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We explored patterns of concomitant psychiatric disorders in a large sample of treatment-seeking children and adolescents with autism spectrum disorder (ASD). Participants were 658 children with ASD (age 3–17 years; mean = 7.2 years) in one of six federally-funded multisite randomized clinical trials (RCT) between 1999 and 2014. All children were referred for hyperactivity or irritability. Study designs varied, but all used the Child and Adolescent Symptom Inventory or Early Childhood Inventory to assess Attention Deficit Hyperactivity Disorder (ADHD), Oppositional-Defiant Disorder (ODD), Conduct Disorder (CD), Anxiety Disorders, and Mood Disorders. In addition, several measures in common were used to assess demographic and clinical characteristics. Of the 658 children, 73% were Caucasian and 59% had an IQ >70. The rates of concomitant disorders across studies were: ADHD 81%, ODD 46%, CD 12%, any anxiety disorder 42%, and any mood disorder 8%. Two or more psychiatric disorders were identified in 66% of the sample. Of those who met criteria for ADHD, 50% also met criteria for ODD and 46% for any anxiety disorder. Associations between types of concomitant disorders and a number of demographic and clinical characteristics are presented. In this well-characterized sample of treatment-seeking children with ASD, rates of concomitant psychiatric disorders were high and the presence of two or more co-occurring disorders was common. Findings highlight the importance of improving diagnostic practice in ASD and understanding possible mechanisms of comorbidity. •We observed a high frequency of multiple concomitant DSM-defined disorders.•50% of children who met criteria for ADHD also met criteria for ODD.•46% of children who met criteria for ADHD also met criteria for an anxiety disorder.•Findings highlight the importance of improving diagnostic practices in ASD.

\"The Cognitive Behavioral Workbook for Depression offers a complete program for defeating depressive thinking and other symptoms of depression using cognitive behavioral therapy, a proven effective treatment protocol. This new edition includes new information on relapse prevention, revised worksheets and exercises, and vital information on depression coexisting with other mental health conditions. The entire workbook has been thoroughly updated with the latest depression research. First, readers learn the basics for defeating the most damaging symptoms of depression and create a master plan for overcoming their condition. Later, readers discover the roots of their depression in depressive beliefs, worthlessness beliefs, and helplessness beliefs. The final section of this workbook helps readers anchor these positive changes for long-term relapse prevention and increased motivation. Recommended by therapists nationwide, this second edition of The Cognitive Behavioral Workbook for Depression offers all the skills readers need to overcome depression with cognitive behavioral therapy\"-- Provided by publisher.

The National Institute of Mental Health (NIMH) ‘fast-fail’ approach seeks to improve too-often-misleading early-phase drug development methods by incorporating biomarker-based proof-of-mechanism (POM) testing in phase 2a. This first comprehensive application of the fast-fail approach evaluated the potential of κ-opioid receptor (KOR) antagonism for treating anhedonia with a POM study determining whether robust target engagement favorably impacts the brain circuitry hypothesized to mediate clinical effects. Here we report the results from a multicenter, 8-week, double-blind, placebo-controlled, randomized trial in patients with anhedonia and a mood or anxiety disorder (selective KOR antagonist (JNJ-67953964, 10 mg; n  = 45) and placebo ( n  = 44)). JNJ-67953964 significantly increased functional magnetic resonance imaging (fMRI) ventral striatum activation during reward anticipation (primary outcome) as compared to placebo (baseline-adjusted mean: JNJ-67953964, 0.72 (s.d. = 0.67); placebo, 0.33 (s.d. = 0.68); F (1,86) = 5.58, P  < 0.01; effect size = 0.58 (95% confidence interval, 0.13–0.99)). JNJ-67953964, generally well tolerated, was not associated with any serious adverse events. This study supports proceeding with assessment of the clinical impact of target engagement and serves as a model for implementing the ‘fast-fail’ approach. A phase 2 proof-of-mechanism trial shows that a κ-opioid receptor antagonist improves reward-related functioning in the brain and a clinical measure of anhedonia in patients with mood and anxiety disorders, serving as a model for implementing the ‘fast-fail’ approach to psychiatric treatment development.

