Sleep disturbances, namely insomnia and recurrent nightmares, are ubiquitous following trauma exposure and are considered hallmarks of posttraumatic stress disorder (PTSD). Other sleep disorders frequently co-occur with PTSD. This article describes research examining sleep problems most common in PTSD, including prevalence and clinical characteristics. Sleep disturbances are often robust to trauma-focused treatment; thus, evidence for psychological and pharmacological interventions for insomnia and nightmares in PTSD are discussed. Given the high prevalence of sleep problems in PTSD, more work is needed to empirically study putative mechanisms linking trauma exposure and sleep, as well as how to best target these symptoms in patients with PTSD.

In the United States, 18.9% of the population identifies as Hispanic or Latin. The culture of these communities is as diverse, heterogenous, and rich as the history of this population. Culture shapes the perception of symptoms and psychiatric disorders. To provide culturally sensitive care, it is relevant to understand the history of these communities in the US, recognize cultural humility, and acknowledge aspects and values (eg, culturally bound syndromes, familism, paternalism, stigma of mental illness, machismo, immigration) inherent to the cultural experience and unique barriers to care. Incorporating these aspects into clinical practice is essential for positive outcomes. The purpose of this article is to give a brief historical context, encourage cultural humility, and describe cultural aspects that are essential when providing culturally sensitive care to the Hispanic and Latinx community in the US.

Black people are disproportionately affected by mental illness, including depression. While the prevalence of depression is paradoxically lower among the Black population, the impact of depression on Black people results in greater severity of illness and higher chronicity. The main factors through which Black people experience worse mental health outcomes includes delayed treatment seeking, and poor access to mental health services. Mental illness stigma contributes to the delay in treatment seeking behavior. Stigma refers to negative attitudes, beliefs or behaviors about a particular characteristic of an individual such as their health status. Both patients and mental health professionals experience stigma that impacts health engagement, limits access to effective depression treatments, and compromises positive patient-clinician communication. A commitment to lifelong learning about the role of culture, history, and the psychosocial context of our patients is critical to closing public health gaps in the field of mental health.

Psychotherapy is an important part of managing bipolar depression and its associated impairments. There is considerable evidence that psychotherapies are effective adjuncts to pharmacotherapy in delaying or preventing episodes of bipolar depression. Individuals with bipolar depression may be reticent to consider these treatments. This paper surveys the utility, evidence base, effective treatment components, and controversies surrounding adjunctive psychosocial interventions.

Anxiety and depressive disorders are common psychiatric conditions with high rates of co-occurrence. Although traditional cognitive-behavioral therapy (CBT) protocols targeting individual anxiety and depressive disorder diagnoses have been shown to be effective, such "single-diagnosis" approaches pose challenges for providers who treat patients with multiple comorbidities and for large-scale dissemination of and training in evidence-based psychological treatments. To help meet this need, newer "transdiagnostic" CBT interventions targeting shared underlying features across anxiety, depressive, and related disorders have been developed in recent years. Here we provide a rationale for and description of the transdiagnostic CBT model, followed by an overview of key therapeutic strategies included in transdiagnostic CBT protocols for patients with anxiety disorders and comorbid depression. We conclude with a brief review of the empirical evidence in support of transdiagnostic CBT for individuals with anxiety and depressive disorders and identify directions for future research.

Neurodevelopmental disorders, including autism spectrum disorder (ASD) and attention-deficit/hyper-activity disorder (ADHD), represent a group of conditions that manifest early in child development and produce impairments across multiple domains of functioning. Although a number of pharmacological and psychosocial treatments exist to improve the symptoms associated with these syndromes, treatment advances have lagged. The Precision Medicine Initiative was launched with the goal of revolutionizing medicine by progressing beyond the historical one-size-fits-all approach. In this review, we evaluate current research efforts to personalize treatments for ASD and ADHD. Most pharmacogenetic testing has focused on the cytochrome P450 enzyme family with a particular focus on CYP2D6 and CYP2C19, which are genes that produce an enzyme that acts as a key metabolizer of many prescribed medications. This article provides an update on the state of the field of pharmacogenetics and "therapy-genetics" in the context of ASD and ADHD, and it also encourages clinicians to follow US Food and Drug Administration recommendations regarding pharmacogenetic testing.

Major depression (MD) is a leading cause of disability worldwide; it arises from the action and interaction between genetic and environmental factors, and is often comorbid with other psychiatric and medical conditions. To date, upwards of 100 genetic loci have been associated with MD, giving clues to biological underpinnings. Although recent progress has yielded modest insight into the genetic architecture of MD, most studies have been in populations with European ancestry, seriously limiting precision medicine efforts. Broadening diversity of study populations will empower genomic research by expanding discovery and enhancing our understanding of the role of genomic variation in disease etiology. To fully realize the potential of pharmacogenetics and precision medicine, we will need to address the major gaps in our knowledge of the genetic and environmental risk architecture of MD across ancestries, including sex differences, to improve etiologic understanding, diagnosis, prevention, and treatment for all.

