A systematic review and meta-analysis of the psychosis continuum: evidence for a psychosis proneness-persistence-impairment model of psychotic disorder
There is evidence, however, that transitory developmental expression of psychosis (psychosis proneness) may become abnormally persistent and subsequently clinically relevant (impairment), depending on the degree of environmental risk the person is additionally exposed to.
Abstract:
A systematic review of all reported incidence and prevalence studies of population rates of subclinical psychotic experiences reveals a median prevalence rate of around 5% and a median incidence rate of around 3%. A meta-analysis of risk factors reveals associations with developmental stage, child and adult social adversity, psychoactive drug use, and also male sex and migrant status. The small difference between prevalence and incidence rates, together with data from follow-up studies, indicates that approximately 75-90% of developmental psychotic experiences are transitory and disappear over time. There is evidence, however, that transitory developmental expression of psychosis (psychosis proneness) may become abnormally persistent (persistence) and subsequently clinically relevant (impairment), depending on the degree of environmental risk the person is additionally exposed to. The psychosis proneness-persistence-impairment model considers genetic background factors impacting on a broadly distributed and transitory population expression of psychosis during development, poor prognosis of which, in terms of persistence and clinical need, is predicted by environmental exposure interacting with genetic risk.
TL;DR: The dopamine hypothesis of schizophrenia-version III is synthesized into a comprehensive framework that links risk factors, including pregnancy and obstetric complications, stress and trauma, drug use, and genes, to increased presynaptic striatal dopaminergic function.
TL;DR: The structure of psychopathology is examined, taking into account dimensionality, persistence, co-occurrence, and sequential comorbidity of mental disorders across 20 years, from adolescence to midlife, to explain why it is challenging to find causes, consequences, biomarkers, and treatments with specificity to individual mental disorders.
TL;DR: The HiTOP promises to improve research and clinical practice by addressing the aforementioned shortcomings of traditional nosologies and provides an effective way to summarize and convey information on risk factors, etiology, pathophysiology, phenomenology, illness course, and treatment response.
TL;DR: The results of the meta-analysis confirm that CSA is a global problem of considerable extent, but also show that methodological issues drastically influence the self-reported prevalence of CSA.
TL;DR: Although heritability is often emphasized, onset is associated with environmental factors such as early life adversity, growing up in an urban environment, minority group position and cannabis use, suggesting that exposure may have an impact on the developing ‘social’ brain during sensitive periods.
TL;DR: While I have not until recently begun any systematic research efforts on this baffling disorder, I felt that to share with you some of my thoughts, based though they are upon clinical impressions in the context of selected research by others, might be an acceptable use of this occasion.
TL;DR: The research addressing the relationship of childhood trauma to psychosis and schizophrenia is reviewed, and the theoretical and clinical implications are discussed.
TL;DR: Differences between children destined to develop schizophrenia as adults and the general population were found across a range of developmental domains, and the origins of schizophrenia may be found in early life.
TL;DR: This is the first prospective longitudinal study of adolescent cannabis use as a risk factor for adult schizophreniform disorder, taking into account childhood psychotic symptoms, and the Dunedin multidisciplinary health and development study has a 96% follow up rate at age 26.
TL;DR: Findings of previous studies implicating migration as a risk factor for the development of schizophrenia and a quantitative index of the associated effect size are synthesized to suggest a role for psychosocial adversity in the etiology of schizophrenia.
Q1. What contributions have the authors mentioned in the paper "A systematic review and meta-analysis of the psychosis continuum: evidence for a psychosis proneness–persistence–impairment model of psychotic disorder" ?
The small difference between prevalence and incidence rates, together with data from follow-up studies, indicates that approximately 75–90 % of developmental psychotic experiences are transitory and disappear over time.
Q2. What is the robust finding in the literature?
In the offspring of parents with schizophrenia, impaired cognition, particularly with regard to verbal memory, is one of the more robust findings (Owens & Johnstone, 2006).
Q3. What are some of the non-genetic risk factors associated with schizophrenia?
Some of the non-genetic risk factors associated with schizophrenia such as urbanicity (Krabbendam & van Os, 2005), ethnic minority status (Cantor-Graae & Selten, 2005), childhood trauma (Read et al. 2005) and cannabis (Henquet et al. 2005) may also impact on the rate of subclinical psychotic experiences.
Q4. What is the median prevalence of experience without clinical impact?
in the studies reviewed here, the median prevalence of experience that has a clinical impact was 1.5% (IQR 0.4–3.0%) whereas the median rate derived without this or similar restrictions (e.g. on the number of experiences or frequency or probability criteria) was 8.4% (IQR 3.5–20.9%).