508 research outputs found

    Schizotypy and psychosis-like experiences from recreational cannabis in a non-clinical sample

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    Background. The relationship between cannabis use and psychosis is still a matter for debate. Accounting for the individual differences in subjective experiences to recreational cannabis use in the general population may hold some clues to the aetiological relationship between cannabis and psychotic symptoms. We hypothesized that schizotypy would account for the individual differences in subjective experiences after cannabis use but not in patterns of use. Method. In a sample of 532 young people who had used cannabis at least once, we examined the relationship between the Cannabis Experiences Questionnaire (CEQ) and the Schizotypal Personality Questionnaire (SPQ). Additionally, we examined the psychometric properties of the CEQ. Results. We replicated our previously reported findings that schizotypy was associated with increased psychosis-like experiences and after-effects, but also found that high-scoring schizotypes reported more pleasurable experiences when smoking cannabis. Using new subscales derived from principal components analysis (PCA), we found that the psychosis-like items were most related to varying rates of schizotypy both during the immediate use of cannabis and in the after-effects of cannabis use. High-scoring schizotypes who used cannabis experienced more psychosis-like symptoms during and after use.Conclusions. Our results suggest that cannabis use may reveal an underlying vulnerability to psychosis in those with high schizotypal traits

    What causes aberrant salience in schizophrenia? A role for impaired short-term habituation and the GRIA1 (GluA1) AMPA receptor subunit.

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    The GRIA1 locus, encoding the GluA1 (also known as GluRA or GluR1) AMPA glutamate receptor subunit, shows genome-wide association to schizophrenia. As well as extending the evidence that glutamatergic abnormalities have a key role in the disorder, this finding draws attention to the behavioural phenotype of Gria1 knockout mice. These mice show deficits in short-term habituation. Importantly, under some conditions the attention being paid to a recently presented neutral stimulus can actually increase rather than decrease (sensitization). We propose that this mouse phenotype represents a cause of aberrant salience and, in turn, that aberrant salience (and the resulting positive symptoms) in schizophrenia may arise, at least in part, from a glutamatergic genetic predisposition and a deficit in short-term habituation. This proposal links an established risk gene with a psychological process central to psychosis and is supported by findings of comparable deficits in short-term habituation in mice lacking the NMDAR receptor subunit Grin2a (which also shows association to schizophrenia). As aberrant salience is primarily a dopaminergic phenomenon, the model supports the view that the dopaminergic abnormalities can be downstream of a glutamatergic aetiology. Finally, we suggest that, as illustrated here, the real value of genetically modified mice is not as ‘models of schizophrenia’ but as experimental tools that can link genomic discoveries with psychological processes and help elucidate the underlying neural mechanisms

    A systematic review of cognitive failures in daily life: healthy populations

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    Cognitive failures are minor errors in thinking reported by clinical and non-clinical individuals during everyday life. It is not yet clear how subjectively-reported cognitive failures relate to objective neuropsychological ability. We aimed to consolidate the definition of cognitive failures, outline evidence for the relationship with objective cognition, and develop a unified model of factors that increase cognitive failures. We conducted a systematic review of cognitive failures, identifying 45 articles according to the PRISMA statement. Failures were defined as reflecting proneness to errors in \u27real world\u27 planned thought and action. Vulnerability to failures was not consistently associated with objective cognitive performance. A range of stable and variable factors were linked to increased risk of cognitive failures. We conclude that cognitive failures measure real world cognitive capacity rather than pure \u27unchallenged\u27 ability. Momentary state may interact with predisposing trait factors to increase the likelihood of failures occurring. Inclusion of self-reported cognitive failures in objective cognitive research will increase the translational relevance of ability into more ecologically valid aspects of real world functioning

    A Transdiagnostic Perspective on Social Anhedonia

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    Humans are highly social beings, yet people with social anhedonia experience reduced interest in or reward from social situations. Social anhedonia is a key facet of schizotypal personality, an important symptom of schizophrenia, and increasingly recognized as an important feature in a range of other psychological disorders. However, to date, there has been little examination of the similarities and differences in social anhedonia across diagnostic borders. Here, our goal was to conduct a selective review of social anhedonia in different psychological and life course contexts, including the psychosis continuum, depressive disorder, posttraumatic stress disorder, eating disorders, and autism spectrum disorders, along with developmental and neurobiological factors. Current evidence suggests that the nature and expression of social anhedonia vary across psychological disorders with some groups showing deficient learning about, enjoyment from, and anticipation of the pleasurable aspects of social interactions, while for others, some of these components appear to remain intact. However, study designs and methodologies are diverse, the roles of developmental and neurobiological factors are not routinely considered, and direct comparisons between diagnostic groups are rare—which prevents a more nuanced understanding of the underlying mechanisms involved. Future studies, parsing the wanting, liking, and learning components of social reward, will help to fill gaps in the current knowledge base. Consistent across disorders is diminished pleasure from social situations, subsequent withdrawal, and poorer social functioning in those who express social anhedonia. Nonetheless, feelings of loneliness often remain, which suggests the need for social connection is not entirely absent. Adolescence is a particularly important period of social and neural development and may provide a valuable window on the developmental origins of social anhedonia. Adaptive social functioning is key to recovery from mental health disorders; therefore, understanding the intricacies of social anhedonia will help to inform treatment and prevention strategies for a range of diagnostic categories

