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Background: Autism and psychosis co-occur at elevated rates, with implications for clinical outcomes, functioning, and suicidality. The PANSS-Autism-Severity-Score (PAUSS) is a measure of autism trait severity which has not yet been validated externally or longitudinally. Study Design: Participants were derived from the GROUP and SCOPE datasets. Participants included 1448 adults with schizophrenia spectrum disorder (SSD), 800 SSD-siblings, 103 adults diagnosed with an autistic spectrum condition (ASC), and 409 typically-developing controls (TC). Analyses from the original validation study were conducted with SSD participants, and extended into ASC, SSD-sibling, and TC participants. Test-retest reliability of the PAUSS at 2-weeks and long-term stability 3 and 6-years was also examined.Study Results: Results differed in important ways from the original validation. SSD participants reported higher PAUSS scores than other groups, with only a fraction of ASC participants scoring as ‘PAUSS-Autistic’. Cronbach’s alpha was acceptable for the SSD cohort only. Two-week stability of the PAUSS was fair to good for all PAUSS scores. Long-term stability was poor for most PAUSS items but fair for total PAUSS score.Conclusions: Results suggest, firstly, the cut-off proposed in the original PAUSS paper may need further evaluation. Secondly, the PAUSS does not appear appropriate for assessing autism in non-psychosis populations, with the low rate of PAUSS-Autistic in the ASC population suggesting the PAUSS may not accurately reflect characteristics of autism. Finally, the relative lack of long-term stability is cause for concern and may suggest that the PAUSS is capturing features of schizophrenia rather than autism traits.

Psychotic and autistic symptoms are related to social functioning in individuals with psychotic disorders (PD). The present study used a network approach to (1) evaluate the interactions between autistic symptoms, psychotic symptoms, and social functioning, and (2) investigate whether relations are similar in individuals with and without PD. We estimated an undirected network model in a sample of 504 PD, 572 familial risk for psychosis (FR), and 337 typical comparisons (TC), with a mean age of 34.9 years. Symptoms were assessed with the Autism Spectrum Quotient (AQ; 5 nodes) and the Community Assessment of Psychic Experiences (CAPE; 9 nodes). Social functioning was measured with the Social Functioning Scale (SFS; 7 nodes). We identified statistically significant differences between the FR and PD samples in global strength (P < .001) and network structure (P < .001). Our results show autistic symptoms (social interaction nodes) are negatively and more closely related to social functioning (withdrawal, interpersonal behavior) than psychotic symptoms. More and stronger connections between nodes were observed for the PD network than for FR and TC networks, while the latter 2 were similar in density (P = .11) and network structure (P = .19). The most central items in strength for PD were bizarre experiences, social skills, and paranoia. In conclusion, specific autistic symptoms are negatively associated with social functioning across the psychosis spectrum, but in the PD network symptoms may reinforce each other more easily. These findings emphasize the need for increased clinical awareness of comorbid autistic symptoms in psychotic individuals.

BackgroundPrevalence estimates of autistic traits in individuals with psychotic disorders (PD) vary greatly and it is unclear whether individuals with a familial risk (FR) for psychosis have an increased propensity to display autistic traits. Furthermore, it is unknown whether the presence of comorbid autism traits disproportionally affects the cognitive and behavioral aspects of social functioning in PD.MethodsIn total, 504 individuals with PD, 587 unaffected siblings with FR, and 337 typical comparison (TC) individuals (16–50 years) were included. Autistic and psychotic traits were measured with the Autism Spectrum Quotient (AQ) and the Community Assessment of Psychic Experiences (CAPE). Social cognition was assessed with the Picture Sequencing Task (PST) and social behavior with the Social Functioning Scale (SFS).ResultsFor PD 6.5% scored above AQ clinical cut-off (⩾32), 1.0% for FR, and 1.2% for TC. After accounting for age, sex, and IQ, the PD group showed significantly more autistic traits and alterations in social behavior and cognition, while FR and TC only displayed marginal differences. Within the PD group autistic traits were a robust predictor of social behavior and there were no interactions with positive psychotic symptoms.ConclusionsLevels of autistic traits are substantially elevated in PD and have a profoundly negative association with social functioning. In contrast, autistic traits above the clinical cut-off are not elevated in those with FR, and only marginally on a dimensional level. These findings warrant specific clinical guidelines for psychotic patients who present themselves with autistic comorbidity to help address their social needs.

BackgroundParent–child interaction is essential in the development of attentional control (AC) and executive functioning (EF). Educating parents in AC and EF development may help them to respond more adaptively to their child's developmental needs.AimThis study aimed to investigate whether parents can be educated to improve interactions with their child through a compact psycho‐educational programme that focuses on fostering the development of AC and EF.SampleParents and their children in a low‐risk sample of four‐ to eight‐year‐olds were randomly assigned to either the educational programme condition (N = 34) or the control condition (N = 36).MethodsParental supportive presence and intrusiveness were observed during home visits, and children's performance‐based AC and EF were assessed before and after the four‐session programme.ResultParents in the educational programme improved significantly in support ( = .19) and intrusiveness ( = .09) compared to controls. There was no short‐term programme mediation effect on child AC and EF through parental support and intrusiveness. This study showed, however, that parents who improved after the educational programme had children who improved on AC and EF.ConclusionParent–child interaction can be enhanced in a low‐risk sample of four‐ to eight‐year‐olds using a compact educational group programme within the school community. Future studies should aim at examining variations in programme responsiveness and assessing associations between parent–child interaction and AC and EF over time.

