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Query: UMLS:C0018991 (hemiplegia)
 3,997 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hemiplegic migraine was observed in a boy aged 16 years. The family history was unquestionable and the duration of hemiplegia was prolonged. Carotid angiography after regression of clinical signs showed a particularly profuse passage of the contrast to the contralateral side and to the area of vascularization of the basilar artery. It is supposed that particularly favourable connections existed in this case in the arterial vascular bed of the brain, with possible hypotonia of the arterial walls in this area.
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PMID:[Case of hemiphlegic migraine with atypical angiographic findings]. 71 33

Eight patients with hemiplegic migraine are described. Majority were in their second decade and suffered two or more episodes of dense hemiplegia outlasting the headache. Complete recovery was the rule.
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PMID:Hemiplegic migraine. 239 3

The cases of a woman and her son with a long history (24 and 9 years, respectively) of hemiplegic migraine are presented. The mother demonstrated exclusively right-sided paralysis; in the son, paralysis occurred on each side. Electroencephalograms recorded during the attacks were characterized by pseudoperiodic slow sharp waves over the hemisphere contralateral to the hemiplegia. Between attacks the neurological examination and EEG were normal. CT scans performed during and between attacks showed no abnormalities.
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PMID:Familial hemiplegic migraine: EEG and CT scan study of two cases. 731 92

A mother and son suffer from hemiplegic migraine with onset in childhood. Both have nystagmus which has not changed for many years, but the date of onset is uncertain. They have an asymmetrical tremor, clinically indistinguishable from essential tremor. Neuroophthalmological examination revealed inability to produce smooth pursuit, gaze-paretic nystagmus, rebound nystagmus, failure of fixation suppression of the vestibuloocular reflex both horizontally and vertically, and low gain of the optokinetic system. These abnormalities, confirmed by electrooculography, are commonly seen in disease of the cerebellum and brainstem. Treatment with propranolol and pizotyline lessened the number of episodes of hemiplegia and improved the tremor. Hemiplegic migraine has been reported in association with nystagmus, retinal degeneration, deafness, and ataxia in varying combinations in three other families with autosomal dominant inheritance. These associated neurological manifestations likely represent system degenerations rather than the effect of repeated ischemia imputable to the migraine itself. The syndrome of hemiplegic migraine, tremor, and ocular smooth pursuit system disorder seen in this family appears to be inherited as a single autosomal dominant trait, although more than one autosomal dominant gene may be involved.
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PMID:An autosomal dominant syndrome of hemiplegic migraine, nystagmus, and tremor. 743 78

The authors use the term "complicated migraine" to describe the onset of neurological disorder occurring during an acute attack in a patient with chronic migraine. The disturbance may last for long periods or may be permanent, and these irreversible cerebral lesions have to be differentiated from the transient neurological effects characteristic of ophthalmic on secondary migraine. Patients with migraine and retinal lesions, as well as those with ophthalmoplegic or familial hemiplegic migraine, were excluded from the study. The seven cases reported included 5 women and 2 men with an average age of 30 years (from 14 to 51 years). A more or less severe lesion in a hemisphere was present, which led to sensory-motor signs of a hemiplegia (4 cases), an aphasia (4 cases), and a homonymous lateral hemianopia (3 cases). Exploration revealed the presence of an ischemic cerebral lesion in all cases. One or more arterial occlusions were also noted in 5 out of the 6 patients who were investigated by angiography. All cases showed the presence of the criteria thought to be essential for associating the cerebral ischemic lesion with migraine. 1) the patient had true migraine, 2) there was a close chronological relationship between the migraine attack and the lasting neurological disorder, 3) no other associated vascular disease was present (atheroma, cardiopathy). The very severe and prolonged spasm, which could be the cause of neurological disturbances in secondary and ophthalmic migraine, does not appear to be sufficient for producing an irreversible ischemic lesion and, more especially, a persistent vascular obstruction. The roles played by edema of the arterial wall and parietal changes in the vessels are discussed. It could be that thrombosis formation is encouraged by the changes in blood coagulability which may be associated with a migraine attack. The fact that anomalies in platelet aggregation have been demonstrated merits closer study.
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PMID:[Cerebral ischemic accidents during migraine attacks. A report on "complicated migraine"]. 746 14

Familial hemiplegic migraine and its associated signs and symptoms have previously been well described. The condition demonstrates autosomal dominant inheritance and has been recently assigned to a locus on chromosome 19. Previous reports of familial hemiplegic migraine have indicated that expression always occurs early in life. We describe a patient who presented with multiple episodes of reversible hemiplegia followed by headache at the age of 75. Seven other family members were found to have been affected in a similar manner. We believe this case represents a unique description of familial hemiplegic migraine presenting in later life.
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PMID:Adult onset familial hemiplegic migraine. 767 61

