Journal of Abnormal Child Psychology最新文献

Individuals diagnosed with autism spectrum disorder (ASD) have difficulty perceiving and expressing emotions. Since prosodic changes in speech (i.e. changes in intonation, stress, rhythm, etc.) are crucial for extracting information about the emotional state of a speaker, an inability to perceive and interpret these prosodic changes may be related to impairments in social communication. This study used non-verbal emotional voice-clips to examine the ability of autistic and typically-developing children (7-13 years old) to extract affect from changes in prosody. This research also explored whether difficulty extracting affective intent from changes in prosody may be related to social competence. Autistic (n = 26) and typically-developing (n = 26) children accurately matched emotional voice-clips to emotion words, suggesting autistic children can accurately extract the affective meaning conveyed by changes in prosody. Autistic children were less accurate at matching the voice-clips to emotional faces, suggesting that autistic children may struggle to make use of prosodic information in a social context. Across both autistic and typically-developing children, prosody-face matching accuracy was found to predict overall social competence, as well as social inferencing abilities, suggesting that the inability to utilize affective information derived from a speaker's voice may interfere with effective social communication.

The present study tested the moderating role of interparental relationship quality and child inhibitory control on the stability of paternal depression over time and associations between paternal depression and child internalizing problems in early childhood. Participants were a subsample (n = 166) of families from the Early Steps Multisite study, a longitudinal study of low-income parents and children. Interparental relationship quality (age 2) attenuated the association between paternal depressive symptoms at age 2 and paternal depressive symptoms at age 3. Both interparental relationship quality (age 3) and child inhibitory control (age 3) attenuated the association between paternal depressive symptoms (age 3) and age 4 child internalizing problems. Results suggest that high interparental relationship quality may be a protective factor in terms of lessening the stability of paternal depressive symptoms over time, as well as the association between paternal depression and later child internalizing problems. Similarly, high levels of inhibitory control may buffer children from the negative effects of paternal depression on the development of internalizing problems.

Burns et al. (this issue) have shown that the application of the symmetrical bifactor model to attention-deficit/hyperactivity disorder (ADHD) and oppositional defiant disorder (ODD) symptoms leads to anomalous and inconsistent results across different rater groups. In contrast to the symmetrical bifactor model, applications of the bifactor S-1 model showed consistent and theoretically well-founded results. The implications of the bifactor S-1 model for individual clinical assessment are discussed. It is shown that individual factor scores of the bifactor S-1 model reveal important information about the profile of individual symptoms that is not captured by factor scores of the multidimensional model with correlated first-order factors. It is argued that for individual clinical assessment factor scores from both types of model (multidimensional model with correlated first-order factors, bifactor S -1 model) should be estimated and compared. Finally, a general strategy for choosing an appropriate model for analyzing multi-faceted constructs is presented that compares areas of applications for (1) the multidimensional model with correlated first-order factors, (2) the bifactor S-1 model with a general reference factor, and (3) the bifactor S - 1 model with a directly assessed general factor.

To examine the construct validity of attention-deficit/hyperactivity disorder (ADHD) and oppositional defiant disorder (ODD), the bifactor S-1 approach has been applied as an alternative to the fully symmetrical bifactor models in order to eliminate anomalous results and to allow for an unambiguous interpretation of g- and s-factors. We compared and contrasted our results with those of Burns et al. (2019) and extended their analyses by taking into account a two- vs. a three-factor structure of ADHD. Data from our previous research were reanalyzed and reinterpreted in accordance with the bifactor S-1 approach, constructing different models with hyperactivity (HY), impulsivity (IM) or hyperactivity/impulsivity (HI) as the general factor. No anomalous results were observed. All factor loadings were significant. Our results were comparable to those reported by Burns et al. (2019), although items from the specific subscales inattention (IN) and ODD accounted for more variance in our sample. Model fit for our HI model was comparable to that in Burns et al. (2019). In our sample, model fit was best when solely HY or IM was chosen as a general reference factor. However, in these cases, the remaining specific factor IM or HY was weakly defined. Overall, we were able to replicate the results found by Burns et al. 2019), although our factor loadings on the g-factor were slightly lower and our specificity regarding IN and ODD was slightly higher. Our results support a two-factor structure of ADHD/ODD in a clinical population.

Questions persist about whether attention deficit hyperactivity disorder (ADHD), oppositional defiant disorder (ODD), and conduct disorder are in fact distinct from one another. When such questions arise, ODD is often suggested to be subsumed under one or the other condition. Modeling approaches that can evaluate whether specific subfactors can be distinguished from general psychopathology are of great interest, and the general bifactor model has been increasingly applied in studies evaluating the structure of psychopathology. However, evidence for bias in the model, the frequency of anomalous indicators, and theoretical concerns about the applicability of the general bifactor model to these questions raise doubts about whether it is reliable or appropriate to do so. Burns and colleagues propose the bifactor S-1 model as a psychometrically sounder alternative. Their systematic examination provides a compelling argument that it is psychometrically sounder, but it is not clear that it is a true alternative. It may not be answering the same questions, cannot test hypotheses regarding the same sets of specific subfactors, and relies on a priori decisions on the part of the researcher that may change the interpretation of the results. The bifactor S-1 model approach appears to be a valuable, psychometrically sound approach to test the structure of psychopathology, particularly in regard to ADHD and ODD.

