Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sixty-four patients with atypical transient cerebral or visual symptoms that could not be classified as unequivocal TIAs nor as migraine, epilepsy or neurosis, were followed up for a mean of 3.75 years (range 11 months and 9 years, 240 patient years). Their mean age was 55 years. Only two patients suffered a (non-disabling) stroke, but eight patients had a major cardiac event: fatal myocardial infarction in three, sudden death in one and non-fatal myocardial infarction in four patients. Seven of these eight patients were known to have cardiovascular risk factors. Visual symptoms were relatively benign with regard to cardiac events (2 events in 28 patients), whereas dizziness alone and focal sensory symptoms alone were more strongly associated with subsequent cardiac complications (2 out of 4, and 4 out of 13 patients, respectively). In a control group of 185 patients with 'typical' TIAs or minor strokes, followed for a total of 233 patient years, seven patients had a ischaemic stroke, and only one a cardiac event. Our results suggest that patients with atypical transient cerebral deficits and cardiovascular risk factors may carry a low risk of subsequent stroke, but a high risk of major cardiac events.
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PMID:'Atypical TIAs' may herald cardiac rather than cerebral events. 165 90

This report concerns seven children who had at least one episode of infarct, possibly during an attack of migraine. They fulfilled the following criteria: presence of acute neurological deficit associated with headache or other symptoms characteristic of migraine attacks; a history of migraine; evidence of infarct on CT scan; and no other evident cause of the stroke. CT showed that the area of infarction was in the distribution of the posterior cerebral artery in three cases. Four of the children have been followed for at least 23 months and none has severe residual deficit. An aetiological relationship between migraine and stroke could not be demonstrated. However, epidemiological data suggest that childhood migraine can be a contributory risk-factor for strokes.
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PMID:Does migraine-related stroke occur in childhood? 170 43

We studied 65 consecutive patients with a first stroke who had an appropriate CT-proven small infarct in the territory of the lateral (61 patients), medial (3 patients) or both lateral and medial lenticulostriate arteries (1 patient) from the middle cerebral artery. While more than 75% of these patients were either hypertensive or diabetic (having at least one cause for small-artery disease), embolic sources were encountered in 35%, either from large vessels (28%), and/or from the heart (15%). Other causes (angiitis, migraine) were found in only 9%. The neurologic deficit was purely motor in more than 50% of the patients (in half of them with neuropsychological dysfunctions), a sensori-motor deficit was present in 30% (in half of them with neuropsychological dysfunctions), and only 20% had ataxic hemiparesis. No one had pure sensory stroke. None of the classical lacunar syndrome or the modality of sensory, motor or ataxic deficits were specific for any topographic subdivision of LS territory, but there was a tendency for clinical features to be linked with the involved basal ganglia and the topography of pathways in the internal capsule as delineated by anatomical studies. Pure motor deficits were associated with infarcts in the medial and posterior part of LS territory, visual field deficits and hemineglect always corresponded to posteriorly situated infarcts. Neuropsychological deficits were common in infarcts in the anterior and posterior subdivisions of LS territory, with a major effect of the size of infarct. Sensory deficits were not correlated with any location in LS territory, probably because thalamo-efferent fibres have a more diffuse course through the internal capsule.
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PMID:Infarcts in the territory of lenticulostriate branches from the middle cerebral artery. Etiological factors and clinical features in 65 cases. 170 98

I studied 9 patients with migraine and posterior circulation ischemia. Inclusion criteria were (1) brainstem or cerebellar infarcts or transient ischemic attacks, (2) satisfactory vertebrobasilar angiograms, and (3) migraine. Excluded were patients with only occipital lobe ischemia, known arteriosclerosis, or other nonmigrainous vascular disease. Two women and 7 men, ages 6 to 58 years (mean, 34.7), had transient attacks only (2), single strokes (4), single stroke followed by attacks (1), or multiple strokes (2). Five had antecedent classic, 2 common migraine, and classic migraine began only after the initial ischemic event in the other two. The 7 stroke patients all had CT- or MRI-documented brainstem (4) or cerebellar (6) infarcts. Angiography was normal (3) or demonstrated basilar artery (BA) narrowing (2) or occlusion (4), or branch occlusion (1). In 3 patients the initially occluded BA later reopened. At follow-up (average 4.3 years, range 1 to 9 years), 5 were normal and 4 had important clinical deficits. I conclude that (1) "basilar migraine" is not always benign; it affects both sexes and a wide age range; (2) the pattern of headaches, attacks, and strokes varies; (3) migraine may appear only after ischemia; (4) some patients have BA occlusion or diffuse narrowing; and (5) BA occlusion can be temporary.
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PMID:Migraine and vertebrobasilar ischemia. 192 34

