Sexual dysfunction is a frequently encountered comorbid condition in patients with many medical and psychiatric conditions, such as epilepsy and depression. Most depressed patients experience some type ofsexual dysfunction, decreased sexual desire being the most common. The association of sexual dysfunction with epilepsy is less clear. Changes in sex hormone levels are common in patients with epilepsy and may be attributable to the disease or to antiepileptic drugs (AEDs). Sexual dysfunction associated with depression or epilepsy is generally treated according to standard guidelines for the management of sexual disorders,since data from special populations are not available. The most common forms of female sexual dysfunction are lack of sexual desire and difficulty achieving orgasm. There are no approved pharmacotherapies forfemale hypoactive sexual desire disorder or female orgasmic disorder. Female sexual arousal disorder is treated with estrogen replacement therapy when indicated or vaginal lubricants. The most common male sexual dysfunction disorders are premature ejaculation and erectile dysfunction.  Phosphodiesterase type-5 inhibitor drugs are now the first-line treatment for erectile dysfunction, and selective serotonin reuptake inhibitors and topical anesthetic creams are nonapproved but effective treatments for premature ejaculation. Testosterone and aromatase inhibitors have been used investigationally to treat sexual dysfunction in men taking AEDs. Patient education and follow-up appointments are essential to ensure optimal outcomes of pharmacologic treatments for sexual dysfunction.

Depression is a common disorder among adolescents and is associated with a high risk of suicide. Suicide is the third leading cause of death among adolescents in the United States. Currently, there are only two evidence-based psychotherapies for adolescence depression: cognitive-behavioral therapy and interpersonal psychotherapy. Furthermore, psychosocial interventions that specifically target suicidal behavior in adolescents are even fewer in number than treatments for depression. This article will review the psychosocial interventions for depression and suicidality in adolescents and will describe a recently developed treatment that is under study for depressed suicidal adolescents.

Dementia is a neuropsychiatric disorder characterized by cognitive impairment and behavioral disturbances. The behavioral and psychological symptoms of dementia (BPSD) are common, contributing to caregiver burden and premature institutionalization. Management of BPSD is complex and often needs recourse to psychotropic drugs. Though widely prescribed, there is a lack of consensus concerning their use, and serious side effects are frequent. This is particularly the case with antidepressant treatment based on the assumption that BPSD is depressive in nature. A better understanding of BPSD etiology could lead to better management strategies. We submit that some BPSD could be the consequence of both dementia and an undiagnosed comorbid bipolar spectrum disorder, or a pre-existing bipolar diathesis pathoplastically altering the clinical expression of dementia. The existence of such a relationship is based on clinical observation, as far as the high frequency of bipolar spectrum disorders in the general population, with a prevalence estimated to be between 5.4% and 8.3%, and the psychopathological similarities between BPSD and mood disorder episodes in bipolar illness. We will review the concept of the bipolar spectrum and explain BPSD before proposing clinical pointers of a possible bipolar spectrum contaminating the phenomenology of dementia, which could lead to the targeted prescription of mood-stabilizing agents in lieu of antidepressant monotherapy. These considerations are of heuristic interest in reconceptualizing the origin of the behavioral manifestations of dementia, with important implications for geriatric practice.

Attentional bias in substance-dependent patients is the tendency to automatically direct attention to substance-related cues in the environment. Preclinical models suggest that attentional bias emerges as a consequence of dopaminergic activity evoked by substance-related cues. The aim of the current review is to describe pharmacological mechanisms underlying attentional bias in humans and to critically review empirical studies that aimed to modulate attentional bias in substance-dependent patients by using pharmacological agents. The findings of the reviewed studies suggest that attentional bias and related brain activation may be modulated by dopamine. All of the reviewed studies investigated acute effects of pharmacological agents, while measurements of chronic pharmacological treatments on attentional bias and clinically relevant measures such as relapse are yet lacking. Therefore, the current findings should be interpreted as a proof of principle concerning the role of dopamine in attentional bias. At the moment, there is too little evidence for clinical applications. While the literature search was not limited to dopamine, there is a lack of studies investigating the role of non-dopaminergic neurotransmitter systems in substance-related attentional bias. A focus on neurotransmitter systems such as acetylcholine and noradrenaline could provide new insights regarding the pharmacology of substance-related attentional bias.

The association between violence and mental illness is well-studied, yet remains highly controversial. Currently, there appears to be a trend of increasing violence in state hospital settings, including both civilly and forensically committed populations. In fact, physical aggression is the primary reason for admission to many state hospitals. Given that violence is now often both a reason for admission and a barrier to discharge, there is a case to be made for psychiatric violence to be re-conceptualized dimensionally, as a primary syndrome, not as the byproduct of one. Furthermore, treatment settings need to be enhanced to address the new types of violence exhibited in inpatient environments, and this modification needs to be geared toward balancing safety with treatment.