Background:Within young individuals, mood disorder onset may be related to changes in trajectory of brain structure development. To date, however, longitudinal prospective studies remain scarce and show partly contradictory findings, with a lack of emphasis on changes at the level of global brain patterns. Cross-sectional adult studies have applied such methods and show that mood disorders are associated with accelerated brain ageing. Currently, it remains unclear whether young individuals show differential brain structure aging trajectories associated with onset of mood disorder and/or presence of familial risk.Methods:Participants included young individuals (15-30 years, 53%F) from the prospective longitudinal Scottish Bipolar Family Study with and without close family history of mood disorder. All were well at time of recruitment. Implementing a structural MRI-based brain age prediction model, we globally assessed individual trajectories of age-related structural change using the difference between predicted brain age and chronological age (brain-predicted age difference (brain-PAD)) at baseline and at 2-year follow-up. Based on follow-up clinical assessment, individuals were categorised into three groups: (i) controls who remained well (C-well,n= 93), (ii) high familial risk who remained well (HR-well,n= 74) and (iii) high familial risk who developed a mood disorder (HR-MD,n= 35).Results:At baseline, brain-PAD was comparable between groups. Results showed statistically significant negative trajectories of brain-PAD between baseline and follow-up for HR-MD versus C-well (β= -0.60,pcorrected< 0.001) and HR-well (β= -0.36,pcorrected= 0.02), with a potential intermediate trajectory for HR-well (β= -0.24 years,pcorrected= 0.06). Conclusions:These preliminary findings suggest that within young individuals, onset of mood disorder and familial risk may be associated with a deceleration in brain structure aging trajectories. Extended longitudinal research will need to corroborate findings of emerging maturational lags in relation to mood disorder risk and onset.

Background: Autism and schizophrenia spectrum disorders both represent severely disabling neurodevelopmental disorders with marked impairments in social functioning. Despite an increased incidence of psychosis in autism, and substantial overlap in symptoms and cognitive markers, it is unclear whether such phenotypes are specifically related to risk for psychosis or perhaps reflect more general, idiosyncratic autism traits. The attenuated psychosis syndrome (APS) is primarily defined by the presence of attenuated psychotic symptoms, which currently constitute the best and most-replicated clinical predictors of psychosis, and are common in clinical youth with and without autism. The aims of this study were to test the hypothesis that facial affect processing is impaired in adolescents with APS and to explore whether such deficits are more indicative of psychotic or autistic phenotypes on a categorical and dimensional level.Materials and Method: Fifty-three adolescents with APS and 81 typically developing controls (aged 12-18) were included. The APS group consisted of adolescents with (n = 21) and without (n = 32) a diagnosis of autism spectrum disorder. Facial affect recognition was assessed with the Amsterdam Neuropsychological Tasks using a cascade model of cognitive processing, in which disturbances in "lower-level" cognitive abilities (pattern recognition), affect "higher-level" cognitive processes (face recognition and facial affect recognition). For associations with schizotypal and autistic-like traits the Schizotypal Personality Questionnaire and Social Communication Questionnaire were used in a confirmatory item factor analysis framework.Results: Contrary to expectation, APS in adolescents was not associated with impairments in pattern, face, or facial affect recognition. However, the APS group with autism spectrum disorder showed a general latency in response time to social and non-social stimuli. Dimensionally assessed schizotypal and autistic-like traits did not predict the accuracy or the speed of face or facial affect recognition.Conclusion: Facial affect processing performance was not associated with APS in adolescence and represents an unlikely early vulnerability marker for psychosis. APS individuals with a more autistic-like profile were characterized by slower responses to social- and non-social stimuli, suggesting that the combined effect of APS and autism spectrum disorder on cognition is larger than for APS alone.

In order to better understand which factors play a role in non-adaptive social behavior in autism spectrum disorder (ASD) we looked into physiological arousal and awareness of one’s own emotions. Heart rate (HR) and heart rate variability (HRV) were measured during a public speaking task in 51 young adults with ASD and 28 typically developing (TD) controls. The results showed no significant group differences in baseline HR/HRV, HR reactivity (change from baseline to the speaking task) or self-reported emotional awareness. However, adults with ASD showed significantly lower HRV reactivity (p = .023, d = 0.6) compared to TD adults. These results suggest a mismatch between arousal regulation and emotional awareness, which may be related to problems in social adaptation in ASD. Electronic supplementary material The online version of this article (10.1007/s10803-019-04000-5) contains supplementary material, which is available to authorized users.

Many students with autism spectrum disorders (ASDs) attending higher education drop out prematurely. The predictive value of self-reported daily executive functioning (EF) and (cognitive) performance-based EF (mental flexibility and working memory) for academic progress was evaluated in 54 young adults with ASD (Mage = 22.5, SD = 2.4, 72% male). Regression analyses showed that autism symptom severity explained 12% of variance in academic progress, which was raised to 36% by adding self-reported daily EF, and to 25% by adding performance-based EF. It is suggested that EF is a candidate marker for academic progress in higher education students with ASD and a candidate target for early intervention.

Good parenting strategies can shape children’s neurocognitive development, yet little is known about the nature of this relation in school-aged children and whether this association shifts with age. We aimed to investigate the relation between parenting strategies observed during a home visit and children’s performance-based attentional control and executive functioning (N = 98, aged 4–8 years). Linear and curvilinear regression analyses showed that children of parents who were more supportive, were less intrusive, and asked more open-ended questions displayed better inhibitory control. In addition, children of parents who asked relatively more open-ended than closed-ended questions showed better performance on inhibition, working memory, and cognitive flexibility tasks. Curvilinear relations indicated the presence of an optimal amount of closed-ended and elaborative questions by parents—that is, not too few and not too many—which is linked to increased performance on attentional and inhibitory control in children. Higher parental intrusiveness and more frequent elaborative questioning were associated with decreased inhibitory control in younger children, whereas no such negative associations were present in older children. These results suggest that susceptibility to certain parenting strategies may shift with age. Our findings underscore the importance of adaptive parenting strategies to both the age and needs of school-aged children, which may positively affect their self-regulation skills.

Contains fulltext : 177940.pdf (Publisher’s version ) (Open Access) BACKGROUND: Autism is generally associated with poor functional outcome but little is known about predictors of quality of life, especially during early adulthood. This study was conducted to assess subjective quality of life during early adulthood in high-functioning autism spectrum disorder and its relation with self-regulating abilities. Individuals with high-functioning autism spectrum disorder who progressed into post-secondary higher education ( N = 75) were compared to a typical peer control group ( N = 28) based on behavioral self-report questionnaires. The results indicated that individuals with high-functioning autism spectrum disorder reported significantly lower subjective quality of life than typical controls ( p < 0.001, effect size ( d) = 1.84). In addition, individuals with high-functioning autism spectrum disorder reported more problems with emotion processing ( p < 0.05, effect size ( d) = 0.79) and daily executive functioning ( p < 0.001, effect size ( d) = 1.29) than controls. A higher level of executive functioning problems was related to lower quality of life in the high-functioning autism spectrum disorder group, but no significant relation between level of emotion processing and subjective quality of life became apparent in the regression analysis. Our findings show that even in high-functioning young adults with autism, executive functioning, emotion processing, and subjective quality of life are low compared to typically developing peers. Furthermore, these results emphasize the importance of targeting executive functioning problems in individuals with autism to improve subjective quality of life.

