Ce projet doctoral s’inscrit dans le contexte de la réhabilitation psychosociale promouvant la lutte contre la stigmatisation des maladies psychiatriques sévères. Il vise à une meilleure compréhension de la stigmatisation de la schizophrénie au travers de l’étude des composantes du stéréotype et de ses effets sur les performances neuropsychologiques. La revue de la littérature sur la thématique nous amène au constat d’une grande hétérogénéité dans les méthodes d’exploration du stéréotype de la schizophrénie, en partie expliquée par un cloisonnement des recherches entre la Psychiatrie et la Psychologie sociale.Les deux études réalisées visaient à : i) explorer le contenu du stéréotype de la schizophrénie chez les familles et dans la population générale en France ; ii) étudier expérimentalement l’impact de la menace du stéréotype sur les performances cognitives des personnes souffrant de schizophrénie.La première étude montre que le stéréotype de la schizophrénie est plus massivement rejeté par les familles, et notamment dans sa dimension « Dangerosité ». Les résultats suggèrent en outre que la dimension « Incompétence » du stéréotype de la schizophrénie occupe une place centrale, autant chez les familles que dans la population générale. L’intégration de nos résultats dans les modèles développés par la Psychologie sociale nous amène à proposer un modèle du contenu du stéréotype de la schizophrénie, dans lequel les dimensions de dangerosité et d’incompétence du stéréotype prédiraient des patterns spécifiques d’émotions et de comportements discriminatoires.La seconde étude, expérimentale, ne permet pas de mettre en évidence un effet négatif de la menace du stéréotype de la schizophrénie sur les performances exécutives. Cette absence de résultat significatif nous amène à discuter des enjeux méthodologiques dans les designs expérimentaux, en particulier quant à leur application dans la schizophrénie. Ainsi, certains facteurs comme le domaine d’identification, le choix des mesures cognitives et la prise en compte des différentes menaces potentielles apparaissent primordiaux pour les recherches futures. / This doctoral research interests the field of psychosocial rehabilitation, promoting the fight of stigma in severe mental disorders. The objective is to better understand the schizophrenia stigma through the study of stereotype components and its effect on current clinical neuropsychological practice. The review of stigma scientific publishing underlines a great methodological heterogeneity regarding schizophrenia stereotype exploration, that can be explain by the scientific partitioning of Social psychology and Psychiatry research. Consequently our doctoral research was aimed at integrating these two bodies of research to enhance the operationalization of schizophrenia stereotype content and its potential effects on cognitive performances.We conducted two studies aimed at: i) exploring schizophrenia content stereotype in families and the general population in France; ii) investigating the impact of stereotype threat on cognitive performances in schizophrenia.The first study shows that schizophrenia stereotype is more strongly rejected by families, especially in its “Dangerousness” dimension. Results also suggest that “Incompetency” is a core dimension of schizophrenia stereotype, both in families and the general population. The integration of our results with the models of Social psychology leads us to propose a model of schizophrenia stereotype content in which the Dangerousness and Incompetency dimensions would both predict specific patterns of emotions and discriminatory behaviors.The second experimental study failed to show any negative effect of schizophrenia stereotype threat on executive performances. Finally, this failure leads us to discuss the methodological issues of experimental designs, especially regarding their application in schizophrenia. Thus, several factors of interest, like the identification domain, the choice of cognitive measures and the consideration for various potential threats appear to be relevant for future research

<p dir="ltr">The development of child temperament during the first year of life, its relationships to neurodevelopmental risk, and its associated psychobiological predictors was examined. Latent curve growth analysis suggested that the first year of life may have two distinct developmental groups with one group characterized by high levels of surgency and orienting/regulating and with one group characterized primarily by lower levels of these traits. These two developmental trajectory groups were unrelated to ADHD family risk, MDD family risk, and frontal asymmetry; however, the groups were associated with current maternal depression. </p>

