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ABSTRACT Why are boys at risk? To address this question, I use the perspective of regulation theory to offer a model of the deeper psychoneurobiological mechanisms that underlie the vulnerability of the developing male. The central thesis of this work dictates that significant gender differences are seen between male and female social and emotional functions in the earliest stages of development, and that these result from not only differences in sex hormones and social experiences but also in rates of male and female brain maturation, specifically in the early developing right brain. I present interdisciplinary research which indicates that the stress-regulating circuits of the male brain mature more slowly than those of the female in the prenatal, perinatal, and postnatal critical periods, and that this differential structural maturation is reflected in normal gender differences in right-brain attachment functions. Due to this maturational delay, developing males also are more vulnerable over a longer period of time to stressors in the social environment (attachment trauma) and toxins in the physical environment (endocrine disruptors) that negatively impact right-brain development. In terms of differences in gender-related psychopathology, I describe the early developmental neuroendocrinological and neurobiological mechanisms that are involved in the increased vulnerability of males to autism, early onset schizophrenia, attention deficit hyperactivity disorder, and conduct disorders as well as the epigenetic mechanisms that can account for the recent widespread increase of these disorders in U.S. culture. I also offer a clinical formulation of early assessments of boys at risk, discuss the impact of early childcare on male psychopathogenesis, and end with a neurobiological model of optimal adult male socioemotional functions. [ABSTRACT FROM AUTHOR]

Psychoanalysis, the science of unconscious processes, has recently undergone a significant transformation. Self psychology, derived from the work of Heinz Kohut, represents perhaps the most important revision of Freud's theory as it has shifted its basic core concepts from an intrapsychic to a relational unconscious and from a cognitive ego to an emotion-processing self. As a result of a common interest in the essential, rapid, bodily based, affective processes that lie beneath conscious awareness, a productive dialogue is now occurring between psychoanalysis and neuroscience. Here I apply this interdisciplinary perspective to a deeper understanding of the nonconscious brain/mind/body mechanisms that lie at the core of self psychology. I offer a neuropsychoanalytic conception of the development and structuralization of the self, focusing on the experience-dependent maturation of the emotion-processing right brain in infancy. I then articulate an interdisciplinary model of attachment trauma and pathological dissociation, an early forming defense against overwhelming affect that is a cardinal feature of self-psychopathologies. I end with some thoughts on the mechanism of the psychotherapeutic change process and suggest that self psychology is, in essence, a psychology of the unique functions of the right brain and that a rapprochement between psychoanalysis and neuroscience is now at hand. [ABSTRACT FROM AUTHOR]

Objective: This review integrates recent advances in attachment theory, affective neuroscience, developmental stress research, and infant psychiatry in order to delineate the developmental precursors of posttraumatic stress disorder. Method: Existing attachment, stress physiology, trauma, and neuroscience literatures were collected using Index Medicus/Medline and Psychological Abstracts . This converging interdisciplinary data was used as a theoretical base for modelling the effects of early relational trauma on the developing central and autonomic nervous system activities that drive attachment functions. Results: Current trends that integrate neuropsychiatry, infant psychiatry, and clinical psychiatry are generating more powerful models of the early genesis of a predisposition to psychiatric disorders, including PTSD. Data are presented which suggest that traumatic attachments, expressed in episodes of hyperarousal and dissociation, are imprinted into the developing limbic and autonomic nervous systems of the early maturing right brain. These enduring structural changes lead to the inefficient stress coping mechanisms that lie at the core of infant, child, and adult posttraumatic stress disorders. Conclusions: Disorganised-disoriented insecure attachment, a pattern common in infants abused in the first 2 years of life, is psychologically manifest as an inability to generate a coherent strategy for coping with relational stress. Early abuse negatively impacts the developmental trajectory of the right brain, dominant for attachment, affect regulation, and stress modulation, thereby setting a template for the coping deficits of both mind and body that characterise PTSD symptomatology. These data suggest that early intervention programs can significantly alter the intergenerational transmission of posttraumatic stress disorders. [ABSTRACT FROM AUTHOR]