Cognitive-behavioral therapy (CBT) is currently the most empirically supported intervention for posttraumatic stress disorder (PTSD) and includes both specific manualized treatments (e.g., cognitive processing therapy, prolonged exposure) and less standardized applications. As CBT for PTSD has become increasingly popular, more advanced questions have emerged regarding its use, including how existing treatments might be enhanced. In the current review, we aimed to discover recent trends in the CBT for PTSD literature by applying rigorous search criteria to peer-reviewed articles published from 2009 to 2012. Results of the 14 studies that were identified are discussed, and future directions for research are suggested.

Recent research shows that single genes do not cause schizophrenia, but that multiple “susceptibility” genes each provide a genetic “bias” towards schizophrenia. Each susceptibility gene codes for a subtle molecular abnormality that hypothetically causes inefficient information processing in brain circuits that mediate the symptoms of this disorder. It is therefore not surprising that many of the susceptibility genes that have been identified for schizophrenia are known to regulate neuronal connectivity, synaptogenesis, and N-methyl-D-aspartate (NMDA) glutamate receptor functions. This includes genes for brain-derived neurotrophic factor (BDNF), dysbindin, also known as dystrobrevin-binding protein 1, neuregulin, disrupted in schizophrenia-1 (DISC-1), D-amino acid oxidase activator (DAOA), and regulator of G-protein signaling (RGS4). Hypothetically, converging molecular abnormalities expressed by defective versions of these genes could cause dysregulation of NMDA receptors and NMDA synapses, leading to vulnerability for schizophrenia due to inefficient information processing at glutamate synapses.

Therapy of bipolar disorders is a rapidly evolving field. Lithium has efficacy in classic bipolar disorders whereas divalproex sodium and carbamazepine may have broader spectrum efficacy that includes non-classic bipolar disorder. In the last 10 years, a series of anticonvulsants have been approved for marketing in the United States. Gabapentin has indirect γ-aminobuytric acid-ergic actions, is generally well tolerated, and appears to have anxiolytic, analgesic, and hypnotic effects. Lamotrigine has antiglutamatergic actions and is generally well tolerated (aside from rash in 1 in 10, and serious rash in 1 in 1,000 patients). Lamotrigine is indicated for maintance treatment in bipolar disorder. Emerging evidence suggests lamotrigine may have utility in bipolar disorder patients with depression and treatment-refractory rapid cycling, as well as analgesic effects. Topiramate and zonisamide may allow both weight loss, while topiramate may have specific efficacy in bulimia, binge eating disorder, and alcohol dependence. Two small studies found oxcarbazepine had similar efficacy to lithium and haloperidol in acute mania. Phenytoin, an older anticonvulsant, may have adjunctive acute mania efficacy. Levetiracetam, a newer anticonvulsant, may be worth exploring and has minimal drug-drug interactions. None of these newer agents has been shown effective in a large placebo controlled trial for acute mania. Although the clinical profiles of these newer anticonvulsants do not appear to overlap markedly with divalproex and carbamazepine (except perhaps for oxcarbazepine), these novel agents may still offer important new options in relieving a variety of specific target symptoms in patients with bipolar disorder.

Depression in older people, especially depression with an older age of onset, may be a manifestation of acquired brain disease. The cerebrovascular model of depression, often referred to as “vascular depression,” hypothesizes that otherwise clinically occult small vessel brain disease contribute to the pathogeneses of some late-life depressive conditions. This paper reviews several lines of evidence supporting the cerebrovascular model and addresses the limitations of the existing literature. Several directions for future research are noted, including empirical testing of the notion that cerebrovascular disease might underlie the pathogeneses of depression with prominent executive dysfunction or other cognitive impairments. At this time, there are no specific therapeutic options for patients with suspected vascular depression beyond standard approaches to depression treatments, although education about the possibly greater risks of chronicity should be included in treatment planning. Therapy of cerebrovascular risk factors and stroke-risk reduction are important as consistent with general practice guidelines, although it is not known whether this will reduce the incidence or improve the outcome of late-life depression.

