Increased ALFF and functional connectivity of the right striatum in bipolar disorder patients

Background: Bipolar disorder (BD) is a serious neuropsychiatric disorder characterized by alternating periods of mania, depression, and euthymia. Abnormal spontaneous brain activity within the cortical-striatal neural circuits has been observed in patients with BD. However, whether the abnormality appears in patients with BD while not in a manic mood state is unclear. Methods: This study collected resting-state fMRI data from 65 patients with BD who were not in a manic mood state and 85 matched healthy controls. First, we examined differences in amplitude of low-frequency fluctuations (ALFF) between the patients with BD and the healthy controls to identify regions that show abnormal local spontaneous activity in the patients. Based on the ALFF results, we conducted seed-based resting-state functional connectivity (rsFC) analysis to identify the changes in brain networks that are centered on the regions showing abnormal local spontaneous activity in the patients. Finally, we repeated these analyses in a sub-sample comprising euthymic BD patients (N = 37) and between the euthymic BD patients and all the other patients who had at least mild depressive symptoms. Results: BD patients exhibited increased ALFF in the right caudate/putamen and increased rsFC in the right caudate/putamen with the right inferior parietal lobe (cluster-level FWE p < 0.05). Further analyses showed that the euthymic BD patients showed similar abnormalities in ALFF and rsFC maps as found in all patients with BD. And the euthymic BD patients were comparable with all the other patients who had at least mild depressive symptoms in ALFF values. Conclusions: Our results indicated the important role of the right striatum in the baseline brain function of BD patients and suggested that the abnormality of spontaneous brain activity in the cortical-striatal neural circuits may be a trait-like variant in patients with BD. The results deepen our understanding of the neurobiological mechanisms associated with BD etiology.