Ca antagonists of the dihydropyridine class (DHPs) are a heterogeneous group of drugs that interfere with Ca entry into vascular smooth muscle cells of resistance arterioles through type-L calcium channels producing arteriolar vasodilation. This leads to a reduction of vascular tone and, therefore, they have been successfully used in the treatment of systemic hypertension, myocardial ischemia (stable, variant, and unstable angina and silent ischemia), and Raynaud's phenomenon. Furthermore, recent clinical trials have indicated that DHPs may induce regression or slowing the progression of atheroma in coronary arteries. The results obtained with DHPs in the prophylaxis of migraine headache and in treating ischemic stroke and cerebral artery vasospasm are encouraging. However, more carefully designed, double-blind, large-scale, long-term studies are needed to better define the therapeutic value of DHPs in these disorders, the severity of adverse effects, and the mechanism responsible for their therapeutic effects.
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PMID:Dihydropyridines and vascular diseases. 179 15

By means of magnetic resonance imaging we investigated a total of 45 patients suffering from classic migraine; 25 patients had been treated in our department for classic migraine over the past 2 years (group A), and 20 other patients investigated between 1976 and 1984 were reexamined for this study (group B). Thirty-two age- and roughly sex-matched healthy volunteers underwent magnetic resonance imaging and served as controls (group C). There was a trend for patients with classic migraine to have more subcortical patchy lesions on T2-weighted magnetic resonance imaging. In a comparison of our control subjects and patients with a history of greater than 20 attacks of classic migraine taken from groups A and B, this difference in number of lesions was significant (p = 0.02). The results suggest that patchy lesions in patients with classic migraine should be interpreted with particular caution before diagnosing a demyelinating disease since the lesions could be ischemic in origin.
Stroke 1991 Aug
PMID:Microinfarction in classic migraine? A study with magnetic resonance imaging findings. 186 46

There has been a recent increase in the number of studies dealing with migraine-stroke. I describe five patients in whom migraine-stroke was the clinical diagnosis but in whom the subsequent clinical events or autopsy showed a different mechanism for the cerebral infarction. Three patients had arterial dissection (one proven at autopsy), one had marantic endocarditis that had been missed on two echocardiograms (proven at autopsy), and one had generalized atherosclerosis and diabetes. These patients demonstrate that important and different etiologies may produce what seems to be the migraine-stroke syndrome. The result may be failure to recognize specific therapeutic measures that could have vitally important benefit to the patient.
Stroke 1991 Aug
PMID:Stroke from other etiologies masquerading as migraine-stroke. 186 54

The aetiology of strokes was studied in a hospital based series of patients aged up to 40 years with precise clinical and radiological criteria. One hundred and forty five patients (75 males and 73 females) aged five to 40 years with cerebral ischaemia were evaluated. Aetiology was heterogeneous and could be classified into seven groups. Cerebral arteriograms were performed in all cases and indicated the aetiological diagnosis in most patients. Embolism was the most frequent recognised abnormality (38.4%). There were no complications of arteriography. Arterial dissections discovered by arteriography were the cause of the stroke in 10.1% of the patients. Atherosclerosis was diagnosed in 32 cases and was the commonest cause (21.6%). In one fifth of cases no cause was found. Contraceptive drugs were considered as potential cause of ischaemic stroke in 11.5%, cardiac diseases in 12.8% and haematological disorders in 8.1%. Other potential causes included migraine, inflammatory diseases, pregnancy and lacunas. Follow up in 126 cases showed that many patients had good functional recovery.
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PMID:Cerebral infarction in young people. A study of 148 patients with early cerebral angiography. 189 19

A 24-year-old male had a deficiency of the complex I (NADH coenzyme-Q-reductase) of the mitochondrial respiratory chain, which clinically presented as a mitochondrial encephalomyopathy, with lactic acidosis and stroke-like episodes (MELAS syndrome). The encephalopathic episodes were preceded by migraine and were characterized by focal deficit signs, motor partial seizures and hypodense areas in the CT scan. An echocardiographic diagnosis of hypertrophic cardiomyopathy without intracavitary thrombi was made. It is suggested that hypertrophic cardiomyopathy is caused by the mitochondrial abnormalities that have been reported in the myocardium, and that migraine and cerebral infarctions are associated with abnormalities in the mitochondria from the endothelium and smooth muscle fibres of the cerebral small arteries and arterioles.
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PMID:[Complex I (NADH coenzyme-Q-reductase) deficiency, MELAS syndrome and hypertrophic cardiomyopathy]. 190 55

Anticardiolipin antibodies (aCL), one of a group of antiphospholipid antibodies which include the lupus anticoagulant (LA), may occur in association with systemic lupus erythematosus (SLE) and are less commonly detected in other diseases. We retrospectively reviewed the clinical and immunological features of 39 consecutive patients with abnormal aCL identified by one laboratory, to examine the spectrum of neurological disease in those patients without SLE. Fourteen patients in this category are described, 6 of whom did not have evidence of LA. All but 1 presented with neurological symptoms. Stroke and migraine dominated the clinical presentation, but many patients had features to suggest the presence of a hypercoagulable state. This study lends support to the concept of a primary antiphospholipid syndrome.
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PMID:Neurological disease associated with anticardiolipin antibodies in patients without systemic lupus erythematosus: clinical and immunological features. 196 May 45


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