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

During the course of hemiplegic migraine in 3 patients, changes in regional cerebral blood flow (rCBF) were recorded by the intracarotid 133Xe method and a 254 multidetector camera covering one hemisphere. The rCBF measurements were performed in conjunction with cerebral angiography. During repeated rCBF measurements all 3 patients developed focal hypoperfusion originating in the frontal lobe, subsequently spreading posteriorly to involve the precentral and postcentral regions. In 2 cases focal hyperperfusion appeared to precede the hypoperfusion. In association with the rCBF changes the patients developed transient motor and/or sensory deficits and subsequently severe headache. No signs of arterial occlusion were found. In the over and underperfused regions blood flow fluctuated rapidly because of instability of cerebrovascular tone, defined as transient constriction of the smallest cerebral vessels (arterioles) alternating with a normal calibre for these vessels and/or short periods of vasodilatation. It is considered to be a primary pathological condition of the vessels. When vasoconstriction was present the blood flow decreased to values consistent with ischaemia, which was probably the cause of the neurological deficits. On the basis of these observations and previous work from our laboratory we conclude that instability of cerebrovascular tone may cause focal ischaemia during the course of attacks of classical and hemiplegic migraine.
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PMID:Focal ischaemia caused by instability of cerebrovascular tone during attacks of hemiplegic migraine. A regional cerebral blood flow study. 365 1

Two cases of non-familial hemiplegic migraine are described. Naloxone reversed the neurological deficits accompanying attacks, whereas the pain was uninfluenced. The possibility that the opiate-antagonist naloxone facilitates regression of neurological symptoms associated with migraine attacks in general is voiced.
Cephalalgia 1983 Jun
PMID:Non-familial hemiplegic migraine responsive to naloxone. 687 87

A 21-year-old man had typical symptoms of hemiplegic migraine. A lumbar puncture demonstrated a significant lymphocytic response and an elevated CSF protein level on the day of and 24 days after the headache despite the absence of any other clinical symptoms. Other reported cases of CSF leukorrhaghia associated with hemiplegic migraine are briefly reviewed.
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PMID:Hemiplegic migraine associated with an aseptic meningeal reaction. 738 69

A 30-year-old woman with hemiplegic migraine and an elevated CSF protein level with considerable pleocytosis is described. Fourteen other cases of hemiplegic migraine with cerebrospinal fluid abnormalities reported in the literature are reviewed.
Headache 1995 Jun
PMID:Hemiplegic migraine with CSF abnormalities. 763 25

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.
Headache
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

Studies of twins, spouses and familial aggregation strongly suggest that migraine without aura (MO) and migraine with aura (MA) are genetically determined. The mode of inheritance is most likely multifactorial in both MO and MA. However, autosomal dominant inheritance with reduced penetrance cannot be excluded in either MO or MA. At present the only evidence for genetic heterogeneity of MA is familial hemiplegic migraine with slowly progressive ataxia. This phenomenon can also be explained by linkage of different genes. All existing studies have been characterized by one or more of the following methodologic shortcomings: selection of probands from clinic populations, information obtained by questionnaire, family history obtained through probands, insufficient description of the attacks, lack of distinction between MO and MA. Useful strategies for future studies of migraine genetics are discussed.
Cephalalgia 1993 Aug
PMID:The genetics of migraine without aura and migraine with aura. 837 38

We studied aura symptoms in 83 patients from 6 unrelated families suffering from familial hemiplegic migraine. Fifty-five of the patients reported symptoms that allowed us to categorize them as basilar migraine (BM) patients, in accordance with the International Headache Society (IHS) criteria. In a control group of 33 patients suffering from migraine with aura and 33 patients suffering from migraine without aura, 9 patients complained of vertigo, and only one patient of diplopia during one of her attacks. None of these control patients fulfilled the IHS criteria for BM. We suggest that familial hemiplegic migraine and BM may share certain pathophysiologic mechanisms, which may consist of a (genetically determined) disturbance of basilar artery blood flow.
Cephalalgia 1995 Dec
PMID:Is familial hemiplegic migraine a hereditary form of basilar migraine? 870 4

We compared the clinical characteristics of 46 patients from three unrelated families with familial hemiplegic migraine (FHM) linked to chromosome 19, with those of 20 patients from two families with FHM not linked to chromosome 19. We found no significant differences for age at onset, frequency and duration of attacks, duration of the paresis, and occurrence of basilar migraine symptoms. In the linked families, significantly more patients reported unconsciousness during attacks (39% vs 15%; p < 0.05) and provocation of attacks by mild head trauma (70% vs 40%; p < 0.05). In one linked family patients also displayed chronic progressive cerebellar ataxia, whereas in one unlinked family benign infantile convulsions occurred in addition to FHM. Interestingly, so far an association with cerebellar ataxia was only described in chromosome 19-linked families. FHM linked to chromosome 19 and FHM unlinked to chromosome 19 do not differ with respect to clinical features.
Cephalalgia 1996 May
PMID:Familial hemiplegic migraine: a clinical comparison of families linked and unlinked to chromosome 19.DMG RG. 873 65

Recent progress in the genetics of migraine and other headache syndromes occurred in three major areas during the past year: systematic family studies of migraine, large-scale population-based twin studies, and linkage and association studies of familial hemiplegic migraine. Studies of linkage between familial hemiplegic migraine and marker 19p13 in 13 extended families have found a total of seven families with linkage to this region. Three large scale population-based twin studies of headache have revealed that approximately one-half of the variation in migraine could be attributable to additive genes, with the remainder primarily caused by unshared rather than shared environmental factors between twins. Migraine is clearly a complex disease characterized by high population prevalence, an inconclusive mode of transmission, and a lack of clear evidence for phenotypic validity. Increasing knowledge from family and twin studies using contemporary diagnostic methods will help to clarify the factors contributing to the heterogeneity of this condition.
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PMID:Genetics of migraine and other headache. 883 11


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