz, J.C. Nature (1982) [Pubmed]
  24. Neurotransmitters and the fifth cranial nerve: is there a relation to the headache phase of migraine? Moskowitz, M.A., Reinhard, J.F., Romero, J., Melamed, E., Pettibone, D.J. Lancet (1979) [Pubmed]
  25. Genomewide significant linkage to migrainous headache on chromosome 5q21. Nyholt, D.R., Morley, K.I., Ferreira, M.A., Medland, S.E., Boomsma, D.I., Heath, A.C., Merikangas, K.R., Montgomery, G.W., Martin, N.G. Am. J. Hum. Genet. (2005) [Pubmed]
  26. The gene for paroxysmal non-kinesigenic dyskinesia encodes an enzyme in a stress response pathway. Lee, H.Y., Xu, Y., Huang, Y., Ahn, A.H., Auburger, G.W., Pandolfo, M., Kwiecinski, H., Grimes, D.A., Lang, A.E., Nielsen, J.E., Averyanov, Y., Servidei, S., Friedman, A., Van Bogaert, P., Abramowicz, M.J., Bruno, M.K., Sorensen, B.F., Tang, L., Fu, Y.H., Ptácek, L.J. Hum. Mol. Genet. (2004) [Pubmed]
  27. Migraine and MTHFR C677T genotype in a population-based sample. Scher, A.I., Terwindt, G.M., Verschuren, W.M., Kruit, M.C., Blom, H.J., Kowa, H., Frants, R.R., van den Maagdenberg, A.M., van Buchem, M., Ferrari, M.D., Launer, L.J. Ann. Neurol. (2006) [Pubmed]
  28. A Cacna1a knockin migraine mouse model with increased susceptibility to cortical spreading depression. van den Maagdenberg, A.M., Pietrobon, D., Pizzorusso, T., Kaja, S., Broos, L.A., Cesetti, T., van de Ven, R.C., Tottene, A., van der Kaa, J., Plomp, J.J., Frants, R.R., Ferrari, M.D. Neuron (2004) [Pubmed]
  29. Effect of subcutaneous sumatriptan, a selective 5HT1 agonist, on the systemic, pulmonary, and coronary circulation. MacIntyre, P.D., Bhargava, B., Hogg, K.J., Gemmill, J.D., Hillis, W.S. Circulation (1993) [Pubmed]
  30. Function and dysfunction of synaptic calcium channels: insights from mouse models. Pietrobon, D. Curr. Opin. Neurobiol. (2005) [Pubmed]
  31. Characterization of 5-hydroxytryptamine receptors in human temporal arteries: comparison between migraine suffers and nonsufferers. Skärby, T., Tfelt-Hansen, P., Gjerris, F., Edvinsson, L., Olesen, J. Ann. Neurol. (1982) [Pubmed]
  32. Calcitonin gene-related peptide does not excite or sensitize meningeal nociceptors: implications for the pathophysiology of migraine. Levy, D., Burstein, R., Strassman, A.M. Ann. Neurol. (2005) [Pubmed]
  33. Association between dopamine receptor genes and migraine without aura in a Sardinian sample. Del Zompo, M., Cherchi, A., Palmas, M.A., Ponti, M., Bocchetta, A., Gessa, G.L., Piccardi, M.P. Neurology (1998) [Pubmed]
  34. Recent developments on KCNQ potassium channel openers. Wua, Y.J., Dworetzky, S.I. Current medicinal chemistry. (2005) [Pubmed]
  35. No mutations in CACNA1A and ATP1A2 in probands with common types of migraine. Jen, J.C., Kim, G.W., Dudding, K.A., Baloh, R.W. Arch. Neurol. (2004) [Pubmed]
  36. Genetics of migraine: an update with special attention to genetic comorbidity. Stam, A.H., van den Maagdenberg, A.M., Haan, J., Terwindt, G.M., Ferrari, M.D. Curr. Opin. Neurol. (2008) [Pubmed]
  37. Tolfenamic acid is as effective as ergotamine during migraine attacks. Hakkarainen, H., Vapaatalo, H., Gothoni, G., Parantainen, J. Lancet (1979) [Pubmed]
  38. Coronary angiography in migraine patient after subcutaneous sumatriptan. Evers, S., Husstedt, I.W., Enbergs, A. Lancet (1995) [Pubmed]
  39. No increase of calcitonin gene-related peptide in jugular blood during migraine. Tvedskov, J.F., Lipka, K., Ashina, M., Iversen, H.K., Schifter, S., Olesen, J. Ann. Neurol. (2005) [Pubmed]
  40. Functional 1H-MRS findings in migraine patients with and without aura assessed interictally. Sarchielli, P., Tarducci, R., Presciutti, O., Gobbi, G., Pelliccioli, G.P., Stipa, G., Alberti, A., Capocchi, G. Neuroimage (2005) [Pubmed]
  41. Prophylaxis of menstrual migraine with triptans: problems and possibilities. Loder, E. Neurology (2002) [Pubmed]
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