23 research outputs found

    Small Vessel Disease and Subcortical Vascular Dementia

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    Atherothromboembolism and intracranial small vessel disease are considered to be the main causes of cerebrovascular injury, which may lead to cognitive impairment and vascular dementia (VaD). VaD appears to be the second most common type of dementia with prevalence estimates of 10-15%. Cortical or multi-infarct dementia and subcortical vascular dementia (SVD) are suggested to be the two main forms of VaD. The main clinical features of SVD comprise decreased motor performance, early impairment of attention and executive function with slowing of information processing. SVD results from lacunar infarcts or multiple microinfarcts in the basal ganglia, thalamus, brainstem and white matter and are associated with more than 50% of the VaD cases. White matter changes including regions of incomplete infarction are usually widespread in VaD but their contribution to impairment of subcortical regions is unclear. While most of VaD occurs sporadically only a small proportion of cases bear clear familial traits. CADASIL is likely the most common form of hereditary VaD, which arises from subcortical arteriopathy. SVD needs unambiguous definition to impact on preventative and treatment strategies, and critical for selective recruitment to clinical trials

    Acoustic neuroma with malignant transformation

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    Expanding Lacunae Causing Triventricular Hydrocephalus

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    A New Three-Dimensional Echocardiography Method to Quantify Aortic Valve Calcification

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    Background: Aortic valve calcification (AVC) quantification is computed from multidetector computed tomography (MDCT). The aim of this study was to test the hypothesis that three-dimensional (3D) transthoracic echocardiography can be used to provide a bedside method to assess AVC. Methods: The study included 94 patients (mean age, 78 ± 12 years; mean aortic valve [AV] area, 1.0 ± 0.6 cm2) referred for MDCT and echocardiography for AV assessment. Apical 3D full-volume data sets focused on the AV region were acquired during transthoracic echocardiography, and a region-growing algorithm was applied offline to compute 3D transthoracic echocardiographic AVC (AVC-3DEcho). AVC-3DEcho was compared with AVC by MDCT and with calcium weight in the subgroup of patients referred for surgery, with explanted AVs analyzed by a pathologist (n = 22). Results: In the explanted valve group, AVC-3DEcho score exhibited fair correlations with MDCT score (r = 0.85, P <.001), calcium load (r = 0.81, P <.001), and peak AV velocity (r = 0.64, P <.001). In the overall population, AVC-3DEcho score correlated modestly with MDCT score (r = 0.61, P <.001) but had similar accuracy to identify severe aortic stenosis (area under the curve = 0.94). AVC-3DEcho > 1,054 mm3 identified severe aortic stenosis with specificity of 100% and sensitivity of 76%. In addition, AVC-3DEcho was associated with the presence of significant paravalvular regurgitation after transcatheter aortic valve implantation. Finally, intraobserver and interobserver variability for AVC-3DEcho score was 4.2% and 8.9%, respectively. Conclusions: AVC-3DEcho correlated with calcium weight obtained from pathologic analysis and MDCT. These data suggest that a bedside method for quantifying AV calcification with ultrasound is feasible
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