Formal thought disorder (FTD) is a disruption in the flow of thought and a common feature in psychotic disorders and autism spectrum disorder (ASD). Executive dysfunction has often been associated with FTD, yet for ASD convincing evidence is lacking. This study investigated FTD and three core executive functions in 50 young children and adolescents with high-functioning ASD and 56 matched controls. Higher overall levels of FTD marked ASD compared to controls. Furthermore, in ASD decreased performance on verbal working memory was correlated with increased FTD ratings and explained a significant amount of variance of objective and subjective FTD. Verbal working memory is currently the most promising target executive function for understanding the development of idiosyncratic thought disorders in ASD. Electronic supplementary material The online version of this article (doi:10.1007/s10803-017-3104-6) contains supplementary material, which is available to authorized users.

Background Autism and schizophrenia spectrum disorders both represent severely disabling neurodevelopmental disorders with marked impairments in social functioning. Despite an increased incidence of psychosis in autism, and substantial overlap in symptoms and cognitive markers, it is unclear whether such phenotypes are specifically related to risk for psychosis or perhaps reflect more general, idiosyncratic autism traits. Attenuated positive symptoms (APS) currently constitute the best and most-replicated clinical predictors of schizophrenic psychosis, and are common in clinical youth with and without autism. The aims of this study were to test the hypothesis that facial affect processing is impaired in adolescents with APS and to explore whether such deficits are more indicative of psychotic or autistic phenotypes on a categorical and dimensional level. Methods Fifty-three adolescents with APS and 81 typically developing controls (aged 12–18) were included. The APS group consisted of adolescents with (n = 21) and without (n = 32) a diagnosis of autism spectrum disorder. Facial affect recognition and ‘lower-level’ cognitive skills, namely pattern and face recognition, were assessed with the Amsterdam Neuropsychological Tasks. For associations with schizotypal and autistic-like traits the Schizotypal Personality Questionnaire and Social Communication questionnaire were used and one-dimensional factor scores were generated with confirmatory factor analysis. Results Our preliminary findings suggest that APS in adolescents is not associated with impairments in pattern, face, or emotion recognition. However, the APS group with autism spectrum disorder generally showed slower reaction times for face/emotional stimuli and they were significantly worse in recognizing fearful expressions than APS participants without autism spectrum disorder and controls. There were no dimensional correlations with schizotypal traits and marginal correlations between autistic-like traits and speed of recognizing faces. Discussion Contrary to our expectations, APS demonstrated limited use in identifying cognitive deficits typical to schizophrenic psychosis. A more autistic-like profile may be characterized by slower reaction times to facial stimuli, suggesting that more complicated and dynamic social cognitive stimuli have a better chance of discerning between autistic and psychotic-like phenotypes.

BackgroundThe prevalence of psychotic experiences (PEs) is higher in low-and-middle-income-countries (LAMIC) than in high-income countries (HIC). Here, we examine whether this effect is explicable by measurement bias.MethodsA community sample from 13 countries (N = 7141) was used to examine the measurement invariance (MI) of a frequently used self-report measure of PEs, the Community Assessment of Psychic Experiences (CAPE), in LAMIC (n = 2472) and HIC (n = 4669). The CAPE measures positive (e.g. hallucinations), negative (e.g. avolition) and depressive symptoms. MI analyses were conducted with multiple-group confirmatory factor analyses.ResultsMI analyses showed similarities in the structure and understanding of the CAPE factors between LAMIC and HIC. Partial scalar invariance was found, allowing for latent score comparisons. Residual invariance was not found, indicating that sum score comparisons are biased. A comparison of latent scores before and after MI adjustment showed both overestimation (e.g. avolition, d = 0.03 into d = −0.42) and underestimation (e.g. magical thinking, d = −0.03 into d = 0.33) of PE in LAMIC relative to HIC. After adjusting the CAPE for MI, participants from LAMIC reported significantly higher levels on most CAPE factors but a significantly lower level of avolition.ConclusionPrevious studies using sum scores to compare differences across countries are likely to be biased. The direction of the bias involves both over- and underestimation of PEs in LAMIC compared to HIC. Nevertheless, the study confirms the basic finding that PEs are more frequent in LAMIC than in HIC.

This study investigated whether parents can be educated to alter parent-child interactions and whether this can improve children's reasoning abilities. Parents of four- to eight-year-olds were randomly assigned to a compact psycho-educational program (N = 34) or control condition (N = 36). Parental questioning style was observed during problem-solving interactions at home and children's scientific and social reasoning were assessed using performance-based tasks. Parents in the educational condition asked significantly more open-ended, observational and explanatory questions at post-test than controls did. Asking relatively more open-ended questions at post-test was associated with improved aspects of scientific reasoning in their children. Asking more observational or explanatory questions was not associated with improved reasoning abilities. Educating parents to adaptively modify their parent-child interactions can positively influence their questioning style, which in turn may benefit their child's reasoning abilities.

BACKGROUND: Autism traits are present at elevated rates in individuals with psychotic disorders (PD). However, prevalence varies across clinical samples and it is unclear whether individuals with a genetic risk for psychosis (GR) also report more symptoms. Furthermore, it is unknown to what extent comorbid autism symptoms may have an impact on social functioning in psychotic disorders. METHODS: A large sample of 504 individuals with a PD, 572 individuals with GR (siblings) and 337 typical comparison (TC) individuals was recruited. Autism traits were assessed with the Autism Spectrum Quotient (AQ) and social functioning was measured with the Social Functioning Scale. RESULTS: The proportion of AQ scores >32 (indicative of autism diagnosis) was 6.6% for PD, 1.1% for GR and 1.2% for TC. For AQ scores >26 (indicative of high autism traits) respective percentages were: 21.4%, 2.8% and 2.4%. Mean group differences for autism traits (PD > GR > TC) and social functioning (PD < GR < TC) were all significant, albeit with small effect sizes for GR vs TC. Within the PD and GR group, autistic traits showed a negative impact on overall social functioning above and beyond the effect of positive psychotic symptoms. DISCUSSION: At least 1 in 5 individuals with a psychotic disorder is characterized by elevated levels of autism traits. In addition, levels of social functioning are negatively affected by autisms traits in individuals with (a genetic predisposition to) psychotic disorders. These findings warrant specific clinical guidelines for psychotic patients who present themselves with autistic comorbidity.