Four of five members of a family complained of repeated attacks of hemiplegic migraine, migraine with aura of different types, or migraine without aura. The hemiplegia always outlasted the headache and was often accompanied by altered consciousness, aphasia, and, in one patient, coma; in this latter patient, the ictal EEG, recorded during two attacks, showed delta activity in the hemisphere contralateral to the hemiplegia. At least 2 months after their latest attacks, three patients showed dyscalculia, attentional disturbances, and impaired long-term verbal memory on neuropsychologic assessment. There were no cognitive disturbances in the unaffected relative. The severity of cognitive impairment appears to be correlated with migraine history. We attempt to classify these cases according to the criteria of the International Headache Society.
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PMID:Familial hemiplegic migraine versus migraine with prolonged aura: an uncertain diagnosis in a family report. 782 30

Familial hemiplegic migraine is an autosomal dominant disorder of unknown pathogenesis in which the migrainous attacks are marked by the occurrence of a transient hemiplegia during the aura. The aim of our study was the identification of the affected gene. The first step was the chromosomal mapping of the affected gene, for which we used a "candidate gene" strategy. The first candidate gene was the gene responsible for CADASIL. While investigating CADASIL, mapped previously to chromosome 19, we observed that some patients had recurrent attacks of migraine with aura. Although the clinical and neuroimaging features of familial hemiplegic migraine differ markedly from CADASIL, we hypothesized that the same gene could be involved in the pathogenesis of both conditions. We chose two large pedigrees for linkage analysis of familial hemiplegic migraine. A maximum lodsore > 8 was found with two markers that are strongly linked to CADASIL. Multilocus linkage analysis located the affected gene within an interval of about 30 cM on chromosome 19, containing the gene responsible for CADASIL. At this step it's not possible to conclude that CADASIL and familial hemiplegic migraine are due to the same mutated gene. It will be necessary to analyse other familial hemiplegic migraine and CADASIL families in order to reduce the size of their respective interval and ultimately identify the mutated gene(s).
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PMID:[Familial hemiplegic migraine. Localization of a responsible gene on chromosome 19]. 787 19

By analogy with ophthalmic migraine, hemiplegic migraine is defined by the occurrence during the attacks of unilateral weakness. This simple definition is however far from reflecting the wide range of clinical situations reported under this term. Familial hemiplegic migraine (FHM) is a well individualized autosomal dominant condition. Attacks start in childhood, adolescence, or early adulthood. They invariably include a unilateral weakness lasting 30 to 60 minutes and almost always associated with visual, sensory, or speech disturbances. They are occasionally very severe with a dense hemiplegia, confusion, coma or fever, but they always completely recover. Brain neuroimaging is normal. In 20% of the families, migraine is associated with permanent neurological signs, mainly nystagmus and cerebellar ataxia. FHM is a genetically heterogeneous condition, with half of the families linked to chromosome 19 and the other half in which this link is excluded. By contrast to FHM, which is a well defined entity, other varieties of so called hemiplegic migraine do not deserve to be individualized as such. They include attacks of migraine with typical aura when a unilateral weakness is part of the aura, severe hemiplegic attacks similar to those reported in FHM but sporadic, migrainous infarcts with hemiplegia, and, for some authors, alternating hemiplegia of childhood. The pathogenesis of all these conditions and of migraine itself remaining largely unknown, it is currently impossible to know whether or not they share common pathophysiologic mechanisms. The identification of the gene on chromosome 19 and the discovery of other genes will be major steps to elucidate this question.
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PMID:[Hemiplegic migraine]. 789 22

Familial hemiplegic migraine is an autosomal dominant disorder of unknown pathogenesis in which the migrainous attacks are marked by the occurrence of a transient hemiplegia during the aura. While investigating CADASIL, mapped previously to chromosome 19, we observed that some patients had recurrent attacks of migraine with aura. Although the clinical and neuroimaging features of familial hemiplegic migraine differ markedly from CADASIL, we hypothesized that the same gene could be involved in the pathogenesis of both conditions. We chose two large pedigrees for linkage analysis of familial hemiplegic migraine. A maximum lod score > 8 was found with two markers that are also strongly linked to CADASIL. Multilocus linkage analysis suggested that the loci responsible for the two diseases reside within an interval of about 30 cM on chromosome 19.
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PMID:A gene for familial hemiplegic migraine maps to chromosome 19. 822 Apr 21


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