RT Journal Article
SR Electronic
T1 Isolated Acute Nontraumatic Cortical Subarachnoid Hemorrhage
JF American Journal of Neuroradiology
JO Am. J. Neuroradiol.
FD American Society of Neuroradiology
SP 1355
OP 1362
DO 10.3174/ajnr.A1986
VO 31
IS 8
A1 V. Cuvinciuc
A1 A. Viguier
A1 L. Calviere
A1 N. Raposo
A1 V. Larrue
A1 C. Cognard
A1 F. Bonneville
YR 2010
UL http://www.ajnr.org/content/31/8/1355.abstract
AB SUMMARY: Our aim was to review the etiologic background of isolated acute nontraumatic cSAH. While SAH located in the basal cisterns originates from a ruptured aneurysm in approximately 85% of cases, a broad spectrum of vascular and even nonvascular pathologies can cause acute nontraumatic SAH along the convexity. Arteriovenous malformations or fistulas, cortical venous and/or dural sinus thrombosis, and distal and proximal arteriopathies (RCVS, vasculitides, mycotic aneurysms, Moyamoya, or severe atherosclerotic carotid disease) should be sought by noninvasive imaging methods or/and conventional angiography. Additionally, PRES may also be a source of acute cSAH. In elderly patients, cSAH might be attributed to CAA if numerous hemorrhages are demonstrated by GRE T2 images. Finally, cSAH is rarely observed in nonvascular disorders, such as abscess and primitive or secondary brain tumors. CAAcerebral amyloid angiopathycSAHcortical subarachnoid hemorrhageCTACT angiographyCTVCT venographyCVTcerebral venous thrombosisDSAdigital subtraction angiographyDWIdiffusion-weighted imagingFLAIRfluid-attenuated inversion recoveryGdgadoliniumGRE T2gradient echo T2-weighted imagingMRAMR angiographyMRVMR venographyPRESposterior reversible encephalopathy syndromeRCVSreversible cerebral vasoconstriction syndromeSAHsubarachnoid hemorrhageSWIsusceptibility-weighted imagingTIAtransient ischemic attackTOFtime of flight