An important focus of studies of individuals at ultra-high risk (UHR) for psychosis has been to identify biomarkers to predict which individuals will transition to psychosis. However, the majority of individuals will prove to be resilient and go on to experience remission of their symptoms and function well. The aim of this study was to investigate the possibility of using structural MRI measures collected in UHR adolescents at baseline to quantitatively predict their long-term clinical outcome and level of functioning. We included 64 UHR individuals and 62 typically developing adolescents (12–18 years old at recruitment). At six-year follow-up, we determined resilience for 43 UHR individuals. Support Vector Regression analyses were performed to predict long-term functional and clinical outcome from baseline MRI measures on a continuous scale, instead of the more typical binary classification. This led to predictive correlations of baseline MR measures with level of functioning, and negative and disorganization symptoms. The highest correlation (r = 0.42) was found between baseline subcortical volumes and long-term level of functioning. In conclusion, our results show that structural MRI data can be used to quantitatively predict long-term functional and clinical outcome in UHR individuals with medium effect size, suggesting that there may be scope for predicting outcome at the individual level. Moreover, we recommend classifying individual outcome on a continuous scale, enabling the assessment of different functional and clinical scales separately without the need to set a threshold. Hum Brain Mapp, 2016. © 2016 Wiley Periodicals, Inc.

Background Little is known about the role of behavioural executive functioning (EF) skills and level of intelligence (IQ) on math abilities in children with mild to borderline intellectual disabilities. Method Teachers of 63 children attending a school for special education (age: 10 to 13 years; IQ: 50 to 85) filled out a Behaviour Rating Inventory for Executive Function for each student. Furthermore, students took a standardised national composite math test and a specific math test on measurement and time problems. Information on level of intelligence was gathered through school records. Multiple regression analyses were performed to test direct, moderating and mediating effects of EF and IQ on math performance. Results Behavioural problems with working memory and flexibility had a direct negative effect on math outcome, while concurrently, level of intelligence had a positive effect. The effect of IQ on math skills was moderated by problems with inhibition: in children with a clinical level of inhibition problems, there was no effect of level of intelligence on math performance. Conclusions Findings suggest that in students with mild to borderline intellectual disabilities and math difficulties, it is important to address their strengths and weaknesses with respect to EF and adjust instruction and remedial intervention accordingly.

BackgroundAccelerated biological ageing has been proposed as a mechanism underlying mood disorder, but has been predominantly studied cross-sectionally in adult populations. It remains unclear whether differential ageing/maturation trajectories emerge earlier in life, in particular during the neurodevelopmental period of adolescence, and whether they are associated with onset of mood disorder and/or presence of familial risk.MethodsParticipants were young individuals (16-25 years) from the prospective longitudinal Scottish Bipolar Family Study (SBFS) with and without family history of mood disorder. All were well at time of recruitment. Implementing a structural MRI-based brain age prediction model, individual maturational trajectories were captured by the difference between predicted brain age and chronological age (brain-PAD) at baseline and two-year follow-up. Based on clinical assessment at follow-up, individuals were categorised into three groups: (i) controls who remained well (C-well,n=94), (ii) high familial risk who remained well (HR-well,n=73) and (iii) high familial risk who developed a mood disorder (HR-MD,n=38).ResultsResults showed no differences in brain-PAD between groups at baseline or follow-up. However, we found negative trajectories of brain-PAD for HR-MD versus C-well (β= −0.68 years,pp=.01), and for HR-well versus C-well (β= −0.30 years,p=.03).ConclusionsThese findings suggest that within young individuals, onset of mood disorder and familial risk may be associated with a deceleration in brain maturation trajectory. However, without significantly differential status of brain maturation at follow-up, extended longitudinal research will need to show whether this marks the emergence of maturational lag.

Background Impaired social cognition represents a common feature in both the autism and psychosis spectrum, but direct comparisons are sparse and assessments typically restricted to a few tasks with limited ecological validity. The first aim of the present study was to compare the social cognitive profile of young individuals with autism spectrum disorder (ASD) or a first episode psychosis (FEP) with a group of typical comparisons (TC) on a comprehensive social cognition test battery. The second aim was to explore the relative contribution of autistic and psychotic traits to social cognitive performance across groups. Methods In total 90 young individuals (M = 21.9 y, SD = 3.1 y, range = 16–30 y, 67% male) were recruited. Groups (31 FEP, 21 ASD, 38 TC) were matched for age and sex. Social cognition assessment included measures for static and dynamic emotion recognition & social inference / Theory of Mind, social attention (eye-tacking), empathy and alexithymia. Autistic and psychotic traits were assessed with self-report questionnaires (AQ-28 & SPQ-br). Results Data collection is completed at the time of abstract submission and analyses are expected to be finalized in February 2020. Discussion Pending the outcome of our analyses, we expect our results will provide a more complete and detailed picture of shared and unique aspects in the social cognitive profile of autism and psychosis. In general we hypothesize that both ASD and FEP, on a group-level, will significantly underperform compared to TC, but that the respective trait dimensions will each explain a unique amount of variance in social cognitive performance.

Background Both psychotic and autistic traits are related to poor social outcome in individuals with psychotic disorders (PD). However, it is unknown how specific trait clusters relate to each other and which are pivotal to social functioning. The aim of the present study was to use a network approach to address this issue and to investigate whether relations are similar in individuals with a familial risk for psychosis (FR) or typical comparisons (TC). Methods The total sample consisted of 1413 individuals (504 PD, 572 FR, and 337 TC). Traits were assessed with the Autism Spectrum Quotient (AQ; 5 nodes) and the Community Assessment of Psychic Experiences (CAPE; 9 nodes). Social functioning was measured with the Social Functioning Scale (7 nodes). Results Overall our results show that autistic traits are more negatively and closely related to social functioning, particularly in the interpersonal environment, than psychotic traits. These relations are more intrinsically connected for the PD network, as more and stronger connections between nodes were observed than for the FR and TC networks. In addition, the latter two networks appeared strikingly similar with only few unique relations. Discussion Presence of autistic traits generally have a negative effect on social functioning, but in PD they may have a disproportional detrimental effect on psychopathology and levels of social functioning. These findings emphasize the need for increased clinical awareness of autistic comorbidity in psychotic patients to help enrich their daily social environments.

