Altered default mode network connectivity in basal ganglia intracerebral hemorrhage: A resting-state fMRI study.

Objective: This study investigates the impact of basal ganglia intracerebral hemorrhage (ICH) on default mode network (DMN) connectivity and its relationship with cognitive impairment using resting-state functional magnetic resonance imaging (rs-fMRI).

Method: DMN differences between left/right basal ganglia ICH patients and healthy controls were analyzed respectively. Co-altered brain region were obtained by overlapping the differential brain regions of bilateral basal ganglia ICH. Gene and functional decoding analyses validated the role of co-altered brain regions in cognition. Whole-brain functional connectivity (FC) analysis was conducted using the co-altered brain region as a seed, and correlation analysis was performed with the Mini-Mental State Examination (MMSE) to obtain the cognitive representation brain network of patients in basal ganglia ICH. Finally, it was nested with the DMN of basal ganglia ICH patients to obtain the important brain regions regulating cognitive function in the DMN of basal ganglia ICH patients.

Result: A total of 89 basal ganglia ICH patients were enrolled. Compared to healthy controls, bilateral basal ganglia ICH patients showed significant alterations in DMN connectivity. The co-altered brain region mainly involved the medial prefrontal cortex (mPFC). Additionally, gene and functional decoding analyses revealed strong association with chemical synaptic transmission, synaptic signaling, cognition, and intelligence. The left parahippocampal gyrus, the left superior temporal gyrus, right temporal regions, the cerebellar, and posterior cingulate cortex exhibited significant correlation with MMSE. Furthermore, the left parahippocampal gyrus emerged as a key node in the DMN of basal ganglia ICH patients involved in cognitive regulation.

Conclusion: The mPFC-left parahippocampal circuit in the DMN plays a crucial role in cognitive regulation following basal ganglia ICH. These findings provide new insights into neural mechanisms underlying cognitive changes after basal ganglia ICH and suggest potential therapeutic targets for cognitive rehabilitation.