A number of studies have examined the association of the three major eating disorders - anorexia nervosa, bulimia nervosa, and binge-eating disorder - with metabolic syndrome, or with individual components of metabolic syndrome, such as obesity, type 2 diabetes, hypertension, and dyslipidemia. Present evidence suggests that anorexia nervosa confers no excess risk of metabolic syndrome and may be associated with lower risk of certain metabolic syndrome components, including obesity and type 2 diabetes. Bulimia nervosa shows associations with increased risk for metabolic syndrome components in some studies, but not in others. Binge-eating disorder, however, is strongly associated with increased risk for both metabolic syndrome and its components - and these associations appear to be mediated not only through elevated body weight, but also possible body-weight-independent factors. Given that binge-eating disorder is the most common eating disorder, treatment and prevention of metabolic syndrome in this group represents a significant clinical and public health challenge.

Transcranial direct current stimulation (tDCS) is a non-invasive brain stimulation technique that has grown in popularity over the past two decades as an alternative treatment option for various neuropsychiatric disorders. tDCS modulates cortical excitability through the application of a weak direct current to the scalp via electrodes placed over cortical regions of interest. It has been shown to be a promising and relatively safe treatment tool with few adverse events. In this article, we will briefly review the efficacy of tDCS in depression, bipolar disorder, schizophrenia, and obsessive-compulsive disorder. We will also discuss biomarkers of tDCS efficacy in depression, as it is the most studied neuropsychiatric disorder using tDCS application. We will then offer suggestions for future directions. Although efficacy results show promise, more studies with larger samples and longer treatment periods are needed to better understand the benefits of using tDCS as an alternative treatment option for neuropsychiatric disorders.

Sleep disturbances are common in adults with PTSD and range from insomnia and nightmares to periodic leg movements and disruptive nocturnal behaviors. Together these findings suggest profound disturbances in rapid eye movement (REM) and non-REM (NREM) sleep, although there is a lack of consensus regarding a distinct profile of objective sleep disturbances associated with PTSD. Prospective, longitudinal studies have established that sleep disturbances represent a risk factor for the development and course of PTSD, suggesting that sleep is an important neurobiological mechanism in the etiology and maintenance of this disorder. This research highlights the importance of early identification and treatment of sleep disturbances in at-risk and trauma exposed populations. A number of psychological and pharmacological treatments are effective at treating sleep disturbances in PTSD. Additional research is needed to further develop clinical guidelines informing when and how to integrate sleep-specific treatment with PTSD focused clinical care.

Established treatments for obsessive-compulsive disorder (OCD) are of benefit in approximately 3 of every 4 patients, but refractory disease remains distressingly common, and many treatment responders continue to experience considerable morbidity. This motivates a search for new insights into pathophysiology that may inform novel treatment strategies. Much recent work has focused on the neurotransmitter glutamate. Several lines of neurochemical and genetic evidence suggests that glutamate dysregulation may contribute to OCD, although much remains unclear. The off-label use of a number of pharmacological agents approved for other indications has been investigated in refractory OCD. We summarize investigations of memantine, riluzole, ketamine, D-cycloserine, glycine, N-acetylserine, topiramate, and lamotrigine. Evidence exists for benefit from each of these in some patients; though none has been proven effective with sufficient clarity to be considered part of standard care, these agents are options in individuals whose symptoms are refractory to better-established therapeutic strategies.

Psychopathy is theorized as a disorder of personality and affective deficits while antisocial personality disorder (ASPD) diagnosis is primarily behaviorally based. While ASPD and psychopathy are similar and are highly comorbid with each other, they are not synonymous. ASPD has been well studied in community samples with estimates of its lifetime prevalence ranging from 1-4% of the general population. In contrast, psychopathy is almost exclusively investigated within criminal populations so that its prevalence in the general population has been inferred by psychopathic traits rather than disorder (1%). Differences in etiology and comorbidity with each other and other psychiatric disorders of these two disorders are also evident. The current article will briefly review the epidemiology, etiology, and comorbidity of ASPD and psychopathy, focusing predominately on research completed in community and clinical populations. This paper aims to highlight ASPD and psychopathy as related, but distinct disorders.

Following the earlier versions of the diagnostic manual, the DSM-IV set a higher symptom and duration threshold for the diagnosis of major depression in individuals who have experienced recent bereavement-the bereavement exclusion criterion. This criterion excludes a diagnosis of major depression among those whose symptoms persist for less than two months, as long as they do not have marked functional impairment, morbid preoccupation with worthlessness, suicidal ideation, psychotic symptoms, or psychomotor retardation. The DSM-5 committee, however, has proposed to remove this criterion from the upcoming DSM-5. The committee's decision was based on reviews of past literature. However, few past studies directly compared DSM-excluded bereavement-related depression to other major depressive disorder in representative population samples and had adequate power to detect differences. The results of these studies, therefore, did not provide strong evidence for the validity of bereavement exclusion. In this paper, we review three recently published analyses based on large epidemiologic samples that found significant differences between those with bereavement-excluded episodes and episodes meeting major depression criteria with regard to short-term risk of future depressive episodes, psychiatric comorbidity and other clinical and socio-demographic characteristics. In follow-ups ranging from 1 to 3 years, individuals with bereavement-excluded depressive episodes were significantly less likely to experience new episodes than those who met criteria for depression, and were not more likely to experience future episodes than those without any past history of depression. The findings from these new studies support the validity of the DSM-IV bereavement exclusion criterion and argue for preserving it in the new edition of the manual.

