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

The etiology of migrainous cerebral infarction is unknown, but may involve prothrombotic coagulation abnormalities. Therefore, we studied resistance to activated protein C and the presence of the Arg506Gln factor V Leiden mutation in 20 patients with migrainous cerebral infarction. Only one heterozygous carrier of the mutation was found, whereas other patients did not carry the mutation. This indicates that the factor V Leiden mutation is not a major risk factor for migrainous cerebral infarction.
Cephalalgia 1997 Aug
PMID:The factor V Leiden mutation (R506Q) is not a major risk factor for migrainous cerebral infarction. 925 78

From January 1978 to December 1995, 92 cases of Moyamoya disease were collected from seven major medical centers in Taiwan. The data gave an annual incidence rate of 0.048 per 100,000 population. There were 40 males and 52 females and the ages ranged from 2 to 62 years with the peak incidence in the 31-40 year age group (23 cases). Cerebral infarction occurred in 20 out of 24 juvenile patients (83%), and in 24 out of 68 adult patients (35%). The difference was statistically significant. Haemorrhagic stroke was more frequent in adult patients. Computed tomographic scans following stroke showed cerebral infarction in 44 cases, ventricular haemorrhage in 26 cases, intracerebral haemorrhage in 14 cases and pure subarachnoid haemorrhage in eight. The most frequent initial symptom was motor disturbance (59%), followed by headache (49%) and impaired consciousness (35%). This survey showed an incidence rate much lower than that in Japan, but comparable with those in other Oriental countries and higher than those in Western countries. The male-to-female ratio once differed considerably from that of the Japanese series, but from the present study is now quite similar.
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PMID:Epidemiological study of moyamoya disease in Taiwan. 940 99

Carotid artery dissection is a major cause of cerebral infarction in the young. The extracranial portion of the internal carotid artery is much more frequently involved than the intracranial portion. In up to 20% of cases it is bilateral or associated with vertebral artery dissection. It is mainly characterised by local signs such as headache or facial pain, Horner's syndrome, lower cranial nerve palsies and pulsatile tinnitus, followed a few hours or days later by signs of cerebral or retinal ischemia. Ultrasound investigations show signs of distal stenosis or occlusion, highly suggestive of dissection, but the best diagnostic tool is presently the association of magnetic resonance imaging (MRI) and MR angiography which tend to replace intra-arterial angiography. The prognosis is highly variable: excellent in cases limited to local signs, but very poor leading to death or major sequelae in about 15% of cases. Various treatments have been suggested but no controlled trial has ever been performed in this condition. Heparin in the acute stage followed by warfarin or aspirin for 3 to 6 months is most commonly used.
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PMID:Internal carotid artery dissection: an update. 951 74

Internal carotid artery involvement and dementia occur infrequently in patients with giant cell (temporal) arteritis. A 75-year-old woman admitted with progressive cognitive decline, drowsiness and headache was diagnosed as having giant cell arteritis by temporal artery biopsy (TAB). High dose corticosteroid improved inflammatory reaction but did not improve his cognitive function. Cerebral angiograms showed obstruction of both internal carotid arteries at the siphon. Brain MRI showed only small cerebral infarcts in the basal ganglia and corona radiata bilaterally. However, brain SPECT disclosed reduced cerebral blood flow in the frontal lobe bilaterally. A postmortem examination revealed bilateral parietal infarcts and isolated giant cell arteritis involving the both internal carotid arteries at the siphon. We speculated that perfusion insufficiency and multiple cerebral infarction due to bilateral internal carotid artery occlusion had caused this neurologic deterioration.
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PMID:[Giant cell arteritis with bilateral obstruction of the internal carotid artery--report of an autopsy case]. 974 80

Spontaneous dissection of the internal carotid artery is rarely submitted to surgery. We report a case successfully operated on with complete restoration of the cerebral blood flow. A 43-year-old male was admitted to our hospital 10 days after an episode of amaurosis fugax of the left eye, left sided headache and paresis of the right arm of a few hours duration. A diagnosis of dissection of the left internal carotid artery was made by duplex and triplex ultrasound examination and was confirmed by cerebral arteriography in contrast to magnetic resonance angiography which was misleading. Due to the slow arterial flow from the right to the left cerebral hemisphere through only the posterior communicating arteries we envisaged the possibility of a cerebral infarction if the dissection were to be extended. For this reason a surgical procedure was performed by excising the dissected segment and inserting a venous graft for the re-establishment of the arterial flow. Surgical treatment of spontaneous internal carotid dissection should be considered very carefully when the clinical and laboratory findings suggest the possibility of an impending stroke.
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PMID:Surgical treatment of spontaneous internal carotid dissection. 975 2

Cerebral amyloid angiopathy affects the cerebral vasculature selectively, and there is no systemic amyloidosis. Amyloid is deposited in small and medium-sized vessels of the cortex and leptomeninges. Cerebral amyloid angiopathy is a common cause of spontaneous lobar haemorrhage in elderly patients. However, cerebral amyloid angiopathy may have atypical clinical and radiological presentations. We report on five patients (three males and two females, aged 43-77 years) with histologically verified cerebral amyloid angiopathy. One patient experienced an acute headache attack and classical lobar haemorrhage. The other patients had various neurological symptoms and signs, such as seizure, disturbed vision, pareses, aphasia, and dementia that were initially diagnosed as cerebral infarction or tumour. Two patients with cerebral amyloid angiopathy and granulomatous angiitis responded to immunosuppressive treatment.
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PMID:[Cerebral amyloid angiopathy]. 976 Aug 54