Reduced empathy and alexithymic traits are common across the autism spectrum, but it is unknown whether this is also true for intellectually advanced adults with autism spectrum disorder. The aim of this study was to examine whether college students with autism spectrum disorder experience difficulties with empathy and alexithymia, and whether this is associated with their cognitive levels of executive functioning. In total, 53 college students with autism spectrum disorder were compared to a gender-matched group of 29 neurotypical students on cognitive and affective dimensions of empathy and alexithymia. In addition, cognitive performance on executive functioning was measured with computerized and paper-and-pencil tasks. The autism spectrum disorder group scored significantly lower on cognitive empathy and higher on cognitive alexithymia (both d = 0.65). The difference on cognitive empathy also remained significant after controlling for levels of cognitive alexithymia. There were no group differences on affective empathy and alexithymia. No significant relations between executive functioning and cognitive alexithymia or cognitive empathy were detected. Together, these findings suggest that intellectually advanced individuals with autism spectrum disorder experience serious impairments in the cognitive processing of social–emotional information. However, these impairments cannot be attributed to individual levels of cognitive executive functioning.

The increasing interest in dimensional approaches towards schizophrenia spectrum pathology calls for instruments that can be used to study developmental markers conveying risk for psychopathology prior to onset of the disorder. In this study we evaluated the Dutch child version (SPQ-C-D) of the Schizotypal Personality Questionnaire (SPQ) developed by Raine, in terms of reliability and factorial structure in comparison to SPQ data from two studies with adults. The 74-item SPQ-C-D was completed by 219 children and adolescents aged 9 to 18 years. Internal consistency was assessed and the factorial structure was analyzed using principal component analysis (PCA) and confirmatory factor analysis. Results showed that most of the subscales had high Cronbach’s alphas, indicating good internal consistency. PCA resulted in three components, similar to the adult studies: Cognitive-Perceptual, Interpersonal, and Disorganization. The pattern of individual subscales loading on each of the components was identical to the original Raine study, except for one additional subscale loading on the Disorganization component. In addition, forcing Raine’s factorial structure on our data with confirmatory factor analysis resulted in an overall adequate model fit. In conclusion, the SPQ-C-D appears to be a suitable dimensional measure of schizotypal traits in populations aged 9 to 18 years.

Studies of individuals at ultra-high risk (UHR) for psychosis have mostly reported on long-term outcome of those individuals who develop psychosis compared to those who do not. However, these studies show that a large number of UHR individuals no longer meet criteria for UHR at follow-up. Therefore, this study aimed to investigate functioning at 6-year follow-up in remitted individuals, and to explore the course of their clinical symptoms. Forty-four UHR adolescents completed extensive clinical assessments at baseline and participated in long-term follow-up approximately six years later. UHR adolescents who had either converted to psychosis or who still met UHR criteria (n=26) at follow-up were compared to individuals who had remitted from their UHR status (n=18) on clinical and psychosocial variables. Results show that more than 40% of UHR individuals had fully remitted from their UHR status. At six-year follow-up, remitted individuals had improved clinically on most symptoms. The course of their symptoms showed that the most substantial reduction in positive symptoms occurred within the first two years, while improvements in general, mood and anxiety symptoms occurred at a later stage. Baseline socio-demographic characteristics and clinical symptoms did not distinguish between remitters and non-remitters. Although remitters no longer met criteria for UHR, they did meet diagnostic criteria for a wide range of psychiatric disorders. Our findings suggest that, when related to long-term outcome, UHR criteria capture non-specific psychotic symptoms rather than risk for psychosis per se and relate more to general psychopathology.

Background:Within young individuals, mood disorder onset may be related to changes in trajectory of brain structure development. To date, however, longitudinal prospective studies remain scarce and show partly contradictory findings, with a lack of emphasis on changes at the level of global brain patterns. Cross-sectional adult studies have applied such methods and show that mood disorders are associated with accelerated brain ageing. Currently, it remains unclear whether young individuals show differential brain structure ageing trajectories associated with onset of mood disorder and/or presence of familial risk.Methods:Participants included young individuals (15-30 years, 53%F) from the prospective longitudinal Scottish Bipolar Family Study with and without close family history of mood disorder. All were well at time of recruitment. Implementing a structural MRI-based brain age prediction model, we globally assessed individual trajectories of age-related structural change using the difference between predicted brain age and chronological age (brain-predicted age difference (brain-PAD)) at baseline and at 2-year follow-up. Based on follow-up clinical assessment, individuals were categorised into three groups: (i) controls who remained well (C-well,n= 93), (ii) high familial risk who remained well (HR-well,n= 74) and (iii) high familial risk who developed a mood disorder (HR-MD,n= 35).Results:At baseline, brain-PAD was comparable between groups. Results showed statistically significant negative trajectories of brain-PAD between baseline and follow-up for HR-MD versus C-well (β= -0.60,pcorrected< 0.001) and HR-well (β= -0.36,pcorrected= 0.02), with a potential intermediate trajectory for HR-well (β= -0.24 years,pcorrected= 0.06). Conclusions:These preliminary findings suggest that within young individuals, onset of mood disorder and familial risk may be associated with a deceleration in brain structure ageing trajectories. Extended longitudinal research will need to corroborate findings of emerging maturational lags in relation to mood disorder risk and onset.

Psychotic-like experiences (PLEs) are sub-psychotic expressions of the psychosis continuum. Several studies have suggested multifactorial models, including a bifactor model, of the putative PLEs assessed with the popular Community Assessment of Psychic Experiences (CAPE) questionnaire. Our confirmatory results in a gender-balanced population of adolescents and young adults support a three-factor Paranoia-Delusions-Hallucinations structure of PLEs, which excludes Grandiosity and Common Paranormal Beliefs. The best latent models achieved excellent fit when taking the categorical nature of the responses into consideration.

