| Management of sporadic and familial hemiplegic migraine. | |
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MedLine Citation:
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PMID: 20187861 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Sporadic and familial hemiplegic migraines (SHM and FHM) are rare paroxysmal disorders characterized by motor aura and headache. The distinction is based on whether other family members are affected. The majority of FHM families have a mutation in one of the ion channels CACNA1A, ATP1A2 and SCN1A. SHM is sometimes caused by a de novo mutation in one of the genes. Clinical trials of SHM and FHM have not been conducted. Seizure in FHM is secondary to cerebral edema and fever among other factors. The regional cerebral blood flow is reduced during the reversible aura symptoms. Triptans and ergotamine are contraindicated in the management of SHM and FHM based on the pathophysiology. Nimodipine is contraindicated. Acute and prophylactic management are otherwise based on the management principle of the migraine without aura and migraine with aura. |
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Authors:
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Michael Bj?rn Russell |
Publication Detail:
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Type: Journal Article; Review |
Journal Detail:
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Title: Expert review of neurotherapeutics Volume: 10 ISSN: 1744-8360 ISO Abbreviation: Expert Rev Neurother Publication Date: 2010 Mar |
Date Detail:
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Created Date: 2010-03-01 Completed Date: 2010-05-18 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 101129944 Medline TA: Expert Rev Neurother Country: England |
Other Details:
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Languages: eng Pagination: 381-7 Citation Subset: IM |
Affiliation:
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Head and Neck Research Group, Department of Neurology, Research Centre, Akershus University Hospital, Dr. Kobros vei 39, 1474 Nordbyhagen, Oslo, Norway. m.b.russell@medisin.uio.no |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Calcium Channels / genetics Clinical Trials as Topic Cortical Spreading Depression / physiology Humans Ion Channels / genetics Migraine Disorders / diagnosis*, genetics, physiopathology, therapy* Mutation / genetics Sodium-Potassium-Exchanging ATPase / genetics |
| Chemical | |
Reg. No./Substance:
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0/CACNA1A protein, human; 0/Calcium Channels; 0/Ion Channels; EC 3.6.1.-/ATP1A2 protein, human; EC 3.6.3.9/Sodium-Potassium-Exchanging ATPase |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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