Subarachnoid Hemosiderosis and Superficial Cortical Hemosiderosis in Cerebral Amyloid Angiopathy

Linn, Jennifer; Herms, Jochen; Dichgans, Martin; Brückmann, H.; Fesl, G.; Freilinger, Tobias; Wiesmann, Martin

doi:10.3174/ajnr.a0783

Cited by 145 publications

(121 citation statements)

References 15 publications

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“…Indeed, in CAA, cSS has a characteristic predilection for the cerebral convexities, reflecting linear blood residues in the superficial layers of the cerebral cortex or in the subarachnoid space. 8,30,31 Our study has several strengths including the systematic evaluation of MRI scans by trained raters using validated scales for a range of imaging markers of small vessel disease and the testing of a prespecified hypothesis. The main limitation is the potential selection bias because of the requirement for MRI done as part of routine clinical care; hence, our results can only be extrapolated to patient populations in a similar clinical context with available MRI and need to be validated using larger independent cohorts.…”

Section: Discussionmentioning

confidence: 99%

White Matter Perivascular Spaces Are Related to Cortical Superficial Siderosis in Cerebral Amyloid Angiopathy

Charidimou

Jäger

Peeters

et al. 2014

Stroke

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Consecutive CAA patients (according to the original Boston criteria 9 ; ie, not including cSS as a criterion) from an ongoing multicenter Background and Purpose-We set out to investigate whether MRI-visible centrum semiovale perivascular spaces (CSO-PVS), a potential biomarker of impaired interstitial fluid drainage in sporadic cerebral amyloid angiopathy, is associated with cortical superficial siderosis (cSS), reflecting recurrent hemorrhage from severe leptomeningeal and superficial cortical vascular amyloid. Methods-Retrospective multicenter cohort study of possible/probable cerebral amyloid angiopathy according to the Boston criteria. PVS were rated in basal ganglia and CSO (CSO-PVS) on axial T2-weighted sequences, using a validated 4-point visual rating scale and were classified as high (score >2) or low degree (score ≤2) for prespecified analyses. Independent risk factors for high CSO-PVS degree were investigated in logistic regression. Results-The

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Section: Discussionmentioning

confidence: 99%

White Matter Perivascular Spaces Are Related to Cortical Superficial Siderosis in Cerebral Amyloid Angiopathy

Charidimou

Jäger

Peeters

et al. 2014

Stroke

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“…[5][6][7][8] In CAA, cSS has a characteristic predilection for the cerebral convexities, reflecting linear blood residues in the superficial layers of the cerebral cortex or in the subarachnoid space. [8][9][10] cSS may have clinical relevance as an important cause of transient focal neurologic episodes (sometimes called "amyloid spells"), 11,12 and a potential "warning sign" for future symptomatic ICH. 13 Although cSS is a promising diagnostic neuroimaging marker of CAA, 8 the strength of the association and underlying mechanisms have not been systematically studied.…”

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confidence: 99%

Prevalence and mechanisms of cortical superficial siderosis in cerebral amyloid angiopathy

et al. 2013

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Objective: We investigated the prevalence and clinical-radiologic associations of cortical superficial siderosis (cSS) in patients with probable cerebral amyloid angiopathy (CAA) compared to those with intracerebral hemorrhage (ICH) not attributed to CAA. Methods:We conducted a retrospective multicenter cohort study of 120 patients with probable CAA and 2 comparison groups: 67 patients with either single lobar ICH or mixed (deep and lobar) hemorrhages; and 22 patients with strictly deep hemorrhages. We rated cSS, ICH, white matter changes, and cerebral microbleeds.

