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There have been several attempts to identify individuals potentially at high risk for psychotic-spectrum disorders using brief screening measures. However, relatively few studies have tested the psychometric properties of the psychosis screening measures in representative samples of adolescents. The main purpose of the present study was to analyse the prevalence, factorial structure, measurement invariance across gender, and reliability of the Youth Psychosis At-Risk Questionnaire - Brief (YPARQ-B) in a community-derived sample of adolescents. Additionally, the relationship between YPARQ-B, depressive symptoms, psychopathology, stress manifestations, and prosocial skills was analysed. One thousand and twenty students from high schools participated in a cross-sectional survey. The YPARQ-B, the Reynolds Adolescent Depression Scale, the Strengths and Difficulties Questionnaire, and the Student Stress Inventory - Stress Manifestations were used. A total of 85.1% of the total sample self-reported at least one subclinical psychotic experience. We observed a total of 10.9% of adolescents with a cutoff score of 11 or 6.8% with a cutoff score of 13. The analysis of internal structure of the YPARQ-B yielded an essentially unidimensional structure. The YPARQ-B scores showed measurement invariance across gender. The internal consistency of the YPARQ-B total score was 0.94. Furthermore, self-reported subclinical psychotic experiences were associated with depressive symptoms, emotional and behavioural problems, poor prosocial skills, and stress manifestations. These results would appear to indicate that YPARQ-B is a brief and easy tool to assess self-reported subclinical psychotic experiences in adolescents from the general population. The assessment of these experiences in community settings, and its associations with psychopathology, may help us to enhance the possibility of an early identification of adolescents potentially at risk for psychosis and mental health problems. © 2016 John Wiley & Sons, Ltd.

In this review article, we outline the evidence linking attachment adversity to psychosis, from the premorbid stages of the disorder to its clinical forms. To better understand the neurobiological mechanisms through which insecure attachment may contribute to psychosis, we identify at least five neurobiological pathways linking attachment to risk for developing psychosis. Besides its well documented influence on the hypothalamic-pituary-adrenal (HPA) axis, insecure attachment may also contribute to neurodevelopmental risk through the dopaminergic and oxytonergic systems, as well as bear influence on neuroinflammation and oxidative stress responses. We further consider the neuroscientific and behavioral studies that underpin mentalization as a suite of processes potentially moderating the risk to transition to psychotic disorders. In particular, mentalization may help the individual compensate for endophenotypical impairments in the integration of sensory and metacognitive information. We propose a model where embodied mentalization would lie at the core of a protective, resilience response mitigating the adverse and potentially pathological influence of the neurodevelopmental cascade of risk for psychosis. ispartof: Frontiers in Human Neuroscience vol:10 pages:1-22 ispartof: location:Switzerland status: published

In this review article, we outline the evidence linking attachment adversity to psychosis, from the premorbid stages of the disorder to its clinical forms. To better understand the neurobiological mechanisms through which insecure attachment may contribute to psychosis, we identify at least five neurobiological pathways linking attachment to risk for developing psychosis. Besides its well documented influence on the hypothalamic-pituary-adrenal (HPA) axis, insecure attachment may also contribute to neurodevelopmental risk through the dopaminergic and oxytonergic systems, as well as bear influence on neuroinflammation and oxidative stress responses. We further consider the neuroscientific and behavioral studies that underpin mentalization as a suite of processes potentially moderating the risk to transition to psychotic disorders. In particular, mentalization may help the individual compensate for endophenotypical impairments in the integration of sensory and metacognitive information. We propose a model where embodied mentalization would lie at the core of a protective, resilience response mitigating the adverse and potentially pathological influence of the neurodevelopmental cascade of risk for psychosis.

