Background: There is limited data on the effects of Childhood Maltreatment (CM) on pediatric mood disorders in general and pediatric Bipolar Disorder (BD) in particular. We aimed to compare clinical and family characteristics of youth with CM and Mood Disorder Not Otherwise Specified (MD) to youth with CM and BD and to follow the youth with MD longitudinally to determine their course of illness. Methods: Twenty-two youths (ages 8-18 years) with mood symptoms (11 with BD and 11 with MD) and histories of CM prior to the age of 5 years were assessed using a structured clinical interview. A follow-up assessment was conducted with 8 of the 11 parents of youth with MD. Results: 11 subjects (5 females, mean age 13 ± 2.4 sd) met DSMIV-TR criteria for BD and 11 subjects (4 females, mean age 12.5 ± 3.1 sd) met DSM-IV-TR criteria for MD. BD subjects had a higher number of lifetime major depressive episodes (BD=18.9 versus MD=4, z(20)=-2.5, p=0.01) and lifetime manic episodes (BD=17.7 MD=0.3, z(19)=-5.1,p<0.001). Age at first reported trauma exposure was similar for both groups youth with BD (BD=3.1 ± 1.7 MD 3.4 ± 1.8 t(19.9)=-0.4, p=0.7), as were types of trauma, number of incidents, and PTSD symptoms. There were higher rates of schizophrenia, BD and major depressive disorder in the families of youth with BD compared to youth with MD. At follow up, 4/8 (50%) youth with MD at baseline either received a different diagnosis (n=2), or experienced a manic episode (n=2). Conclusions: The results suggest higher rates of schizophrenia, BD, and MDD in the families of youth with BD. These preliminary results suggest potential biological and genetic vulnerabilities, which may predispose children with histories of CM to develop specific mood disorders under certain circumstances.

Affect dysregulation, defined as the impaired ability to regulate or tolerate negative emotional states, has been associated with interpersonal trauma and posttraumatic stress. Affect-regulation difficulties play a role in many psychiatric conditions, including anxiety and mood disorders, and especially major depression in youth and bipolar disorder throughout the life span. Exposure to traumatic events and interpersonal trauma in childhood is associated with wide-ranging psychosocial, developmental, and medical impairments in children, adolescents, and adults, with emotional dysregulation being a core feature that may help to account for this heightened risk. In order to understand how the developmental effects of childhood maltreatment contribute to emotional dysregulation and psychiatric sequelae, we review emotional regulation and its developmental neurobiology, and examine the research evidence of associations between childhood trauma, emotional dysregulation, and psychiatric comorbidities in children, adolescents, and adults.

Activity Date: This activity will be available as an online learning module starting August 30, 2013, and will be available for one year. material for a maximum of 1.0 AMA PRA Category 1 Credits™. Physicians should only claim credit commensurate with the extent of their participation in the activity.  Identify the biological role of oxytocin in forming attachments.  Evaluate the relationship between various neuropsychiatric disorders and oxytocin.  Identify clinical implications of using oxytocin to treat various neuropsychiatric disorders.

LEARNING OBJECTIVES:After participating in this educational activity, the physician should be better able to 1. Identify the biological role of oxytocin in forming attachments. 2. Evaluate the relationship between various neuropsychiatric disorders and oxytocin. 3. Identify clinical implications of using oxytocin to treat various neuropsychiatric disorders. Oxytocin is a peptide hormone integral in parturition, milk letdown, and maternal behaviors that has been demonstrated in animal studies to be important in the formation of pair bonds and in social behaviors. This hormone is increasingly recognized as an important regulator of human social behaviors, including social decision making, evaluating and responding to social stimuli, mediating social interactions, and forming social memories. In addition, oxytocin is intricately involved in a broad array of neuropsychiatric functions and may be a common factor important in multiple psychiatric disorders such as autism, schizophrenia, and mood and anxiety disorders. This review article examines the extant literature on the evidence for oxytocin dysfunction in a variety of psychiatric disorders and highlights the need for further research to understand the complex role of the oxytocin system in psychiatric disease and thus pave the way for developing new therapeutic modalities. Articles were selected that involved human participants with various psychiatric disorders and that either compared oxytocin biology to healthy controls or examined the effects of exogenous oxytocin administration.

Objectives: Mood dysregulation in traumatized children may be misdiagnosed as bipolar disorder (BD) and conversely, the diagnosis of BD overlooked. Our aim is to characterize the relationship between trauma and mood dysregulation and pediatric BD. Methods: We are assessing youths ages 8-18 who present with mood symptoms and past trauma divided into two groups: 1. Trauma+Unmodified DSM-IV-TR BD (T+BD) and 2. Trauma+Mood Disorder NOS (T+MD). Differences in clinical variables between groups are analyzed using t-tests for continuous and chi-square tests for categorical variables (α= 0.05). Results: Age at onset of trauma for youth with T+BD (n=10) compared with T+MD (n=10) was similar (2.6±1.8 versus 3.3±1.9 years; p=0.4) as were types of trauma and number of incidents, and age at onset of mood symptoms (T+BD 7±2.5 versus T+MD 7.8±1.8 p=0.4). The T+BD group had higher scores on the sexual abuse subscale of the Childhood Trauma Questionnaire (p=0.04) and BPRS mania subscale (p=0.02), and higher total number of major depressive episodes (p=0.04) and manic episodes (p=0.03) per the KSCID. Youth with T+BD reported a trend toward higher rates of ideation to self-harm compared to youth with T+MD (p=0.08). Both groups had similar PTSD and ADHD symptoms, and similar number of psychotrophic medications (BD 3.6±2.9 MD 2.7±2.1 p=0.4). Finally, family history findings suggest a trend towards higher rates of any Axis I disorder in the T+BD families (p=0.07), and significantly higher rates of anxiety disorders (p=0.05), BD (p=0.04), and schizophrenia (p=0.02). Conclusions: Results suggest differences in clinical presentation and higher rates of BD and schizophrenia in the T+BD families. Taken together, these preliminary results suggest potential biological and genetic vulnerabilities which may predispose children to develop specific mood disorders under certain circumstances; the ability to identify these children early on could change their prognostic trajectory.