title: Extensive white matter hyperintensities may increase brain volume in cerebral autosomal-dominant arteriopathy with subcortical infarcts and leukoencephalopathy.
abstract: OBJECTIVE
  The extent of white matter hyperintensities (WMH) is associated with cerebral atrophy in elderly people. WMH is a radiological hallmark of cerebral autosomal-dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL), but their relationship with brain volume remains poorly understood. The association between WMH and brain volume was analyzed in a large population of patients with CADASIL.
  
  
  METHODS
  Demographic and MRI data of 278 patients recruited from a prospective cohort study were analyzed. Volumes of WMH and lacunar infarcts, number of cerebral microbleeds, and brain parenchymal fraction were measured. Multivariate analysis was used to study the impact of WMH on brain volume at baseline.
  
  
  RESULTS
  In univariate analyses, brain parenchymal fraction was negatively associated with age, male sex, and all MRI markers. Multiple regression modeling showed that brain parenchymal fraction was inversely related to age, number of cerebral microbleeds, and normalized volume of lacunar infarcts but positively related to normalized volume of WMH (P<0.001). This positive relationship was independent of the presence/absence of lacunar infarcts or of cerebral microbleeds. Subgroup analysis showed that this association was significant in subjects having normalized volume of WMH ≥6.13 or brain parenchymal fraction ≥86.37% (median values, both P≤0.001).
  
  
  CONCLUSIONS
  The results of the present study suggest that extensive WMH may be associated with increase of brain volume in CADASIL. In this disorder, WMH may be related not only to loss of white matter components, but also to a global increase of water content in the cerebral tissue.
authors.affiliation: University Paris Diderot, INSERM UMR 740, and Department of Neurology, Lariboisière Hospital, 2 rue Ambroise Paré, 75010 Paris, France.
authors.forename: Ming
authors.initials: M
authors.lastname: Yao
authors.forename: Eric
authors.initials: E
authors.lastname: Jouvent
authors.forename: Marco
authors.initials: M
authors.lastname: During
authors.forename: Ophélia
authors.initials: O
authors.lastname: Godin
authors.forename: Dominique
authors.initials: D
authors.lastname: Hervé
authors.forename: Jean Pierre
authors.initials: JP
authors.lastname: Guichard
authors.forename: Yi-Cheng
authors.initials: YC
authors.lastname: Zhu
authors.forename: Andreas
authors.initials: A
authors.lastname: Gschwendtner
authors.forename: Christian
authors.initials: C
authors.lastname: Opherk
authors.forename: Martin
authors.initials: M
authors.lastname: Dichgans
authors.forename: Hugues
authors.initials: H
authors.lastname: Chabriat
mesh_terms: D000328:Adult; D000367:Age Factors; D000368:Aged; D001284:Atrophy; D001921:Brain / Q000378:metabolism / Q000473:pathology*; D046589:CADASIL / Q000473:pathology*; D002543:Cerebral Hemorrhage / Q000473:pathology; D005260:Female; D006801:Humans; D056784:Leukoencephalopathies / Q000473:pathology*; D008279:Magnetic Resonance Imaging; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D059409:Stroke, Lacunar / Q000473:pathology*; D014867:Water / Q000378:metabolism; D055815:Young Adult
chemical_list: D014867:Water