Infratentorial stroke disrupts functional network connectivities across the whole brain and affects multidomain cognition. Pontine stroke patients have decreased functional connectivities within the primary perceptual and higher cognitive control networks, and increased functional connectivities between the primary perceptual and higher cognitive control networks. The dysfunctional connectivity of the primary perceptual and higher cognitive control networks may be attributable to the neural substrates of multidomain cognitive deficits in pontine stroke patients.Abstract
Cognitive dysfunction in patients with infratentorial stroke has been paid little attention. Brainstem stroke may disrupt network connectivity across the whole brain and affect multidomain cognition, but the details of this process remain unclear. The study aimed to investigate the effects of stroke-induced pontine injury on whole-brain network connectivity and cognitive function. We included 47 patients with pontine stroke and 56 healthy comparisons (HC), who underwent cognitive tests and functional magnetic resonance imaging (fMRI). Seven meaningful brain networks were identified using independent component analysis (ICA). Patients with pontine stroke had decreased intra-network functional connectivities (FCs) in the primary perceptual and higher cognitive control networks, including sensorimotor network (SMN), visual network (VIS), default mode network (DMN), and salience network (SAN), as well as decreased inter-network FCs in the primary perceptual (VIS-SMN) and higher cognitive control networks (bilateral frontoparietal networks, rFPN-lFPN). While the FCs between the primary perceptual and higher cognitive control networks (VIS-DMN, VIS-rFPN, VIS-lFPN) were increased. Furthermore, the alterations in these FCs correlated with patients' cognitive measurements. These findings suggested that the infratentorial stroke can induce dysfunctional connectivity in both primary perceptual and higher cognitive control networks at the whole-brain level, which may be attributable to the neural substrates of multidomain cognitive deficits in these patients.