Are symptoms of daytime sleepiness relevant among patients with insomnia? Patients with insomnia frequently report daytime consequences secondary to their difficulty initiating and maintaining sleep. The purpose of this study was to determine the frequency of daytime sleepiness as defined by a self-reported measure of daytime sleepiness (the Epworth Sleepiness Scale). In addition, the study characterized the patients' psychological status using the Symptom Checklist-90-Revised. The study corroborated a relatively high frequency of excessive daytime sleepiness and psychiatric conditions among patients with insomnia. Furthermore, the results of the study suggest variation in psychological distress levels, according to the different levels of sleepiness/alertness.

Anxiety disorders are the most prevalent mental disorders and are associated with substantial healthcare costs and a high burden of disease. In this article, changes in the new Diagnostic and Statistical Manual for Mental Disorders (the DSM–5) with respect to panic disorder/agoraphobia, generalized anxiety disorder, social anxiety disorder, specific phobias, and selective mutism are compared with the International Classification of Diseases (ICD–10) system.

Approximately 20%–30% of schizophrenia patients are resistant to current standard pharmacotherapies. Recent schizophrenia research aims to identify specific pathophysiological abnormalities and novel targets in the disease, with the goals of identifying at-risk individuals, facilitating diagnosis, prompting early and personalized interventions, and helping predict response to treatment. Metabolomics involves the systematic study of the profile of biochemical alterations early in the course of a given disorder. Major aspects of the schizophrenia metabolome have been characterized, uncovering potential selective biomarkers for the disease that may change how the disorder is diagnosed, and how patients are stratified and treated. This review focuses on the most common metabolomic fingerprints of the different pathways involved in the pathophysiology of schizophrenia, and the potential development of novel metabolomic-related pharmacotherapies for improved treatment of schizophrenia and other related idiopathic psychotic disorders.

The received wisdom is that there is no known effective treatment for psychopathic disorders. Although outcome studies have not identified an effective programmatic treatment for psychopathic disorders, such studies tend to leave the question open. If behavioral science has not established that psychopathic disorders respond to a particular programmatic approach, neither are psychopathic disorders convincingly proven to be absolutely resistant to treatment. If no treatment is known to be effective in psychopathic disorders, then any treatment seems to squander resources. What is often missing from the discussion is effective therapeutic measures to treat other behaviors that often co-occur, if they do not represent a domain of pathology of psychopathic disorders, such as impulsive aggression. After a brief summary of results of programmatic treatment of psychopathic offenders, this review focuses on the pharmacotherapy of impulsive aggression in psychopathic disorders. If the impulsive aggression that occurs with psychopathic disorders can be better controlled, treatment can have substantial benefits and would be most appropriate.

The newly introduced Mixed Features Specifier of Major Depressive Episode and Disorder (MDE/MDD) is especially challenging in terms of pharmacological management. Prior to the publication of the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, the symptoms of the mixed features specifier were intradepressive hypomanic symptoms, always and only associated with bipolar disorder (BD).

Intradepressive hypomanic symptoms, mostly referred to as depressive mixed states (DMX), have been poorly characterized, and their treatment offers significant challenges. To understand the diagnostic context of DMX, we trace the nosological changes and collocation of intradepressive hypomanic symptoms, and examine diagnostic and prognostic implications of such mixed features.

One of the reasons so little is known about the treatment of DMX is that depressed patients with rapid cycling, substance abuse disorder, and suicidal ideation/attempts are routinely excluded from clinical trials of antidepressants. The exclusion of DMX patients from clinical trials has prevented an assessment of the safety and tolerability of short- and long-term use of antidepressants. Therefore, the generalization of data obtained in clinical trials for unipolar depression to patients with intradepressive hypomanic features is inappropriate and methodologically flawed.

A selective review of the literature shows that antidepressants alone have limited efficacy in DMX, but they have the potential to induce, maintain, or worsen mixed features during depressive episodes in BD. On the other hand, preliminary evidence supports the effective use of some atypical antipsychotics in the treatment of DMX.

