Semantic hyperpriming in schizophrenic patients: increased facilitation or impaired inhibition in semantic association processing?

International audiencePrevious studies analyzing semantic priming in schizophrenic patients have reported conflicting results. In the present study, we explored semantic priming in a sample of schizophrenic patients with mild thought disorders. We wondered if distinct cognitive processes, such as facilitation and/or inhibition, underlie semantic hyperpriming and are variously impaired in schizophrenic patients. Using a lexical decision task, we evaluated semantic priming in 15 schizophrenic patients (DSM-IV) with mild thought disorders and 15 healthy controls matched for sex, age, and education level. The task was designed to divide semantic priming into two additive components, namely facilitation effect and inhibition effect. One-sample t-tests were performed to investigate differences in semantic priming, facilitation, and inhibition within each group. ANOVAs were performed to compare the effects of semantic priming, facilitation, and inhibition between groups. Patients displayed greater semantic priming than controls (i.e., hyperpriming), but this was not due to increased facilitation in processing semantically related pairs. On the contrary, hyperpriming was the result of prolonged response time to process semantically unrelated pairs, corresponding to a requirement to inhibit unrelated information. We demonstrated semantic hyperpriming in stabilized schizophrenic patients with mild severity of symptoms. Thus, semantic hyperpriming may be an intrinsic feature of schizophrenia that is not related to the clinical state of patients. Semantic hyperpriming was due to an inhibition effect involved in processing semantically unrelated information not to increased facilitatory effect for related pairs

Cognitive and affective Theory of Mind in mild to moderate Alzheimer's disease.

International audienceTheory of Mind (ToM) allows one's own and others' cognitive and emotional mental states to be inferred. Although many patients with Alzheimer's disease (AD) display impaired social functioning as their disease progresses, very few studies have investigated ToM in AD. Those that have done so suggest that patients' ToM deficits are the consequence of other cognitive impairments. The aim of this study was thus to investigate changes in both the cognitive and the affective dimensions of ToM in AD, using tasks designed to circumvent the patients' comprehension difficulties. Sixteen mild to moderate AD patients and 15 healthy controls matched on age, sex and education level underwent cognitive (preference judgment and first- and second-order false belief) and affective (Reading the Mind in the Eyes) ToM assessments. Comprehension of false belief stories was verified and an additional neuropsychological examination was undergone. We observed impaired performances by AD patients on all the ToM tasks. While working memory and executive functioning impairments contributed to the deterioration in the more complex aspects of cognitive ToM abilities as highlighted by a correlation analysis, we failed to observe any comprehension difficulties in patients who performed poorly on simple cognitive ToM tasks, which suggests that AD truly affects cognitive ToM

Does hyperpriming reveal impaired spreading of activation in schizophrenia?

International audienceEnhancement of semantic priming effects (hyperpriming) has been well documented in schizophrenic patients (Minzenberg et al. 2002). In a previous study, we demonstrated that hyperpriming was related to a more pronounced requirement to inhibit unrelated information (Lecardeur et al. 2007). On the other hand, several authors have suggested that hyperpriming could reflect enhanced spreading of semantic activation in schizophrenia (Spitzer et al. 1993; Spitzer 1997; Moritz et al. 2001). So far, there are few reports that attempted to study the spreading of activation in schizophrenic patients compared to healthy controls, when the links between semantically related information were manipulated. Notably, authors stated that activation could consequently spread farther and further in the semantic networks of schizophrenic patients. Moreover, enhanced spreading of activation was hypothesized to be responsible of the appearance of thought and language disorders in schizophrenic patients. Consequently, we examined whether the manipulation of the type of connection and the semantic distance between prime and target can modulate semantic priming effects in schizophrenic patients compared to healthy controls

Sense of identity in advanced Alzheimer's dementia: a cognitive dissociation between sameness and selfhood?