A 12-year-old boy currently is followed by multiple sub-specialists for problems caused by the chromosome 22q11.2 deletion syndrome (22q11DS) (Figure). He was born via spontaneous vaginal delivery, weighing 3033 g, to a 31-year-old G3P3 mother after a full-term pregnancy complicated only by mild polyhydramnios. Family history was non-contributory. Apgar scores were 8 at 1 minute and 9 at 5 minutes. With the exception of a weak cry, the results of the infant’s initial examination were unremarkable, and he was moved to the well-baby nursery. Shortly thereafter, a cardiac murmur was noted, the cardiology department was consulted, and the child was transferred to a local tertiary care facility with a diagnosis of tetralogy of Fallot. Stable, he was discharged home at 3 days of life. Figure Mild dysmorphic facial features of a boy aged 11 years with 22q11.2DS, including a short forehead, hooded eyelids with upslanting palpebral fissures, malar flatness, bulbous nasal tip with hypoplastic alae nasi, and protuberant ears. At 5 days of life, he had jerky movements. On presentation to the local emergency department, his total calcium level was 4.7 mg/dL, and later partial hypoparathyroidism was diagnosed. At that time, a consulting geneticist suggested the diagnosis of chromosome 22q11DS. Weeks later, the family received a telephone call confirming the diagnosis with fluorescence in situ hybridization (FISH). No additional information about the diagnosis, prognosis, etiology, or recurrence risk was provided until the child was 5 months of age, when he underwent cardiac repair at a third hospital, where a comprehensive 22q11DS program was in operation. In the interim, the child had feeding difficulties requiring supplemental nasogastric tube feeds, nasal regurgitation, and gastroesophageal reflux, while the parents searched the internet for reliable information about their son’s diagnosis. Subsequent notable abnormalities and interventions included: recurrent otitis media with bilateral myringotomy tube placement at 6 months; angioplasty with left pulmonary artery stent placement after the identification of pulmonary artery stenosis with bilateral pleural effusions at age 6 years; chronic upper respiratory infections with significant T cell dysfunction requiring live viral vaccines to be held until age 7 years; velopharyngeal incompetence necessitating posterior pharyngeal flap surgery at 7 years; enamel hypoplasia and numerous caries resulting in 3 separate dental procedures under general cardiac anesthesia beginning at age 7 years; multiple cervical and thoracic vertebral anomalies with thoracic levoconvex scoliosis and upper lumbar dextroscoliosis requiring growing rod placement at age 11 years with subsequent rod extension at ages 11.5 and 12 years; postoperative hypocalcemia; short stature; constipation; and persistent idiopathic thrombocytopenia. Pertinent negative test results included normal renal ultrasound scanning and parental 22q11.2 deletion studies. On physical examination, the boy’s height and weight have consistently tracked just below the fifth percentile, with no evidence of growth hormone deficiency. His head circumference is within reference range at the 25th percentile. Dysmorphic features include: a low anterior hairline; hooded eyelids; malar flatness; normally formed but protuberant ears with attached lobes; a mildly deviated nose with a bulbous nasal tip and hypoplastic alae nasi; asymmetric crying facies with a thin upper lip; mild micrognathia; a sacral dimple; and soft tissue syndactyly of the second and third toes. Developmentally, the boy had mild delays in achieving motor milestones, sitting at 11 months and walking at 18 months. However, he exhibited significant delays in the emergence of language: he never babbled, spoke his first words at age 3 years, and only achieved full conversational speech at 7 years. However, he had relative strengths in receptive language and communicated appropriately by the use of sign language. Now quite conversant, he is mainstreamed in the seventh grade with resource room supports. Moreover, he is affable, but exhibits anxiety and perseverations. Lastly, despite numerous medical, academic, and social challenges, he participates in assisted athletics, is an avid wrestling fan, and enjoys travel. However, his exceptionally supportive parents, siblings, and extended family continue to worry about his long-term outcome and transition of care as he approaches adulthood. As demonstrated by this boy’s complicated course, practical multi-system guidelines are needed to assist the general practitioner and specialists in caring for patients with 22q11DS. Although still under-recognized, detection, including in the prenatal setting, is increasing. Moreover, the phenotypic spectrum is highly variable, and patients may present at any age. Thus, initial guidelines developed by an international panel of experts present the best practice recommendations currently available across the lifespan, with a major focus on the changing issues through childhood development.

INTRODUCTION Velocardiofacial syndrome (VCFS) is a neurogenetic disorder caused by a microdeletion on chromosome 22q11. Among other cognitive impairments and learning difficulties affected individuals show difficulties in estimating time intervals (Debbané et al. 2005). Interestingly neuroimaging studies have found an increased volume of the basal ganglia of people with VCFS (Eliez et al. 2002; Kates et al. 2004; Campbell et al. 2006). Given that the caudate nucleus represents a central component of the cerebral network underlying temporal perception skills the present report proposes to examine potential relationships between cerebral alteration to the caudate nucleus and time estimation in individuals with VCFS. METHODS A group of 30 patients with VCFS and 38 age matched healthy individuals participated in time perception and time reproduction tasks. In the time perception task individuals listened to two sequential stimuli and had to choose the longer of both stimuli by pressing a button. In the time reproduction task subjects listened to a succession of sounds and once this succession had stopped they had to reproduce the same rhythm with their dominant index. Cerebral MRI images were also obtained for each participant. A manual tracing procedure was performed to measure the basal ganglia volume. RESULTS Participants with VCFS demonstrated significantly poorer performances during the time perception and time reproduction tasks in comparison to the control participants. Further increased volume of the caudate nucleus was found in individuals with VCFS. Correlational analyses revealed a significant relationship between the caudate nucleus's volume and the performances obtained in the time perception task for control participants. This correlation was not found for individuals with VCFS. CONCLUSION The present results suggest that cerebral alterations to the caudate nucleus in VCFS may alter the temporal perception function it sustains.