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1/197. rupture mechanism of a thrombosed slow-growing giant aneurysm of the vertebral artery--case report.

    A 76-year-old male developed left hemiparesis in July 1991. The diagnosis was thrombosed giant vertebral artery aneurysm. He showed progressive symptoms and signs of brainstem compression, but refused surgery and was followed up without treatment. He died of rupture of the aneurysm and underwent autopsy in March 1995. Histological examination of the aneurysm revealed fresh clot in the aneurysmal lumen, old thrombus surrounding the aneurysmal lumen, and more recent hemorrhage between the old thrombus and the inner aneurysmal wall. The most important histological feature was the many clefts containing fresh blood clots in the old thrombus near the wall of the distal neck. These clefts were not lined with endothelial cells, and seemed to connect the lumen of the parent artery with the most peripheral fresh hemorrhage. However, the diameter of each of these clefts is apparently not large enough to transmit the blood pressure of the parent artery. Simple dissection of the aneurysmal wall by blood flow in the lumen through many clefts in the old thrombus of the distal neck may be involved in the growth and rupture of thrombosed giant aneurysms of the vertebral artery.
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2/197. Angiographical extravasation of contrast medium in hemorrhagic infarction. Case report.

    Leakage of the contrast medium was noted on angiograms of a patient whose autopsied brain disclosed typical pathological findings of hemorrhagic infarction. The case was a 63-year old woman with mitral valve failure, who suddenly had loss of consciousness and right-sided hemiplegia. The left carotid angiography performed six hours after onset demonstrated middle cerebral arterial axis occlusion, and the second angiography performed three days after onset displayed recanalization of the initially occluded artery as well as extravasation of the contrast medium. Fourteen days after onset the patient died and an autopsy was performed. The brain demonstrated perivascular punctate hemorrhages in the area supplied by the middle cerebral artery, and neither hematoma nor microaneurysm was disclosed pathologically. A short discussion is given on the possible relationship between recanalization and hemorrhagic infarction. The clinical assessment of hemorrhagic infarction has not been established successfully.
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3/197. basilar artery occlusion due to spontaneous basilar artery dissection in a child.

    basilar artery occlusion (BAO) causing brainstem infarction occurred in a 7-year-old boy without any basic disorders. A diagnosis of BAO due to basilar artery dissection (BAD) was suspected at angiography, and this was confirmed by gadolinium-enhanced magnetic resonance imaging (MRI). These investigations clearly showed all the typical diagnostic signs such as a pseudolumen, double lumen and intimal flap, and a pseudolumen in resolution. The spontaneous healing of the dissection was clearly demonstrated during 10 months of follow-up. We stress that BAD can occur in young children and that combined diagnosis with gadolinium-enhanced MRI and angiography is conclusive for diagnosis of dissecting aneurysms. Wider use of these combined diagnostic methods will allow the detection of less severe basilar artery dissection, thus extending the spectrum of presentation and prognosis.
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4/197. Fatal haemorrhagic infarct in an infant with homocystinuria.

    Thrombotic and thromboembolic complications are the main causes of morbidity and mortality in patients with homocystinuria. However, it is unusual for thrombosis and infarction to be the presenting feature leading to investigation for homocystinuria and cerebrovascular lesions in the first year of life. We describe a previously healthy 6-month-old infant who presented with a large middle-cerebral-artery territory infarction and died of massive brain swelling. homocystinuria due to cystathionine beta-synthase (CBS) deficiency was diagnosed by metabolite analysis and confirmed by enzymatic activity measurement in a postmortem liver biopsy. homocystinuria should be considered in the differential diagnosis of venous or arterial thrombosis, regardless of age, even in the absence of other common features of the disease. We recommend systematic metabolic screening for hyperhomocysteinemia in any child presenting with vascular lesions or premature thromboembolism.
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5/197. Cerebellar infarct caused by spontaneous thrombosis of a developmental venous anomaly of the posterior fossa.

    Spontaneous thrombosis of a posterior fossa developmental venous anomaly (DVA) caused a nonhemorrhagic cerebellar infarct in a 31-year-old man who also harbored a midbrain cavernous angioma. DVA thrombosis was well depicted on CT and MR studies and was proved at angiography by the demonstration of an endoluminal clot.
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6/197. Cerebral and renal embolization after lymphography in a patient with non-Hodgkin lymphoma: case report.

