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Query: UMLS:C0018681 (headache)
 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Migraine is a common, disabling, complex brain disorder, presenting in attacks that may have up to 3 phases: a prodromal phase, the aura phase, and the headache phase. The pathogenesis of the aura and headache phases is reasonably well understood, but the mechanism by which migraine attacks are triggered is unknown. Most likely, migraineurs have a genetically determined reduced threshold for migraine triggers. Identifying "threshold genes" and deciphering their function will help to unravel the triggering mechanisms for migraine attacks. Familial hemiplegic migraine is a rare monogenic subtype of migraine with aura. Three genes have been identified for familial hemiplegic migraine. Recently, knock-in mice carrying human pathogenic FHM1 mutations were generated, which show behavioral, electrophysiological, and neurobiological characteristics in line with prevailing views of migraine physiological processes. Genetic migraine models will be useful in unraveling the triggering mechanisms for migraine attacks and in identifying novel migraine prophylactic targets and therapies.
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PMID:Genetic models of migraine. 1750 63

Liability to spontaneous and experimental pain is genetically determined and there is considerable variability in the antinociceptive effects of drugs commonly used in treating pain conditions and migraine attacks. The causes for variability involve still unknown genetic aspects. Recently, a third gene, SCN1A, was discovered as a cause of familial hemiplegic migraine (FHM). Recent advances in the genetics of pain and pain disorders include the discovery of the role of the sodium ion channel SCN9A in neuropathic pain as well as in inability to experience pain, and of GTP cyclohydrolase (GCH1) in setting the sensitivity to pain in normal individuals and modulating liability to chronic pain. Catechol-O-methyltransferase (COMT) and the cytochrome P450 variant allele CYP3A5 modulate the genetic response to opioid medications in humans. Variability in drug pharmacokinetics and adverse drug reactions of pain medications are also very much related to genetic variation, especially in CYP genes. Pharmacogenomic studies of headache and pain are still in their infancy, but these recent advances in the genetics of migraine and pain arguably hold the promise of individualised treatments and prevention of adverse drug reactions.
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PMID:Recent advances in the pharmacogenomics of pain and headache. 1750 72

This tutorial describes different methods and results of genetic studies of primary headaches. A positive family history is imprecise, because it does not specify the number of affected, family size or relation to the proband. Nor does it include an interview of the possibly affected family members. Calculation of the familial aggregation after confirmation of the diagnosis by a physician is more precise. Compared to the general population, first-degree relatives of probands with migraine without aura, migraine with aura, chronic tension-type headache and cluster headache has a significantly increased risk of the proband's disorder. These data are confirmed in twin studies. The primary headaches are caused by a combination of genetic and environmental factors. A major breakthrough was identification of 3 different genes all causing the rare autosomal dominant inherited familial hemiplegic migraine. The genes encode ion channels. So far no genes have been identified to cause the more common types of primary headaches.
J Headache Pain 2007 Jun
PMID:Genetics in primary headaches. 1756 38

Clinical and pathophysiological evidences connect migraine and the cerebellum. Literature on documented cerebellar abnormalities in migraine, however, is relatively sparse. Cerebellar involvement may be observed in 4 types of migraines: in the widespread migraine with aura (MWA) and migraine without aura (MWoA) forms; in particular subtypes of migraine such as basilar-type migraine (BTM); and in the genetically driven autosomal dominant familial hemiplegic migraine (FHM) forms. Cerebellar dysfunction in migraineurs varies largely in severity, and may be subclinical. Purkinje cells express calcium channels that are related to the pathophysiology of both inherited forms of migraine and primary ataxias, mostly spinal cerebellar ataxia type 6 (SCA-6) and episodic ataxia type 2 (EA-2). Genetically driven ion channels dysfunction leads to hyperexcitability in the brain and cerebellum, possibly facilitating spreading depression waves in both locations. This review focuses on the cerebellar involvement in migraine, the relevant ataxias and their association with this primary headache, and discusses some of the pathophysiological processes putatively underlying these diseases.
Headache 2007 Jun
PMID:The cerebellum and migraine. 1757 30