Binge eating disorder (BED) is the most common eating disorder, with an estimated lifetime prevalence of 2.6% among U.S. adults, yet often goes unrecognized. In the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5), BED is defined by recurrent episodes of binge eating (eating in a discrete period of time an amount of food larger than most people would eat in a similar amount of time under similar circumstances and a sense of lack of control over eating during the episode), occurring on average at least once a week for 3 months, and associated with marked distress. It can affect both men and women, regardless if they are at normal weight, overweight, or obese, and regardless of their ethnic or racial group. Psychiatric comorbidities are very common, with 79% of adults with BED also experiencing anxiety disorders, mood disorders, impulse control disorders, or substance use disorders; almost 50% of persons with BED have ≥3 psychiatric comorbidities. Multiple neurobiological explanations have been proffered for BED, including dysregulation in reward center and impulse control circuitry, with potentially related disturbances in dopamine neurotransmission and endogenous μ‐opioid signaling. Additionally, there is interplay between genetic influences and environmental stressors. Psychological treatments such as cognitive behavioral interventions have been recommended as first line and are supported by meta-analytic reviews. Unfortunately, routine medication treatments for anxiety and depression do not necessarily ameliorate the symptoms of BED; however, at present, there is one approved agent for the treatment of moderate to severe BED—lisdexamfetamine, a stimulant that was originally approved for the treatment of attention deficit hyperactivity disorder.

This article summarizes results of all pharmacotherapy trials for obsessive-compulsive disorder (OCD) published from 2006 to 2008 as well as studies on markers for predicting response to treatment and neurobiological changes induced by pharmacotherapy. Results show that recent developments in the treatment of OCD have been modest and primarily involve evidence for the efficacy of escitalopram and other selective serotonin reuptake inhibitors (SSRIs); augmentation with antipsychotics in treatment-refractory patients and combination treatment with D-cycloserine and cognitive-behavioral therapy has also been effective. The efficacy of serotonin-norepinephrine reuptake inhibitors remains inconclusive. Studies on markers of clinical response have shown inconsistent results, however, duration and severity of OCD and the presence of comorbidities can often identify patients at risk for nonresponse. Lastly, successful treatment with an SSRI results in both serotonergic and dopaminergic changes, but more research is necessary in order to define the biological characteristics of responders and nonresponders.

The excessive and chronic use of alcohol is associated with a variety of neurocognitive changes in a substantial number of detoxified alcoholics. These deficits extend across a wide variety of neuropsychological domains and can be observed over a period of months following detoxification. Furthermore, they are seen in both male and female alcoholics, despite the fact that female alcoholics often have shorter drinking histories. Although these deficits are widely observed, there is considerable heterogeneity both within and across studies. Currently, the sources of this variability are only poorly understood. In this article, we review these neurocognitive and neurophysiological deficits, their pattern of recovery, potential contributing or confounding factors, and some of the clinical implications of these findings.

While obsessive-compulsive (OC) symptoms in schizophrenia have been reported for many years, they have achieved only limited recognition and, perhaps for this reason, few studies their pharmacological treatment have been carried out. One suggested treatment approach is the use of different agents for different symptoms. In this article, we review the small number of published studies and case reports regarding this multi-pharmacological method of treatment for OC symptoms in schizophrenia. While each study used a somewhat different patient population and provided varying and limited information concerning patient sample, study design, and results, some tentative conclusions and treatment recommendations may be drawn from their findings.

The unique clinical presentation of Tourette syndrome (TS) and its symptomatic response to dopamine antagonists are widely cited as evidence for the central role of the limbic-motor interface in the pathophysiology of TS. Nonetheless, the true neuropathology of TS remains elusive, even though significant advances have been made in understanding complex interconnected circuitries within the limbic system and basal ganglia. Neuropathologic and neuroimaging studies—plagued by small samples, clinical heterogeneity, and a number of interpretative problems—are generally supportive of pathology within the orbitofrontal cortex, striatum, and their efferent projections in TS. The specific patterns of abnormalities vary widely across these studies, clouding attempts to define a unifying neuropathology for this disorder. Converging yet circumstantial evidence for frontal cortical, and basal ganglia pathology in TS comes also from studies infields ranging from neuroimmunology to neuropsychology, and from the clinical overlap between TS and disorders such as obsessive-compulsive disorder, attention-deficit/hyperactivity disorder, and Sydenhams chorea. As a “model” neuropsychiatric disorder, TS has stimulated advances in several areas of neurobiology research, yet we still await a real understanding of its pathophysiology in order to move from empirically driven therapeutics to the development of targeted effective treatments.

Can a medical illness or its treatment qualify as an emotionally traumatic event and can it cause posttraumatic stress disorder symptoms? If so, can the view of a medical illness as a traumatic experience enhance our ability to understand patients' adjustment to illness and their emotional reactions to it? Is it important to identify posttraumatic symptoms and try to address them in medically ill patients? These questions form the backbone for this review. Because many questions remain unanswered (or the answers are not definitive yet), we concisely summarize the issues and present our own view of the most pressing questions for further research.

