Progression of white matter hyperintensities and incidence of new lacunes over a 3-year period: the Leukoaraiosis and Disability study.
OBJECTIVE
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.
Gouw
Alida A
AA
Department of Neurology, Alzheimer Center and Image Analysis Center, Vrije Universiteit Medical Center, PO Box 7057, 1007 MB Amsterdam, The Netherlands. AA.Gouw@vumc.nl
van der Flier
Wiesje M
WM
Fazekas
Franz
F
van Straaten
Elisabeth C W
EC
Pantoni
Leonardo
L
Poggesi
Anna
A
Inzitari
Domenico
D
Erkinjuntti
Timo
T
Wahlund
Lars O
LO
Waldemar
Gunhild
G
Schmidt
Reinhold
R
Scheltens
Philip
P
Barkhof
Frederik
F
D000368:Aged; D000369:Aged, 80 and over; D001479:Basal Ganglia / Q000098:blood supply / Q000473:pathology / Q000503:physiopathology; D001921:Brain / Q000098:blood supply / Q000473:pathology* / Q000503:physiopathology; D020520:Brain Infarction / Q000453:epidemiology* / Q000473:pathology* / Q000503:physiopathology; D002545:Brain Ischemia / Q000453:epidemiology / Q000473:pathology / Q000503:physiopathology; D002318:Cardiovascular Diseases / Q000453:epidemiology; D002536:Cerebral Arteries / Q000473:pathology / Q000503:physiopathology; D015897:Comorbidity; D018450:Disease Progression; D005260:Female; D005500:Follow-Up Studies; D005625:Frontal Lobe / Q000098:blood supply / Q000473:pathology / Q000503:physiopathology; D006801:Humans; D006949:Hyperlipidemias / Q000453:epidemiology; D015994:Incidence; D049292:Leukoaraiosis / Q000453:epidemiology* / Q000473:pathology* / Q000503:physiopathology; D008279:Magnetic Resonance Imaging; D008297:Male; D009413:Nerve Fibers, Myelinated / Q000473:pathology*; D015995:Prevalence; D012307:Risk Factors; D013997:Time Factors