Bonivento, Carolina (2012)
Ph.D. thesis, University of Birmingham.
Humans appear to show an innate tendency to imitate, and this may provide one of the foundations of social communication. Several studies have been carried out in social and cognitive science in order to understand how imitation works, which parts of the brain are involved, and what the role of imitation might be in social behaviour. Previous brain imaging and neuropsychological studies
report data that favour a dual process account of imitation, according to which actions are imitated
through different mechanisms on the basis of whether they are meaningful and familiar (MF actions) or meaningless/unfamiliar (ML actions). However many questions remain to be clarified – such as which brain areas mediate these different actions. In addition to the distinction between MF and ML gestures, there is considerable interest in the production of different types of known gestures – particularly between actions involving tools (i.e. transitive actions) and those subserving communicative (intransitive) gestures, and in how the production of these gestures relates to the processes involved in recognizing the gestures as input. This thesis reports a neuropsychological examination of the functional and neural bases of imitation using converging data from behavioural
studies with different patient groups (stroke patients, patients with Parkinson’s Disease, PD) and structural brain imaging (particularly using voxel-based morphometric [VBM] analyses) to examine lesion-symptom relations.
The first empirical chapter (Chapter 2) describes a neuropsychological study on the recognition and production of MF actions and the imitation of ML gestures, in patients with unilateral left or rightside brain damage (respectively: LBD and RBD patients). At a group level, LBD patient were worse in imitation than RBD patients only when novel transitive actions had to be reproduced, when both LBD and RBD differed from healthy participants, while intransitive gestures were generally easier to be executed. Also both transitive and intransitive action imitation tasks were correlated to action recognition. At a single subject level, however, there was evidence for some dissociated symptoms, suggesting that at least partially different mechanisms mediate the imitation of transitive and intransitive gestures and gesture production as opposed to recognition.
Chapter 3 presents a first attempt to use VBM to evaluate the relations between brain lesions and the symptoms of apraxia, contrasting the imitation of meaningful (familiar) and meaningless (unfamiliar) transitive and intransitive actions in a consecutive series of brain damaged patients.
Chapters 4 and 5 describe two investigations where VBM was again used in a large-scale lesionsymptom analysis of deficits in i) the recognition and generation to command of MF actions and the imitation of ML actions, and ii) the generation to command of different types of learned action
(transitive or intransitive gestures). All three investigations using VBM revealed common and differential neural substrates involved in the execution of the tasks considered, and the data are compatible with a model which posits that different processes are involved in MF and ML action execution, as well as in action understanding. The results also suggest that the distinction between transitive and intransitive actions may be included in an action reproduction system. In the final empirical chapter (Chapter 6), I report a study on PD patients tested for imitation of transitive and intransitive MF and ML actions, also relating their performance to the neurological/peripheral symptoms of the disease. This study revealed that PD patients were impaired in imitation, and they also had different pattern of deficit for transitive and intransitive actions. The correlation with peripheral symptoms was not significant, though there were correlations with underlying cognitive processes likely to support action production. Chapter 7 summarizes the different results and links them back to functional and neural accounts of action recognition, production and imitation. The relations between action production and recognition and other cognitive processes are discussed, as
are methodological issues concerning lesion-symptom mapping.
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