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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cerebral angiography, performed after a seizure in a patient with a life-long history of typical hemiplegic migraine, disclosed markedly dolichoectatic anterior and middle cerebral arteries. No abnormality of the adjacent capillary or venous structures was present. A positive brain scan was attributed to ischemia induced by vasospasm rather than to the corresponding large tortuous anterior and middle cerebral arteries. There were no permanent sequelae and the patient has been free of seizures on Dilantin and phenobarbital over a 3-year follow-up period. Angiographic demonstration or description of a similar ectatic set of anterior and middle cerebral arteries could not be found in the literature. The concurrence of seizures and hemiplegic migraine adds to the peculiarity of this case.
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PMID:Cerebral arterial dolichoectasia with seizure. Case report. 125 41

EEG abnormalities in migraine have been reported by a number of authors during the last 50 years. Prevalences vary considerably in the older literature. A number of unspecific rhythms related to drowsiness or hyperventilation have probably been counted as "abnormal", and the reported numbers of definitely abnormal EEG rhythms have been consistently low. In a few controlled and blinded studies, however, slight excess of various EEG rhythms has been found in migraine patients. Similar prevalences of interictal EEG abnormalities have generally been found in patients with classic and common migraine, but the diagnostic classification may not have been precise enough in some studies. During visual aura, either slow waves, depression of background activity amplitude or normal EEG have been reported. The most definitely abnormal EEGs with unilateral or bilateral delta activity have been recorded during attacks of hemiplegic migraine, and during attacks of migraine with disturbed consciousness. The relationship between migraine and epilepsy has still not been adequately clarified. The connection seems to exist in several small entities (e.g. migraine-like headache as an epileptic manifestation, epileptic seizures triggered by epileptic attacks, and possibly in epilepsies with occipital spike waves), but it is seemingly not "fundamental". Newer methods, i.e. EEG frequency analysis and topographic brain mapping, are promising tools in this field. So far, mostly small studies have been published with somewhat inconsistent results. A pattern of increased alpha rhythm variability (and/or asymmetry) in the headache-free phase seems to emerge, however. Significant asymmetry of alpha and theta during headache has been reported in one topographic brain mapping study. Magnetoencephalographic studies of migraine patients have demonstrated slow wave-shifts (similar to those observed in animals with spreading depression). The EEG patterns observed in migraine patients seem to suggest a possible physiological connection between sleep, hyperventilation and migraine. The study of such relationship may shed new light on migraine pathophysiology.
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PMID:EEG in migraine: a review of the literature. 205 54

A family had a dominantly inherited amyloid angiopathy that involved the meninges of the brain and spinal cord, retina, vitreous humor, peripheral nerves, and systemic organs. Clinical features included hemiplegic migraine, periodic obtundation, psychosis, seizures, intracerebral hemorrhage, myelopathy, visual impairment, deafness, and peripheral neuropathy. Pathological findings consisted of amyloid deposition in the leptomeningeal and retinal vessels, in the vitreous humor, and in perivascular tissue throughout the body. Evaluation of the amyloid showed it to be a transthyretin (prealbumin). A brief course of plasmapheresis produced a short-lived decrease concentration in circulating transthyretin.
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PMID:Familial oculoleptomeningeal amyloidosis. Report of a new family with unusual features. 317 32

Tottering and leaner, two mutations of the mouse tottering locus, have been studied extensively as models for human epilepsy. Here we describe the isolation, mapping, and expression analysis of Cacnl1a4, a gene encoding the alpha subunit of a proposed P-type calcium channel, and also report the physical mapping and expression patterns of the orthologous human gene. DNA sequencing and gene expression data demonstrate that Cacnl1a4 mutations are the primary cause of seizures and ataxia in tottering and leaner mutant mice, and suggest that tottering locus mutations and human diseases, episodic ataxia 2 and familial hemiplegic migraine, represent mutations in mouse and human versions of the same channel-encoding gene.
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PMID:Mutations in the Cacnl1a4 calcium channel gene are associated with seizures, cerebellar degeneration, and ataxia in tottering and leaner mutant mice. 906 Apr 10

A 6-year-old boy with a family history of hemiplegic migraine had a hemiplegic migraine lasting for 6 days complicated by prolonged fever, lethargy, and two brief focal seizures. An acute single photon emission computerized tomogram (SPECT) demonstrated decreased blood flow in the symptomatic cerebral hemisphere as well as crossed cerebellar diaschisis not previously documented in migraine. Another unique finding was the MRI with enhancement of the meninges and pial vessels over the symptomatic cerebral hemisphere. These findings suggest cerebellar and extra-axial involvement as components of hemiplegic migraine.
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PMID:Familial hemiplegic migraine with crossed cerebellar diaschisis and unilateral meningeal enhancement. 938 60

Familial hemiplegic migraine is a distinctive form of migraine with autosomal dominant inheritance. The patients undergo attacks of migraine complicated by hemiplegia. Seizures have not been reported as comprising a part of this syndrome. We describe three generations of a family with hemiplegic migraine and focal seizures occurring concurrently with the migrainous attacks. There were five affected family members whose clinical features included unilateral headache and transient hemiplegia. Two family members also had focal seizures during the migrainous attacks. One of the patients was treated with carbamazepine with good results. The only associated neurological finding was ataxia which was found in the oldest patient. The presence of focal seizures during an episode of hemiplegic migraine suggests that the two phenomena of migraine and focal seizures may share the same underlying pathophysiology.
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PMID:A family with hemiplegic migraine and focal seizures. 1072 90

