Evidence map›Paper›PMID 30869563›Full record

ArticleStroke2019

Cortical Superficial Siderosis Evolution.

Andreas Charidimou, Gregoire Boulouis, Li Xiong, Marco Pasi, Duangnapa Roongpiboonsopit, Alison Ayres, Kristin M Schwab, Jonathan Rosand, M Edip Gurol, Anand Viswanathan and 1 more

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Stroke, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.3field-weighted citation impact, top 12% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

14 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
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  10. Cortical superficial siderosis in the general population: The Framingham Heart and Rotterdam studies.International journal of stroke : official journal of the International Stroke Society · 2021
    Article
  11. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 2 institutions in 2 countries.

Andreas CharidimouFrom the Hemorrhagic Stroke Research Program, Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston (A.C., G.B., L.X., M.P., D.R., A.A., K.M.S., J.R., M.E.G., A.V., S.M.G.).
Gregoire BoulouisFrom the Hemorrhagic Stroke Research Program, Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston (A.C., G.B., L.X., M.P., D.R., A.A., K.M.S., J.R., M.E.G., A.V., S.M.G.).
Li XiongFrom the Hemorrhagic Stroke Research Program, Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston (A.C., G.B., L.X., M.P., D.R., A.A., K.M.S., J.R., M.E.G., A.V., S.M.G.).
Marco PasiFrom the Hemorrhagic Stroke Research Program, Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston (A.C., G.B., L.X., M.P., D.R., A.A., K.M.S., J.R., M.E.G., A.V., S.M.G.).
Duangnapa RoongpiboonsopitFrom the Hemorrhagic Stroke Research Program, Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston (A.C., G.B., L.X., M.P., D.R., A.A., K.M.S., J.R., M.E.G., A.V., S.M.G.).
Alison AyresFrom the Hemorrhagic Stroke Research Program, Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston (A.C., G.B., L.X., M.P., D.R., A.A., K.M.S., J.R., M.E.G., A.V., S.M.G.).
Kristin M SchwabFrom the Hemorrhagic Stroke Research Program, Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston (A.C., G.B., L.X., M.P., D.R., A.A., K.M.S., J.R., M.E.G., A.V., S.M.G.).
Jonathan RosandFrom the Hemorrhagic Stroke Research Program, Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston (A.C., G.B., L.X., M.P., D.R., A.A., K.M.S., J.R., M.E.G., A.V., S.M.G.).
M Edip GurolFrom the Hemorrhagic Stroke Research Program, Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston (A.C., G.B., L.X., M.P., D.R., A.A., K.M.S., J.R., M.E.G., A.V., S.M.G.).
Anand ViswanathanFrom the Hemorrhagic Stroke Research Program, Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston (A.C., G.B., L.X., M.P., D.R., A.A., K.M.S., J.R., M.E.G., A.V., S.M.G.).
Steven M GreenbergFrom the Hemorrhagic Stroke Research Program, Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston (A.C., G.B., L.X., M.P., D.R., A.A., K.M.S., J.R., M.E.G., A.V., S.M.G.).
Harvard University · USMassachusetts General Hospital · US

Funding

Vascular Dysfunction in Cerebral Amyloid AngiopathyR01AG026484 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI GREENBERG, STEVEN M · 2005 to 2019
$7.5M
NIA NIH HHS R01 AG026484
6 · The paper itself

Abstract

Background and Purpose- We investigated cortical superficial siderosis (cSS) progression and its clinical relevance for incident lobar intracerebral hemorrhage (ICH) risk, in probable cerebral amyloid angiopathy presenting with neurological symptoms and without ICH at baseline. Methods- Consecutive patients meeting modified Boston criteria for probable cerebral amyloid angiopathy from a single-center cohort who underwent magnetic resonance imaging (MRI) at baseline and during follow-up were analyzed. cSS progression was assessed by comparison of the baseline and follow-up images. Patients were followed prospectively for incident symptomatic ICH. cSS progression and first-ever ICH risk were investigated in Cox proportional hazard models adjusting for confounders. Results- The cohort included 118 probable cerebral amyloid angiopathy patients: 72 (61%) presented with transient focal neurological episodes and 46 (39%) with cognitive complaints prompting the baseline MRI investigation. Fifty-two patients (44.1%) had cSS at baseline. During a median scan interval of 2.2 years (interquartile range, 1.2-4.4 years) between the baseline (ie, first) MRI and the latest MRI, cSS progression was detected in 33 (28%) patients. In multivariable logistic regression, baseline cSS presence (odds ratio, 4.04; 95% CI, 1.53-10.70; P=0.005), especially disseminated cSS (odds ratio, 9.12; 95% CI, 2.85-29.18; P<0.0001) and appearance of new lobar microbleeds (odds ratio, 4.24; 95% CI, 1.29-13.9; P=0.017) were independent predictors of cSS progression. For patients without an ICH during the interscan interval (n=105) and subsequent follow-up (median postfinal MRI time, 1.34; interquartile range, 0.3-3 years), cSS progression independently predicted increased symptomatic ICH risk (hazard ratio, 3.76; 95% CI, 1.37-10.35; P=0.010). Conclusions- Our results suggest that cSS evolution may be a useful biomarker for assessing disease progression and ICH risk in cerebral amyloid angiopathy patients and a candidate biomarker for clinical studies and trials.

Indexed as

AgedAged, 80 and overCerebral Amyloid AngiopathyCerebral CortexCerebral HemorrhageDisease ProgressionFemaleHumansIncidenceMagnetic Resonance ImagingMaleMiddle AgedRiskSiderosiscerebral amyloid angiopathycerebral hemorrhagedisease progressionmagnetic resonance imagingsiderosis

Identifiers

PMID30869563
PMCPMC6433512
OpenAlexW2941878772

What OpenQuestion holds

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LicenceTDM
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.