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000164283 0247_ $$2doi$$a10.1016/j.jns.2020.117173
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000164283 037__ $$aDZNE-2022-00937
000164283 041__ $$aEnglish
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000164283 1001_ $$aScheumann, Vincent$$b0
000164283 245__ $$aMRI phenotyping of underlying cerebral small vessel disease in mixed hemorrhage patients.
000164283 260__ $$aAmsterdam [u.a.]$$bElsevier Science$$c2020
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000164283 520__ $$aTo investigate underlying cerebral small vessel disease (CSVD) in patients with mixed cerebral hemorrhages patterns and phenotype them according to the contribution of the two most common sporadic CSVD subtypes: cerebral amyloid angiopathy (CAA) vs. hypertensive arteriopathy (HA).Brain MRIs of patients with intracerebral hemorrhages (ICHs) and/or cerebral microbleeds (CMBs) were assessed for the full spectrum of CSVD markers using validated scales: ICHs, CMBs, cortical superficial siderosis (cSS), white matter hyperintensities, MRI-visible perivascular spaces (PVS). PVS predominance pattern was grouped as centrum-semiovale (CSO)-PVS predominance, basal-ganglia (BG)-PVS predominance, CSO-PVS and BG-PVS equality. Patients with mixed cerebral hemorrhages were classified into mixed CAA-pattern or mixed HA-pattern according to the existence of cSS and/or a CSO-PVS predominance pattern and comparisons were performed.We included 110 patients with CAA (strictly lobar ICHs/CMBs), 33 with HA (strictly deep ICHs/CMBs) and 97 with mixed lobar/deep ICHs/CMBs. Mixed patients were more similar to HA with respect to their MRI-CSVD markers, vascular risk profile and cerebrospinal fluid (CSF) measures. In the mixed patients, 33 (34%) had cSS, a CSO-PVS predominance pattern, or both, and were defined as mixed CAA-pattern cases. The mixed CAA-pattern patients were more alike CAA patients regarding their MRI-CSVD markers, CSF and genetic profile.Our findings suggest that the heterogeneous group of patients with mixed cerebral hemorrhages distribution can be further phenotyped according to the predominant underlying CSVD. cSS presence and a CSO-PVS predominance pattern could serve as strongly suggestive markers of a contribution from CAA among patients with mixed hemorrhages.
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000164283 650_7 $$2Other$$aCerebral amyloid angiopathy
000164283 650_7 $$2Other$$aCerebral small vessel diseases
000164283 650_7 $$2Other$$aCerebrospinal fluid
000164283 650_7 $$2Other$$aIntracerebral hemorrhage
000164283 650_7 $$2Other$$aMRI
000164283 650_7 $$2Other$$aVascular dementia
000164283 650_2 $$2MeSH$$aCerebral Amyloid Angiopathy
000164283 650_2 $$2MeSH$$aCerebral Hemorrhage: complications
000164283 650_2 $$2MeSH$$aCerebral Hemorrhage: diagnostic imaging
000164283 650_2 $$2MeSH$$aCerebral Small Vessel Diseases: complications
000164283 650_2 $$2MeSH$$aCerebral Small Vessel Diseases: diagnostic imaging
000164283 650_2 $$2MeSH$$aHumans
000164283 650_2 $$2MeSH$$aMagnetic Resonance Imaging
000164283 650_2 $$2MeSH$$aSiderosis
000164283 7001_ $$0P:(DE-2719)9000986$$aSchreiber, Frank$$b1$$udzne
000164283 7001_ $$0P:(DE-2719)9000985$$aPerosa, Valentina$$b2$$udzne
000164283 7001_ $$0P:(DE-2719)2812914$$aAssmann, Anne$$b3$$udzne
000164283 7001_ $$aMawrin, Christian$$b4
000164283 7001_ $$0P:(DE-2719)2813207$$aGarz, Cornelia$$b5$$udzne
000164283 7001_ $$0P:(DE-2719)2260426$$aHeinze, Hans-Jochen$$b6$$udzne
000164283 7001_ $$0P:(DE-2719)2811292$$aGörtler, Michael$$b7$$udzne
000164283 7001_ $$0P:(DE-2719)2000005$$aDüzel, Emrah$$b8$$udzne
000164283 7001_ $$0P:(DE-2719)2000035$$aVielhaber, Stefan$$b9$$udzne
000164283 7001_ $$aCharidimou, Andreas$$b10
000164283 7001_ $$0P:(DE-2719)2812631$$aSchreiber, Stefanie$$b11$$udzne
000164283 773__ $$0PERI:(DE-600)1500645-1$$a10.1016/j.jns.2020.117173$$gVol. 419, p. 117173 -$$p117173$$tJournal of the neurological sciences$$v419$$x0022-510X$$y2020
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