Patients at Ultra-High Risk (UHR) for developing a first psychosis vary widely in their symptom presentation and illness course. An important aim in UHR research concerns the characterization of the clinical heterogeneity in this population. We aimed to identify qualitatively and quantitatively different clinical symptom profiles at baseline and at 2-year follow-up in a group of UHR subjects and healthy controls. We employed a Latent Class Factor Analysis (LCFA) to the 19 items of the Structured Interview for Prodromal Syndromes (SIPS) ratings at baseline and at 2-year follow-up in a sample of 147 UHR subjects and 141 controls from the Dutch Prediction of Psychosis Study (DUPS) in the Netherlands. Additionally, a stepwise logistic regression analysis was performed with transition to psychosis as a dependent variable and baseline latent variable scores as predictors. Variation in symptomatology at baseline was explained by both quantitative and qualitative differences; at 2-year follow-up qualitative differences between individuals were no longer observed. Quantitative differences showed moderate stability over time (range=0.109–0.42). Within the UHR sample, transition to psychosis was significantly associated with quantitative differences in baseline SIPS scores. The results of our study suggest a ‘quasi'-continuous extended psychosis phenotype, a finding that merits replication in other samples.

Very little is known about the relative influence of cognitive performance-based executive functioning (EF) measures and behavioral EF ratings in explaining differences in children's school achievement. This study examined the shared and unique influence of these different EF measures on math and spelling outcome for a sample of 84 first and second graders. Parents and teachers completed the Behavior Rating Inventory of Executive Function (BRIEF), and children were tested with computer-based performance tests from the Amsterdam Neuropsychological Tasks (ANT). Mixed-model hierarchical regression analyses, including intelligence level and age, showed that cognitive performance and teacher's ratings of working memory and shifting concurrently explained differences in spelling. However, teacher's behavioral EF ratings did not explain any additional variance in math outcome above cognitive EF performance. Parent's behavioral EF ratings did not add any unique information for either outcome measure. This study provides support for the ecological validity of performance- and teacher rating-based EF measures, and shows that both measures could have a complementary role in identifying EF processes underlying spelling achievement problems. The early identification of strengths and weaknesses of a child's working memory and shifting capabilities, might help teachers to broaden their range of remedial intervention options to optimize school achievement.

BACKGROUND: The Valine158Methionine (Val158Met) polymorphism of the COMT gene leads to lower enzymatic activity and higher dopamine availability in Met carriers. The Met allele is associated with b ...

Studies of individuals at ultra high risk (UHR) for psychosis have revealed deviations in cognitive and neural development before the onset of psychosis. As affective impairments are among the core dysfunctions in psychotic disorders such as schizophrenia, this study assessed emotion processing and the relationship with social competence in adolescents at risk for psychosis. Thirty-four adolescents at UHR for psychosis and twenty-three non-clinical controls completed the Bermond-Vorst Alexithymia Questionnaire, a measure of emotion awareness. Social inadequacy was measured using the Dutch Personality Questionnaire. Schizophrenia spectrum psychopathology was assessed using self-report and clinical instruments. The Wechsler Adult Intelligence Scale (WAIS) was used to evaluate intellectual functioning. UHR adolescents showed difficulties in identifying and verbalizing their own emotions, independent of intelligence scores. Emotion awareness problems were related to social inadequacy and schizotypal traits in the high risk group. These findings suggest that UHR adolescents may have reduced emotion awareness, independent of intellectual functioning. The relationship with social inadequate behavior fits with the idea that emotion awareness is a prerequisite for the regulation of emotions in social contexts. In the search for early vulnerability markers of risk for psychosis, studying emotion processing besides cognitive abilities might increase our understanding of 'at risk' developmental pathways. (C) 2010 Elsevier Ireland Ltd. All rights reserved.

BackgroundThe peak in age of onset of psychotic disorders such as schizophrenia during puberty and early adulthood suggests a relationship between the expression of psychopathology and the changes in the brain and body that take place during this dynamic maturational period, including a dramatic increase in circulating oestrogens and androgens. This study examined levels of salivary testosterone and oestradiol in adolescents with prepsychotic, prodromal symptoms, as this may mediate risk for psychosis by having an impact on brain development.MethodIn 21 male adolescents with prodromal symptoms and 21 male non-clinical controls levels of testosterone and oestradiol were measured in saliva. Tanner pubertal stage and prodromal symptoms were also assessed.ResultsLevels of testosterone were significantly lower in adolescents with prodromal symptoms as compared with non-clinical controls. No group differences in oestradiol were found. In the total sample, level of testosterone was significantly correlated with age and Tanner pubertal stage.ConclusionsOur observations are in line with current hypotheses stressing the role of neuroendocrine factors during adolescence in the expression of psychotic symptoms. From a developmental perspective, susceptibility to psychotic disorders increases during adolescence. Our data suggest that testosterone might, in part, mediate this increased vulnerability. Further research is needed to assess the mediating, neural, mechanisms through which testosterone may have an impact on the development of psychotic symptoms. In the search for early risk markers for psychosis, studying neuroendocrine factors might increase our understanding of ‘at-risk’ developmental pathways.

BackgroundBy studying behavior, cognitive abilities and brain functioning in adolescents at high risk for psychosis, we can gain an insight into the vulnerability markers or protective factors in the development of psychotic symptoms. Although many high-risk studies have focused on impairments in neurocognitive functions, such as memory and attention, very few studies have investigated problems in processing social cues such as facial expressions as a possible vulnerability marker for psychosis.MethodThirty-six adolescents at ultra-high risk (UHR) for psychosis and 21 non-clinical controls completed a face recognition test, a facial affect labeling test and an inhibitory control test. Schizotypal traits and schizophrenia symptoms were assessed using a schizotypy questionnaire and the Positive and Negative Syndrome Scale (PANSS).ResultsThe UHR group showed impairments in labeling facial expressions of others, in addition to a spared ability to recognize facial identity. More specifically, the UHR group made more errors in labeling neutral expressions compared to the controls, and an analysis of error types indicated that neutral faces were misattributed as being angry. The degree of misattribution of neutral-as-angry faces correlated significantly with reduced inhibitory control.ConclusionsOur findings suggest that misattributing social cues might contribute to vulnerability for psychosis. This social cognitive deficit may be related to problems in inhibitory control, which potentially plays an important role in the selection of appropriate social meaning. These findings may have relevance for understanding the mechanisms underlying prodromal social dysfunction, which should be targeted in future remediation interventions.

