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It is known that unpleasant emotions can modulate the speed of involuntary movements, yet the effects of aversive stimulation on voluntary motor acts have not been systematically investigated. The effects of aversive stimulation on subsequent movement-related cortical activity were examined using a task invalving compatible and incompatible movements. Negative shifts in the timing of two motor event-related potentials were found subsequent to aversive stimulation for compatible movements only. With analogy to the Fear-Potentiated Startle Reflex, a reactive mechanism affecting covert action, these Fear-Potentiated Movement-Related Potentials (FPMPs) reflect preparation for overt actions performed to cope with particular types of danger. Further analysis revealed a positive deflection in the left frontal cortex prior the execution of incompatible movements, which may reflect inhibitory suppression of externally-triggered imitative tendencies.

The hypothesis that semantic deficits in dementia may contribute in producing changes in eating preferences has never been experimentally investigated despite this association has been clinically observed. We administered tasks assessing semantic memory and the Appetite and Eating Habits Questionnaire (APEHQ) to 23 patients with dementia (behavioural frontotemporal dementia, primary progressive aphasia, and Alzheimer's disease) and to 21 healthy controls. We used voxel-based morphometry and diffusion tensor imaging to identify regions and white matter tracts of significant atrophy associated with the performance at the semantic tasks and the pathological scores at the APEHQ. We observed that the lower the patients' scores at semantic tasks, the higher their changes in eating habits and preferences. Both semantic disorders and eating alterations correlated with atrophy in the temporal lobes and white matter tracts connecting the temporal lobe with frontal regions such as the arcuate fasciculus, the cingulum, and the inferior longitudinal fasciculus. These results confirm that semantic deficits underlie specific eating alterations in dementia patients.

Food constitutes a fuel of life for human beings. It is therefore of chief importance that their recognition system readily identifies the most relevant properties of food by drawing on semantic memory. One of the most relevant properties to be considered is the level of processing impressed by humans on food. We hypothesized that recognition of raw food capitalizes on sensory properties and that of transformed food on functional properties, consistently with the hypothesis of a sensory-functional organization of semantic knowledge. To test this hypothesis, patients with Alzheimer’s disease, frontotemporal dementia, primary progressive aphasia, and healthy controls performed lexical-semantic tasks with food (raw and transformed) and non-food (living and nonliving) stimuli. Correlations between task performance and local grey matter concentration (VBM) and white matter fractional anisotropy (TBSS) led to two main findings. First, recognition of raw food and living things implicated occipital cortices, typically involved in processing sensory information and, second, recognition of processed food and nonliving things implicated the middle temporal gyrus and surrounding white matter tracts, regions that have been associated with functional properties. In conclusion, the present study confirms and extends the hypothesis of a sensory and a functional organization of semantic knowledge.

Although deep brain stimulation of the subthalamic nucleus is an effective surgical treatment for Parkinson's disease, it may expose patients to non-motor side effects such as increased impulsivity and changes in decision-making behavior. Even if several studies have shown that stimulation of the subthalamic nucleus increases the incentive salience of food rewards in both humans and animals, temporal discounting for food rewards has never been investigated in patients who underwent STN-DBS. In this study, we measured inter-temporal choice after STN-DBS, using both primary and secondary rewards. In particular, PD patients who underwent STN-DBS (in ON medication/ON stimulation), PD patients without STN-DBS (in ON medication) and healthy matched controls (C) performed three temporal discounting tasks with food (primary reward), money and discount vouchers (secondary rewards). Participants performed also neuropsychological tests assessing memory and executive functions. Our results show that STN-DBS patients and PD without DBS behave as healthy controls. Even PD patients who after DBS experienced weight gain and/or eating alterations did not show an increased temporal discounting for food rewards. Interestingly, patients taking a higher dosage of dopaminergic medications, fewer years from DBS surgery and, unexpectedly, with better episodic memory were also those who discounted rewards more. In conclusion, this study shows that STN-DBS does not affect temporal discounting of primary and secondary rewards. Furthermore, by revealing interesting correlations between clinical measures and temporal discounting, it also shed light on the clinical outcomes that follow STN-DBS in patients with PD.

Background Parkinson's disease (PD) patients who are treated with dopamine replacement therapy are at risk of developing impulse control disorders (ICDs) (such as gambling, binge eating, and others). According to recent evidence, compulsive reward seeking in ICDs may arise from an excessive attribution of incentive salience (or ‘wanting’) to rewards. Objectives In this study, we tested this hypothesis in patients with PD who developed binge eating (BE). Methods Patients with BE, patients without BE, and healthy controls performed different experimental tasks assessing food liking and wanting. Participants first rated the degree of liking and wanting for different foods using explicit self-report measures. They then performed an affective priming task that measured participants' affective reactions towards foods (liking), and a grip-force task that assessed their motivation for food rewards (wanting). All participants also completed several questionnaires assessing impulsivity, reward sensitivity, anxiety and depression, and underwent a neuropsychological evaluation. Results Patients with BE displayed an altered liking for sweet foods compared to controls but not to patients without BE. Furthermore, this difference emerged only when implicit measures were used. Importantly, an increased wanting was not associated with binge eating even if wanting, but not liking scores significantly correlated with LED levodopa, confirming the hypothesis of a distinction between the two components of rewards. Lastly, binge eating was associated with depression and lower working memory scores. Conclusions Take together these results suggest that binge eating in PD is associated with cognitive abnormalities, and to lesser extent affective abnormalities, but not with an increased incentive salience.

Previous studies have suggested that imitators can reproduce known gestures shown by a model using a semantic, indirect route, and novel gestures using a sublexical, direct route. In the present study we aimed at testing the validity of such a dual-route model of action imitation. Patients with either left-brain damage (LBD) or right-brain damage (RBD) were tested on an action imitation task. Actions were either meaningful (n ¼ 20) or meaningless (n ¼ 20), and were presented in an intermingled list and, on a different day, in separate lists. We predicted that, in the mixed condition, patients would use a direct route to imitate meaningful and meaningless actions, as it allows the imitation of both action types. In the blocked condition, patients were expected to select the semantic route for meaningful actions and the direct route for meaningless actions. As hypothesized, none of the 32 patients showed dissociations between imitation of meaningful and meaningless actions in the mixed presentation. In contrast, eight patients showed a dissociation between imitation of meaningful actions and imitation of meaningless actions in the blocked presentation. Moreover, two of these patients showed a classical double dissociation between the imitation of the two action types. Results were interpreted in support of the validity of a dual-route model for explaining action imitation. We argue that the decrease in imitation of meaningful actions, relative to meaningless actions, is caused by a damage of the semantic route, and that the decline in imitation of meaningless actions, relative to meaningful actions, is produced by a breakdown of the direct route. The brain areas that were lesioned in all six LBD patients who showed a dissociation were in the superior temporal gyrus and the angular gyrus, whereas the two RBD subjects had common lesions of the pallidum and of the putamen. The brain structures affected in our patients with selective apraxia are consistent with those reported before in other neuropsychological reports. They are also in agreement with areas found activated in imaging studies in which the neural mechanisms underlying imitation were examined.

The effects of learning on strategy selection in the context of action imitation have been investigated in two experiments conducted with healthy individuals. It was predicted that, once learnt, meaningless actions are processed by the cognitive system as meaningful and this new representational status might influence the process selection in action imitation. Results showed that not only were learnt meaningless actions processed in the same way as known, meaningful actions, but that they were imitated even better, probably due to their being represented only once in the episodic, long-term memory system. Our findings are interpreted in the light of a multiple route model for action imitation.