Prolonged migraine auras can be disabling and potentially can cause permanent neurologic deficits. Several medicinal agents have shown some efficacy in aborting prolonged auras, but results are inconsistent. Greater occipital nerve blockade can alleviate the pain of migraine and in 1 case report the migraine aura. Hemiplegic migraine attacks are marked by motor weakness that can last for minutes to days. Two case patients with a history of hemiplegic migraine with prolonged auras are presented, who both had complete alleviation of their aura symptoms with GON blockade. A hypothesis on how GON blockade may inhibit cortical spreading depression is also presented.
Headache 2007 Jun
PMID:Cessation of hemiplegic migraine auras with greater occipital nerve blockade. 1820 98

A 20-year-old female with hemiplegic migraine was treated during an acute attack with intravenous verapamil, which reproducibly resolved the headache within 20 min but did not affect her hemiplegia. Magnetic resonance (MR) and computed tomographic (CT) angiography and perfusion performed during the attack showed vasodilation and hyperperfusion. Cerebral hyperperfusion concurrent with hemiplegia suggests a dissociation between cerebral perfusion and neuronal function in hemiplegic migraine. The beneficial effect of verapamil on headache but not hemiplegia suggests a distinct mechanism for pain and neuronal dysfunction in hemiplegic migraine, with the beneficial effect on pain not due to vasodilation.
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PMID:Hemiplegic migraine: hyperperfusion and abortive therapy with intravenous verapamil. 1761 29

We present genetically identical twin patients who experienced late-onset migraine with visual and somatosensory auras and later developed hemiplegic migraines associated with severe cortical oedema and enhancement. Both positron emission tomography and electroencephalography showed an increase in activity contralateral to the hemiplegic side. Brain biopsy during the attack showed reactive astrogliosis and microgliosis. Mutations in CACNA1A, ATP1A2, SLC1A3 and NOTCH3 were ruled out by sequencing. This report shows the clinical and genetic evaluation of a severe form of familial hemiplegic migraine as well as the evolution of the imaging changes.
Cephalalgia 2007 Oct
PMID:Adult-onset hemiplegic migraine with cortical enhancement and oedema. 1764 64

Hemiplegic migraine is an unusual variant of migraine, characterised by a temporary hemiparesis or hemiplegia associated with headache. We report a patient with hemiplegic migraine who developed atypical migraine with apnoeic spells, aphasia and hemiparesis following general anaesthesia. We review the clinical features of hemiplegic migraine and the considerations for its anaesthetic management.
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PMID:Apnoeic spells following general anaesthesia in a patient with familial hemiplegic migraine. 1769 27

Hemiplegic migraine (HM) is characterized by motor weakness and at least one other aura symptom or sign that is fully reversible within 24 hours. While prolonged neurological impairment lasting weeks has been observed, persistent attack-related neurological deficits have not been described. This case illustrates the potential for permanent neurological deficits to occur as a sequelae of HM in the absence of infarction, and highlights potentially important pathophysiological and treatment implications.
Headache 2007 Sep
PMID:Familial hemiplegic migraine: permanent attack-related neurologic deficits. 1788 29

A cross-sectional study to determine the prevalence of migraine in seventh grade Thai students in 4 junior high schools in Bangkok, Thailand, according to the diagnostic criteria of the second edition of the Classification of Headache of the International Headache Society was conducted in July 2004. The study included a screening self-administered questionnaire and face-to-face interview with physical examination. The diagnosis of migraine was made and confirmed by 2 pediatric neurologists. All of 1789 students in participating schools completed the questionnaire. After 2 interviews, 248 students (13.8%) were diagnosed with migraine. The prevalence in girls was higher than that in boys (16.2% vs 11.7%). Migraine as having aura was diagnosed in 34 students (13.7%). One student had sporadic hemiplegic migraine. Among 248 children, 176 (71%) reported the duration of headache between 1 and 2 hours. The leading precipitating factor of migraine was the stress related to daily school activities (17.7%). There were 32 students (12.9%) with frequent and intense headache who were referred to their primary physicians for further management. This study had disclosed a high prevalence of migraine in seventh grade Thai students in Bangkok City and reflected the existing burden of this illness in Thai students.
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PMID:Migraine in Thai children: prevalence in junior high school students. 1789 Apr 11


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