The Barcelona Stroke Registry was established to collect clinical data of hospitalized patients with stroke, in order to study their clinical characteristics and outcome. Data were collected over a 17-year period in 3,577 consecutive patients with first-ever stroke admitted to a stroke unit in two university hospitals in the city of Barcelona (Catalonia, Spain). Patients were generally admitted within 48 h from stroke onset, were evaluated by a neurologist, and clinical data were collected using a standardized protocol. All subjects underwent computerized tomography (CT) examination. Data on the 3,577 patients revealed the following stroke subtypes: cerebral infarction (81%), corresponding to the varieties of atherothrombotic (39.5%), cardioembolic (17.5%), lacunar (11%), unusual (5%), or unknown (8%); and cerebral hemorrhage. We analyzed age distribution (mean age 66 years); risk factors (the most frequent being hypertension, present in 54% of cerebral infarctions and in 65% of hemorrhages); clinical manifestations (the most salient being abrupt onset in one half of the cases; high frequency of decreased consciousness in cardioembolic infarction; headache, seizures and nuclear palsy in 'unusual' cerebral infarctions; vomiting and coma in hemorrhage); localizations by vascular territories; mechanisms of the various stroke subtypes; complications (present in one third of patients, with a mortality of 14%), and outcome. Two out of 3 hospitalized stroke patients are first-ever stroke sufferers. Neuroimaging shows a cerebral infarct in 86.5% of cases. Clinical and laboratory investigations cannot determine the mechanism of 8% of infarcts and of 23% of hemorrhages. The high frequency of medical complications, mortality, and disability highlights the need to establish stroke units and stroke registries in order to perform further research into the diagnosis and management of patients with cerebrovascular disease.
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PMID:The Barcelona Stroke Registry. 1020 44

Cerebral infarction is a well-documented complication of systemic lupus erythematosus (SLE), that usually occurs several years after the diagnosis of SLE. To our knowledge, however, strokes associated with vertebrobasilar artery involvement were not reported to present as an initial manifestation of SLE. We report two patients, who presented with vertebrobasilar territory infarction as an initial manifestation of SLE. Patient 1 was a 16-year-old girl, who developed dysarthria and ataxia. MRI showed multiple infarcts in the pons, cerebellum and thalamus. Four-vessel cerebral angiography showed multifocal stenoses in the vertebral and basilar arteries with beaded appearance. Patient 2 was a 26-year-old woman, who developed headache associated with dysarthria, dizziness and ataxia. MRI showed multiple infarcts in the cerebellum, medulla, pons, midbrain and thalamus. Cerebral angiography revealed occlusion of both vertebral arteries at the first cervical vertebral level with non-visualization of the basilar artery. Both patients were diagnosed as having SLE supported by laboratory results. Although rare, posterior circulation stroke can present as an initial manifestation of SLE, which may be attributed to vasculitis or dissection in the vertebral/basilar artery.
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PMID:Vertebrobasilar artery territory infarction as an initial manifestation of systemic lupus erythematosus. 1035 Feb 8

A 49-year-old woman was admitted to our hospital because of severe headache. She had a 10-month history of migraine with aura-like headache that occurred every 7 to 10 days and was preceded by photopsia. Brain CT showed cerebral infarction of the left occipital lobe. Bilateral carotid angiograms showed vascular occlusions in the supraclinoid portion of the bilateral internal carotid arteries with telangiectatic vessels acting as collateral channels to the occluded distal carotid arteries, which were consistent with the diagnosis of moyamoya disease. Headache resolved gradually and has never developed again after the infarct of the left occipital lobe. Pathophysiological mechanisms of migraine-like headache were discussed. We conclude that borderline perfusion of occipital lobe cortex could be a trigger for the development of migraine with aura-like headache in susceptible patients. In the case of atypical attack of migraine detailed investigation should be done to detect underlying vascular diseases such as moyamoya disease.
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PMID:Migraine with aura-like headache associated with moyamoya disease. 1044 55

A case of intracerebral hemorrhage which probably had been caused by a rupture of abnormal "moyamoya vessels" due to tuberculous arteritis was reported. A 42-year-old female had a history of tuberculous meningitis at the age of 2 years and suffered from a sudden onset of severe headache in January of 1998. CT scan disclosed a medium-sized intracerebral hematoma in the left frontal base and many calcifications in the basal cistern. Subsequent angiography demonstrated high-grade stenosis in the terminal portion of the right internal carotid artery and near-by "moyamoya vessels". No surgery was performed on the patient. A second angiography was carried out two months later and it newly disclosed ophthalmic artery-feeding "moyamoya vessels" in the place where the intracerebral hematoma had been located. This led us to conclude that a rupture of "moyamoya vessels" was the cause of the intracerebral hemorrhage and "moyamoya vessels" were not visible in the first angiograms because they had been compressed by the hematoma. Although cerebral infarction is common in tuberculous arteritis, cerebral hemorrhage is uncommon. The pathogenesis of cerebral hemorrhage due to tuberculous arteritis and its difference from that of hemorrhage caused by moyamoya disease is discussed.
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PMID:[Intracerebral hemorrhage in a patient with moyamoya phenomenon caused by tuberculous arteritis: a case report]. 1045 40


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