This is particularly important when the recommended agent is a new and/or infrequently employed drug.ĭisclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher.ĭrug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. Callosal atrophy was correlated with dementia severity in patients with AD but not PDD.Ĭopyright: All rights reserved. We conclude that PD and PDD patients do not have callosal atrophy in contrast to other neurodegenerative diseases, including AD. Dementia severity was correlated with total callosal atrophy in AD (R = 0.66, p 0.1). The AD patients had a significant loss of callosal area compared to controls (d = –0.58, –1.01 to –0.15). We found that PD and PDD patients did not show statistically significant callosal atrophy compared to controls (effect size d, 95% CI, d = 0.13, –0.26 to 0.52, and d = 0.05, –0.44 to 0.33, respectively) or AD. The meta-analysis combined results from all publications (Medline or PubMed) representing unique samples and measuring callosal area in AD, FTD, PSP, and CBD. For the imaging study, midsagittal T 1-weighted MRIs were analyzed and the callosal area was determined in patients with PD (n = 24), PDD (n = 25), AD (n = 16) and controls (n = 27). We subsequently compared our results to a meta-analysis of studies examining callosal area in AD, frontotemporal dementia (FTD), progressive supranuclear palsy (PSP), and corticobasal degeneration (CBD). We compared callosal area in patients with PD and PD with dementia (PDD) to healthy controls and patients with Alzheimer’s disease (AD). Corpus callosum area has been examined in neurodegenerative diseases as a marker for cortical pathology and for differential diagnosis however, it has not been examined in Parkinson’s disease (PD).
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