Relationship between white matter T2 hyperintensity and cortical volume changes on magnetic resonance imaging in healthy elders
✍ Scribed by Miho Ota; Kiyotaka Nemoto; Noriko Sato; Katsutoshi Mizukami; Fumio Yamashita; Takashi Asada
- Book ID
- 102845216
- Publisher
- John Wiley and Sons
- Year
- 2010
- Tongue
- English
- Weight
- 555 KB
- Volume
- 26
- Category
- Article
- ISSN
- 0885-6230
- DOI
- 10.1002/gps.2618
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✦ Synopsis
Abstract
Objective
T2 white matter hyperintensity (WMH) on magnetic resonance imaging (MRI) is associated with brain atrophy. Some previous studies examined the relation between the WMH and cortical atrophy, however, little is known about how the WMHs affect the pattern of cortical atrophy. Recent studies have revealed that patho‐physiological role of WMH in affecting cortical atrophy may be different between hyperintensities in basal ganglia and thalami (B&T) and those in other regions. Based on a longitudinal study up to 5 years, we attempt to examine the temporal relation between the WMHs and cortical atrophy with special attention to the hyperintensities in the B&T.
Methods
We evaluated the temporal pattern of cortical atrophy in 74 cognitively normal subjects lacking hyperintensities in B&T (first analysis) and 13 cognitively normal subjects with hyperintensities in B&T (second analysis). The relationship between the baseline WMH severity and the cortical volume change during the observation period (mean: 3.8 years) was voxel basically evaluated on the images.
Results
The first analysis showed fairly axisymmetrical atrophy pattern in parietal, occipital, and precentral cortices, while the findings gained from the second appear to lack such systematic orderliness of the atrophy.
Conclusion
This result shows that WMH may affect atrophy in multiple cerebral cortices even in cognitively normal subjects. Understanding the impact of WMH on the shrinkage shown in the brains of cognitively healthy older individuals is an important base for assessing the temporal pattern of atrophy of the individual with neurodegenerative disorder like AD. Copyright © 2010 John Wiley & Sons, Ltd.