White Matter Lesions and Lacunar Infarcts Are Independently and Differently Associated with Brain Atrophy: The SMART-MR Study

Appelman, Auke P.A.; Vincken, Koen L.; Graaf, Yolanda van der; Vlek, A. L. M.; Witkamp, Theo D.; Mali, Wptm; Geerlings, Mirjam I.

doi:10.1159/000255971

Cited by 52 publications

(52 citation statements)

References 67 publications

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“…Previous studies have reported correlations of WML with both subcortical and cortical atrophy. 8,36 Even though WML and brain atrophy are obviously interrelated processes, our results suggest that they independently and differentially contribute to cognitive impairment.…”

Section: Figure 2 Combined Effects Of White Matter Lesions (Wml) and mentioning

confidence: 76%

Brain atrophy accelerates cognitive decline in cerebral small vessel disease

Jokinen¹,

Lipsanen²,

Schmidt

et al. 2012

Neurology

133

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Objective: To examine the independent contributions and combined interactions of medial temporal lobe atrophy (MTA), cortical and subcortical atrophy, and white matter lesion (WML) volume in longitudinal cognitive performance. Methods:A total of 477 subjects with age-related WML were evaluated with brain MRI and annual neuropsychological examinations in 3-year follow-up. Baseline MRI determinants of cognitive decline were analyzed with linear mixed models controlling for multiple confounders.Results: MTA and subcortical atrophy predicted significantly steeper rate of decline in global cognitive measures as well as compound scores for psychomotor speed, executive functions, and memory after adjusting for age, gender, education, lacunes/infarcts, and WML volume. Cortical atrophy independently predicted decline in psychomotor speed. WML volume remained significantly associated with cognitive decline even after controlling for the atrophy scores. Moreover, significant synergistic interactions were found between WML and atrophy measures in overall cognitive performance across time and the rate of cognitive decline. Synergistic effects were also observed between baseline lacunar infarcts and all atrophy measures on change in psychomotor speed. The main results remained robust after exclusion of subjects with clinical stroke or incident dementia, and after additional adjustments for progression of WML and lacunes.Conclusions: Brain atrophy and WML are independently related to longitudinal cognitive decline in small vessel disease. MTA, subcortical, and cortical atrophy seem to potentiate the effect of WML and lacunes on cognitive decline. Neurology ® 2012;78:1785-1792

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Section: Figure 2 Combined Effects Of White Matter Lesions (Wml) and mentioning

confidence: 76%

Brain atrophy accelerates cognitive decline in cerebral small vessel disease

Jokinen¹,

Lipsanen²,

Schmidt

et al. 2012

Neurology

133

View full text Add to dashboard Cite

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“…Moreover, MR measures of brain atrophy are related to the accrual of subcortical vascular lesions [18,19], thus suggesting that neuroaxonal loss could be the final common pathway of the pathological process underlying CADASIL [20,21]. Finally, the burden of subcortical lesions has been related to cortical apoptosis, confirming that cortical atrophy may follow the axonal damage in the underlying white matter [22].…”

Section: Discussionmentioning

confidence: 99%

Retinal Nerve Fiber Layer Thinning in CADASIL: An Optical Coherence Tomography and MRI Study

Rufa¹,

Pretegiani²,

Frezzotti

et al. 2010

Cerebrovasc Dis

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Background and Purpose: Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is considered a genetic form of small-vessel disease causing subcortical dementia. A relevant role of axonal injury was recently proposed to explain disability and cognitive decline in this disease. The retinal nerve fiber layer (RNFL) is the only part of the brain where unmyelinated axons can be visualized and quantified in vivo. Their assessment may be an easily reproducible marker of neurodegenerative processes. The aim of this study was to investigate axonal degeneration in CADASIL by measuring RNFL thickness and correlating it with MRI measures of global and regional cerebral atrophy. Methods: RNFL thickness was measured using optical coherence tomography in 17 CADASIL patients. Average values per quadrant (temporal, superior, nasal, inferior) and overall values were compared with those of normal sex- and age-matched subjects. Data of 13 patients were analyzed for correlations with MRI-based global and regional brain volumes normalized for head size. Results: RNFL thickness was significantly reduced in CADASIL patients with respect to controls (p < 0.05). No significant correlations were found between RNFL thinning and brain atrophy. Conclusions: RNFL thinning suggests that retinal axonal loss occurs in CADASIL, even in the absence of subjective visual deficit.

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“…6 Some studies 2,10 render these classifications artificial. Others claim that they are arbitrary 11 and contrary to pathologic evidence of common vascular mechanisms, or they have suggested that PVWMH and DWMH volumes are highly correlated and have found that their spatial analysis failed to identify distinct subpopulations for PVWMH and DWMH. 12 Thus, a robust analysis of PVWMH morphology, distribution, and clinical correlates is required to determine a more appropriate classification of these hyperintense regions and their associations.…”

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confidence: 99%