The epilepsies have been regarded as clinically distinct from the paroxysmal movement disorders. Recently, a variety of ion channel defects have been identified as the biological basis of certain familial epilepsies and paroxysmal movement disorders. We studied two families with the co-occurrence of epilepsy, movement disorders and migraine. Information was obtained on 147 individuals in the two families. In family WF, there was a co-occurrence of epilepsy (benign infantile convulsions, idiopathic generalized epilepsy), episodic ataxia (with cerebellar atrophy and without myokymia) and common migraine. In family CL, epilepsy (febrile seizures, febrile seizures plus), kinesigenic paroxysmal dyskinesia and migraine (including hemiplegic migraine) were observed in various combinations over 3 generations. The observations in these two families, together with review of the literature, suggest that the co-occurrence of epilepsy (particularly benign infantile convulsions), paroxysmal movement disorders and migraine is not due to chance. Thus, these distinct clinical phenomena could have a shared biological basis and ion channel defects are an attractive possibility.
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PMID:Epilepsy and paroxysmal movement disorders in families: evidence for shared mechanisms. 1093 38

The rare forms of migraine should be studied so that they can be recognized, thereby avoiding diagnostic errors and unnecessary complementary investigations. These rare forms can be divided into three categories: 1) atypical auras, characterized by the following: their semiology (visual or sensory illusions or hallucinations); their manner of onset (sudden onset of aura, with development of migraine in under four minutes); their duration (aura prolonged for between 60 minutes and seven days); aura with absence of accompanying cephalgia. This form of migraine could be confused with a case of partial epilepsy or AIT and raises a problem of differential diagnosis requiring an etiological investigation to ensure correct diagnosis; 2) clinical forms which are for the most part recognized by the International Headache Society's (IHS) classification, i.e., basilar artery migraine, familial hemiplegic migraine, ophthalmoplegic migraine and the rare occurrence of retinal migraine. Confusional migraine, a disorder which is mainly encountered in childhood, has not been categorized by the IHS but may be part of the symptomatology of the above-described forms; and 3) secondary migraines, in which a triggering mechanism causes migraine attacks to appear in a subject who was not previously affected by this disorder. This category covers post-traumatic migraine, migraine of cervical origin, the co-morbidity of migraine and epileptic seizures, and rare cases of symptomatic migraine which are indicative of underlying general disease or an intracranial lesion, i.e., a tumor or arteriovenous malformation.
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PMID:[Rare and atypical forms of migraine]. 1107 45

There are three categories of rare forms of migraine headache. Atypical aura can raise difficult diagnostic questions due to their clinical expression (visual or sensorial illusions and hallucinations), their mode of onset (sudden aura, developing in less than 4 minute), their duration (prolonged aura lasting more than 60 minutes), and the lack of an accompanying headache. Differential diagnostics include partial epilepsy or AIT, requiring careful search for the underlying cause. Rare migraine syndromes are separate clinical entities, most of which are recognized by the International Headache Society (IHS). These syndromes include basilar migraine, familial hemiplegic migraine, ophthalmoplegic migraine and the exceptional retinal migraine. Confusional migraine, usually observed in children, is no individualized by the IHS but can be included here. For secondary migraines there is a triggering factor leading to migraine in patients with no history of migraine previously. These include post-traumatic migraine and cervical migraine as well as migraine occurring with epileptic seizures and rare symptomatic migraine headache disclosing a general disease or an intracranial neurological lesion.
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PMID:[Rare and atypical forms of migraine]. 1113 47

Several inherited human neurological disorders can be caused by mutations in genes encoding Ca2+ channel subunits. This review deals with known human and mouse calcium channelopathies of the central nervous system (CNS). The human diseases comprise: 1) a recessive retinal disorder, X-linked congenital stationary night blindness, associated with mutations in the CACNA1F gene, encoding alpha(1)1.4 subunits of L-type channels; and 2) a group of rare allelic autosomal dominant human neurological disorders including familial hemiplegic migraine, episodic ataxia type 2, and spinocerebellar ataxia type 6, all associated with mutations in the CACNA1A gene, encoding alpha(1)2.1 subunits of P/Q-type calcium channels. Mutations at the mouse orthologue of the CACNA1A gene cause a group of recessive neurological disorders, including the tottering, leaner, and rocker phenotypes with ataxia and absence epilepsy, and the rolling Nagoya phenotype with ataxia without seizures. Two other spontaneous mouse mutants with ataxia and absence epilepsy, lethargic and stargazer, have mutations in genes encoding a calcium channel auxiliary beta subunit and a putative calcium channel auxiliary gamma subunit. For each channelopathy, the review describes disease phenotype, channel genotype, and known functional consequences of the pathological mutations; in some cases, it also describes working hypothesis and/or speculations addressing the challenging question of how the alterations in channel function lead to selective cellular dysfunction and disease.
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PMID:Calcium channels and channelopathies of the central nervous system. 1189 Apr 56


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