Abnormal coordination of executive control network and default mode network in cognitive impairment after deep nuclei intracerebral hemorrhage
This study investigated the macroscopic neural mechanisms of cognitive impairment after Deep Nuclei Intracerebral Hemorrhage (DNICH) from the dimensions of brain activity and brain networks, and further identified characteristic fingerprints of cognitive representation. Patients with cognitive impairment after DNICH and healthy controls (HC) were prospectively and consecutively enrolled. Resting-state fMRI (rs-fMRI) data and the cognitive scale Mini-Mental State Examination (MMSE) were collected. Spontaneous brain activity measured by fractional Amplitude of Low-Frequency Fluctuations (fALFF) was used to identify hub brain regions of cognitive representation, which were then used as Regions of Interest (ROI) for Functional Connectivity (FC) analysis, in order to investigate the potential mechanisms after DNICH cognitive impairment and identify characteristic fingerprints for distinguishing patients with dementia (dementia was defined as MMSE ≤ 17). This study enrolled 139 patients with DNICH and 100 HC. There were no significant differences in baseline characteristics including age, gender, years of education, height, and weight between the two groups. Hematomas were predominantly located in the bilateral basal ganglia, more commonly on the left side, with varying degrees of thalamic and white matter involvement. Whole-brain zfALFF analysis showed that MMSE scores were significantly correlated with zfALFF values in brain regions including right dorsolateral prefrontal cortex (R-DLPFC) and posterior cingulate cortex (PCC), with R-DLPFC positively correlated and PCC negatively correlated with cognition (AlphaSim correction, p < 0.01; cluster size >19). In addition, FC within the executive control network (ECN) and default mode network (DMN) was abnormally altered in patients with cognitive impairment and was closely associated with cognitive function ( r = −0.29–0.51). FC fingerprints demonstrated stable predictive ability for dementia status (AUC = 0.70–0.73). Abnormal coordination of intra-network and inter-network FC of ECN and DMN may represent a shared neural mechanism of cognitive impairment after DNICH. Modulating FC between these hub brain regions (R-DLPFC and PCC) may provide new therapeutic strategies for cognitive recovery after DNICH.