Journal of Child Psychology and Psychiatry最新文献

In this commentary, I argue that including and operationalizing allostatic processes will become increasingly important in future research on parent–child biobehavioral coregulation. In particular, the conceptualization and modeling of dyadic oscillatory rhythms that align in expected ways with the child's developmental stage and that distinguish typical and atypical development will be useful in future work. Despite the inherent asymmetry characteristic of parent–child relationships, we should not forget to consider the child's effects on the parent within and across time, the additional environmental demands upon parents that shape parent–child coregulation, and variations in parent–child asymmetry by parental risk factors. Studying risk factors that are dyadic in nature, such as child maltreatment, may be particularly informative in gaining a deeper understanding of how parent–child coregulation interfaces with developmental psychopathology. To best model parent–child coregulation as a dynamic system, it will be critical to employ more nonlinear analytic models and better represent the multiple hierarchical domains of coregulation and their interactions, including affect, cognition, behavior, and biology. Finally, in future research, a deeper application of existing dyadic and dynamic theories, as well as the generation of new dyadic developmental theories, will aid us in obtaining a stronger understanding of the developmental function and intervention implications of parent–child biobehavioral coregulation.

Work by many groups demonstrate links between peripheral markers of inflammation and symptoms of depression. Here, Nusslock and colleagues present an update to their neuroimmune network model to incorporate a developmental lens. They propose that specific neural circuits may be responsible for causing heightened inflammation. One principal circuit includes the amygdala and prefrontal cortex and is proposed to be involved in threat detection. Thus, heightened threat sensitivity resulting from early life stress is suggested to cause increases in inflammatory signaling. Second, the authors suggest that reward circuits, including the striatum, may be targets of increased inflammation leading to symptoms of anhedonia. In this commentary, I add context to the model proposed by Nusslock et al., suggesting that taking a learning perspective and considering additional circuits, including the hippocampus and midline structures may be necessary to more fully account for the phenomena described by the authors.

Anhedonia is a symptom encompassing reduced or absence of motivation and pleasure that often emerges in adolescence and conveys risk for different mental illnesses and other difficulties. In their review, Gupta, Eckstrand, and Forbes (Journal of Child Psychology and Psychiatry, 2024) present an empirically-based conceptual neurodevelopmental model of anhedonia whereby brain development and pubertal maturation create openness to vulnerability to anhedonia that is influenced by early life adversity and chronic inflammation. This commentary considers anhedonia as a paradox of adolescence given its juxtaposition to the expected developmental milestones of adolescence. It highlights the need to consider anhedonia in terms of both variability and universality of children's experiences and biological development, missed opportunities for social relationships and experiences, and forms and functions of rewards and anhedonia.

This commentary highlights the limitations of many existing population-based studies examining the utility of the Modified Checklist for Autism in Toddlers, Revised/Follow-Up (M-CHAT-R/F) in screening for autism. We expound on three major factors: (a) the limited number of screen-negative children who undergo diagnostic evaluations, (b) the substantial number of children who screen positive and were subsequently lost to follow-up (i.e. without further diagnostic evaluations), and (c) the sizeable number of children who did not complete the full two-stage screening process as intended. Each of these factors can lead to erroneous estimates of the psychometric properties, specifically, the sensitivity, specificity, and negative predictive value. Hence, we emphasize the need for future studies to increase the number of children who screen negative and receive a diagnostic evaluation and ensure that these children are selected at random without a higher likelihood for the presence of autism. It is also imperative that concrete steps are taken to minimize the number of screen-positive children who are lost to follow-up both within and after the screening process. Both of these will play a major role in ensuring more robust results from empirical research that can guide the clinical implementation of the M-CHAT-R/F.