ABSTRACT
Recent embodied cognition research shows that access to action verbs in shallow-processing tasks becomes selectively compromised upon atrophy of the cerebellum, a critical motor region. Here we assessed whether cerebellar damage also disturbs explicit semantic processing of action pictures and its integration with ongoing motor responses. We evaluated a cognitively preserved 33-year-old man with severe dysplastic cerebellar gangliocytoma (Lhermitte-Duclos disease), encompassing most of the right cerebellum and the posterior part of the left cerebellum. The patient and eight healthy controls completed two semantic association tasks (involving pictures of objects and actions, respectively) that required motor responses. Accuracy results via Crawford's modified t-tests revealed that the patient was selectively impaired in action association. Moreover, reaction-time analysis through Crawford's Revised Standardized Difference Test showed that, while processing of action concepts involved slower manual responses in controls, no such effect was observed in the patient, suggesting that motor-semantic integration dynamics may be compromised following cerebellar damage. Notably, a Bayesian Test for a Deficit allowing for Covariates revealed that these patterns remained after covarying for executive performance, indicating that they were not secondary to extra-linguistic impairments. Taken together, our results extend incipient findings on the embodied functions of the cerebellum, offering unprecedented evidence of its crucial role in processing non-verbal action meanings and integrating them with concomitant movements. These findings illuminate the relatively unexplored semantic functions of this region while calling for extensions of motor cognition models.
ABSTRACT
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.
