Regional brain atrophy in overactive bladder syndrome: a voxel based morphometry study

Objectives To investigate whether patients with overactive bladder syndrome (OAB) have brain volume changes using voxel-based morphometry (VBM) and correlations with clinical tests. Methods With institutional review board approval and after obtaining written informed consent, structural magnetic res...

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Veröffentlicht in:International urology and nephrology 2021, Vol.53 (1), p.27-33
Hauptverfasser: Zuo, Long, Zhou, Yang, Wang, Shuangkun, Wang, Biao, Gu, Hua, Chen, Jingnan
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Sprache:eng
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Zusammenfassung:Objectives To investigate whether patients with overactive bladder syndrome (OAB) have brain volume changes using voxel-based morphometry (VBM) and correlations with clinical tests. Methods With institutional review board approval and after obtaining written informed consent, structural magnetic resonance imaging data were prospectively acquired in 28 patients and 28 control subjects. OAB symptoms were assessed using the OAB symptom score (OABSS) scale. The gray matter volume (GMV) of each voxel was compared between the two groups while controlling for the effects of age, sex, and education level. Correlation analysis was performed to identify correlations between abnormal GMV regions and OABSS scores in patients. Multiple comparisons were corrected using a false discovery rate (FDR) method. Results Patients with OAB exhibited a GMV reduction in the right cerebellum, bilateral hippocampus, left insula, right superior temporal gyrus, left anterior cingulate gyrus, bilateral caudate nucleus and right middle frontal gyrus. Furthermore, there was a significant negative correlation between the local GMV of the right cerebellar hemisphere and OABSS score. Conclusions Patients with OAB have abnormal GMV in brain regions localized within the brain-bladder control network. It deepens our understanding of the structural changes in the brain area of the network. The patterns of structural reorganization in patients with OAB may provide useful information in the neuropathological mechanisms of the OAB.
ISSN:0301-1623
1573-2584
DOI:10.1007/s11255-020-02614-8