Abnormal coordination of executive control network and default mode network in cognitive impairment after deep nuclei intracerebral hemorrhage
Xiwen Fan, Yuchen Lei, Yongbing Deng, Yi Xiang, Chao Sun, Xing Yu, Jun Zhang, Chang Li, Peng Chen
Frontiers in Neurology September 16, 2026 DOI: 10.3389/fneur.2026.1915567 (opens in new tab)
Study at a glance
AI-extracted from the abstract| Characteristics | Observational case-control study Peer reviewed |
|---|---|
| Sample size | 239 |
| Population | 139 patients with cognitive impairment after deep nuclei intracerebral hemorrhage and 100 healthy controls |
| Measures | Mini-Mental State Examination (MMSE), fractional Amplitude of Low-Frequency Fluctuations (fALFF), functional connectivity (FC) |
| Topics | Default mode network |
| Key findings | Cognitive impairment after deep nuclei intracerebral hemorrhage was associated with altered spontaneous activity in the right dorsolateral prefrontal cortex and posterior cingulate cortex and with abnormal functional connectivity within and between the executive control and default mode networks. Connectivity fingerprints distinguished patients with dementia (MMSE ≤ 17) from others with areas under the curve of 0.70 to 0.73. The authors argue that abnormal coordination of these networks may be a shared neural mechanism of post-hemorrhage cognitive impairment. |
Abstract
Objective: 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.
Method: 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).
Result: 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).
Conclusion: 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.