650 research outputs found

    Diagnostically homeless and needing appropriate placement

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    An Observational Study With the Janssen Autism Knowledge Engine (JAKE((R))) in Individuals With Autism Spectrum Disorder

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    Objective: The Janssen Autism Knowledge Engine (JAKE(R)) is a clinical research outcomes assessment system developed to more sensitively measure treatment outcomes and identify subpopulations in autism spectrum disorder (ASD). Here we describe JAKE and present results from its digital phenotyping (My JAKE) and biosensor (JAKE Sense) components. Methods: An observational, non-interventional, prospective study of JAKE in children and adults with ASD was conducted at nine sites in the United States. Feedback on JAKE usability was obtained from caregivers. JAKE Sense included electroencephalography, eye tracking, electrocardiography, electrodermal activity, facial affect analysis, and actigraphy. Caregivers of individuals with ASD reported behaviors using My JAKE. Results from My JAKE and JAKE Sense were compared to traditional ASD symptom measures. Results: Individuals with ASD (N = 144) and a cohort of typically developing (TD) individuals (N = 41) participated in JAKE Sense. Most caregivers reported that overall use and utility of My JAKE was easy (69%, 74/108) or very easy (74%, 80/108). My JAKE could detect differences in ASD symptoms as measured by traditional methods. The majority of biosensors included in JAKE Sense captured sizable amounts of quality data (i.e., 93-100% of eye tracker, facial affect analysis, and electrocardiogram data was of good quality), demonstrated differences between TD and ASD individuals, and correlated with ASD symptom scales. No significant safety events were reported. Conclusions: My JAKE was viewed as easy or very easy to use by caregivers participating in research outside of a clinical study. My JAKE sensitively measured a broad range of ASD symptoms. JAKE Sense biosensors were well-tolerated. JAKE functioned well when used at clinical sites previously inexperienced with some of the technologies. Lessons from the study will optimize JAKE for use in clinical trials to assess ASD interventions. Additionally, because biosensors were able to detect features differentiating TD and ASD individuals, and also were correlated with standardized symptom scales, these measures could be explored as potential biomarkers for ASD and as endpoints in future clinical studies. Clinical Trial Registration: https://clinicaltrials.gov/ct2/show/NCT02668991 identifier: NCT02668991

    Neurobiology of pediatric mood disorders: Part II

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    Neurobiology of pediatric mood disorders:are we there yet

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    Mood Disorders and Trauma – What are the Associations? Future Directions

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    Background: Mood dysregulation in traumatized children often is misdiagnosed as Bipolar Disorder (BD) and conversely the diagnosis of BD is often overlooked. This presents a diagnostic quagmire that is critical to understand in more depth and to date has received little attention in the literature. We aim to characterize the relationship between childhood trauma and mood dysregulation and between childhood trauma and pediatric BD by describing clinical correlates of children with trauma and comorbid mood disorders in a community mental health setting. Methods: 40 youth between the ages of 8-18 years, who present to child psychiatry at Community Healthlink clinics with symptoms of mood dysregulation and history of trauma will be assessed. Children will be divided into two groups: (1) Mood Disorder NOS (MD NOS) (n=20); and (2) Unmodified DSM-IV-TR BD (n=20) At the end of 6 months, youth with MD NOS will be re-evaluated to determine if progressed to the diagnosis of BD Future Directions Better understanding the association between trauma and development of mood disorders will increase our knowledge of the diverse effects of such events on youths’ emotional and behavioral development Identifying clinical correlates that help predict later development of BD in mood dsyregulated, traumatized youth, will promote future research aimed at identifying biological markers and preventive treatment interventions Presented at the UMass Department of Psychiatry Research Day, October 2010

    Mood Disorders and Trauma – What are the Associations?

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    Objectives: To characterize the relationship between childhood trauma/abuse, and mood dysregulation, and between childhood trauma/abuse and pediatric bipolar disorder (BD). To describe the clinical correlates and demographics of children with trauma/abuse and comorbid mood disorders in a community mental health setting. To explore associations between the diagnosis of BD in youth with histories of trauma and a family history of BD, the presence of specific symptom clusters, the presence of pretrauma mood symptoms. Methods We are assessing youths ages 8-18 who present with mood symptoms and past trauma divided into two groups: (1) Trauma Mood Disorder NOS (T+MD); (2) Trauma+Unmodified DSM-IV-TR BD (T+BD). Differences in clinical variables between groups are analyzed using t-tests for continuous and chi-square tests for categorical variables (α= 0.05). Youth are evaluated using the following psychiatric rating scales: (1) Structured Clinical Interview for DSM Disorders, Childhood Disorders Form (KID-SCID) mood module to establish the diagnosis of BD; (2) Brief Psychiatric Rating Scale for Children (BPRS-C); (3)Young Mania Rating Scale (YMRS); (4)Children’s Depression Rating Scale-Revised (CDRS-R); (5) Childhood Trauma Questionnaire (CTQ); (6) PTSD CheckList –Civilian Version (PCL-C); (7)Attention Deficit Hyperactivity Disorder IV (ADHD-IV) Rating Scale; (8) Substance Abuse (SA) screen: CRAFFT Other information obtained includes: Demographic characteristics and socioeconomic status; Number of medications and types; Percent of with a lifelong history of psychiatric hospitalization/out of home placement; Family history of psychiatric illness and substance use disorders Results - Clinical presentations: Mood Symptoms: BD\u3eMD in BPRS total score (p=0.06), BPRS Mania subscale (p=0.05),YMRS total score (p=0.06) BD\u3eMD in total number of mood episodes identified with KID-SCID: •MDE (p=0.04) Mania (without high outlying value) (p = 0.07) Substance use: No difference as assessed using CRAFT PTSD and trauma recollection: No differences in PTSD symptoms as assessed by PCL-C BD\u3eMD abuse identified with CTQ. Sexual abuse (without high outlying value) (p = 0.05). Physical neglect (p=0.07) Medications: BD\u3eMD 1.33 fewer medications (t=11.9, p=0.17) Conclusions Further data collection is ongoing to achieve our targeted sample size in order to identify clinical correlates in mood dsyregulated, traumatized youth. This will promote future research aimed at identifying biomarkers and preventive interventions

    PARENTS' DESCRIPTIONS OF BARRIERS FACED AND STRATEGIES USED TO OBTAIN DENTAL CARE *

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    Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/65428/1/j.1752-7325.1974.tb00670.x.pd

    Risperidone-induced psychosis and depression in a child with a mitochondrial disorder

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    OBJECTIVE: To our knowledge, this is the first published case report of an adolescent girl with a mitochondrial disorder and depression who displayed both new-onset psychotic and increased mood symptoms during treatment with risperidone. DATA: A 16-year-old girl was treated with risperidone for mood lability and impulsivity at a community hospital. Within days, she developed paranoid ideation, profound psychomotor retardation, increased depression, and fatigue. She was transferred to an inpatient psychiatric hospital, where she was taken off risperidone. Within 48 hours after discontinuation of the medication, she had complete resolution of psychotic symptoms, fatigue, and psychomotor retardation, and her depression improved. CONCLUSIONS: This observation of on-off risperidone treatment suggests that risperidone may have worsened both psychiatric and physical manifestations of the mitochondrial disorder in this adolescent. These findings are consistent with recent in vitro literature, which implicate a series of neuroleptic medications with mitochondrial dysfunction. Furthermore, the authors provide diagnostic and treatment options that are available for mitochondrial disorders, which are of interest to child psychiatrists due to the central nervous system manifestations of these disorders

    Mood Disorders and Trauma: What are the Associations?

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    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
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