Simple SummaryGliomas that infiltrate eloquent areas can damage the corresponding cortical or subcortical structures, leading to language dysfunction. A total of 20–40% of eloquent area glioma patients have language deficits. Gliomas anchored in eloquent areas cause varying degrees of language impairment. A tumor’s size, grade, location, and contralesional compensation may explain these differences. This study aimed to retrospectively explore gray and white matter plasticity in the contralesional hemisphere of patients with gliomas in the eloquent area using VBM and DTI network analysis.Lower-grade Gliomas anchored in eloquent areas cause varying degrees of language impairment. Except for a tumor’s features, contralesional compensation may explain these differences. Therefore, studying changes in the contralateral hemisphere can provide insights into the underlying mechanisms of language function compensation in patients with gliomas. This study included 60 patients with eloquent-area or near-eloquent-area gliomas. The participants were grouped according to the degree of language defect. T1 and diffusion tensor imaging were obtained. The contralesional cortical volume and the subcortical network were compared between groups. Patients with unimpaired language function showed elevated cortical volume in the midline areas of the frontal and temporal lobes. In subcortical networks, the group also had the highest global efficiency and shortest global path length. Ten nodes had intergroup differences in nodal efficiency, among which four nodes were in the motor area and four nodes were in the language area. Linear correlation was observed between the efficiency of the two nodes and the patient’s language function score. Functional compensation in the contralesional hemisphere may alleviate language deficits in patients with gliomas. Structural compensation mainly occurs in the contralesional midline area in the frontal and temporal lobes, and manifests as an increase in cortical volume and subcortical network efficiency.