Longitudinal follow-up of individual white matter hyperintensities in a large cohort of elderly

Pauline Maillard, Fabrice Crivello, Carole Dufouil, Nathalie Tzourio-Mazoyer, Christophe Tzourio, Bernard Mazoyer
Neuroradiology. 2009-01-13; 51(4): 209-220
DOI: 10.1007/s00234-008-0489-0

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1. Neuroradiology. 2009 Apr;51(4):209-20. doi: 10.1007/s00234-008-0489-0. Epub 2009
Jan 13.

Longitudinal follow-up of individual white matter hyperintensities in a large
cohort of elderly.

Maillard P(1), Crivello F, Dufouil C, Tzourio-Mazoyer N, Tzourio C, Mazoyer B.

Author information:
(1)Centre d’Imagerie-Neurosciences et Applications aux Pathologies, CI-NAPS,
UMR6232, CNRS, CEA, Université de Caen, Université Paris Descartes, GIP Cyceron,
Caen cedex, France.

INTRODUCTION: We report on a method for the longitudinal follow-up of individual
white matter hypersignals (WMH) and on its application to the study of WMH
natural evolution in a cohort of 1,118 elderly over a 4-year period.
MATERIALS AND METHODS: For each subject, automated WMH detection was performed on
T2-weighted MR images acquired both at baseline and at follow-up after
registration in a common space. The detection algorithm was designed both to
track WMH previously existing at baseline and to identify newly formed WMH.
RESULTS: The average annual change in WMH load was found to be 0.25 cm(3)/year,
36% of this change being attributable to newly formed WMH. Quantitative analyses
showed that change in WMH was mainly explained by progression of juxtaventricular
and periventricular WMH while the load of WMH in the deep white matter zones was
found stable over 4 years of the study. Statistical parametric mapping confirmed
these spatial WMH change distributions in the juxta- and periventricular zones.
High blood pressure was not a significant predictor of the annual change in WMH.
CONCLUSION: This study proposes a new scheme for the longitudinal study of WMH
change by dissociating worsening of existent WMH from surfacing of new WMH and
may thus contribute to help understanding and characterizing the neurological and
etiological bases of these two processes and their potential differences.

DOI: 10.1007/s00234-008-0489-0
PMID: 19139875 [Indexed for MEDLINE]

Auteurs Bordeaux Neurocampus