Attempted suicide is the main risk factor for suicide and repeated suicide attempts. However, the evidence for follow-up treatments reducing suicidal behavior in these patients is limited. The objective of the present study was to evaluate the efficacy of the Attempted Suicide Short Intervention Program (ASSIP) in reducing suicidal behavior. ASSIP is a novel brief therapy based on a patient-centered model of suicidal behavior, with an emphasis on early therapeutic alliance. Patients who had recently attempted suicide were randomly allocated to treatment as usual (n = 60) or treatment as usual plus ASSIP (n = 60). ASSIP participants received three therapy sessions followed by regular contact through personalized letters over 24 months. Participants considered to be at high risk of suicide were included, 63% were diagnosed with an affective disorder, and 50% had a history of prior suicide attempts. Clinical exclusion criteria were habitual self-harm, serious cognitive impairment, and psychotic disorder. Study participants completed a set of psychosocial and clinical questionnaires every 6 months over a 24-month follow-up period. The study represents a real-world clinical setting at an outpatient clinic of a university hospital of psychiatry. The primary outcome measure was repeat suicide attempts during the 24-month follow-up period. Secondary outcome measures were suicidal ideation, depression, and health-care utilization. Furthermore, effects of prior suicide attempts, depression at baseline, diagnosis, and therapeutic alliance on outcome were investigated. During the 24-month follow-up period, five repeat suicide attempts were recorded in the ASSIP group and 41 attempts in the control group. The rates of participants reattempting suicide at least once were 8.3% (n = 5) and 26.7% (n = 16). ASSIP was associated with an approximately 80% reduced risk of participants making at least one repeat suicide attempt (Wald χ21 = 13.1, 95% CI 12.4-13.7, p < 0.001). ASSIP participants spent 72% fewer days in the hospital during follow-up (ASSIP: 29 d; control group: 105 d; W = 94.5, p = 0.038). Higher scores of patient-rated therapeutic alliance in the ASSIP group were associated with a lower rate of repeat suicide attempts. Prior suicide attempts, depression, and a diagnosis of personality disorder at baseline did not significantly affect outcome. Participants with a diagnosis of borderline personality disorder (n = 20) had more previous suicide attempts and a higher number of reattempts. Key study limitations were missing data and dropout rates. Although both were generally low, they increased during follow-up. At 24 months, the group difference in dropout rate was significant: ASSIP, 7% (n = 4); control, 22% (n = 13). A further limitation is that we do not have detailed information of the co-active follow-up treatment apart from participant self-reports every 6 months on the setting and the duration of the co-active treatment. ASSIP, a manual-based brief therapy for patients who have recently attempted suicide, administered in addition to the usual clinical treatment, was efficacious in reducing suicidal behavior in a real-world clinical setting. ASSIP fulfills the need for an easy-to-administer low-cost intervention. Large pragmatic trials will be needed to conclusively establish the efficacy of ASSIP and replicate our findings in other clinical settings. ClinicalTrials.gov NCT02505373.

\"Introducing a breakthrough, integrative approach to managing your borderline personality disorder (BPD). If you've been diagnosed with BPDyou may feel a number of emotions--including shock, shame, sadness, abandonment, emptiness, or even anger. Even worse, you may be tempted to research your diagnosis online, only to find doomsday scenarios and terrible prognoses everywhere you click. Take a deep breath. You can get through this--and this workbook will help guide you. Despite what you may have read or been told, BPD is not the worst thing that can happen to you. Like many mental health issues, it manifests on a continuum, and while some people may experience extreme symptoms and consequences on one end, others may be less affected on the other. What do you all have in common? You likely experience difficulty balancing your emotions, thoughts, and behaviors that disrupt how you see yourself and the success you have in relationships. And you may even have trouble seeing yourself clearly--continuously switching from the hero to the villain of the story you've written about your life. So, how can you make sense of it all and start on the road to healing? Rather than utilizing a one-size-fits-all treatment, this groundbreaking and comprehensive workbook meets you where you are on your therapeutic journey, and provides an integrative approach to treating BPD drawing on evidence-based dialectical behavior therapy (DBT), acceptance and commitment therapy (ACT), cognitive behavioral therapy (CBT), and interpersonal therapy. With this compassionate workbook, you'll gain a greater understanding of your BPD, uncover your own emotional triggers, and discover your own personal motivators for positive change. Your BPD has determined how you see and live your life, but it doesn't have to define you forever. With this workbook as your guide, you'll be ready to face your diagnosis head-on, and take those important first steps toward lasting wellness\"-- Provided by publisher.

Objectives. To estimate the economic burden of untreated perinatal mood and anxiety disorders (PMADs) among 2017 births in the United States. Methods. We developed a mathematical model based on a cost-of-illness approach to estimate the impacts of exposure to untreated PMADs on mothers and children. Our model estimated the costs incurred by mothers and their babies born in 2017, projected from conception through the first 5 years of the birth cohort’s lives. We determined model inputs from secondary data sources and a literature review. Results. We estimated PMADs to cost$14 billion for the 2017 birth cohort from conception to 5 years postpartum. The average cost per affected mother–child dyad was about $ 31 800. Mothers incurred 65% of the costs; children incurred 35%. The largest costs were attributable to reduced economic productivity among affected mothers, more preterm births, and increases in other maternal health expenditures. Conclusions. The US economic burden of PMADs is high. Efforts to lower the prevalence of untreated PMADs could lead to substantial economic savings for employers, insurers, the government, and society.

Social Signal Transduction Theory of Depression is a biologically plausible, multi-level theory that describes neural, physiologic, molecular, and genomic mechanisms that link experiences of social-environmental adversity with internal biological processes that drive depression pathogenesis, maintenance, and recurrence. Central to this theory is the hypothesis that interpersonal stressors involving social threat (e.g., social conflict, evaluation, rejection, isolation, and exclusion) upregulate inflammatory processes that can induce several depressive symptoms, including sad mood, anhedonia, fatigue, psychomotor retardation, and social-behavioral withdrawal. The original article describing this formulation (Psychol Bull 140:774–815, 2014) addressed critical questions involving depression onset and recurrence, as well as why depression is strongly predicted by early life stress and comorbid with anxiety disorders and certain physical disease conditions, such as asthma, rheumatoid arthritis, chronic pain, and cardiovascular disease. Here, we extend the theory to help explain sex differences in depression prevalence, which is a defining feature of this disorder. Central to this extension is research demonstrating that ovarian hormone fluctuations modulate women’s susceptibility to stress, brain structure and function, and inflammatory activity and reactivity. These effects are evident at multiple levels and are highly context-dependent, varying as a function of several factors including sex, age, reproductive state, endogenous versus exogenous hormones, and hormone administration mode and dose. Together, these effects help explain why women are at greater risk for developing inflammation-related depressed mood and other neuropsychiatric, neurodevelopmental, and neurodegenerative disorders during the reproductive years, especially for those already at heightened risk for depression or in the midst of a hormonal transition period.