scholarly journals Susceptibility-weighted imaging in familial cerebral cavernous malformations

Neurology ◽  
2008 ◽  
Vol 71 (5) ◽  
pp. 382-382 ◽  
Author(s):  
A. D. Cooper ◽  
N. G. Campeau ◽  
I. Meissner
2021 ◽  
Vol 30 (12) ◽  
pp. 106130
Author(s):  
Pablo Iruzubieta ◽  
David Campo-Caballero ◽  
Jon Equiza ◽  
Inés Albajar ◽  
Naroa Sulibarría ◽  
...  

Neurosurgery ◽  
2000 ◽  
Vol 46 (5) ◽  
pp. 1272-1279 ◽  
Author(s):  
Jun Zhang ◽  
Richard E. Clatterbuck ◽  
Daniele Rigamonti ◽  
Harry C. Dietz

Radiology ◽  
2017 ◽  
Vol 284 (2) ◽  
pp. 443-450 ◽  
Author(s):  
Corinne D. Strickland ◽  
Steven C. Eberhardt ◽  
Mary R. Bartlett ◽  
Jeffrey Nelson ◽  
Helen Kim ◽  
...  

2010 ◽  
Vol 29 (3) ◽  
pp. E5 ◽  
Author(s):  
Philipp Dammann ◽  
Markus Barth ◽  
Yuan Zhu ◽  
Stefan Maderwald ◽  
Marc Schlamann ◽  
...  

High-resolution susceptibility weighted MR imaging at high field strength provides excellent depiction of venous structures, blood products, and iron deposits, making it a promising complementary imaging modality for cerebral cavernous malformations (CCMs). Although already introduced in 1997 and being constantly improved, susceptibility weighted imaging is not yet routine in clinical neuroimaging protocols for CCMs. In this article, the authors review the recent literature dealing with clinical and scientific susceptibility weighted imaging of CCMs to summarize its prospects and drawbacks and provide their first experience with its use in ultra–high field (7-T) MR imaging.


2012 ◽  
Vol 84 (2) ◽  
pp. 194-200 ◽  
Author(s):  
Philipp Dammann ◽  
Karsten H Wrede ◽  
Stefan Maderwald ◽  
Nicolai El Hindy ◽  
Oliver Mueller ◽  
...  

2006 ◽  
Vol 21 (1) ◽  
pp. 1-5 ◽  
Author(s):  
Shervin R. Dashti ◽  
Alan Hoffer ◽  
Yin C. Hu ◽  
Warren R. Selman

✓Cerebral cavernous malformations (CMs) are angiographically occult neurovascular lesions that consist of enlarged vascular channels without intervening normal parenchyma. Cavernous malformations can occur as sporadic or auto-somal-dominant inherited conditions. Approximately 50% of Hispanic patients with cerebral CMs have the familial form, compared with 10 to 20% of Caucasian patients. There is no difference in the pathological findings or presentation in the sporadic and familial forms. To date, familial CMs have been attributed to mutations at three different loci: CCM1 on 7q21.2, CCM2 on 7p15-p13, or CCM3 on 3q25.2-q27. The authors summarize the current understanding of the molecular events underlying familial CMs.


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