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Theories of embodied cognition suggest that perceiving an emotion involves somatovisceral and motoric re-experiencing. Here we suggest taking such an embodied stance when looking at emotion processing deficits in patients with Huntington's Disease (HD), a neurodegenerative motor disorder. The literature on these patients' emotion recognition deficit has recently been enriched by some reports of impaired emotion expression. The goal of the study was to find out if expression deficits might be linked to a more motoric level of impairment. We used electromyography (EMG) to compare voluntary emotion expression from words to emotion imitation from static face images, and spontaneous emotion mimicry in 28 HD patients and 24 matched controls. For the latter two imitation conditions, an underlying emotion understanding is not imperative (even though performance might be helped by it). EMG measures were compared to emotion recognition and to the capacity to identify and describe emotions using alexithymia questionnaires. Alexithymia questionnaires tap into the more somato-visceral or interoceptive aspects of emotion perception. Furthermore, we correlated patients' expression and recognition scores to cerebral grey matter volume using voxel-based morphometry (VBM). EMG results replicated impaired voluntary emotion expression in HD. Critically, voluntary imitation and spontaneous mimicry were equally impaired and correlated with impaired recognition. By contrast, alexithymia scores were normal, suggesting that emotion representations on the level of internal experience might be spared. Recognition correlated with brain volume in the caudate as well as in areas previously associated with shared action representations, namely somatosensory, posterior parietal, posterior superior temporal sulcus (pSTS) and subcentral sulcus. Together, these findings indicate that in these patients emotion deficits might be tied to the "motoric level" of emotion expression. Such a double-sided recognition and expression impairment may have important consequences, interrupting empathy in nonverbal communication both ways (understanding and being understood), independently of intact internal experience of emotion., (Copyright © 2017 Elsevier Ltd. All rights reserved.)

Second person social cognition cannot be restricted to dyadic interactions between two persons (the "I" and the "you"). Many instances of social communication are triadic, and involve a third person (the "him/her/it"), which is the object of the interaction. We discuss neuropsychological and brain imaging data showing that triadic interactions involve dedicated brain networks distinct from those of dyadic interactions.

Humans usually point at objects to communicate with other persons, although they generally avoid pointing at the other's body. Moreover, patients with heterotopagnosia after left parietal damage cannot point at another person's body parts, although they can point at objects and at their own body parts and although they can grasp the others' body parts. Strikingly, their performance gradually improves for figurative human body targets. Altogether, this suggests that the body of another real person holds a specific status in communicative pointing. Here, we test in healthy individuals whether performance for communicative pointing is influenced by the communicative capacity of the target. In Experiment 1, pointing at another real person's body parts was compared to pointing at objects, and in Experiment 2, the person was replaced by a manikin. While reaction times for pointing at objects were shorter compared to pointing at other person's body parts, they were similar for objects and manikin body parts. By adapting Experiment 1 to PET-scan imaging (Experiment 3), we showed that, compared to pointing at objects, the brain network for pointing at other person's body parts involves the left posterior intraparietal sulcus, lesion of which could cause heterotopagnosia. Taken together, our results indicate that the specificity of pointing at another person's body goes beyond the visuo-spatial features of the human body and might rather rely on its communicative capacity., (Copyright © 2012 Elsevier Ltd. All rights reserved.)

Declarative memory is a long-term store for facts, concepts and words. Procedural memory subserves the learning and control of sensorimotor and cognitive skills, including the mental grammar. In this study, we report a single-case study of a mild aphasic patient who showed procedural deficits in the presence of preserved declarative memory abilities. We administered several experiments to explore rule application in morphology, syntax and number processing. Results partly support the differentiation between declarative and procedural memory. Moreover, the patient's performance varied according to the domain in which rules were to be applied, which underlines the need for more fine-grained distinctions in cognition between procedural rules.

Heterotopagnosia is the acquired inability of brain-lesioned patients to point at someone else's body parts when prompted. The cognitive basis of this disorder is unclear. It might result from a biological function deficit critical for communication in human beings; alternatively, it could result from the disruption of a body representation. Here, we report three patients with heterotopagnosia following a recent left parieto-occipital stroke and a previous insular lesion. The patients were tested on their ability to name, point out and grasp several targets including body parts (own, real others' and figurative others'). Language, visuo-spatial deficits or any confounding neuropsychological disorders were controlled for. We found that the patients erroneously pointed to their own body parts when asked to point at someone else's. Strikingly, their ability to grasp someone else's body parts was largely unimpaired. The dissociation between their grasping and communicative pointing abilities supports the hypothesis that heterotopagnosia is a disorder of communicative function conveyed by pointing but not by grasping. In addition, pointing performance in our patients varied according to the target: the more similar the target was to a real person, the worse the patients' pointing performance. We suggest that communicative pointing might require a specific representation of the addressee's body and point of view, a heterocentric representation. In the patients described here this phenomenon resulted from a combined insulo-parietal lesion, which may explain why, in contrast to other patients described previously, the heterotopagnosia was long-lasting.

Objective: To assess the natural progression of cognitive impairment in Huntington's disease (HD) and to reveal factors that may mask this progression., Background: Although numerous cross-sectional studies reported cognitive deterioration at different stages of the disease, progressive cognitive deterioration has been, up to now, difficult to demonstrate in neuropsychological longitudinal studies., Methods: The authors assessed 22 patients in early stages of HD at yearly intervals for 2 to 4 years (average, 31.2 +/- 10 months), using a comprehensive neuropsychological battery based on the Core Assessment Program for Intracerebral Transplantation in Huntington's Disease (CAPIT-HD)., Results: The authors observed a significant decline in different cognitive functions over time: these involved primarily attention and executive functions but also involved language comprehension, and visuospatial immediate memory. Episodic memory impairment that was already present at the time of enrollment did not show significant decline. The authors found a significant retest effect at the second assessment in many tasks., Conclusion: Many attention and executive tasks adequately assess the progression of the disease at an early stage. For other functions, the overlapping of retest effects and disease progression may confuse the results. High interindividual and intraindividual variability seem to be hallmarks of the disease.

Background: Huntington's disease is a neurodegenerative disease of genetic origin that mainly affects the striatum. It has severe motor and cognitive consequences and, up to now, no treatment. Motor and cognitive functions can be restored in experimental animal models by means of intrastriatal transplantation of fetal striatal neuroblasts. We explored whether grafts of human fetal striatal tissue could survive and have detectable effects in five patients with mild to moderate Huntington's disease., Methods: After 2 years of preoperative assessment, patients were grafted with human fetal neuroblasts into the right striatum then, after a year, the left striatum. Final results were assessed 1 year later on the basis of neurological, neuropsychological, neurophysiological, and psychiatric tests. The results obtained were compared with those of a cohort of 22 untreated patients at similar stages of the disease who were followed up in parallel. Repeated magnetic resonance imaging (MRI) and positron emission tomography (PET) scanning with fluorine-18-labelled fluorodeoxyglucose was also done to assess metabolic activity., Findings: The final PET-scan assessment showed increased metabolic activity in various subnuclei of the striatum in three of five patients, contrasting with the progressive decline recorded in the two other patients in the series, as seen in patients with untreated Huntington's disease. Small areas of even higher metabolic activity, coregistering with spherical hyposignals on MRI were also present in the same three patients, suggesting that grafts were functional. Accordingly, motor and cognitive functions were improved or maintained within the normal range, and functional benefits were seen in daily-life activities in these three patients, but not in the other two., Interpretation: Fetal neural allografts could be associated with functional, motor, and cognitive improvements in patients with Huntington's disease.