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Query: UMLS:C0917798 (cerebral ischemia)
 17,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

On the basis of 100 patients operated during the last ten years at the Neurosurgical University Clinic of Zurich the experiences with the extra-intracranial bypass anastomosis for stroke patients are examined. The risks of this surgery are low (morbidity 2%, mortality 3%) and the patency rate is high (94.3%). The main purpose of this intervention is to prevent or minimize further strokes. This risk was decreased from 40% of non operated cases in the literature to 4.2% in this series. Severe neurological deficits are not improved by surgery. The procedure is therefore indicated for mild forms of cerebral ischemia (TIA's and mild strokes), when the disease is caused by an appropriate obstruction of the internal carotid artery and/or middle cerebral artery which are inaccessible to surgery of the neck. For this latter reason preoperative carotid angiography is mandatory. To avoid unnecessary angiography, the carotid Doppler ultrasound test and dynamic brain scanning are valuable, non invasive screening methods for indicating angiography in eah individual case.
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PMID:[Improvement in brain circulation by microsurgical bypass anastomoses]. 742 6

Patent foramen ovale (PFO) and atrial septal aneurysm (ASA) have been identified as potential risk factors for stroke, but information about the risk of recurrent cerebral ischemia is scarce. The aim of this retrospective study was to assess the absolute risk of recurrent cerebrovascular events in 132 patients under 60 years of age with patent foramen ovale, atrial septal aneurysm (diagnosed by transesophageal echocardiography with a contrast study), or both and an otherwise unexplained stroke or transient ischemic attack (TIA). During a mean follow-up of 22.6 +/- 16 months, six patients had a recurrent stroke (n = 2) or a TIA (n = 4). No systemic embolism was observed. The actuarial risk of having a recurrent stroke was 2.3% (95% confidence interval, 0.6% to 8.2%) at 2 years, whereas the risk of having a stroke or a TIA was 6.7% (95% confidence interval, 3.1% to 14.2%) at 2 years. The average annual rates of recurrence were 1.2% and 3.4%, respectively. In patients with both PFO and ASA, the actuarial risk of a first recurrent stroke was 9.0% (95% confidence interval, 2.4% to 28.5%) at 2 years, with an average annual rate of recurrence of 4.4%. As a group, patients with patent foramen ovale, atrial septal aneurysm, or both and an otherwise unexplained stroke or TIA appear to have a low risk of recurrent stroke whatever the prophylactic antithrombotic therapy used. The association of ASA and PFO may be an indicator of a higher risk of recurrent stroke.
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PMID:Recurrent cerebrovascular events in patients with patent foramen ovale, atrial septal aneurysm, or both and cryptogenic stroke or transient ischemic attack. French Study Group on Patent Foramen Ovale and Atrial Septal Aneurysm. 748 40

Anticardiolipin antibodies (ACL-A) are acquired antiphospholipid antibodies characteristically found in patients with systemic lupus erythematosus or related autoimmune diseases. Several reports have shown that there may be an association between ACL-A and various neurological disorders, in particular cerebral ischemia. Using a micropin enzyme linked immunosorbent assay we measured the levels of ACL-A in the sera of 225 unselected patients with various neurological disorders. The prevalence of ACL-A in the whole group was 4.0% (9/225). However, the prevalence in patients with ischemic cerebrovascular disorders was 9.1% (5/55). With one exception (thrombocytopenia was found more often in ACL-A-positive cases) there was no difference with respect to the prevalence of risk factors for stroke and associated diseases between ACL-A-positive and ACL-A-negative patients with TIA/stroke. High titers of ACL-A were also found in a few patients with epilepsy (n = 2), migraine (n = 1), and intracranial meningioma (n = 1). In patients with ischemic cerebrovascular disorders search for ACL-A may help to identify patients with a possibly higher risk of thrombosis.
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PMID:Anticardiolipin-antibodies in stroke and in other neurological disorders. 754 77