Post-traumatic stress disorder (PTSD) is classified as an anxiety disorder in the Diagnostic and Statistical Manual IV of the American Psychiatric Association. It is characterised by three main symptom clusters: re-experiencing (of which flashbacks are the hallmark symptom); hyperarousal; and avoidance. Diagnosis requires not only the occurrence of a traumatic event but also an intense emotional (fear, horror, or helplessness) reaction to it. Epidemiological data suggest that 80% of people will experience at least one qualifying event in their lifetime. However, prevalence rates of PTSD are much lower. Additionally, individuals with PTSD tend to experience flashbacks of only two or three particular ‘hot-spots’ of the entire trauma. Therefore, the question arises: why do some moments of trauma flash back and not others? Clinical-cognitive theories of PTSD suggest that shifts in information processing at the time of the trauma (i.e. peri-traumatically) are the mechanism whereby flashbacks are created. However, for ethical and practical reasons peri-traumatic processes in real trauma are seldom studied. An analogue traumatic event has been developed to help study peri-traumatic processes – the trauma film paradigm. This paradigm is used through-out this thesis with the goal of investigating peri-traumatic cognitive mechanisms in flashback formation. Studies 1 and 2 extend previous work using dual tasks to manipulate intrusions in-line with clinical-cognitive theories. Studies 3 and 4 use neuroimaging techniques to investigate brain regions involved in real-time peri-traumatic encoding of analogue flashbacks. Chapter 9 presents heart rate data relating to peri-traumatic physiological response to flashback encoding. All of these studies support the notion that peri-traumatic shifts in processing are involved in flashback formation. In particular, Study 3 suggests that there may be a particular neural signature associated with the formation of flashbacks. Investigation of these brain areas may help solve the questions of why some individuals are more vulnerable to PTSD and why only a few specific moments of a trauma subsequently flashback. Furthermore, an improved understanding of the cognitive mechanisms involved in flashback formation may allow theory and evidence led improvements in PTSD treatments.

Background: Adolescence and young adulthood are particularly vulnerable periods for the development of mental health disorders, including bipolar disorder (BD). Mental health screening at universities could aid in the early identification of particularly at- risk individuals, with the long-term aim of providing early treatment interventions to improve clinical outcomes. However, further research into the identification of appropriate behavioral and biological markers for vulnerability to psychiatric disorders – as well as into the acceptability and efficacy of mental health screening - is warranted. Methods: Young adults were recruited via an already existing Internet-based mental health screening survey of undergraduate students at the University of Oxford. In Study 1, qualitative interviews of young adults with and without previous mental health problems were conducted to assess the acceptability and efficacy of mental health screening within a university setting. In Studies 2-5 we explored the hypotheses of altered emotional decision-making, reward processing and neurostructural integrity as behavioral and neurobiological markers for vulnerability to bipolar disorder via the study of young adults with a common bipolar phenotype (BPP) - some of whom meet diagnostic criteria for bipolar II or not-otherwise-specified disorder (BD II/NOS). To that end, we employed a diverse range of methodologies: alcohol challenge (Study 2); neuropsychological task performance (Study 3); functional magnetic resonance imaging (fMRI; Study 4); diffusion tensor imaging (DTI) and voxel-based morphometry (VBM; Study 5). Results: Findings from Study 1 suggest that young adults are willing to participate in mental health screening within a university setting, and that such screening may be used to offer subsequent treatment interventions. Taken together, findings from Studies 2 and 4 suggest a general blunted reward response among unmedicated young adults at increased risk for BD during euthymia, and additionally suggest pathophysiological similarities between BD and alcohol use disorders (AUDs) that may provide a causal link between the elevated co-occurrence rates of the two disorders. Finally, findings from Study 5 suggest widespread white matter microstructural alterations – which are likely to be neurodevelopmental in origin – among antipsychotic- and mood-stabilizer naïve young adults with BD II/NOS. Conclusions: These data support the hypothesis of neurodevelopmental alterations identifiable prior to significant clinical impairment among young adults at increased risk of – or already meeting DSM-IV criteria for – bipolar disorder. They also suggest that young adults in higher education are willing to participate in mental health screening. Future studies should aim to identify more specific markers for individual disorders such as BD.

Thesis (M.A.)--The University of North Carolina at Greensboro, 2008. / Directed by Thomas Kwapil; submitted to the Dept. of Psychology. Title from PDF t.p. (viewed Jan. 28, 2010). Includes bibliographical references (p. ).

Thesis (Ph. D.)--University of California, San Diego, 2000. / Vita. Includes bibliographical references (leaves 148-160).