Psychiatrists are increasingly called upon to care for individuals with cognitive, emotional, and behavioral disturbances after TBI, especially in settings serving military service personnel and Veterans. In both the early and late post-injury periods, cognitive impairments contribute to disability among persons with TBI and are potentially substantial sources of suffering for persons with TBI and their families. In this article, the differential diagnosis, evaluation, and management of posttraumatic cognitive complaints is reviewed. The importance of pre-treatment evaluation as well as consideration of non-cognitive contributors to cognitive problems and functional limitations is emphasized first. The course of recovery after TBI, framed as a progression through posttraumatic encephalopathy, is reviewed next and used to anchor the evaluation and treatment of posttraumatic cognitive impairments in relation to injury severity as well as time post-injury. Finally, pharmacologic and rehabilitative interventions that may facilitate cognitive and functional recovery at each stage of posttraumatic encephalopathy are presented.

Increasingly, multiple outcomes are collected in order to characterize treatment effectiveness or to evaluate risk factors. These outcomes tend to be correlated because they are measuring related quantities in the same individuals. While the analysis of outcomes measured in the same scale (commensurate outcomes) can be undertaken with standard statistical methods, outcomes measured in different scales (non-commensurate outcomes), such as mixed binary and continuous outcomes, present more difficult challenges.In this paper we contrast some statistical approaches to analyze non-commensurate multiple outcomes. We discuss the advantages of a multivariate method for the analysis of non-commensurate outcomes including situations of missing data. A real data example from a clinical trial, comparing different treatments for depression in low-income women, is used to illustrate the differences between the statistical approaches.

While much psychiatric research is based on randomized controlled trials (RCTs), where patients are randomly assigned to treatments, sometimes RCTs are not feasible. This paper describes propensity score approaches, which are increasingly used for estimating treatment effects in non-experimental settings. The primary goal of propensity score methods is to create sets of treated and comparison subjects who look as similar as possible, in essence replicating a randomized experiment, at least with respect to observed patient characteristics. A study to estimate the metabolic effects of antipsychotic medication in a sample of Florida Medicaid beneficiaries with schizophrenia illustrates methods.

In the last decade, the number of publications in psychiatric genetics has nearly tripled but little attention has been paid to the role of genetic factors in the etiology of posttraumatic stress disorder (PTSD). The present review summarizes the current state of genetic research on PTSD. First, we outline information regarding genetic influences provided by family investigations and by twin studies. Second, we propose the fear-conditioning model of PTSD as a framework for the nomination of candidate genes that may be related to the disorder. Third, we review lines of evidence from three neurobiological systems involved in fear conditioning, and we summarize published investigations of genetic variants studied in association with PTSD in these three systems. Finally, we review gene-by-environment interaction research, a promising novel approach to genetic research in PTSD.

We reviewed the literature from 2010 to 2016 on the relationship between posttraumatic stress disorder (PTSD) and cardiometabolic health conditions, including metabolic syndrome, coronary artery disease, stroke, and myocardial infarction, among others. Collectively, PTSD was associated with increased risk of cardiometabolic health problems, with pre-clinical and clinical studies offering evidence of behavioral (e.g., poor sleep, cigarette use, poor diet and insufficient exercise) and biological (e.g., autonomic reactivity, inflammation) mediators of these associations. We discuss the possibility that these behavioral and biological mechanisms lead to accelerated cellular aging, as regulated in the epigenome, which contributes to premature cardiometabolic health decline. This has implications for the assessment, prevention, and treatment of cardiometabolic conditions among those with PTSD. It also highlights the need to better understand the mechanisms linking PTSD to accelerated aging and to develop interventions to attenuate or reverse this phenomenon.

There is evidence that doxazosin is effective in the treatment of posttraumatic stress disorder (PTSD). Doxazosin is a "me-too" drug of prazosin. Doxazosin has an improved absorption profile and this likely minimizes the risk for unintended adverse hypotensive effects. The availability of doxazosin in the gastrointestinal therapeutic system (GITS) form permits a higher initial daily dose (4 mg/day) while avoiding significant first-dose side effects. The treatment of PTSD with prazosin has several disadvantages due to its short duration of action (6-8 hours), which results in multiple doses being required. Prazosin may wear off and this may lead to nightmares in the latter half of the sleep. Doxazosin has significant advantages over prazosin in clinical practice because it has a long half-life and requires only once-daily dosing. This may lead to better adherence and greater effectiveness in the treatment of PTSD.