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Cerebral Emboli (cerebral + emboli)
Selected AbstractsRoutine Transesophageal Echocardiography for the Evaluation of Cerebral Emboli in Elderly PatientsECHOCARDIOGRAPHY, Issue 9 2005Sergey Vitebskiy M.D. Background: Approximately 20% of cerebral infarctions are cardioembolic in nature. Transesophageal echocardiography (TEE) is widely regarded as the initial study of choice for evaluating cardiac source of embolism. Although the majority of cerebrovascular accidents occur in elderly patients, the value of TEE in this population is poorly defined. Methods: We compared 491 patients older than 65 years with suspected embolic stroke or transient ischemic attack (TIA) who had undergone TEE evaluation between April 2000 and February 2004 to an age-, sex-, and time-matched control group that consisted of 252 patients. Studies were reviewed for abnormalities associated with thromboembolic disease. Results: The overall incidence of stroke risk factors was significantly higher in the study than in the control group. However, the four patients with left atrial thrombi had a history of atrial fibrillation. Although ascending and aortic arch sessile atheromata were observed more frequently in the study than control group, there were no significant differences in the incidence of either complex or mobile aortic atheromata. The incidence of atrial septal aneurysm was higher in the stroke/TIA group, but not in association with patent foramen ovale. Finally, there were also no differences in the incidence of spontaneous echocontrast, and/or patent foramen ovale between study and control groups. Conclusions: We conclude: (1) There is a higher incidence of abnormalities implicated as sources of thromboembolic disease on TEE in elderly patients with cerebral infarctions, but (2) this incidence is driven by the presence of sessile aortic atheroma and atrial septal aneurysm. Until the benefits of specific therapies for these conditions are known, routine TEE in elderly patients with suspected embolic neurological events appears to be unwarranted. [source] Cerebral emboli and paradoxical embolisation in dementia: a pilot studyINTERNATIONAL JOURNAL OF GERIATRIC PSYCHIATRY, Issue 1 2005Nitin Purandare Abstract Background The causes of the common dementias remain unknown. Paradoxical embolisation of the cerebral circulation by venous thrombi passing through venous to arterial shunts (v-aCS) in the heart or pulmonary circulation is known to occur in cryptogenic stroke and post-operative confusion following hip replacement. Objectives To explore the role of paradoxical embolisation in dementia by investigating for cerebral emboli, venous to arterial circulation shunt (v-aCS) and carotid artery disease. Methods Forty-one patients with dementia (24 Alzheimer's AD and 17 vascular VaD) diagnosed using DSM-IV criteria and 16 controls underwent transcranial Doppler (TCD) detection of spontaneous cerebral emboli in both middle cerebral arteries. A v-aCS was detected by intravenous injection of an air/saline ultrasound contrast at rest and after provocation by coughing and Valsalva's manoeuvre. Carotid artery disease was assessed by duplex imaging. Results Cerebral emboli were detected in 11 (27.5%) dementia patients compared with one (7%) control (p,=,0.15) with emboli being most frequent in VaD (41%) compared to controls [OR (95% CI): 10.5 (1.1, 98.9), p,=,0.04]. A v-aCS was detected in 25 (61%) patients and seven (44%) controls (p,=,0.24). In dementia patients with cerebral emboli; v-aCS was detected in seven (64%) and moderate to severe carotid stenosis was present in three (30%). Conclusion Cerebral emboli and v-aCS may be more frequent in patients with both VaD and AD than in controls, which suggest paradoxical embolisation as a potential mechanism for cerebral damage. This pilot study justifies a definitive case-control study. Copyright © 2004 John Wiley & Sons, Ltd. [source] Microemboli may link spreading depression, migraine aura, and patent foramen ovaleANNALS OF NEUROLOGY, Issue 2 2010Ala Nozari MD Objective Patent foramen ovale and pulmonary arteriovenous shunts are associated with serious complications such as cerebral emboli, stroke, and migraine with aura. The pathophysiological mechanisms that link these conditions are unknown. We aimed to establish a mechanism linking microembolization to migraine aura in an experimental animal model. Methods We introduced particulate or air microemboli into the carotid circulation in mice to determine whether transient microvascular occlusion, insufficient to cause infarcts, triggered cortical spreading depression (CSD), a propagating slow depolarization that underlies migraine aura. Results Air microemboli reliably triggered CSD without causing infarction. Polystyrene microspheres (10,m) or cholesterol crystals (<70,m) triggered CSD in 16 of 28 mice, with 60% of the mice (40% of those with CSD) showing no infarcts or inflammation on detailed histological analysis of serial brain sections. No evidence of injury was detected on magnetic resonance imaging examination (9.4T; T2 weighted) in 14 of 15 selected animals. The occurrence of CSD appeared to be related to the magnitude and duration of flow reduction, with a triggering mechanism that depended on decreased brain perfusion but not sustained tissue damage. Interpretation In a mouse model, microemboli triggered CSD, often without causing microinfarction. Paradoxical embolization then may link cardiac and extracardiac right-to-left shunts to migraine aura. If translatable to humans, a subset of migraine auras may belong to a spectrum of hypoperfusion disorders along with transient ischemic attacks and silent infarcts. ANN NEUROL 2010;67:221,229 [source] |