Predictors for cognitive decline in patients with confluent white matter hyperintensities.
BACKGROUND
Although patients harboring confluent white matter hyperintensities (WMH) are at high risk of cognitive decline, this risk varies among individuals. We investigated the predictors for cognitive decline in stroke patients with confluent WMH.


METHODS
We followed up 100 stroke patients with confluent WMH who were participants of the VITAmins TO Prevent Stroke study for 2 years. We investigated the association between clinical features, apolipoprotein E status, imaging measures (infarcts, microbleeds, volumes of WMH, cortical gray matter [cGM], lateral ventricles, and hippocampi), and B vitamins with changes in cognitive measures (clinical dementia rating scale, Mini-Mental State Examination, Mattis dementia rating scale--initiation/perseveration subscale). We performed Pittsburgh compound B imaging among dementia converters.


RESULTS
Multivariate regression analysis showed that increase in clinical dementia rating scale grade was associated with cGM atrophy, absence of hyperlipidemia, and lower diastolic blood pressure at baseline. cGM atrophy and absence of hyperlipidemia were also associated with deterioration in Mini-Mental State Examination and Mattis dementia rating scale--initiation/perseveration subscale scores. Pittsburgh compound B retention typical of Alzheimer's disease was found only in 10% of dementia converters. Incident stroke and B vitamins were not associated with cognitive decline.


CONCLUSIONS
Among stroke patients with confluent WMH, cGM atrophy and absence of hyperlipidemia are important predictors for cognitive decline. Significant cognitive decline can occur in the absence of incident stroke or Alzheimer's pathology.
Department of Medicine and Therapeutics, The Chinese University of Hong Kong, Shatin, Hong Kong Special Administrative Region, People's Republic of China. vctmok@cuhk.edu.hk
Vincent
V
Mok
Yunyun
Y
Xiong
Kelvin K
KK
Wong
Adrian
A
Wong
Reinhold
R
Schmidt
Winnie W C
WW
Chu
Xintao
X
Hu
Eric Yim
EY
Lung Leung
Sirong
S
Chen
Yangkun
Y
Chen
Wai Kwong
WK
Tang
Xiangyan
X
Chen
Chi Lai
CL
Ho
Ka Sing
KS
Wong
Stephen T C
ST
Wong
D000368:Aged; D001284:Atrophy / Q000473:pathology; D001921:Brain / Q000473:pathology* / Q000503:physiopathology; D003072:Cognition Disorders / Q000209:etiology / Q000473:pathology* / Q000503:physiopathology; D004311:Double-Blind Method; D005260:Female; D005492:Folic Acid / Q000627:therapeutic use; D006801:Humans; D008279:Magnetic Resonance Imaging; D008297:Male; D009413:Nerve Fibers, Myelinated / Q000473:pathology*; D055502:Secondary Prevention; D020521:Stroke / Q000150:complications / Q000188:drug therapy / Q000473:pathology*; D014805:Vitamin B 12 / Q000627:therapeutic use; D025101:Vitamin B 6 / Q000627:therapeutic use; D014803:Vitamin B Complex / Q000627:therapeutic use
D014803:Vitamin B Complex; D025101:Vitamin B 6; D005492:Folic Acid; D014805:Vitamin B 12