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Background: The Washington Early Recognition Center Affectivity and Psychosis (WERCAP) Screen was developed to assess risk for developing psychosis. Its validity has not been investigated in a large population-based study or with longitudinal analyses., Methods: 825 participants, aged 14-25, were recruited from Kenya. Symptoms were assessed using the WERCAP Screen, as experienced over the prior 3-months (3MO), 12-months (12MO) or lifetime (LIF). ROC curve analysis was used to determine the validity of the WERCAP Screen against the Structured Interview of Psychosis-Risk Syndromes. Longitudinal validity was assessed by comparing baseline p-WERCAP scores in psychotic disorder converters and non-converters, and using ROC curve analysis. Relationship of the p-WERCAP was examined against clinical variables., Results: ROC curve analyses against SIPS showed an AUC of 0.83 for 3MO, 0.79 for 12MO and 0.65 for LIF psychosis scores. The optimal cut-point on 3MO was a score of >12 (sens: 0.78; spec: 0.77; ppv: 0.41), and >32 for 12MO (sens: 0.71; spec: 0.74; ppv: 0.24). Baseline 3MO scores (but not LIF scores) were higher in converters compared to high-risk non-converters (p = 0.02). 3MO scores against conversion status had an AUC of 0.75, with an optimal cutoff point of >16 (sens: 1.0; spec: 0.53). All p-WERCAP scores significantly correlated with substance use and stress severity. 12 MO scores were most related to cognitive impairment., Conclusions: The WERCAP Screen is a valid instrument for assessing psychosis severity and conversion risk. It can be used in the community to identify those who may require clinical assessment and care, and for recruitment in psychosis-risk research., (Copyright © 2022 The Authors. Published by Elsevier B.V. All rights reserved.)

Background: Malhi et al. in this issue critique the clinical high risk (CHR) syndrome for psychosis., Method: Response to points of critique., Results: We agree that inconsistency in CHR nomenclature should be minimized. We respectfully disagree on other points. In our view: a) individuals with CHR and their families need help, using existing interventions, even though we do not yet fully understand disease mechanisms; b) substantial progress has been made in identification of biomarkers; c) symptoms used to identify CHR are specific to psychotic illnesses; d) CHR diagnosis is not "extremely difficult"; e) the pattern of progression, although heterogenous, is discernible; f) "psychosis-like symptoms" are common but are not used to identify CHR; and g) on the point described as 'the real risk,' CHR diagnosis does not frequently cause harmful stigma., Discussion: Malhi et al.'s arguments do not fairly characterize progress in the CHR field nor efforts to minimize stigma. That said, much work remains in areas of consistent nomenclature, mechanisms of disease, dissecting heterogeneity, and biomarkers. With regard to what the authors term the "real risk" of stigma associated with a CHR "label," however, our view is that avoiding words like "risk" and "psychosis" reinforces the stigma that both they and we mean to oppose. Moreover, patients and their families benefit from being given a term that describes what is happening to them., (Copyright © 2020 Elsevier B.V. All rights reserved.)

The schizophrenia prodrome has not been extensively studied in Africa. Identification of prodromal behavioral symptoms holds promise for early intervention and prevention of disorder onset. Our goal was to investigate schizophrenia risk traits in Kenyan adolescents and identify predictors of psychosis progression. 135 high-risk (HR) and 142 low-risk (LR) adolescents were identified from among secondary school students in Machakos, Kenya, using the structured interview of psychosis-risk syndromes (SIPS) and the Washington early recognition center affectivity and psychosis (WERCAP) screen. Clinical characteristics were compared across groups, and participants followed longitudinally over 0-, 4-, 7-, 14- and 20-months. Potential predictors of psychosis conversion and severity change were studied using multiple regression analyses. More psychiatric comorbidities and increased psychosocial stress were observed in HR compared to LR participants. HR participants also had worse attention and better abstraction. The psychosis conversion rate was 3.8%, with only disorganized communication severity at baseline predicting conversion (p=0.007). Decreasing psychotic symptom severity over the study period was observed in both HR and LR participants. ADHD, bipolar disorder, and major depression diagnoses, as well as poor occupational functioning and avolition were factors relating to lesser improvement in psychosis severity. Our results indicate that psychopathology and disability occur at relatively high rates in Kenyan HR adolescents. Few psychosis conversions may reflect an inadequate time to conversion, warranting longer follow-up studies to clarify risk predictors. Identifying disorganized communication and other risk factors could be useful for developing preventive strategies for HR youth in Kenya., (Copyright © 2016 The Authors. Published by Elsevier B.V. All rights reserved.)

