Lateralization-specific motor network reorganization in pontine infarction revealed by resting-state functional connectivity magnetic resonance imaging.

Background: Pontine infarction (PI) accounts for 7% of ischemic strokes, yet motor recovery varies significantly despite comparable lesion topography. The neural mechanisms underlying this heterogeneity remain unclear. This study aimed to investigate lesion laterality-dependent functional reorganization within the motor execution network following PI through the use of region of interest (ROI)-based resting-state functional magnetic resonance imaging (rs-fMRI). Methods: A total of 31 patients with acute unilateral PI [19 with left PI (LPI) and 12 with right PI (RPI)] and 31 matched controls underwent rs-fMRI. Seed-based functional connectivity (FC) analysis of the motor execution network was performed with spherical ROIs (6-mm radius). Group differences in FC were tested with one-way analysis of variance (ANOVA) and post hoc Bonferroni correction [cluster-level family-wise error (FWE)-corrected P<0.05]. Correlations between FC, infarct volume, and National Institute of Health Stroke Scale (NIHSS) scores were assessed. Results: No significant intergroup differences were observed in age, education years, head motion parameters, or gender distribution (P>0.05). Lesion volumes during the acute phase and NIHSS scores did not differ significantly between the LPI and RPI groups (P>0.05). In patients with LPI, FC was enhanced between the right dorsolateral prefrontal cortex (DLPFC) and the thalamus/basal ganglia, between the right supplementary motor area (SMA)/precentral gyrus and ipsilateral basal ganglia, and between the thalamus and bilateral cerebellum (all cluster-level FWE-corrected P values <0.05). In contrast, FC was reduced within the ipsilateral motor cortex and between the ventral premotor cortex and sensory cortex (all cluster-level FWE-corrected P values <0.05). In patients with RPI, FC was enhanced between the posterior cingulate cortex (PCC)/precuneus and thalamus and between the left SMA and contralateral basal ganglia (all cluster-level FWE-corrected P values <0.05). Within the LPI group, the FC between the right DLPFC and thalamus correlated positively with infarct volume (r=0.575; P=0.012). However, no significant correlations were observed between FC alterations and NIHSS scores or the NIHSS motor subscores (upper and lower extremity items), respectively, in either the LPI or RPI groups (all P values >0.05). Conclusions: Motor recovery post-PI may be influenced by dynamic imbalances in multinetwork early alterations and potentially shaped by lesion laterality: left-sided lesions primarily show recruitment of contralateral prefrontal cognitive resources, whereas right-sided lesions appear to engage default mode network (DMN)-mediated spatial remapping. The thalamo-basal ganglia hub may orchestrate transhemispheric integration, and its FC alterations, such as those within the DLPFC-thalamic pathway, might reflect compensatory potential, potentially offering insights into rehabilitation strategies. However, longitudinal studies are needed to validate these preliminary findings.