Introduction: Because major depressive disorder (MDD) is often chronic and recurrent, even pediatric patients who are treated successfully during an acute episode may need longer-term treatment. Yet, data on long-term treatment with antidepressants in pediatric MDD are limited.

Objective: To evaluate long-term effectiveness and safety of treatment with venlafaxine extended-release (ER) in children and adolescents with MDD.

Methods: Subjects (n=86) 7–17 years of age with MDD entered a multicenter, open-label study of flexible-dose venlafaxine ER for 6 weeks of acute treatment, followed by continuation treatment for up to 6 months total treatment. The primary efficacy variable was the Children's Depression Rating Scale-Revised (CDRS-R) total score (intent-to-treat population).

Results: Mean CDRS-R total score decreased from 60.1±10.0 at baseline to 36.3±13.1 at week 6, and to 33.8±15.0 at 6 months (last observation carried forward). Among completers (n=36), the mean CDRS-R total score was 24.3±7.6 at the end of 6 months of treatment. The most frequent treatment-emergent adverse events were headache (53%), nausea (26%), infection (24%), abdominal pain (22%), vomiting (21%), and pharyngitis (19%). Fifteen (17%) participants discontinued due to adverse events, 9 of whom did so within the first 6 weeks. Serious adverse events (suicide attempt [two], hostility [two], hallucinations, depression, and pharyngitis) occurred in seven patients. There were no suicides.

Conclusion: Most improvement with venlafaxine ER occurs during the first 6 weeks of treatment. Prescribers should be alert to signs of suicidal ideation and hostility in pediatric patients.

Sexual health is important to overall health and quality of life. Sexual problems have been associated with relationship problems and may interfere with overall health and they may also be a marker for other undiagnosed comorbid medical conditions. In order for healthcare professionals to manage the sexual health concerns of their patients, it is important for them to understand what constitutes good sexual health. To that end, it is necessary to have a working knowledge of the evolving theoretical models offered to describe a healthy sexual response as well as an understanding of the neurobiology of sexual function. The Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Revised lists six primary female sexual disorders: hypoactive sexual desire disorder, sexual aversion disorder, female sexual arousal disorder, female orgasmic disorder,dyspareunia, and vaginismus. Despite a growing awareness of the high prevalence of sexual disorders they are not typically identified nor treated. There are a number of reasons why clinicians fail to identify and treat sexual problems including insufficient training in sexual medicine and communication skills, time-constraints, and embarrassment. Treatment for female sexual problems is usually individualized and may include a combination of office-based education and basic counseling, cognitive-behavioral psychotherapy, pharmacotherapy, and treatment of concomitant medical conditions.

The proportion of pregnancies exposed to either second-generation antipsychotics (SGAs) or first-generation antipsychotics (FGAs) varies between 0.3%–2% of all pregnancies, but, until now, little is known about the potential neurobehavioral teratogenicity of antipsychotics. Assessing this safety facet is the aim of this article. PubMed, Scopus, and Google Scholar were searched for eligible articles. PubMed (1954 to May 2016) was searched using several medical subject headings, variously combined. PubMed search results were also limited using the search filter for human studies published in English. Scopus and Google Scholar searches were filtered for article title (antipsychotics/neuroleptics, pregnancy). After excluding duplicates, 9,250 articles were identified and 29 met the following inclusion criteria: only articles that provided original/primary data on neurodevelopmental outcome in human offspring older than 4 months of age, independently of the study design, were selected for review. Indeed, some relevant neurodevelopmental milestones are achieved at this time. Length of study and neurodevelopmental assessment methodology did not influence the study selection. Unfortunately, published data on neurodevelopmental teratogenicity of SGAs mainly derive from case reports and small case-series studies. Even findings emerging from case-control and prospective/retrospective studies are of limited clinical relevance because of their small sample sizes. Limited data are also available on FGAs. Hence, we have to conclude that the long-term neurodevelopmental outcomes for children exposed in utero remain unclear. Low to very low quality evidence of retrieved data makes impossible to confirm or exclude potential long-lasting untoward effects on infant neurocognitive development associate with antenatal exposure to either SGAs or FGAs.