Autism spectrum disorders (ASD) are neurodevelopmental disorders with multiple neurobiological aetiologies, which could be genetic, structural, metabolic or immune-mediated. ASDs are diagnosed with deficits in social communication and restricted and repetitive behaviours, and are associated with sensorial atypicalities. 30% of cases have co-existing epilepsy. A series of in vitro, in vivo and post-mortem investigations were undertaken to examine sensory atypicalities in ASD. In vitro characterisation of hippocampal neuronal cultures using immunofluorescence demonstrated the presence of multiple cell types including neurons, astrocytes and microglia. The distribution of ion channels of the Shaker family and tumour necrosis factor α receptors in astrocytes and neurons were identified but not explored further. Neuroanatomical and neuropathological investigations of primary olfactory cortex, using post-mortem stereology, demonstrated a specific increase in glial cell densities in layer II, which was negatively associated with age in ASD. Increases in glia were also associated with symptom severity and often co-localised with the presence of corpora amylacea in layer I. Qualitative analysis of the olfactory tubercle demonstrated that corpora amylacea did not extend to this neighbouring region of the primary olfactory cortex in ASD. These changes were independent of co-existing epilepsy and not observed in epilepsy without ASD. Preliminary pilot studies of the hippocampus provided a stereological sampling strategy to quantify cell densities in future investigations of this area in ASD. Neurophysiological investigations using collected magnetoencephalography data demonstrated diminished occipital gamma oscillatory synchrony in ASD in a visual time perception task. This did not always predict behavioural outcome but was specific to ASD and could not be explained simply in terms of changes in task performance. Moreover, changes in oscillatory synchrony were associated with symptom severity. These observations in primary sensory domains in post-mortem tissue and in patients suggest possible novel mechanisms in ASD and extend knowledge of the neurobiological bases of these disorders.

Recurrent and intrusive distressing recollections of trauma are a hallmark symptom of Posttraumatic Stress Disorder (PTSD). The term ‘flashback’ is used in this thesis to refer to vivid, sensory perceptual (predominantly visual images), emotional memories from a traumatic event that intrude involuntarily into consciousness. Furthermore, intrusive image based memories occur in a number of other psychological disorders, for example, bipolar disorder and depression. Clinically, the presence and occurrence of flashbacks and flashback type memories are well documented. However, in terms of the neural underpinnings there is limited understanding of how such flashback memories are formed or later involuntarily recalled. An experimental psychopathology approach is taken whereby flashbacks are viewed on a continuum with other involuntary autobiographical memories and are studied using analogue emotional events in the laboratory. An initial review develops a heuristic clinical neuroscience framework for understanding flashback memories. It is proposed that flashbacks consistent of five component parts – mental imagery, autobiographical memory, involuntary recall, attention hijacking and negative emotion. Combining knowledge of the component parts helped provide a guiding framework, at both a neural and behavioural level, into how flashback memories may be formed and how they return to mind unbidden. Four studies (1 neuroimaging, 3 behavioural) using emotional film paradigms were conducted. In the first study, the trauma film paradigm was combined with neuroimaging (n = 35) to investigate the neural basis of both the encoding and the involuntary recall of flashback memories. Results provided a first replication of a specific pattern of brain activation at the encoding of memories that later returned as flashbacks. This included elevation in the rostral anterior cingulate cortex, insula, thalamus, ventral occipital cortex and left inferior frontal gyrus (during just the encoding of scenes that returned as flashbacks) alongside suppressed activation in the left inferior frontal gyrus (during the encoding of scenes that returned as flashbacks in other participants, but not that individual). Critically, this is also the first study to show the brain activation at the moment of flashback involuntary recall in the scanner. Activation in the middle and superior frontal gyri and the left inferior frontal gyrus was found to be associated with flashback involuntary recall. In the second study, control conditions from 16 behavioural trauma film paradigm experiments were combined (n = 458) to investigate commonly studied factors that may be protective against flashback development. Results indicated that low emotional response to the traumatic film footage was associated with an absence of flashbacks over the following week. The third study used a positive film to consider the emotional valence of the emotion component of the framework. Positive emotional response at the time of viewing the footage was associated with positive involuntary memories over the following week. The fourth study aimed to replicate and extend this finding, comparing the impact of engaging in two cognitive tasks after film viewing (equated for general load). Predictions were not supported and methodological considerations are discussed. Results may have implications for understanding flashbacks and involuntary autobiographical memories occurring in everyday life and across psychological disorders. Further understanding of the proposed components of the clinical neuroscience framework may even help inform targeted treatments to prevent, or lessen, the formation and frequency of distressing involuntary memories.

M.A. (Counselling Psychology) / The treatment of learning- and associated socio-emotional problems as found in ADHD has long been researched and practiced. The treatment still doesn't seem 100% effective since it helps in some cases but worsens effects in others. The literature aroused the possibility that other disorders could occur under the same behavioural symptoms as displayed in ADHD. One of these is Tourette's disorder ...

Thesis (doctoral)--University of Limburg, Maastricht, 1992. / Summary in Dutch. Includes bibliographical references (p. 109-119)