Background: The comparison of high-risk populations with different developmental pathways to psychosis may lend more insight into the heterogeneity of the manifestation of the psychotic syndrome, and possible differing etiological pathways.Aim: To compare high-risk traits and symptoms in two populations at risk for psychosis, i.e. (1) help-seeking adolescents presenting with prodromal symptoms meeting the criteria for At Risk Mental State (ARMS), and (2) adolescents with Multiple Complex Developmental Disorder (MCDD), a PDD-NOS subtype characterized by severe, early childhood-onset deficits in affect regulation, anxieties, disturbed social relationships, and thought disorder.Method: 80 ARMS- and 32 MCDD-adolescents (12-18 years) were compared on prodromal symptoms (Structured Interview of Prodromal Symptoms, and Bonn Scale for the Assessment of Basic Symptoms-Prediction list), and autism traits (Social Communication Questionnaire). In addition, both high-risk groups were compared with 82 healthy controls on schizotypal traits (Schizotypal Personality Questionnaire-Revised).Results: Although the high-risk groups clearly differed in early developmental and treatment histories as well as autism traits, they did not differ with regard to schizotypal traits and basic symptoms, as well as disorganized and general prodromal symptoms. There were, however, group differences in positive and negative prodromal symptoms. Interestingly, 78% of the adolescents with MCDD met criteria for ARMS.Conclusion: These findings suggest that children diagnosed with MCDD are at high risk for developing psychosis later in life, and support the notion that there are different developmental pathways to psychosis. Follow-up research is needed to compare the rates of transition to psychosis in both high-risk groups. (C) 2007 Elsevier B.V. All rights reserved.

OBJECTIVE: The dopamine transporter (DAT1) gene has been implicated in attention-deficit/hyperactivity disorder (ADHD), although the mechanism by which it exerts its effects remains unknown. The polymorphism associated with ADHD has been shown to affect expression of the transporter in vitro and in vivo. Dopamine transporters are predominantly expressed in the striatum, but also in the cerebellar vermis. Stimulant medication is often effective in ADHD and is believed to exert its effects by blocking dopamine transporters in the striatum. We set out to investigate the effect of the DAT1 genotype in ADHD in a small, preliminary study. We hypothesized that the DAT1 genotype would affect brain activation patterns in a manner similar to that of stimulant medication, with the lesser expressing allele mirroring its effects.METHOD: We investigated DAT1 gene effects on brain activation patterns in an all-male sample of sibling pairs discordant for ADHD (n = 20) and controls (n = 9). All of the subjects participated in a functional magnetic resonance imaging session using a go/no-go paradigm and provided a DNA sample for analysis.RESULTS: DAT1 genotype affected activation in the striatum and cerebellar vermis. The genotype interacted with familial risk of ADHD in the striatum but not the vermis.CONCLUSIONS: These preliminary results suggest that the DAT1 gene effects in the striatum are involved in translating the genetic risk of ADHD into a neurobiological substrate. As such, this study represents a first step in elucidating the neurobiological mechanisms underlying genetic influences in ADHD. Furthermore, these results may contribute to long-term possibilities for the development of new treatments: If the DAT1 genotype has differential effects on striatal activation, then it may be useful as a surrogate endpoint in individualized treatments targeting genotype/functional magnetic resonance imaging activation profiles.

IMPORTANCE Individuals can be classified as being at clinical high risk (CHR) for psychosis if they meet at least one of the ultra-high-risk (UHR) inclusion criteria (brief limited intermittent psychotic symptoms [BLIPS] and/or attenuated psychotic symptoms [APS] and/or genetic risk and deterioration syndrome [GRD]) and/or basic symptoms [BS]. Themeta-analytical risk of psychosis of these different subgroups is still unknown. OBJECTIVE To compare the risk of psychosis in CHR individuals who met at least one of the major inclusion criteria and in individuals not at CHR for psychosis (CHR-). DATA SOURCES Electronic databases (Web of Science, MEDLINE, Scopus) were searched until June 18, 2015, along with investigation of citations of previous publications and a manual search of the reference lists of retrieved articles. STUDY SELECTION We included original follow-up studies of CHR individuals who reported the risk of psychosis classified according to the presence of any BLIPS, APS and GRD, APS alone, GRD alone, BS, and CHR-. DATA EXTRACTION AND SYNTHESIS Independent extraction by multiple observers and random-effects meta-analysis of proportions. Moderators were tested with meta-regression analyses (Bonferroni corrected). Heterogeneity was assessed with the I2 index. Sensitivity analyses tested robustness of results. Publication biases were assessed with funnel plots and the Egger test. MAIN OUTCOMES AND MEASURES The proportion of each subgroup with any psychotic disorder at 6, 12, 24, 36, and 48 or more months of follow-up. RESULTS Thirty-three independent studies comprising up to 4227 individualswere included. The meta-analytical proportion of individuals meeting each UHR subgroup at intakewas: 0.85 APS (95%CI, 0.79-0.90), 0.1 BLIPS (95%CI, 0.06-0.14), and 0.05 GRD (95%CI, 0.03-0.07). There were no significant differences in psychosis risk at any time point between the APS and GRD and the APS-alone subgroups. Therewas a higher risk of psychosis in the any BLIPS greater than APS greater than GRD-alone subgroups at 24, 36, and 48 or more months of follow-up. Therewas no evidence that the GRD subgroup has a higher risk of psychosis than the CHR- subgroup. There were too fewBS or BS and UHR studies to allowrobust conclusions. CONCLUSIONS AND RELEVANCE There is meta-analytical evidence that BLIPS represents separate risk subgroup compared with the APS. The GRD subgroup is infrequent and not associated with an increased risk of psychosis. Future studies are advised to stratify their findings across these different subgroups. The CHR guidelines should be updated to reflect these differences.

A developmental increase in working memory capacity is an important part of cognitive development, and low working memory (WM) capacity is a risk factor for developing psychopathology. Brain activity represents a promising endophenotype for linking genes to behavior and for improving our understanding of the neurobiology of WM development. We investigated gene–brain–behavior relationships by focusing on 18 single-nucleotide polymorphisms (SNPs) located in six dopaminergic candidate genes (COMT, SLC6A3/DAT1, DBH, DRD4, DRD5, MAOA). Visuospatial WM (VSWM) brain activity, measured with functional magnetic resonance imaging, and VSWM capacity were assessed in a longitudinal study of typically developing children and adolescents. Behavioral problems were evaluated using the Child Behavior Checklist (CBCL). One SNP (rs6609257), located ∼6.6 kb downstream of the monoamine oxidase A gene (MAOA) on human chromosome X, significantly affected brain activity in a network of frontal, parietal and occipital regions. Increased activity in this network, but not in caudate nucleus or anterior prefrontal regions, was correlated with VSWM capacity, which in turn predicted externalizing (aggressive/oppositional) symptoms, with higher WM capacity associated with fewer externalizing symptoms. There were no direct significant correlations between rs6609257 and behavioral symptoms. These results suggest a mediating role of WM brain activity and capacity in linking the MAOA gene to aggressive behavior during development.

