title: Association of Key Magnetic Resonance Imaging Markers of Cerebral Small Vessel Disease With Hematoma Volume and Expansion in Patients With Lobar and Deep Intracerebral Hemorrhage.
abstract: OBJECTIVE
  Hematoma expansion is an important determinant of outcome in spontaneous intracerebral hemorrhage (ICH) due to small vessel disease (SVD), but the association between the severity of the underlying SVD and the extent of bleeding at the acute phase is unknown to date.
  
  
  OBJECTIVE
  To investigate the association between key magnetic resonance imaging (MRI) markers of SVD (as per the Standards for Reporting Vascular Changes on Neuroimaging [STRIVE] guidelines) and hematoma volume and expansion in patients with lobar or deep ICH.
  
  
  METHODS
  Analysis of data collected from 418 consecutive patients admitted with primary lobar or deep ICH to a single tertiary care medical center between January 1, 2000, and October 1, 2012. Data were analyzed on March 4, 2016. Participants were consecutive patients with computed tomographic images allowing ICH volume calculation and MRI allowing imaging markers of SVD assessment.
  
  
  METHODS
  The ICH volumes at baseline and within 48 hours after symptom onset were measured in 418 patients with spontaneous ICH without anticoagulant therapy, and hematoma expansion was calculated. Cerebral microbleeds, cortical superficial siderosis, and white matter hyperintensity volume were assessed on MRI. The associations between these SVD markers and ICH volume, as well as hematoma expansion, were investigated using multivariable models.
  
  
  RESULTS
  This study analyzed 254 patients with lobar ICH (mean [SD] age, 75 [11] years and 140 [55.1%] female) and 164 patients with deep ICH (mean [SD] age 67 [14] years and 71 [43.3%] female). The presence of cortical superficial siderosis was an independent variable associated with larger ICH volume in the lobar ICH group (odds ratio per quintile increase in final ICH volume, 1.49; 95% CI, 1.14-1.94; P = .004). In multivariable models, the absence of cerebral microbleeds was associated with larger ICH volume for both the lobar and deep ICH groups (odds ratios per quintile increase in final ICH volume, 1.41; 95% CI, 1.11-1.81; P = .006 and 1.43; 95% CI, 1.04-1.99; P = .03; respectively) and with hematoma expansion in the lobar ICH group (odds ratio, 1.70; 95% CI, 1.07-2.92; P = .04). The white matter hyperintensity volumes were not associated with either hematoma volume or expansion.
  