International audienceWe looked at whether sense of identity persists in patients with Alzheimer's disease (AD) and if its profile remains the same between two examinations. A specifically designed protocol was administered to 16 AD patients in the mild to severe stages of dementia and to 16 matched healthy controls, both living in the same institution. We showed that sense of identity was broadly preserved in AD patients. The patterns of their responses were similar to those of controls, and remained consistent over a two-week period. However, some qualitative characteristics of sense of identity in AD patients differed significantly from those of controls, suggesting that AD patients may not be able to update their self-knowledge, probably because of their episodic memory deficit. These results are discussed in the light of both current models of the self and philosophical concepts such as sameness and selfhood

Theory of mind impairments in patients with semantic dementia.: ToM in semantic dementia

International audienceSemantic dementia is characterized by semantic deficits and behavioural abnormalities that occur in the wake of bilateral inferolateral and predominantly left-sided anterior temporal lobe atrophy. The temporal poles have been shown to be involved in theory of mind, namely the ability to ascribe cognitive and affective mental states to others that regulates social interactions by predicting and interpreting human behaviour. However, very few studies have examined theory of mind in semantic dementia. In this study, we investigated both cognitive and affective theory of mind in a group of patients with semantic dementia, using separate objective and subjective assessment tasks. Results provided objective evidence of an impact of semantic dementia on cognitive and affective theory of mind, consistent with the patients' atrophy in the left temporal lobe and hypometabolism in the temporal lobes and the medial frontal cortex. However, the subjective assessment of theory of mind suggested that awareness of the affective but not cognitive theory of mind deficit persists into the moderate stage of the disease

Neurocognitive determinants of theory of mind across the adult lifespan

International audienceAlthough theory of mind (ToM) has been extensively explored in aging, few studies have used the same tool to simultaneously assess and compare its cognitive and affective components. When we administered the Movie for Assessment of Social Cognition, a dynamic sequence of social scenes, to 60 healthy participants (20-75 years), we observed no different age-related decreases in both cognitive and affective ToM. While each component was associated with cognitive measures (i.e., episodic memory and processing speed were predictive of cognitive ToM, and recognition of facial emotion expressions and inhibition were predictive of affective ToM), mediation analyses showed that these measures only mediated the effect of age on affective ToM. Voxelwise regressions with grey-matter volume showed that the components partly rely on the same neural substrates, reflecting either ToM per se or other cognitive processes elicited by this multi-determinant task. We discuss the specific substrates of each ToM component, emphasising the importance of considering the impact of other aspects of cognition, present in more ecological situations, on ToM functioning

Pathophysiology of the behavioral variant of frontotemporal lobar degeneration: A study combining MRI and FDG-PET

International audienceGray matter (GM) lobar atrophy and glucose hypometabolism are well-described hallmarks of frontotemporal lobar degeneration (FTLD), but the relationships between them are still poorly understood. In this study, we aimed to show the patterns of GM atrophy and hypometabolism in a sample of 15 patients with the behavioral variant of FTLD (bv-FTD), compared to 15 healthy controls, then to provide a direct comparison between GM atrophy and hypometabolism, using a voxel-based method specially designed to statistically compare the two imaging modalities. The participants underwent structural magnetic resonance imaging and 18F-fluorodeoxyglucose (FDG) positron emission tomography examinations. First, between-group comparisons of GM volume and metabolism were performed. Then, in the patient group, correlations between regional alterations and direct between-modality voxelwise comparison were performed. Finally, we examined individual patterns of brain abnormalities for each imaging modality and each patient. The observed patterns of GM atrophy and hypometabolism were consistent with previous studies. We found significant voxelwise correlations between changes in GM and FDG uptake, mainly in the frontal cortex, corresponding to the typical profile of alterations in bv-FTD. The direct comparison revealed regional variability in the relationship between hypometabolism and atrophy. This analysis revealed greater atrophy than hypometabolism in the right putamen and amygdala, and left insula and superior temporal gyrus, whereas hypometabolism was more severe than GM atrophy in the left caudate nucleus and anterior cingulate cortex. Finally, GM atrophy affected the right amygdala/hippocampus and left insula in 95% of the patients. These findings provide evidence for regional variations in the hierarchy of hypometabolism and GM atrophy and the relationships between them, and enhance our understanding of the pathophysiology of bv-FTD