Plasticity of language networks in patients with brain tumors: A positron emission tomography activation study

TLDR

The study examined language‑network plasticity in patients with slowly evolving left‑hemisphere brain tumors, aiming to identify compensatory mechanisms. Using O‑15‑water PET, 61 right‑handed tumor patients and 12 controls were scanned, revealing intra‑hemispheric recruitment of left frontolateral areas and inter‑hemispheric frontolateral activation as compensatory strategies. Compared to controls, patients displayed additional activation of left BA46/47, anterior insula, and left cerebellum, with frontolateral activation in the nondominant hemisphere occurring only in frontal or posterior temporal lesions, 18 % showing reversed language dominance, and cerebellar laterality indices negatively correlating with language performance.

Abstract

Abstract We investigated plasticity of language networks exposed to slowly evolving brain damage. Single subject O‐15‐water language activation positron emission tomography studies were analyzed in 61 right‐handed patients with brain tumors of the left hemisphere, and 12 normal controls. In controls, activations were found in left Brodmann's Area (BA)44 and BA45, superior posterior temporal gyrus bilaterally, and right cerebellum. Patients additionally activated left BA46, BA47, anterior insula, and left cerebellum. Superior temporal activation was less frequent, and activations in areas other than posterior temporal gyrus were found bilaterally. Frontolateral activations within the nondominant hemisphere were only seen in patients (63%) with frontal or posterior temporal lesions. Laterality indices of frontolateral cortex showed reversed language dominance in 18% of patients. Laterality indices of the cerebellum were negatively correlated with language performance. Two compensatory mechanisms in patients with slowly evolving brain lesions are described: An intrahemispheric mechanism with recruitment of left frontolateral regions other than classic language areas; and an interhemispheric compensatory mechanism with frontolateral activation in the nondominant hemisphere. The latter one was only found in patients with frontal or posterior temporal lesions, thus supporting the hypothesis that right frontolateral activations are a disinhibition phenomenon.