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

We report four cases of a new variant of cluster headache associated with hemiparesis. Clinical similarities with hemiplegic migraine suggest that hemiplegic cluster, too, may be a channelopathy. One of our patients had a family history suggestive of an autosomal dominant inheritance.
Headache 2002 Feb
PMID:Hemiplegic cluster. 1200 89

The objective of the present study was to use systematic nation-wide case-finding methods to establish the prevalence and sex ratio of hemiplegic migraine (HM) in the entire Danish population of 5.2 million inhabitants. Affected patients were identified from three different recruitment sources: the National Patient Register, case records from private practising neurologists and advertisements. Based on the observed number of affected patients from each case-finding method, it was attempted to estimate the total number of affected patients by means of the statistical method known as capture-recapture. Two hundred and ninety-one affected patients were identified; 147 were familial HM from 44 different families, 105 were sporadic HM and 39 were unclassifiable HM. The HM sex ratio (M:F) was 1:3. Based on the identified number of affected patients the prevalence of HM at the end of 1999 was estimated to be 0.01% in Denmark, where the familial and sporadic form were equally frequent.
Cephalalgia 2002 Jun
PMID:An epidemiological survey of hemiplegic migraine. 1211 Jan 12

Migraine is a common episodic headache disorder. A comprehensive headache treatment plan includes acute attack treatment to relieve pain and impairment and long-term preventive therapy to reduce attack frequency, severity, and duration. Circumstances that might warrant preventive treatment include: (i) migraine that significantly interferes with the patient's daily routine despite acute treatment; (ii) failure, contraindication to, or troublesome side-effects from acute medications; (iii) overuse of acute medications; (iv) special circumstances, such as hemiplegic migraine; (v) very frequent headaches (more than two a week); or (vi) patient preference. Start the drug at a low dose. Give each treatment an adequate trial. Avoid interfering, overused, and contraindicated drugs. Re-evaluate therapy. Be sure that a woman of childbearing potential is aware of any potential risks. Involve patients in their care to maximize compliance. Consider co-morbidity. Choose a drug based on its proven efficacy, the patient's preferences and headache profile, the drug's side-effects, and the presence or absence of coexisting or co-morbid disease. Drugs that have documented high efficacy and mild to moderate adverse events (AEs) include beta-blockers, amitriptyline, and divalproex. Drugs that have lower documented efficacy and mild to moderate AEs include selective serotonin reuptake inhibitors (SSRIs), calcium channel antagonists, gabapentin, topiramate, riboflavin, and non-steroidal anti-inflammatory drugs.
Cephalalgia 2002 Sep
PMID:Migraine: preventive treatment. 1537 26

In Western communities, 15 to 20% of the general population experiences migraine headaches. In Japan, 3 to 9% of the population experience migraine headaches. Quality of life in headache patients is impaired. The International Headache Society (IHS) published the new headache classification in 1988. Chronic daily headache (CDH) is a common problem in headache clinics. Recently, the problems in classifying CDH have been discussed. CDH is not easily classified within the IHS criteria. For migraine attacks, triptans are effective. The genetic analysis in migraine is progressing. Point mutations in the P/Q-type Ca2+ channel alpha 1 subunit gene in familial hemiplegic migraine and in Notch 3 gene in cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL), have been identified. Although CADASIL patients in Europe often show migraine headache, migraine attacks are less common in Japanese CADASIL patients.
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PMID:[Clinical progress in headache]. 1223 33

Headache attacks and autonomic dysfunctions characterize migraine, a very common, disabling disorder with a prevalence of 12% in the general population of Western countries. About 20% of individuals affected with migraine experience aura, a visual or sensory-motor neurological dysfunction that usually precedes or accompanies the headache. Although the mode of transmission is controversial, population-based and twin studies have implicated genetic factors, especially in migraine with aura. Familial hemiplegic migraine is a hereditary form of migraine characterized by aura and some hemiparesis. Here we show that mutations in the gene ATP1A2 that encodes the alpha2 subunit of the Na+/K+ pump are associated with familial hemiplegic migraine type 2 (FHM2) linked to chromosome 1q23 (OMIM 602481). Functional data indicate that the putative pathogenetic mechanism is triggered by a loss of function of a single allele of ATP1A2. This is the first report associating mutations of Na+K+ pump subunits to genetic diseases.
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PMID:Haploinsufficiency of ATP1A2 encoding the Na+/K+ pump alpha2 subunit associated with familial hemiplegic migraine type 2. 1253 47

A 43 year old man with thirty years history of recurrent hemiplegic migraine, consistently occurring on one side (left sided paresthesia and weakness of less than forty five minutes followed by right sided headache) and lately increasing to once in three days was investigated. CT head and carotid angiogram showed gyral calcification with prominent medullary and subependymal veins confirming the diagnosis of leptomeningeal angiomatosis. Management and followup is discussed.
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PMID:A case of hemeplegic migraine with leptomeningeal angiomatosis. 1257 15