  
  CONCLUSIONS
  In patients admitted with primary lobar or deep ICH to a single tertiary care medical center, the presence of cortical superficial siderosis was an independent variable associated with larger lobar ICH volume, and the absence of cerebral microbleeds was associated with larger lobar and deep ICHs. The absence of cerebral microbleeds was independently associated with more frequent hematoma expansion in patients with lobar ICH. We provide an analytical framework for future studies aimed at limiting hematoma expansion.
authors.affiliation: Hemorrhagic Stroke Research Program, Department of Neurology, Massachusetts General Hospital Stroke Research Center, Harvard Medical School, Boston.
authors.forename: Gregoire
authors.initials: G
authors.lastname: Boulouis
authors.affiliation: Hemorrhagic Stroke Research Program, Department of Neurology, Massachusetts General Hospital Stroke Research Center, Harvard Medical School, Boston2Department of Neurology, Leiden University Medical Center, Leiden, the Netherlands.
authors.forename: Ellis S
authors.initials: ES
authors.lastname: van Etten
authors.affiliation: Hemorrhagic Stroke Research Program, Department of Neurology, Massachusetts General Hospital Stroke Research Center, Harvard Medical School, Boston.
authors.forename: Andreas
authors.initials: A
authors.lastname: Charidimou
authors.affiliation: Hemorrhagic Stroke Research Program, Department of Neurology, Massachusetts General Hospital Stroke Research Center, Harvard Medical School, Boston.
authors.forename: Eitan
authors.initials: E
authors.lastname: Auriel
authors.affiliation: Hemorrhagic Stroke Research Program, Department of Neurology, Massachusetts General Hospital Stroke Research Center, Harvard Medical School, Boston.
authors.forename: Andrea
authors.initials: A
authors.lastname: Morotti
authors.affiliation: Hemorrhagic Stroke Research Program, Department of Neurology, Massachusetts General Hospital Stroke Research Center, Harvard Medical School, Boston.
authors.forename: Marco
authors.initials: M
authors.lastname: Pasi
authors.affiliation: Hemorrhagic Stroke Research Program, Department of Neurology, Massachusetts General Hospital Stroke Research Center, Harvard Medical School, Boston.
authors.forename: Kellen E
authors.initials: KE
authors.lastname: Haley
authors.affiliation: Hemorrhagic Stroke Research Program, Department of Neurology, Massachusetts General Hospital Stroke Research Center, Harvard Medical School, Boston3Brain Center Rudolf Magnus, Department of Neurosurgery, University Medical Center Utrecht, Heidelberglaan, Utrecht, the Netherlands.
authors.forename: H Bart
authors.initials: HB
authors.lastname: Brouwers
authors.affiliation: Hemorrhagic Stroke Research Program, Department of Neurology, Massachusetts General Hospital Stroke Research Center, Harvard Medical School, Boston.
authors.forename: Alison M
authors.initials: AM
authors.lastname: Ayres
authors.affiliation: Hemorrhagic Stroke Research Program, Department of Neurology, Massachusetts General Hospital Stroke Research Center, Harvard Medical School, Boston.
authors.forename: Anastasia
authors.initials: A
authors.lastname: Vashkevich
authors.affiliation: Hemorrhagic Stroke Research Program, Department of Neurology, Massachusetts General Hospital Stroke Research Center, Harvard Medical School, Boston.
authors.forename: Michael J
authors.initials: MJ
authors.lastname: Jessel
authors.affiliation: Hemorrhagic Stroke Research Program, Department of Neurology, Massachusetts General Hospital Stroke Research Center, Harvard Medical School, Boston.
authors.forename: Kristin M
authors.initials: KM
authors.lastname: Schwab
authors.affiliation: Hemorrhagic Stroke Research Program, Department of Neurology, Massachusetts General Hospital Stroke Research Center, Harvard Medical School, Boston.
authors.forename: Anand
authors.initials: A
authors.lastname: Viswanathan
authors.affiliation: Hemorrhagic Stroke Research Program, Department of Neurology, Massachusetts General Hospital Stroke Research Center, Harvard Medical School, Boston.
authors.forename: Steven M
authors.initials: SM
authors.lastname: Greenberg
authors.affiliation: Hemorrhagic Stroke Research Program, Department of Neurology, Massachusetts General Hospital Stroke Research Center, Harvard Medical School, Boston.
authors.forename: Jonathan
authors.initials: J
authors.lastname: Rosand
authors.affiliation: Hemorrhagic Stroke Research Program, Department of Neurology, Massachusetts General Hospital Stroke Research Center, Harvard Medical School, Boston4Division of Neurocritical Care and Emergency Neurology, Massachusetts General Hospital, Harvard Medical School, Boston.
authors.forename: Joshua N
authors.initials: JN
authors.lastname: Goldstein
authors.affiliation: Hemorrhagic Stroke Research Program, Department of Neurology, Massachusetts General Hospital Stroke Research Center, Harvard Medical School, Boston.
authors.forename: M Edip
authors.initials: ME
authors.lastname: Gurol
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D015415:Biomarkers; D001900:Boston / Q000453:epidemiology; D002540:Cerebral Cortex / Q000000981:diagnostic imaging*; D002543:Cerebral Hemorrhage / Q000000981:diagnostic imaging* / Q000453:epidemiology; D059345:Cerebral Small Vessel Diseases / Q000000981:diagnostic imaging* / Q000453:epidemiology; D005260:Female; D006406:Hematoma / Q000000981:diagnostic imaging* / Q000453:epidemiology; D006486:Hemosiderosis / Q000000981:diagnostic imaging*; D006801:Humans; D008279:Magnetic Resonance Imaging / Q000379:methods*; D008297:Male; D008875:Middle Aged
chemical_list: D015415:Biomarkers