Transient ischaemic attacks (TIA) are defined by the focal and sudden loss of a cerebral function or the vision of one eye, resolving without sequelae within 24 hours and related to a vascular cause, thromboembolic much more frequently than haemodynamic. TIA represent between 9% and 25% of all cerebrovascular accident (CVA) with a variable global incidence from one study to another, between 0.2 and 3.3/1,000/year. The natural history of TIA is characterized by an excess mortality and an increased risk of cerebral infarction and myocardial infarction. It is therefore essential to recognize these events in order to prescribe effective preventive treatment. The clinical picture is characterized by a usually brief focal deficit (2 to 30 min, on average) and a normal clinical examination. The diagnosis is therefore exclusively based on the clinical interview. Complementary investigations have a dual objective: 1) to eliminate other diseases likely to cause transient neurological manifestations, and 2) to detect the mechanism and cause of cerebral ischaemia; the commonest causes are atheromatous stenosis and emboligenic heart disease. In addition to the routine laboratory examinations, basic complementary investigations consist of cerebral CT scan, cervical ultrasound and echocardiography. Conventional angiography is performed less and less frequently due to the progress in ultrasound and vascular imaging (helicoidal CT scan and magnetic resonance angiography). The treatment of TIA is designed to prevent cerebral and myocardial infarction, and to decrease the cardiovascular mortality [2]. In the short-term, it is essentially based on heparin, while waiting for the results of the aetiological assessment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Transient cerebral ischemic complications. The neurologist's point of view]. 763 3

Several studies reported that the annual incidence of stroke in patients with sick sinus syndrome ranges from 6 to 10% while the incidence of stroke in patients with atrial fibrillation is about 2-4% and about 0.1% in the normal population. We evaluated the prevalence of cerebral ischemia and peripheral embolism and investigated the predictor factors in a population of 80 patients paced for sick sinus syndrome. The implanted pacemakers were 40 ventricular and 40 physiological stimulation mode was based on the physicians judgement. All patients had cerebral computed tomography scan at the time of implant and after 24 months. Statistical analysis included log-rank test and actuarial curve calculated with Mantel-Haenszel method. At the end of follow-up the end-point occurred in 15 patients: 2 patients had asymptomatic cerebral infarction, 2 had fatal stroke, 2 developed peripheral embolysm, 1 to the lower limb and 1 abdominal; in 4 patients a transient ischemic attack occurred, in 2 a minor stroke and in 3 a non invalidant stroke. No statistically significant difference was found among the subgroups; with different pacing modality. In conclusion, multivariate analysis underlines the role of age > 65 years, history of cerebral ischemia, low atrial ejection force and spontaneous echo contrast in the development of embolic episodes.
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PMID:[Stroke in pacemaker users for sinus node disease. Relevance of atrial function and clinical characteristics]. 767 Dec 76

Referral-based studies suggest that patients with cerebral ischemia and mitral valve prolapse are prone to recurrent cerebral ischemic events. Our purpose was to determine the risk of subsequent stroke in a population-based group of patients with ischemic stroke or TIA and mitral valve prolapse. From 1975 through 1990, 49 residents of Olmsted County, MN, had an initial ischemic stroke or TIA and echocardiographically diagnosed mitral valve prolapse. Risk of subsequent stroke in this cohort was compared with the age- and sex-adjusted rates of recurrent stroke after initial cerebral ischemia in the Rochester, MN, population. Mean age of the patients was 72 years. Thirty-one (63%) were women. Nine had subsequent stroke (5.5 per 100 person-years). For Rochester patients who had initial ischemic stroke in the period 1975 through 1984, 10.72 recurrent strokes were expected (relative risk, 0.84; 95% confidence limits, 0.38 to 1.59). For Rochester patients with initial ischemic stroke or TIA in the period 1975 through 1979, 12.31 recurrent strokes were expected (relative risk, 0.73; 95% confidence limits, 0.33 to 1.39). There is no evidence of increased subsequent stroke risk among patients with initial episodes of cerebral ischemia and mitral valve prolapse relative to the age- and sex-adjusted recurrent stroke rates in the community.
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PMID:Mitral valve prolapse and the risk of stroke after initial cerebral ischemia. 778 67