Mild subclinical impairment of neuromuscular transmission can be detected with single-fibre electromyography (SFEMG) in subgroups of patients suffering from migraine and could be due to dysfunctioning Ca2+-channels on motor axons controlling stimulation-induced acetylcholine release. Acetazolamide, which is thought to ameliorate ion channel function, was shown effective in familial hemiplegic migraine and episodic ataxia type 2, both of which are associated with mutations of the neuronal Ca2+-channel gene CACNA1A, as well as in aura status. We treated therefore in an open pilot study five non-hemiplegic migraineurs showing mild SFEMG abnormalities with acetazolamide for several weeks. This was followed by a normalization of SFEMG recordings in all patients and by clinical improvement in four. These results support the assumption that the subclinical impairment of neuromuscular transmission found in certain migraineurs might be due to dysfunctioning Ca2+-channels.
Cephalalgia 2003 Mar
PMID:Acetazolamide acts on neuromuscular transmission abnormalities found in some migraineurs. 1260 61

The pathophysiology of the neurological deficits in hemiplegic migraine remains unclear. Both neurogenic and vascular etiologies have been proposed to explain this phenomenon. We present the case of a patient with hemiplegic migraine in whom there was no diffusion weighted magnetic resonance imaging evidence of cerebral ischemia, despite persistent left hemiplegia and diffuse vasospasm on cerebral angiography, there was no diffusion weighted magnetic resonance imaging evidence of cerebral ischemia. In addition, hypoperfusional changes were seen diffusely, more so on the less symptomatic hemisphere, whereas depression of cortical electrical activity was seen for several days on the right side. These findings support the notion that although both neurogenic and vascular changes occur in hemiplegic migraine, the former seems to be a more likely explanation for the neurological deficits.
Headache 2003 Jan
PMID:Prolonged cortical electrical depression and diffuse vasospasm without ischemia in a case of severe hemiplegic migraine during pregnancy. 1286 63

Amissense mutation of the CACNA1A gene that encodes the alpha1A subunit of the voltage-dependent P/Q-type calcium channel has been discovered in patients suffering from familial hemiplegic migraine. This suggested that calcium channelopathies may be involved in migraine more broadly, and established the importance of genetic mechanisms in migraine. Channelopathies share many clinical characteristics with migraine, and thus exploring calcium channel functions in the trigeminovascular system may give insights into migraine pathophysiology. It is also known that drugs blocking the P/Q- and N-type calcium channels have been successful in other animal models of trigeminovascular activation and head pain. In the present study, we used intravital microscopy to examine the effects of specific calcium channel blockers on neurogenic dural vasodilatation and calcitonin gene-related peptide (CGRP)-induced dilation. The L-type voltage-dependent calcium channel blocker calciseptine significantly attenuated (20 microg kg(-1), n=7) the dilation brought about by electrical stimulation, but did not effect CGRP-induced dural dilation. The P/Q-type voltage-dependent calcium channel blocker omega-agatoxin-IVA (20 microg kg-1, n=7) significantly attenuated the dilation brought about by electrical stimulation, but did not effect CGRP-induced dural dilation. The N-type voltage-dependent calcium channel blocker omega-conotoxin-GVIA (20 microg kg(-1), n=8 and 40 microg kg(-1), n=7) significantly attenuated the dilation brought about by electrical stimulation, but did not effect CGRP-induced dural dilation. It is thought that the P/Q-, N- and L-type calcium channels all exist presynaptically on trigeminovascular neurons, and blockade of these channels prevents CGRP release, and, therefore, dural blood vessel dilation. These data suggest that the P/Q-, N- and L-type calcium channels may be involved in trigeminovascular nociception.
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PMID:Voltage-dependent calcium channels are involved in neurogenic dural vasodilatation via a presynaptic transmitter release mechanism. 1297 82

In order to better understand sporadic hemiplegic migraine (SHM) and particularly its relation to familial hemiplegic migraine (FHM), migraine without aura (MO) and typical migraine with aura (typical MA), we investigated the occurrence of MO and typical MA among probands with SHM and their first-degree relatives. The pattern of familial aggregation of MO and typical MA was assessed by population relative risk calculations. A total of 105 SHM probands and 483 first-degree relatives were identified in the Danish population. Compared with the general population, SHM probands had no increased risk of MO, but a highly increased risk of typical MA. First-degree relatives of all SHM probands had an increased risk of both MO and typical MA, whereas first-degree relatives of probands with exclusively SHM had no increased risk of MO but an increased risk of typical MA. Our data suggest that SHM is a genetically heterogeneous disorder.
Cephalalgia 2003 Nov
PMID:Sporadic hemiplegic migraine is an aetiologically heterogeneous disorder. 1461 35


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