Background: Reduced prepulse inhibition (PPI) of the auditory startle reflex is a hallmark feature of attention-processing deficits in patients with schizophrenia and other psychotic disorders. Recent evidence suggests that these deficits may also be present before the onset of psychosis in individuals at ultra-high risk (UHR) and become progressively worse as psychosis develops. We conducted a longi tudinal follow-up study to observe the development of PPI over time in UHR adolescents and healthy controls. Methods: Two-year followup data of PPI measures were compared between UHR adolescents and a matched control group of typically developing individuals. Results: We included 42 UHR adolescents and 32 matched controls in our study. Compared with controls, UHR individuals showed reduced PPI at both assessments. Clinical improvement in UHR individuals was associated with an increase in PPI parameters. Limitations: A developmental increase in startle magnitude partially confined the interpretation of the association between clinical status and PPI. Furthermore, post hoc analyses for UHR individuals who became psychotic between assessments had limited power owing to a low transition rate (14%). Conclusion: Deficits in PPI are present before the onset of psychosis and represent a stable vulnerability marker over time in UHR individuals. The magnitude of this marker may partially depend on the severity of clinical symptoms.

Background: Ultra-high risk (UHR) for psychosis has been associated with widespread structural brain changes in young adults. The onset of these changes and their subsequent progression over time are not well understood. Methods: Rate of brain change over time was investigated in 43 adolescents at UHR for psychosis compared with 30 healthy controls. Brain volumes (total brain, gray matter, white matter [WM], cerebellum, and ventricles), cortical thickness, and voxel-based morphometry were measured at baseline and at followup (2 y after baseline) and compared between UHR individuals and controls. Post hoc analyses were done for UHR individuals who became psychotic (N 5 8) and those who did not (N 5 35). Results: UHR individuals showed a smaller increase in cerebral WM over time than controls and more cortical thinning in the left middle temporal gyrus. Post hoc, a more pronounced decrease over time in total brain and WM volume was found for UHR individuals who became psychotic relative to controls and a greater decrease in total brain volume than individuals who were not psychotic. Furthermore, UHR individuals with subsequent psychosis displayed more thinning than controls in widespread areas in the left anterior cingulate, precuneus, and temporo-parieto-occipital area. Volume loss in the individuals who developed psychosis could not be attributed to medication use. Conclusion: The development of psychosis during adolescence is associated with progressive structural brain changes around the time of onset. These changes cannot be attributed to (antipsychotic) medication use and are therefore likely to reflect a pathophysiological process related to clinical manifestation of psychosis.

Background Future success of early intervention initiatives to prevent the onset of psychosis will rely on the validity of methods to predict clinical outcome. Proper identification is particularly essential for young adolescents, as psychotic-like symptoms are often transitory during this period and mislabeling can lead to early stigmatization and unnecessary treatment. This article presents results from a prospective, naturalistic 2-year follow-up study of a cohort of young adolescents putatively at ultra-high risk (UHR) for psychosis. Methods Seventy-two adolescents between 12 and 18 years were recruited, fulfilling either UHR criteria or the basic symptom-based criterion cognitive disturbances (COGDIS). Incidence of transition as well as the remission rate from UHR status was calculated. Individuals who made a transition (UHR-P) were compared to those who did not (UHR-NP) and to those who remitted (UHR-R) on socio-demographic and clinical characteristics. Results Fifty-seven UHR individuals completed the 2-year follow-up assessment. The confirmed transition rate was 15.6% and 35.3% still met UHR criteria. The remaining 49.1% had remitted from an initial UHR status. The UHR subgroups did not differ on socio-demographic or clinical variables at baseline. Conclusions Half of young adolescents meeting UHR criteria continue to experience prodromal or psychotic symptoms after 2 years. However, they are at least three times more likely to have remitted from their UHR status than to have made a transition to psychosis. In addition, baseline characteristics are not indicative of clinical outcome at follow-up. Our results emphasize the need for further improvement and stratification of relative risk factors for psychosis.

Objective The onset of psychosis is thought to be preceded by neurodevelopmental changes in the brain. However, the timing of these changes has not been established. We investigated structural brain changes in a sample of young adolescents (12–18 years) at ultra high-risk for psychosis (UHR). Methods Structural MRI data from young UHR subjects ( n = 54) and typically developing, matched controls ( n = 54) were acquired with a 1.5 Tesla scanner and compared. Results None of the measures differed between UHR subjects and controls. Conclusions Our results do not support the presence of gross neuroanatomical changes in young UHR subjects. This suggests that early changes are too subtle to detect with conventional imaging techniques. Therefore, changes observed in older cohorts may only onset later developmentally or occur secondary to prodromal symptoms.

Background Attention-deficit hyperactivity disorder (ADHD) is a heritable neuropsychiatric disorder, associated with atypical patterns of brain activation in functional imaging studies. Neuroimaging measures may serve as an intermediate phenotype in genetic studies of ADHD, as they are putatively more closely linked to gene expression than a clinical diagnosis. Methods We used rapid, mixed-trial, event-related functional magnetic resonance imaging (fMRI) to investigate changes in brain activation during a go no-go task in boys with ADHD, their unaffected siblings, and matched control subjects. Results On the hardest inhibitory trials in our task, children and adolescents with ADHD had lower accuracy than control subjects, whereas their unaffected siblings did not. Control subjects activated a network of regions, including ventral prefrontal and inferior parietal cortex. Both children and adolescents with ADHD and their unaffected siblings showed decreased activation in these areas, as well as fewer correlations between performance and activation. Conclusions These findings suggest that the magnitude of activation during successful inhibitions is sensitive to genetic vulnerability for ADHD in a number of regions, including ventral prefrontal cortex. If this can be replicated in future studies, this suggests that neuroimaging measures related to inhibitory control may be suitable as intermediate phenotypes in studies investigating gene effects in ADHD.