![]() Prostate cancer: diagnosis, parametric imaging and standardized report.ĭiagn Interv Imaging.Understanding Your Pathology Report: Prostate Cancer.PI-RADS Prostate Imaging – Reporting and Data System: 2015, Version 2.Prostate Imaging Reporting & Data System - PI-RADS 2015 version2 (full text document).In case of multiple suspicious findings, the index lesion is the lesion with the highest PI-RADS assessment category. Prior biopsies (quantity, location, Gleason score).Reporting is done according to the checklist as shown in the table.īefore we start the interpretation of the MRI, we need to be informed about: Since then, this classification system has been revised and simplified in 2015 and is still evolving, based on data analysis of multiparametric prostate MRI. The introduction of the Prostate Imaging Reporting and Data System (PI-RADS) classification for prostate MRI in 2012 lead to a more standardized acquisition, interpretation and reporting of prostate MRI. Multiparametric MRI is a combination of T2-weighted, Diffusion and dynamic contrast-enhanced imaging and is an accurate tool in the detection of clinically significant prostate cancer. MRI of the prostate has become increasingly popular with the use of multiparametric MRI and the PI-RADS classification. How to Differentiate Carotid Obstructions.TI-RADS - Thyroid Imaging Reporting and Data System.Esophagus II: Strictures, Acute syndromes, Neoplasms and Vascular impressions.Esophagus I: anatomy, rings, inflammation.Vascular Anomalies of Aorta, Pulmonary and Systemic vessels.Contrast-enhanced MRA of peripheral vessels.Ischemic and non-ischemic cardiomyopathy.Coronary Artery Disease-Reporting and Data System 2.0.Bi-RADS for Mammography and Ultrasound 2013.Transvaginal Ultrasound for Non-Gynaecological Conditions.Acute Abdomen in Gynaecology - Ultrasound.Appendicitis - Pitfalls in US and CT diagnosis.We conclude that it will be difficult to understand AD without understanding why it preferably affects older brains, and that we need a model that accounts for age-related changes in AD-vulnerable regions independently of AD-pathology.Īlzheimer's disease (AD) Amyloid Cerebral cortex Default mode network (DMN) Hippocampus Normal aging.Ĭopyright © 2014 Elsevier Ltd. We suggest that regions characterized by a high degree of life-long plasticity are vulnerable to detrimental effects of normal aging, and that this age-vulnerability renders them more susceptible to additional, pathological AD-related changes. Thus, rather than necessarily reflecting early signs of disease, these changes may be part of normal aging, and may inform on why the aging brain is so much more susceptible to AD than is the younger brain. This normalcy-pathology homology is critical to understand, since aging itself is the major risk factor for sporadic AD. ![]() Importantly, these regions show high levels of amyloid deposition in AD, and are both structurally and functionally vulnerable early in the disease. We argue that prominent cortical reductions are evident in fronto-temporal regions in elderly even with low probability of AD, including regions overlapping the default mode network. We review recent research on changes of the cerebral cortex and the hippocampus in aging and the borders between normal aging and AD. What can be expected in normal aging, and where does normal aging stop and pathological neurodegeneration begin? With the slow progression of age-related dementias such as Alzheimer's disease (AD), it is difficult to distinguish age-related changes from effects of undetected disease. ![]()
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