scholarly journals Tract-based spatial statistics on diffusion tensor imaging in systemic lupus erythematosus reveals localized involvement of white matter tracts

2010 ◽  
Vol 62 (12) ◽  
pp. 3716-3721 ◽  
Author(s):  
Bart J. Emmer ◽  
Ilya M. Veer ◽  
Gerda M. Steup-Beekman ◽  
Tom W. J. Huizinga ◽  
Jeroen van der Grond ◽  
...  
Lupus ◽  
2021 ◽  
pp. 096120332110450
Author(s):  
Cong Zhou ◽  
Man Dong ◽  
Weiwei Duan ◽  
Hao Lin ◽  
Shuting Wang ◽  
...  

Background Systemic lupus erythematosus is often accompanied with neuropsychiatric symptoms. Neuroimaging evidence indicated that microstructural white matter (WM) abnormalities play role in the neuropathological mechanism. Diffusion tensor imaging (DTI) studies allows the assessment of the microstructural integrity of WM tracts, but existing findings were inconsistent. This present study aimed to conduct a coordinate‐based meta‐analysis (CBMA) to identify statistical consensus of DTI studies in SLE. Methods Relevant studies that reported the differences of fractional anisotropy (FA) between SLE patients and healthy controls (HC) were searched systematically. Only studies reported the results in Talairach or Montreal Neurological Institute (MNI) coordinates were included. The anisotropic effect size version of signed differential mapping (AES-SDM) was applied to detect WM alterations in SLE. Results Totally, five studies with seven datasets which included 126 patients and 161 HC were identified. The pooled meta-analysis demonstrated that SLE patients exhibited significant FA reduction in the left striatum and bilateral inferior network, mainly comprised the corpus callosum (CC), bilateral inferior fronto-occipital fasciculus (IFOF), bilateral anterior thalamic projections, bilateral superior longitudinal fasciculus (SLF), left inferior longitudinal fasciculus (ILF), and left insula. No region with higher FA was identified. Conclusions Disorders of the immune system might lead to subtle WM microstructural alterations in SLE, which might be related with cognitive deficits or emotional distress symptoms. This provides a better understanding of the pathological mechanism of microstructural brain abnormalities in SLE.


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