Neonatal Imitation, Intersubjectivity, and Children With Atypical Development: Do Observations on Autism and Down Syndrome Change Our Understanding?

Almost all studies on neonatal imitation to date seem to have focused on typically developing children, and we thus lack information on the early imitative abilities of children who follow atypical developmental trajectories. From both practical and theoretical perspectives, these abilities might be relevant to study in children who develop a neuropsychiatric diagnosis later on or in infants who later show impaired ability to imitate. Theoretical in the sense that it will provide insight into the earliest signs of intersubjectivity—i.e., primary intersubjectivity—and how this knowledge might influence our understanding of children following atypical trajectories of development. Practical in the sense that it might lead to earlier detection of certain disabilities. In the present work, we screen the literature for empirical studies on neonatal imitation in children with an Autism spectrum disorder (ASD) or Down syndrome (DS) as well as present an observation of neonatal imitation in an infant that later was diagnosed with autism and a re-interpretation of previously published data on the phenomenon in a small group of infants with DS. Our findings suggest that the empirical observations to date are too few to draw any definite conclusions but that the existing data suggests that neonatal imitation can be observed both in children with ASD and in children with DS. Thus, neonatal imitation might not represent a useful predictor of a developmental deficit. Based on current theoretical perspectives advocating that neonatal imitation is a marker of primary intersubjectivity, we propose tentatively that an ability to engage in purposeful exchanges with another human being exists in these populations from birth.

Temporal manipulation of KCC3 expression in juvenile or adult mice suggests irreversible developmental deficit in hereditary motor sensory neuropathy with agenesis of the corpus callosum

Hereditary motor sensory neuropathy (HMSN/ACC) with agenesis of the corpus callosum (ACC) has been documented in the French-derived populations of Charlevoix and Saguenay/Lac St. Jean in Quebec, Canada, as well as a few sporadic families throughout the world. HMSN/ACC occurs because of loss-of-function mutations in the potassium-chloride cotransporter 3 (KCC3). In HMSN/ACC, motor deficits occur early in infancy with rapid and continual deterioration of motor and sensory fibers into juvenile and adulthood. Genetic work in mice has demonstrated that the disease is caused by loss of KCC3 function in neurons and particularly parvalbumin (PV)-expressing neurons. Currently, there are no treatments or cures for HMSN/ACC other than pain management. As genetic counseling in Quebec has increased as a preventative strategy, most individuals with HSMN/ACC are now adults. The onset of the disease is unknown. In particular, it is unknown if the disease starts early during development and whether it can be reversed by restoring KCC3 function. In this study, we used two separate mouse models that when combined to the PV-CreERT2 tamoxifen-inducible system allowed us to 1) disrupt KCC3 expression in adulthood or juvenile periods; and 2) reintroduce KCC3 expression in mice that first develop with a nonfunctional cotransporter. We show that disrupting or reintroducing KCC3 in the adult mouse has no effect on locomotor behavior, indicating that expression of KCC3 is critical during embryonic development and/or the perinatal period and that once the disease has started, reexpressing a functional cotransporter fails to change the course of HMSN/ACC.

Sustained ErbB activation causes demyelination and hypomyelination by driving necroptosis of mature oligodendrocytes and apoptosis of oligodendrocyte precursor cells

Oligodendrocytes are vulnerable to genetic and environmental insults and its injury leads to demyelinating diseases. The roles of ErbB receptors in the CNS myelin integrity are largely unknown. Here we overactivate ErbB receptors that mediate signaling of either neuregulin or EGF family growth factors and found their synergistic activation caused deleterious outcomes in white matter. Sustained ErbB activation induced by the tetracycline-dependent mouse tool Plp-tTA resulted in demyelination, axonal degeneration, oligodendrocyte precursor cell (OPC) proliferation, astrogliosis, and microgliosis in white matter. Moreover, there was hypermyelination prior to these pathological events. In contrast, sustained ErbB activation induced by another tetracycline-dependent mouse tool Sox10+/rtTA caused hypomyelination in the corpus callosum and optic nerve, which appeared to be a developmental deficit and did not associate with OPC regeneration, astrogliosis, or microgliosis. By analyzing the differentiation states of cells that were pulse- labeled with a viral reporter, we found that, during juvenile to adolescent development, Plp-tTA targeted mainly mature oligodendrocytes (MOs), while Sox10+/rtTA targeted OPCs and newly-formed oligodendrocytes. The distinct phenotypes of mice with ErbB overactivation induced by Plp-tTA and Sox10+/rtTA supported the reporter pulse-labeling results, and consolidated their non-overlapping targeting preferences in the oligodendrocyte lineage after early development. These features enabled us to demonstrate that ErbB overactivation in MOs induced necroptosis that caused pathological demyelination, whereas in OPCs induced apoptosis that caused developmental hypomyelination. These results established an upstream pathogenic role of ErbB overactivation in oligodendrocytes, providing molecular and cellular insights into the primary oligodendropathy in demyelinating diseases.

Reduction of Recognition of the Orienting Value of the Gaze as a Violation of the Mechanism of Joint Attention among Preschoolers

The article discusses the role of the model of mental and separately the mechanism of joint attention in the normative age development of preschool children. It is shown that children with a lack of joint attention may experience difficulties in acquiring a wide range of developmental skills, and the ability to use the line of sight is part of a general mechanism that will further allow understanding and understanding the meaning of social information, the child’s ability to accumulate normal social experience. The hypothesis was verified that the developmental deficit of the mental model in children may be due to a decrease in the level of intellect: the difficulties of joint attention lead to an unformed component of the “objective-reflexive-normative thinking”. On a sample of 493 children of preschool age (typically developing and with mental retardation), a methodology was tested that assesses children’s understanding of the intentions and desires of others in the direction of gaze. It was found that the differences between typically developing children, children with lower bound and delayed age development can be tied to the fact that children who participate in joint attention can contribute to having more conditions to expand social learning opportunities. Changes in the accuracy of identifying the direction of sight shows the dynamics of the cognitive development of the child, which in comparison makes it possible to assess the characteristic differences not only in pathology, but at a decrease in the overall level of age development.

The Secret Life of Secrets: Deleterious Psychosomatic Effects on Patient and Analyst

The impact and complex nature of keeping secrets deserves greater scrutiny within psychoanalysis. While the capacity to keep a secret is a developmental achievement that furthers conscious choice and healthy boundary setting between self and others, an individual’s need for privacy must be distinguished from untoward costs of collusion and concealment. Clinical case material shows that not all secrets are unconscious or multilayered, as assumed in most of the psychoanalytic literature. Nonetheless, in these cases deleterious effects to psyche and soma took root. These patients assumed that their secret was irreparably destructive to an essential object relationship; shame, guilt, narcissistic vulnerability, unconscious identification with an injured party, and developmental deficit were other factors found to undergird this mode of pathogenic dissembling. Two clinical examples also demonstrate that embodied countertransference reactions may herald the revelation of a secret in treatment that had been hidden, but in plain view. Secrets appear to exert their profound psychological and physical effects on patient and analyst by biological mechanisms that are as yet poorly understood but are readily observed in clinical practice. Psychoanalysts who keep in conscious awareness both the adaptive value and the potential costs of maintaining the confidences of others over the course of a career are better positioned to assist their patients and themselves in rendering essential self-care.