You are seeing this message because your Web browser does not support basic Web standards. Find out more about why this message is appearing and what you can do to make your experience on this site better.


Advertisement

ABOUT ARCHIVES
Advanced Search

Welcome   | My Account | E-mail Alerts | RSS | Access Rights | Sign In


  Vol. 47 No. 6, June 1990 TABLE OF CONTENTS
  Online Only
 •  Online First Table of
Contents
  ORIGINAL CONTRIBUTIONS
 •Online Features
 This Article
 •References
 •Full text PDF
 • Reply to article
 •Send to a friend
 • Save in My Folder
 •Save to citation manager
 •Permissions
 Citing Articles
 •Citation map
 •Citing articles on HighWire
 •Citing articles on Web of Science (67)
 •Contact me when this article is cited
 Related Content
 •Similar articles in this journal
 Social Bookmarking
  Add to CiteULike Add to Connotea Add to Delicious Add to Digg Add to Facebook Add to Reddit Add to Technorati Add to Twitter What's this?

Hereditary Cerebral Hemorrhage With Amyloidosis-Dutch Type

Clinical and Computed Tomographic Analysis of 24 Cases

Joost Haan, MD; Paul R. Algra, MD; Raymund A. C. Roos, MD

Arch Neurol. 1990;47(6):649-653.


Abstract



• Clinical and computed tomographic findings in 24 patients with hereditary cerebral hemorrhage with amyloidosis-Dutch type were reviewed. The common initial symptoms were headache and vomiting. Computed tomographic scans showed 50 hypodense and 49 hyperdense cortical lesions and in 20 patients the scans also showed generalized white matter hypodensity. Impairment of consciousness was related to the size of the hemorrhagic lesion. Dementia, seen in 11 patients, was related to the duration of the disease and the number of focal lesions on the computed tomographic scans, but not to the presence of white matter hypodensity. It is concluded that in hereditary cerebral hemorrhage with amyloidosis-Dutch type, lobar hemorrhages account predominantly for the acute clinical syndromes. The hemorrhages often have an irregular shape and are responsible for progression of the symptoms after an acute onset. Furthermore, cerebral amyloid angiopathy leads to a generalized abnormality of the white matter, probably due to chronic hypoper-fusion.



Author Affiliations



From the Departments of Neurology (Drs Haan and Roos) and Neuroradiology (Dr Algra), University Hospital, Leiden, the Netherlands.


Footnotes



Accepted for publication September 29, 1989.

Reprint requests to the Department of Neurology, University Hospital, PO Box 9600, 2300 RC Leiden, the Netherlands (Dr Haan).



Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Delicious Delicious   Add to Digg Digg   Add to Facebook Facebook   Add to Reddit Reddit   Add to Technorati Technorati   Add to Twitter Twitter     What's this?

THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES

Hypoperfusion and Ischemia in Cerebral Amyloid Angiopathy Documented by 99mTc-ECD Brain Perfusion SPECT
Chung et al.
JNM 2009;50:1969-1974.
ABSTRACT | FULL TEXT  

Descriptive Analysis of the Boston Criteria Applied to a Dutch-Type Cerebral Amyloid Angiopathy Population
van Rooden et al.
Stroke 2009;40:3022-3027.
ABSTRACT | FULL TEXT  

Progression of white matter lesions and hemorrhages in cerebral amyloid angiopathy.
Chen et al.
Neurology 2006;67:83-87.
ABSTRACT | FULL TEXT  

Evidence for a separate type of migraine with aura: Sporadic hemiplegic migraine
Thomsen et al.
Neurology 2003;60:595-601.
ABSTRACT | FULL TEXT  

Familial British dementia with amyloid angiopathy: Early clinical, neuropsychological and imaging findings
Mead et al.
Brain 2000;123:975-991.
ABSTRACT | FULL TEXT  

Microvasculopathy Is Associated With the Number of Cerebrovascular Lesions in Hereditary Cerebral Hemorrhage With Amyloidosis, Dutch Type
Natte et al.
Stroke 1998;29:1588-1594.
ABSTRACT | FULL TEXT  

White Matter Lesions and Cognitive Deterioration in Presymptomatic Carriers of the Amyloid Precursor Protein Gene Codon 693 Mutation
Bornebroek et al.
Arch Neurol 1996;53:43-48.
ABSTRACT  

Cerebral Hemorrhage With Biopsy-Proved Amyloid Angiopathy
Yong et al.
Arch Neurol 1992;49:51-58.
ABSTRACT  





HOME | CURRENT ISSUE | PAST ISSUES | TOPIC COLLECTIONS | CME | PHYSICIAN JOBS | SUBMIT | SUBSCRIBE | HELP
CONDITIONS OF USE | PRIVACY POLICY | CONTACT US | SITE MAP
 
© 1990 American Medical Association. All Rights Reserved.