    Odontologinės ir kraniologinės medžiagos iš Gintarų kapinyno tyrimo duomenys

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    The fragments of a skull and deciduous and permanent teeth, mainly molars, from five graves were investigated. The skull from grave No. 9 belongs to an adult person, and all the teeth belong to children of various ages – from 3–4 to 10–12 years old: from grave No. 3 – younger than 10 years, from grave No. 4 – from 6–7 to 11–12 years old, from grave No. 8 – a child younger than 3–4 years, and from grave No. 19 – younger than 10 years. Only enamel caps of the teeth crowns are mostly preserved. Despite this, due to lack of enamel attrition, it was possible to examine the teeth odontoglyphically. According to the odontoglyphical pattern, the teeth are quite similar to well – investigated modern Lithuanians

    The Effects of Anhedonia in Social Context

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    Purpose of review: Anhedonia is a transdiagnostic symptom comprising reduced subjective reward or pleasure. Anhedonia influences subjective anticipation and in the moment experiences. This review draws together affective, learning and engagement evidence for anhedonia effecting subjective experiences of social environments. Recent findings: While social engagement is diminished consistently, subjective appraisals of social contexts vary across different mental health disorders. Low positive affect during social experiences or stimuli is reported in PTSD, mood, schizophrenia, and anxiety disorders. Diminished neural reward networks underpin the anticipation of social experiences in ADHD, schizophrenia spectrum and autistic spectrum disorders. Multiple theories exist to explain how anhedonia might interfere with social environments. Summary: Anhedonia is a barrier for engagement, motivation and enjoyment of social contexts. While many studies characterise experiences during social contexts, learning theories provide the most promise for developing targeted interventions

    The Presence of Neurological Soft Signs Along the Psychosis Proneness Continuum

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    Neurological soft signs have been observed in patients with schizophrenia and their relatives. However, it has not been considered whether the increased rates of neurological soft signs are related to measures of psychosis proneness in the general population. We tested this hypothesis in a group of normal volunteers (n = 28) who scored highly for positive schizotypy when assessed online and a control group (n = 33) who scored below the mean. Compared with the controls, high psychosis-prone individuals showed significantly higher Total and Other Soft Signs subscale scores on the Neurological Evaluation Scale. It appears that soft signs are also associated with psychosis proneness when measured in the general population, which suggests that soft signs are distributed along a continuum of risk for schizophrenia

    Invited discussant comments during the UCL–Penn Global COVID Study webinar ‘How Do We Trust (Again): Paranoia and Mental Health’: part 1 of 2

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    The article provides commentary on Wong et al.’s investigation of the relationship between schizotypal traits, social mistrust and aggression, mental and physical health outcomes across three waves of data collection commencing in April 2020. The researchers aimed to consider the nature of the relationship between these variables and the stability of these relationships as coronavirus (Covid-19) restrictions fluctuated over time. Their results suggested that loneliness reflects a hub which links the trait variables of schizotypal and social mistrust to aggression and mental and physical health symptoms. Their network did not vary by demographic factors nor wave of data collection, suggesting that stable individual differences were driving results. Their results propose that interventions which increase social connection could provide positive health benefits as well as decreasing aggression (via reductions in social mistrust). Their data contributes to understanding about how schizotypal traits link to outcomes under conditions of social stress

    Genetic Consideration of Schizotypal Traits: A Review

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    Schizotypal traits are of interest and importance in their own right and also have theoretical and clinical associations with schizophrenia. These traits comprise attenuated psychotic symptoms, social withdrawal, reduced cognitive capacity, and affective dysregulation. The link between schizotypal traits and psychotic disorders has long since been debated. The status of knowledge at this point is such schizotypal traits are a risk for psychotic disorders, but in and of themselves only confer liability, with other risk factors needing to be present before a transition to psychosis occurs. Investigation of schizotypal traits also has the possibility to inform clinical and research pursuits concerning those who do not make a transition to psychotic disorders. A growing body of literature has investigated the genetic underpinnings of schizotypal traits. Here, we review association, family studies and describe genetic disorders where the expression of schizotypal traits has been investigated. We conducted a thorough review of the existing literature, with multiple search engines, references, and linked articles being searched for relevance to the current review. All articles and book chapters in English were sourced and reviewed for inclusion. Family studies demonstrate that schizotypal traits are elevated with increasing genetic proximity to schizophrenia and some chromosomal regions have been associated with schizotypy. Genes associated with schizophrenia have provided the initial start point for the investigation of candidate genes for schizotypal traits; neurobiological pathways of significance have guided selection of genes of interest. Given the chromosomal regions associated with schizophrenia, some genetic disorders have also considered the expression of schizotypal traits. Genetic disorders considered all comprise a profile of cognitive deficits and over representation of psychotic disorders compared to the general population. We conclude that genetic variations associated with schizotypal traits require further investigation, perhaps with targeted phenotypes narrowed to assist in refining the clinical end point of significance
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