    An unusual case of lipid embolization to brain and kidney after lymphography in a patient with non-Hodgkin lymphoma of the upper anterior mediastinum is reported. Contrast material-enhanced echocardiography demonstrated a right-to-left shunt to the left atrium without evidence of a patent foramen ovale. Echo contrast particles were transiently present within the tumor surrounding the great vessels.
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7/197. diffusion- and perfusion-weighted magnetic resonance imaging in deep cerebral venous thrombosis.

    BACKGROUND: diffusion-weighted (DWI) and perfusion-weighted (PI) MRI are highly sensitive techniques for early diagnosis of arterial infarction, but little data on venous cerebral ischemia are available. We describe a case in which DWI, PI, and fast T2-weighted sequences were performed in the acute phase of deep cerebral venous thrombosis (CVT). CASE DESCRIPTION: An 11-year-old girl with Crohn's disease developed deep CVT in which extensive edema was shown in the deep gray matter on T2-weighted sequence images. Isotropic echo-planar DWI demonstrated a local augmentation of the apparent diffusion coefficient (1.1 to 1.6x10(-3) mm2/s), consistent with vasogenic edema. In dynamic contrast-enhanced PI, the regional cerebral blood volume was increased and the passage time of the contrast bolus was markedly prolonged. Clinically, the patient recovered totally after intravenous full-dose heparinization. T2 abnormalities, apparent diffusion coefficient values (0.8 to 0.92x10(-3) mm2/s), and brain perfusion alterations resolved without damage to brain tissue. CONCLUSIONS: Unlike arterial infarction, DWI demonstrated vasogenic edema in a patient with deep CVT, which proved to be reversible in follow-up magnetic resonance imaging. PI showed areas with extensive venous congestion, but perfusion deficits were missing. Therefore, we believe that DWI and PI may play a role in detecting venous congestion in CVT and in prospective differentiation of vasogenic edema and venous infarction.
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8/197. Cerebral arterial gas embolism in air force ground maintenance crew--a report of two cases.

    Two cases of cerebral arterial gas embolism (CAGE) occurred after a decompression incident involving five maintenance crew during a cabin leakage system test of a Hercules C-130 aircraft. During the incident, the cabin pressure increased to 8 in Hg (203.2 mm Hg, 27 kPa) above atmospheric pressure causing intense pain in the ears of all the crew inside. The system was rapidly depressurized to ground level. After the incident, one of the crew reported chest discomfort and fatigue. The next morning, he developed a sensation of numbness in the left hand, with persistence of the earlier symptoms. A second crewmember, who only experienced earache and heaviness in the head after the incident, developed retrosternal chest discomfort, restlessness, fatigue and numbness in his left hand the next morning. Both were subsequently referred to a recompression facility 4 d after the incident. Examination by the diving Medical Officer on duty recorded left-sided hemianesthesia and Grade II middle ear barotrauma as the only abnormalities in both cases. Chest x-rays did not reveal any extra-alveolar gas. Diagnoses of Static Neurological decompression Illness were made and both patients recompressed on a RN 62 table. The first case recovered fully after two treatments, and the second case after one treatment. magnetic resonance imaging (MRI) of the brain and bubble contrast echocardiography performed on the first case 6 mo after the incident were reported to be normal. The second case was lost to follow-up. decompression illness (DCI) generally occurs in occupational groups such as compressed air workers, divers, aviators, and astronauts. This is believed to be the first report of DCI occurring among aircraft's ground maintenance crew.
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9/197. Aggravation of brainstem symptoms caused by a large superior cerebellar artery aneurysm after embolization by Guglielmi detachable coils--case report.

    An 81-year-old male presented with right oculomotor nerve paresis and left hemiparesis caused by a mass effect of a large superior cerebellar artery aneurysm. Endovascular treatment was performed using Guglielmi detachable coils. The patient subsequently suffered aggravation of the mass effect 3 weeks after the embolization. Bilateral vertebral artery occlusion was performed, which decreased the cerebral edema surrounding the aneurysm, but his neurological symptoms did not improve. Parent artery occlusion is recommended as the first choice of treatment for an unclippable large or giant aneurysm causing a mass effect on the brainstem.
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10/197. "Pure word deafness": implications for assessment and management in communication disorder--a report of two cases.

    In "pure word deafness" after acquired brain injury, the auditory comprehension of words is much more impaired than other aspects of communication or cognition. Two cases are presented, one early and one late presentation. The key to diagnosis of communication disorders is to remember to assess all six basic aspects of language function and to be vigilant for coexisting diagnoses that can complicate such assessment (especially psychiatric diagnoses). rehabilitation management of impaired communication should emphasize the teaching of specific coping mechanisms to the patient and to all others who are involved.
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