TY - JOUR
T1 - Progression of white matter hyperintensities and incidence of new lacunes over a 3-year period
T2 - the Leukoaraiosis and Disability study
AU - Gouw, Alida A
AU - van der Flier, Wiesje M
AU - Fazekas, Franz
AU - van Straaten, Elisabeth C W
AU - Pantoni, Leonardo
AU - Poggesi, Anna
AU - Inzitari, Domenico
AU - Erkinjuntti, Timo
AU - Wahlund, Lars O
AU - Waldemar, Gunhild
AU - Schmidt, Reinhold
AU - Scheltens, Philip
AU - Barkhof, Frederik
AU - LADIS study group
A2 - Paulson, Olaf Bjarne
PY - 2008/5
Y1 - 2008/5
N2 - BACKGROUND AND PURPOSE: We studied the natural course of white matter hyperintensities (WMH) and lacunes, the main MRI representatives of small vessel disease, over time and evaluated possible predictors for their development.METHODS: Baseline and repeat MRI (3-year follow-up) were collected within the multicenter, multinational Leukoaraiosis and Disability study (n=396). Baseline WMH were scored on MRI by the Fazekas scale and the Scheltens scale. WMH progression was assessed using the modified Rotterdam Progression scale (absence/presence of progression in 9 brain regions). Baseline and new lacunes were counted per region. WMH and lacunes at baseline and vascular risk factors were evaluated as predictors of WMH progression and new lacunes.RESULTS: WMH progressed (mean+/-SD=1.9+/-1.8) mostly in the subcortical white matter, where WMH was also most prevalent at baseline. The majority of new lacunes, which were found in 19% of the subjects (maximum=9), also appeared in the subcortical white matter, mainly of the frontal lobes, whereas most baseline lacunes were located in the basal ganglia. Baseline WMH and lacunes predicted both WMH progression and new lacunes. Furthermore, previous stroke, diabetes, and blood glucose were risk factors for WMH progression. Male sex, hypertension, systolic blood pressure, previous stroke, body mass index, high-density lipoprotein, and triglyceride levels were risk factors for new lacunes.CONCLUSIONS: WMH and lacunes progressed over time, predominantly in the subcortical white matter. Progression was observed especially in subjects with considerable WMH and lacunes at baseline. Moreover, the presence of vascular risk factors at baseline predicted WMH progression and new lacunes over a 3-year period.
AB - BACKGROUND AND PURPOSE: We studied the natural course of white matter hyperintensities (WMH) and lacunes, the main MRI representatives of small vessel disease, over time and evaluated possible predictors for their development.METHODS: Baseline and repeat MRI (3-year follow-up) were collected within the multicenter, multinational Leukoaraiosis and Disability study (n=396). Baseline WMH were scored on MRI by the Fazekas scale and the Scheltens scale. WMH progression was assessed using the modified Rotterdam Progression scale (absence/presence of progression in 9 brain regions). Baseline and new lacunes were counted per region. WMH and lacunes at baseline and vascular risk factors were evaluated as predictors of WMH progression and new lacunes.RESULTS: WMH progressed (mean+/-SD=1.9+/-1.8) mostly in the subcortical white matter, where WMH was also most prevalent at baseline. The majority of new lacunes, which were found in 19% of the subjects (maximum=9), also appeared in the subcortical white matter, mainly of the frontal lobes, whereas most baseline lacunes were located in the basal ganglia. Baseline WMH and lacunes predicted both WMH progression and new lacunes. Furthermore, previous stroke, diabetes, and blood glucose were risk factors for WMH progression. Male sex, hypertension, systolic blood pressure, previous stroke, body mass index, high-density lipoprotein, and triglyceride levels were risk factors for new lacunes.CONCLUSIONS: WMH and lacunes progressed over time, predominantly in the subcortical white matter. Progression was observed especially in subjects with considerable WMH and lacunes at baseline. Moreover, the presence of vascular risk factors at baseline predicted WMH progression and new lacunes over a 3-year period.
KW - Aged
KW - Aged, 80 and over
KW - Basal Ganglia/blood supply
KW - Brain/blood supply
KW - Brain Infarction/epidemiology
KW - Brain Ischemia/epidemiology
KW - Cardiovascular Diseases/epidemiology
KW - Cerebral Arteries/pathology
KW - Comorbidity
KW - Disease Progression
KW - Female
KW - Follow-Up Studies
KW - Frontal Lobe/blood supply
KW - Humans
KW - Hyperlipidemias/epidemiology
KW - Incidence
KW - Leukoaraiosis/epidemiology
KW - Magnetic Resonance Imaging
KW - Male
KW - Nerve Fibers, Myelinated/pathology
KW - Prevalence
KW - Risk Factors
KW - Time Factors
U2 - 10.1161/STROKEAHA.107.498535
DO - 10.1161/STROKEAHA.107.498535
M3 - Journal article
C2 - 18323505
SN - 0039-2499
VL - 39
SP - 1414
EP - 1420
JO - Stroke
JF - Stroke
IS - 5
ER -