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Strategic corpus callosum lesions are associated with worse cognitive performance in cerebral amyloid angiopathy
Author(s) -
Freeze Whitney M.,
Zotin Maria Clara Za,
Warren Andrew D.,
van der Weerd Louise,
Gurol M. Edip,
Viswanathan Anand,
Greenberg Steven M,
Reijmer Yael D.,
van Veluw Susanne J.
Publication year - 2020
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1002/alz.042464
Subject(s) - splenium , cerebral amyloid angiopathy , corpus callosum , hyperintensity , fractional anisotropy , white matter , neuropsychology , fluid attenuated inversion recovery , cognition , psychology , medicine , dementia , neuroimaging , diffusion mri , effects of sleep deprivation on cognitive performance , pathology , magnetic resonance imaging , audiology , neuroscience , radiology , disease
Background Cerebral amyloid angiopathy (CAA) is highly prevalent in Alzheimer’s disease (AD) and is associated with hemorrhagic and ischemic brain lesions. CAA is increasingly recognized as an important independent cause of cognitive impairment. However, the mechanisms underlying cognitive impairment in these patients are poorly understood. We hypothesized that lesions in the corpus callosum (CC), because of their strategic location, are associated with widespread reductions in microstructural white matter integrity and worse cognitive performance, specifically in the domains of attention/information processing speed and executive functioning. Method 57 individuals meeting the modified Boston criteria for probable CAA underwent 3T MRI, including a DTI scan, and neuropsychological testing. Microstructural white matter integrity was quantified by means of fractional anisotropy and mean diffusivity. Test scores on individual neuropsychological tests were converted into Z‐scores and averaged into the following cognitive domains: memory, attention/information processing speed, language, executive functioning, and visuospatial processing. CC lesions were defined as hemorrhagic (microbleeds or larger bleeds) and ischemic (microinfarcts, lacunar infarcts, and FLAIR hyperintensities). Associations between CC lesion presence, microstructural white matter integrity, and cognitive performance were examined with multiple regression models, corrected for age, sex, education (when cognition was the dependent variable), and history of large ICH. False discovery rate corrections for multiple comparisons were applied. Result Demographic and imaging characteristics of cases with and without CC lesions are outlined in table 1. Sixteen cases (28%) had one or two CC lesions (n=18 lesions). Most lesions were located in the splenium (n=8), followed by the genu (n=7) and the midbody (n=3) of the CC. In multivariate regression models, presence of CC lesions was associated with reduced microstructural white matter integrity on DTI within the CC and in the total white matter. Interestingly, cases with CC lesions performed significantly worse on the domains of attention/information processing speed, and executive functioning compared to those without CC lesions, but no differences were found for the other domains (table 2). Conclusion Because of their strategic location, focal CC lesions may significantly contribute to cognitive impairment in CAA, potentially through their negative impact on the microstructural white matter integrity beyond the lesion core (i.e., Wallerian degeneration).