ABSTRACT Background Bilingual individuals with aphasia may exhibit unique patterns of language impairment and recovery. While code-switching (CS) is a common feature of bilingual speech, pathological CS following brain damage can provide insights into the neural mechanisms controlling bilingual language processing. Aims This study aimed to examine language impairment and recovery patterns in IZ, an unbalanced Hebrew-English bilingual with non-fluent aphasia, focusing on the unusual CS behavior observed during his subacute phase of recovery. Methods and procedures IZ underwent language and narrative assessments in both languages during the subacute and chronic phases of recovery. Ten cognitive tests were administered to assess various domains of cognitive function. Language performance was evaluated through naming and syntactic processing tasks in L1-Hebrew and L2-English. The frequency and type of CS were analyzed using the matrix language frame model. Outcomes and results During the subacute phase, IZ displayed significant language deficits in both L1-Hebrew and L2-English, with more severe impairment in L1-Hebrew naming and L2-English syntactic processing. He exhibited frequent involuntary CS, primarily using L1-Hebrew as the matrix language while embedding L2-English content words. Cognitive testing revealed reduced performance across multiple domains. In the chronic phase, IZ showed parallel improvements in both languages, particularly in L1-Hebrew naming and L2-English syntactic processing, along with a marked reduction in CS frequency. Conclusions IZ’s case demonstrates a double dissociation between lexical and syntactic processing across L1 and L2. The results suggest that matrix language selection in bilinguals may be governed by distinct neural mechanisms for each language, with specific brain regions responsible for activating lexical representations. Damage to these regions may lead to pathological CS, as observed in this case. This study underscores the importance of understanding bilingual language control mechanisms in aphasia rehabilitation.
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