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Relationship between regional homogeneity changes and cognitive dysfunction in patients with first-episode drug-naïve
Jun Zhou1, Aijun Liao2, Xiaoqian Ma2
1Medical Department of Changsha Social Work College, Changsha, 410004, Hunan, China; Department of Psychiatry, National Clinical Research Center for Mental Disorders and National Center for Mental Disorders, The Second Xiangya Hospital of Central South University, Changsha, 410011, Hunan, China.
Background:
Cognitive dysfunction is a prevalent symptom in patients with bipolar II disorder (BD-II) depression, yet its underlying neural mechanisms remain insufficiently understood. This study aimed to investigate the relationship between local spontaneous neural activity and cognitive dysfunction in BD-II depression using the Regional Homogeneity (ReHo) method.
Methods:
A total of 77 first-episode drug-naïve patients with BD-II depression and 69 healthy controls (HC) underwent magnetic resonance imaging (MRI) scans. Cognitive function was assessed using the Hopkins Verbal Learning Test-Revised (HVLT-R), Stroop Color and Word Test (SCWT), Verbal Fluency Test (VFT), and Wisconsin Card Sorting Test (WCST).
Results:
Patients with BD-II depression exhibited widespread cognitive impairments across multiple domains, including verbal learning and memory, reaction time, executive function, working memory, semantic retrieval, and cognitive flexibility. Moreover, significant alterations in ReHo values were observed in several key brain regions, such as the precentral and postcentral gyri, precuneus, medial frontal gyrus (MFG), triangular part of inferior frontal gyrus, and Rolandic operculum. Notably, after Bonferroni correction, ReHo values in the right MFG were significantly correlated with both immediate and delayed recall scores on the HVLT-R (all P < 0.0002), suggesting a crucial role of this region in cognitive processes.
Conclusion:
These findings indicate that abnormal neural activity in specific brain regions may serve as potential neurobiological markers of cognitive dysfunction in BD-II depression. Identifying these neural correlates could contribute to a better understanding of the pathophysiology of BD-II and inform the development of targeted therapeutic strategies.
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