My commentary is organized into four sections. First, I summarize the reasons for the original interest in fitting symmetric bifactor models to ADHD data. Second, I summarize the concerns that Burns and colleagues raised with respect to fitting symmetric bifactor models to ADHD item-level data and describe their recommended alternative approach. Third, I raise two concerns that I had with their manuscript. Fourth, I conclude with a caveat and a general question about the merits of the continued study of the factor structure of ADHD symptoms.

The symmetrical bifactor model is often applied to attention-deficit/hyperactivity disorder (ADHD)-hyperactive/impulsive (HI), ADHD-inattentive (IN), and oppositional defiant disorder (ODD) symptoms, but this model frequently yields anomalous or inadmissible results. An alternative model, the bifactor S - 1 model, is more appropriate for examining the hierarchical structure of ADHD/ODD symptoms. Both models were applied to ADHD-HI, ADHD-IN, and ODD symptom ratings by mothers, fathers, and teachers for 2142 Spanish children (49.49% girls; ages 8-13 years). The symmetrical bifactor model yielded the typical anomalous loadings, with a weakly defined ADHD-HI specific factor and difficult to interpret associations of general and specific factors with correlates. In contrast, the bifactor S - 1 model with ADHD-HI symptoms as general reference factor produced clearly interpretable results. For mothers and fathers, slightly more than 50% of true score variance in ADHD-IN and ODD symptoms represented specific residual variance not shared with the general ADHD-HI reference factor. For teachers, approximately 69% and 39% of true score variance in ADHD-IN and ODD symptoms, respectively, represented specific residual variance not shared with the general ADHD-HI reference factor. The general ADHD-HI reference factor and specific ADHD-IN and ODD residual factors showed convergent and discriminant validity across sources, along with unique associations with peer rejection, social impairment, and academic impairment factors. The bifactor S - 1 model also yielded results consistent with predictions from trait-impulsivity theory of ADHD/ODD development. Researchers should use the bifactor S - 1 model rather than the symmetrical bifactor model if hypotheses involve the latent hierarchical structure of ADHD/ODD symptoms.

The commentaries by Burke and Johnston (this issue), Eid (this issue), Junghänel et al. (this issue), and Willoughby (this issue) on Burns et al. (this issue) provide useful context for comparing three latent variable modeling approaches to understanding psychopathology-the correlated first-order syndrome-specific factors model, the bifactor S - 1 model, and the symmetrical bifactor model. The correlated first-order syndrome-specific factors model has proven useful in constructing explanatory models of psychopathology. The bifactor S - 1 model is also useful for examining the latent structure of psychopathology, especially in contexts with clear theoretical predictions. Joint use of correlated first-order syndrome-specific model and bifactor S - 1 model provides leverage for explaining psychopathology, and both models can also guide individual clinical assessment. In this reply, we further clarify reasons why the symmetrical bifactor model should not be used to study the latent structure of psychopathology and also discuss a restricted bifactor S - 1 model that is equivalent to the first-order syndrome-specific factors model.

It is important to establish correlates of sluggish cognitive tempo (SCT) across units of analysis and to better understand how SCT may be conceptualized in models of psychopathology. The current study examined SCT symptoms in relation to automatic nervous system reactivity during social and cognitive stressor tasks. Participants were 61 children ages 8-12 years with a full range of attention-deficit/hyperactivity disorder (ADHD) symptom severity. Parents provided ratings of SCT and parents and teachers completed measures that were used to create composite indices of ADHD symptoms. Children were administered standardized peer rejection and impossible puzzle tasks, during which their respiratory sinus arrhythmia (RSA) and skin conductance level (SCL) reactivity were recorded. Regression analyses indicated that SCT symptoms were unassociated with RSA reactivity to either task. Greater SCT symptoms were significantly associated with greater SCL reactivity to peer rejection. Greater SCT symptoms were not significantly associated with SCL reactivity to the impossible puzzle task. The pattern of findings was unchanged in sensitivity analyses that controlled for ADHD symptoms, internalizing symptoms, medication status, or sex. This study provides the first evidence that SCT symptoms are associated with sympathetic nervous system reactivity. These findings suggest that SCT symptoms may be associated with greater behavioral inhibition system activation, and reactivity may be especially pronounced in social challenges.

Deficits in positive emotionality (PE) have been implicated in the etiology of both social anxiety and depression; however, factors that contribute to divergent social anxiety and depression outcomes among youth low in PE remain unknown. Extant research suggests that parent-child stress and peer stress demonstrate differential patterns of associations with social anxiety and depression. Thus, the present study examined prospective interactive effects of PE and chronic parent-child and peer stress on simultaneously developing trajectories of social anxiety and depression symptoms among 543 boys and girls (age 8-16 at baseline, M[SD] = 11.94[2.32] 55.6% female). Parents reported on youth PE at baseline. Domains of chronic interpersonal (parent-child and peer) stress occurring between baseline and 18-months were assessed via child-report by trained interviews using the Youth Life Stress Interview (Rudolph and Flynn Development and Psychopathology, 19(2), 497-521, 2007). Youth completed self-report measures of depression and social anxiety every three months from 18- to 36- months (7 assessments). Conditional bivariate latent growth curve models indicated that main effects of parent-child stress, but not peer stress, predicted trajectories of depression in boys and girls. In girls, high levels of chronic interpersonal stress in both domains predicted stable, elevated trajectories of social anxiety symptoms regardless of PE. In boys, PE contributed to a pattern of differential susceptibility whereby boys high in PE were particularly susceptible to the effects of chronic interpersonal stress, for better or worse.