Although significant progress has been made over the last decade in the treatment of obsessive-compulsive disorder (OCD), approximately 20% of OCD patients remain refractory to nonsurgical therapies, including pharmacologic and cognitive-behavioral therapy. Because a number of neural circuits involving the basal ganglia, thalamus, limbic system, and frontal lobes have been implicated in the pathophysiology of OCD, the need for an effective intervention in these patients has brought the focus on surgical approaches, including cingulotomy and capsulotomy procedures. Unlike free-hand surgical approaches used in the past, current neurosurgical interventions have been greatly enhanced by advances in technology, which allow lesioning to an accuracy of 1 mm. Today's neurosurgical approaches have shown significant benefit in as many as 60% of refractory patients, while preserving personality and cognitive functioning and limiting morbidity. A study of gamma knife capsulotomy conducted at Brown University School of Medicine showed that 40% of patients undergoing two lesioning procedures were much or very much improved 2 years postsurgery. The inherent obstacles to conducting placebo-controlled studies in these severely ill patients mean that further study is required to identify optimal candidates for surgical intervention.

Much has changed since the two dominant mental health nosological systems, the International Classification of Diseases (ICD) and the Diagnostic and Statistical Manual of Mental Disorders (DSM), were first published in 1900 and 1952, respectively. Despite numerous modifications to stay up to date with scientific and cultural changes (eg, exclusion of homosexuality as a disorder) and to improve the cultural sensitivity of psychiatric diagnoses, the ICD and DSM have only recently renewed attempts at harmonization. Previous nosological iterations demonstrate the oscillation in the importance placed on the biological focus, highlighting the tension between a gender- and culture-free nosology (solely biological) and a contextually relevant understanding of mental illness. In light of the release of the DSM 5, future nosological systems, such as the ICD 11, scheduled for release in 2017, and the Research Development Criteria (RDoC), can learn from history and apply critiques. This article aims to critically consider gender and culture in previous editions of the ICD and DSM to inform forthcoming classifications.

Nonalcoholic fatty liver disease (NAFLD) is a complex metabolic-inflammatory disease associated with poor outcomes and decreased quality of life. NAFLD is overrepresented in patients with psychiatric disorders like depression, bipolar disorder, and schizophrenia; however, a comprehensive review on NAFLD and psychiatric disorders remains to be delineated. This review endeavors to investigate the association of NAFLD with psychiatric disorders, including shared pathogenesis and future clinical derivatives. Extant literature suggests that patients with psychiatric disorders (in particular, mood disorders) are more susceptible to the development of NAFLD due to multiple reasons, including but not limited to hypothalamic–pituitary–adrenal axis dysregulation, metabolic syndrome, and chronic perceived stress. Moreover, the clinical manifestations of mood disorders (e.g., anhedonia, psychomotor retardation, lifestyle modification, etc.), and potentially long-term treatment with weight-gaining agents, differentially affect these patients, making them more prone to NAFLD. Considering the increased morbidity associated with both mood disorders and NAFLD, our review recommends regular screenings for NAFLD in select patients with mood disorders exhibiting signs of increased risk (i.e., obesity, metabolic syndrome, diabetes, or family history of NAFLD) for better diagnosis and holistic care of both potentially interrelated conditions.

There is an ongoing debate about how best to conceptualize the unconscious. Early psychodynamic views employed theories influenced by physics to explain clinical material, while subsequent cognitivist views relied on computational models of the mind to explain laboratory data. More recently, advances in cognitive-affective neuroscience have provided new insights into the workings of unconscious cognition and affect. We briefly review some of this recent work and its clinical implications.

This study investigates lifetime prevalence rates, demographic characteristics, childhood conduct disorder and adult antisocial features, suicide attempts, and cognitive impairment in individuals with obsessive-compulsive disorder (OCD) uncomplicated by or comorbid with any other psychiatric disorder. The data are from the NIMH Epidemiological Catchment Area (ECA) study, and the current analyses compared subjects with uncomplicated OCD (no history of any other lifetime psychiatric disorder) comorbid OCD (with any other lifetime disorder), other lifetime psychiatric disorders, and no lifetime psychiatric disorders across these variables. OCD in its uncomplicated and comorbid form had significantly higher rates of childhood conduct symptoms, adult antisocial personality disorder problems, and of suicide attempts than did no or other disorders. Comorbid OCD subjects had higher rates of mild cognitive impairment on the Mini-Mental Status Exam than did subjects with other disorders. These findings suggest that a subgroup of OCD patients may have impulsive features, including childhood conduct disorder symptoms and an increased rate of suicide attempts; wider clinical attention to these outcomes is needed.