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Within the language domain, movement disorders triggered by frontostriatal damage are characterized by deficits in action verbs, motor-language coupling, and syntax. However, these impairments have not been jointly interpreted under a unifying rationale or integratively assessed in terms of possible clinical implications. To bridge these gaps, here we introduce the “disrupted motor grounding hypothesis”, a new framework to conceive such impairments as disturbances of embodied mechanisms (high-order domains based on the recycling of functionally germane sensorimotor circuits). We focus on two relevant lesion models: Parkinson's and Huntington's disease. First, we describe the physiopathology of both conditions as models of progressive frontostriatal impairment. Then, we summarize works assessing action language, motor-language coupling, and syntax in samples at early and preclinical disease stages. To conclude, we discuss the implications of the evidence for neurolinguistic modeling, identify key issues to be addressed in future research, and discuss potential clinical implications. In brief, our work seeks to open new theoretical and translational avenues for embodied cognition research. [ABSTRACT FROM AUTHOR]

Impairments of action language have been documented in early stage Parkinson's disease (EPD). The action-sentence compatibility effect (ACE) paradigm has revealed that EPD involves deficits to integrate action-verb processing and ongoing motor actions. Recent studies suggest that an abolished ACE in EPD reflects a cortico-subcortical disruption, and recent neurocognitive models highlight the role of the basal ganglia (BG) in motor-language coupling. Building on such breakthroughs, we report the first exploration of convergent cortical and subcortical signatures of ACE in EPD patients and matched controls. Specifically, we combined cortical recordings of the motor potential, functional connectivity measures, and structural analysis of the BG through voxel-based morphometry. Relative to controls, EPD patients exhibited an impaired ACE, a reduced motor potential, and aberrant frontotemporal connectivity. Furthermore, motor potential abnormalities during the ACE task were predicted by overall BG volume and atrophy. These results corroborate that motor-language coupling is mainly subserved by a cortico-subcortical network including the BG as a key hub. They also evince that action-verb processing may constitute a neurocognitive marker of EPD. Our findings suggest that research on the relationship between language and motor domains is crucial to develop models of motor cognition as well as diagnostic and intervention strategies. [ABSTRACT FROM AUTHOR]