Register for email alerts and news feeds:
This journal | BMJ Group
rss
Journal of Neurology, Neurosurgery, and Psychiatry 2004;75:175-178; doi:10.1136/jnnp.2003.025569
Copyright © 2004 by the BMJ Publishing Group Ltd.
Journal of Neurology Neurosurgery and Psychiatry 2004;75:175-178
© 2004 BMJ Publishing Group Ltd

EDITORIAL

Cortical lewy body disease

Cortical Lewy body disease

D J Burn

Correspondence to:
Correspondence to:
Dr David J Burn
Department of Neurology, Regional Neurosciences Centre, Newcastle General Hospital, University of Newcastle upon Tyne NE4 6BE, UK; djburn@ncl.ac.uk


Cortical Lewy body disease reflects the presence of cortical Lewy bodies but without a clear clinical correlation

Keywords: Lewy body; dementia; Parkinson’s disease

Abbreviations: CERAD, consortium to establish a registry for Alzheimer’s disease; CLB, cortical Lewy bodies; DLB, dementia with Lewy bodies; NFT, neurofibrillary tangle; NIA, National Institute on Aging; PDD, Parkinson’s disease with dementia

The first 150 words of the full text of this article appear below.

Cortical Lewy body disease is a pathological observation rather than a distinct clinicopathological entity. Cortical Lewy bodies (CLB) are typically found in Parkinson’s disease and dementia with Lewy bodies (DLB), although they may also occur in other neurological disorders. Unlike their brain stem counterparts, CLB are less distinctive and are poorly visualised using conventional histochemical methods. The protein {alpha}-synuclein is the main component of Lewy bodies and the related dystrophic Lewy neurites1; immunohistochemistry using antibodies raised against this protein has greater sensitivity in demonstrating Lewy pathology within the cerebral cortex than histochemical methods and anti-ubiquitin immunohistochemistry.

Dementia is a common occurrence in Parkinson’s disease, with a prevalence of 20–40% in cross sectional studies,2,3 but a cumulative incidence approaching 80%.4 The clinical phenotype of this dementia shares many features with DLB. In neither condition, however, has the relation between the presence of CLB and the dementing . . . [Full text of this article]


Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati    What's this?

This article has been cited by other articles:

  • Kramer, M. L., Schulz-Schaeffer, W. J. (2007). Presynaptic {alpha}-Synuclein Aggregates, Not Lewy Bodies, Cause Neurodegeneration in Dementia with Lewy Bodies. J. Neurosci. 27: 1405-1410 [Abstract] [Full Text]  

This Article

Services
Citing Articles
Google Scholar
PubMed
Bookmark with

Register for free content

The full back archive is now available for all BMJ Journals. Institutional subscribers may access the entire archive as part of their subscription. Personal subscribers will also have access to all content when logged in. Non-subscribers who register have free access to all articles published before 2006 right back to volume 1 issue 1. Register here to access the free archive of all BMJ Journals.

Don't forget to sign up for content alerts so you keep up to date with all the articles as they are published.

BMJ Careers - Latest neurology and neurosurgery jobs

Neurology and neurosurgery jobs