First symptoms and initial clinical, ultrasonographic and neuroradiological findings ascertained a mean of 5.6 days (SD = 5.6 days), 7.7 days (7.0), and 11.2 days (8.0) after symptom onset were analysed in 44 patients who suffered a spontaneous internal carotid artery dissection (ICD) verified by magnetic resonance imaging, angiography, or both. Common symptoms signalling dissection were unilateral headache in 68%, transient ischaemic attack in 20%, and cerebral infarction in 9%. Severe pain preceded cerebral ischaemia by more than 3 days in 60% of those patients who eventually suffered a stroke. However, only 2 were admitted because of pain alone and 33 for evolving neurological deficits. During the first month, ipsilateral severe headache occurred in 89%, neck pain in 36%, ipsilateral cerebral ischaemia in 82%, ocular ischaemia in 16%, oculosympathetic palsy in 48%, and cranial nerve palsy in 5%. Recent "trivial" head or neck trauma was elicited in 41%. Doppler and duplex sonography confirmed the clinical suspicion of ICD in 91.5% and in 96% of those with a significant stenosis or occlusion. MRI demonstrated a thickened vessel wall in all 33 imaged carotid dissections and a mural haematoma in 30. None of the 32 patients who received anticoagulant treatment subsequently deteriorated. Monitoring anticoagulant treatment with ultrasonographic follow-up studies demonstrated recanalization in 70% and persistent occlusion in 30%. The results demonstrate that familiarity with the initial symptoms, especially headache, and performance of an ultrasonographic study without delay are the cornerstones of an early diagnosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Spontaneous internal carotid artery dissection: early diagnosis and management in 44 patients. 779 22

Immunohistochemical changes of heat shock protein 70 (HSP 70) and glial fibrillary acidic protein (GFAP) were investigated in the gerbil hippocampus 1 h-7 days after 10 min of cerebral ischemia. Transient cerebral ischemia caused HSP 70 expression in GFAP-positive astrocytes in a delayed fashion, as compared with a rapid induction in vulnerable neurons such as hilar neurons. The present results may offer clues to elucidate the mechanisms of ischemic neuronal damage.
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PMID:Induction of heat shock protein 70 and glial fibrillary acidic protein in the postischemic gerbil hippocampus. 789 3

Establishing the cause of a transient ischemic attack (TIA) or minor stroke enables you to institute effective therapy to prevent major stroke. Clinical and radiologic features that help to clarify the cause of cerebrovascular ischemia include characteristics of prior TIAs, temporal progression and nature of the neurologic deficit, and appearance of infarction on CT and MRI of the brain. Carotid and transcranial Doppler ultrasound, magnetic resonance angiography, arterial angiography, and echocardiography are used to confirm the cause of cerebral ischemia. We provide three case studies to illustrate our approach to stroke diagnosis.
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PMID:Ischemic stroke and TIA: clinical clues to common causes. 791 76

Atrial septal aneurysms (ASA) are frequent findings on transesophageal echocardiographies. Whether they are more frequent in patients with cerebral ischemia of unknown cause remains unclear. We investigated this question in 154 consecutive patients with an ischemic stroke or transient ischemic attack. The 16 patients with ASA were younger, less likely to have arterial hypertension and more likely to have a patent foramen ovale (PFO) or an unknown cause of stroke, but they did not differ for number and side of infarcts, other demographic data and vascular risk factors. Patients with ASA unassociated to PFO were also more likely to have an unknown cause of stroke. These findings lead to the hypothesis that ASA might be sources of cerebral emboli.
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PMID:Higher prevalence of atrial septal aneurysms in patients with ischemic stroke of unknown cause. 803 Apr 3


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