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“…cSS reflects linear blood residues in the superficial (subpial) layers of the cerebral cortex. 14 One likely mechanism leading to cSS is repeated episodes of hemorrhage into the subarachnoid space from brittle superficial cortical or leptomeningeal CAA-laden vessels, potentially heralding a high risk of future lobar ICH. A recent study showed that nearly 50% of CAA patients with cSS experienced intracranial hemorrhage over a period of 35 months, 15 but this study did not include patients without cSS as a control group.…”

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confidence: 99%

Cortical superficial siderosis and intracerebral hemorrhage risk in cerebral amyloid angiopathy

et al. 2013

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Objective: To investigate whether cortical superficial siderosis (cSS) on MRI, especially if disseminated (involving more than 3 sulci), increases the risk of future symptomatic lobar intracerebral hemorrhage (ICH) in cerebral amyloid angiopathy (CAA).Methods: European multicenter cohort study of 118 patients with CAA (104 with baseline symptomatic lobar ICH) diagnosed according to the Boston criteria. We obtained baseline clinical, MRI, and follow-up data on symptomatic lobar ICH. Using Kaplan-Meier and Cox regression analyses, we investigated cSS and ICH risk, adjusting for known confounders.Results: During a median follow-up time of 24 months (interquartile range 9-44 months), 23 of 118 patients (19.5%, 95% confidence interval [CI]: 12.8%-27.8%) experienced symptomatic lobar ICH. Any cSS and disseminated cSS were predictors of time until first or recurrent ICH (logrank test: p 5 0.0045 and p 5 0.0009, respectively). ICH risk at 4 years was 25% (95% CI: 7.6%-28.3%) for patients without siderosis; 28.9% (95% CI: 7.7%-76.7%) for patients with focal siderosis; and 74% (95% CI: 44.1%-95.7%) for patients with disseminated cSS (log-rank test: p 5 0.0031). In Cox regression models, any cSS and disseminated cSS were both independently associated with increased lobar ICH risk, after adjusting for $2 microbleeds and age (hazard ratio: 2.53; 95% CI: 1.05-6.15; p 5 0.040 and hazard ratio: 3.16; 95% CI: 1.35-7.43; p 5 0.008, respectively). These results remained consistent in sensitivity analyses including only patients with symptomatic lobar ICH at baseline. Conclusions:Our findings indicate that cSS, particularly if disseminated, is associated with an increased risk of symptomatic lobar ICH in CAA. cSS may help stratify future bleeding risk in CAA, with implications for prognosis and treatment. Neurology ® 2013;81:1666-1673 GLOSSARY CAA 5 cerebral amyloid angiopathy; CI 5 confidence interval; CMB 5 cerebral microbleed; cSS 5 cortical superficial siderosis; FLAIR 5 fluid-attenuated inversion recovery; GRE 5 gradient-recalled echo; HR 5 hazard ratio; ICH 5 intracerebral hemorrhage.Sporadic cerebral amyloid angiopathy (CAA) is a highly prevalent, age-related small-vessel disease 1 caused by amyloid-b deposition in cortical and leptomeningeal vessel walls. 2 CAA is a major cause of lobar intracerebral hemorrhage (ICH), particularly in elderly patients.2-5 Spontaneous ICH is one of the most catastrophic forms of stroke, with a high risk of recurrence [6][7][8] ; CAA-related lobar ICH may carry a greater risk than deep ICH presumed to be due to hypertensive arteriopathy, 8,9 but this is currently difficult to predict. Predisposing factors for lobar ICH and lobar ICH recurrence in CAA include APOE e4 and e2 alleles, 10 hemorrhagic neuroimaging markers of CAA such as lobar cerebral microbleeds (CMBs), 11 and anticoagulant or antiplatelet use. 12 Little is known about cortical superficial siderosis (cSS), a recently identified neuroimaging marker of CAA, 13 and the risk of subsequent

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Subarachnoid Hemosiderosis and Superficial Cortical Hemosiderosis in Cerebral Amyloid Angiopathy

Cited by 145 publications

References 15 publications

White Matter Perivascular Spaces Are Related to Cortical Superficial Siderosis in Cerebral Amyloid Angiopathy

White Matter Perivascular Spaces Are Related to Cortical Superficial Siderosis in Cerebral Amyloid Angiopathy

Prevalence and mechanisms of cortical superficial siderosis in cerebral amyloid angiopathy

Cortical superficial siderosis and intracerebral hemorrhage risk in cerebral amyloid angiopathy

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