Investigating brain tissue T2* relaxation properties in vivo can potentially guide the uncovering of neuropathology in psychiatric illness, which is traditionally examined post mortem. We use an MRI-based Gradient Echo Plural Contrast Imaging (GEPCI) technique that produces inherently co-registered images allowing quantitative assessment of tissue cellular and hemodynamic properties. Usually described as R2* (=1/T2*) relaxation rate constant, recent developments in GEPCI allow the separation of cellular-specific (R2*C) and hemodynamic (BOLD) contributions to the MRI signal decay. We characterize BOLD effect in terms of tissue concentration of deoxyhemoglobin, i.e. CDEOXY, which reflects brain activity. 17 control (CON), 17 bipolar disorder (BPD), 16 schizophrenia (SCZ), and 12 unaffected schizophrenia sibling (SIB) participants were scanned and post-processed using GEPCI protocols. A MANOVA of 38gray matter regions ROIs showed significant group effects for CDEOXY but not for R2*C. In the three non-control groups, 71-92% of brain regions had increased CDEOXY. Group effects were observed in the superior temporal cortex and the thalamus. Increased superior temporal cortex CDEOXY was found in SCZ (p=0.01), BPD (p=0.01) and SIB (p=0.02), with bilateral effects in SCZ and only left hemisphere effects in BPD and SIB. Thalamic CDEOXY abnormalities were observed in SCZ (p=0.003), BPD (p=0.03) and SIB (p=0.02). Our results suggest that increased activity in certain brain regions is part of the underlying pathophysiology of specific psychiatric disorders. High CDEOXY in the superior temporal cortex suggests abnormal activity with auditory, language and/or social cognitive processing. Larger studies are needed to clarify the clinical significance of relaxometric abnormalities., (Copyright © 2015 Elsevier B.V. All rights reserved.)

Background: Alcohol abuse and dependence have been reported to exacerbate the clinical course of schizophrenia. However, the neurobiological basis of this co-morbid interaction is unknown. The aim of this study was to determine the relationship of co-morbid alcohol use disorder (AUD) with brain structure abnormalities in schizophrenia patients., Methods: T1-weighted magnetic resonance images were collected from schizophrenia patients without a history of any substance use disorder (SCZ_0, n=35), schizophrenia patients with a history of AUD only (SCZ_AUD, n=16), and a healthy comparison group without a history of any substance use disorder (CON, n=56). Large-deformation, high-dimensional brain mapping was used to quantify the surface shapes of the hippocampus, thalamus, striatum, and globus pallidus in these subject groups. Analysis of variance was used to test for differences in surface shape measures among the groups., Results: SCZ_AUD demonstrated the greatest severity of shape abnormalities in the hippocampus, thalamus, striatum, and globus pallidus as compared to SCZ_0 and CON. SCZ_AUD demonstrated a combination of exaggerated shape differences in regions where SCZ_0 also showed shape differences, and unique shape differences that were not observed in SCZ_0 or CON., Conclusions: Shape differences in schizophrenia were compounded by a history of co-morbid AUD. Future research is needed to determine whether these differences are simply additive or whether they are due to an interaction between the underlying neurobiology of schizophrenia and alcoholism. The consequences of such shape differences for the clinical course of schizophrenia are not yet understood., (Copyright © 2011 Elsevier B.V. All rights reserved.)

Background: Individuals with schizophrenia use psychoactive substances more frequently than the general population. The genetic vulnerability to develop schizophrenia may also increase risk for the development of substance use disorders. We examine this hypothesis by assessing the rates of substance use disorders and nicotine use in non-psychotic siblings of individuals with schizophrenia., Methods: Participants included 59 individuals with DSM-IV schizophrenia, 53 of their siblings, 80 community controls, and 75 of their siblings. Statistical regression was used to assess the rates of substance use disorders and nicotine use in study participants while controlling for age, gender, lifetime diagnosis of a mood or anxiety disorder, and a family history of substance use disorder., Results: Individuals with schizophrenia and their non-psychotic siblings reported higher rates of alcohol and cannabis use disorders and nicotine use when compared to siblings of comparison subjects., Conclusions: The vulnerability to develop schizophrenia may also extend to substance use disorders. Future research is needed to investigate the neurobiological basis of increased substance use in non-psychotic siblings and the psychosocial mechanisms that may contribute to increased substance use in non-psychotic siblings.

Increases in the total volume of basal ganglia structures have been reported in schizophrenia. However, patterns of basal ganglia shape change, which can reveal localized changes in substructure volumes, have not been investigated. In this study, the total volume and shape of several basal ganglia structures were compared in subjects with and without schizophrenia. T(1)-weighted magnetic resonance scans were collected in 54 schizophrenia and 70 comparison subjects. High-dimensional (large-deformation) brain mapping was used to assess the shape and volume of several basal ganglia structures. The relationships of shape and volume measures with psychopathology, cognition and motor function were also assessed. Left and right volumes of the caudate and putamen, as well as the right globus pallidus volume, were significantly increased in subjects with schizophrenia as compared to comparison subjects after total brain volume was included as a covariate. Significant differences in shape accompanied these volume changes in the caudate, putamen and globus pallidus, after their total volumes were included as covariates. There were few significant correlations between volume or shape measures and either cognitive function or clinical symptoms, other than a positive correlation between an attention/vigilance cognitive dimension and the volume of the caudate and putamen, and a negative correlation between nucleus accumbens volume and delusions. In conclusion, basal ganglia volumes relative to total brain volume were larger in schizophrenia subjects than healthy comparison subjects. Specific patterns of shape change accompanied these volume differences.