Obesity has reached epidemic prevalence, and much research has focused on homeostatic and nonhomeostatic mechanisms underlying overconsumption of food. Mesocorticolimbic circuitry, including dopamine neurons of the ventral tegmental area (VTA), is a key substrate for nonhomeostatic feeding. The goal of the present review is to compare changes in mesolimbic dopamine function in human obesity with diet-induced obesity in rodents. Additionally, we will review the literature to determine if dopamine signaling is altered with binge eating disorder in humans or binge eating modeled in rodents. Finally, we assess modulation of dopamine neurons by neuropeptides and peripheral peptidergic signals that occur with obesity or binge eating. We find that while decreased dopamine concentration is observed with obesity, there is inconsistency outside the human literature on the relationship between striatal D2 receptor expression and obesity. Finally, few studies have explored how orexigenic or anorexigenic peptides modulate dopamine neuronal activity or striatal dopamine in obese models. However, ghrelin modulation of dopamine neurons may be an important factor for driving binge feeding in rodents.

The central nervous system is one of the main target tissues for sex steroid hormones, which act on both through genomic mechanisms, modulating synthesis, release, and metabolism of many neuropeptides and neurotransmitters, and through non-genomic mechanisms, influencing electrical excitability, synaptic function, morphological features, and neuron-glia interactions. During the climacteric period, sex steroid deficiency causes many neuroendocrine changes. At the hypothalamic level, estrogen withdrawal gives rise to vasomotor symptoms, to eating behavior disorders, and altered blood pressure control. On the other hand, at the limbic level, the changes in serotoninergic, noradrenergic, and opioidergic tones contribute to the modifications in mood, behavior, and nociception. Hormone replacement therapy (HRT) positively affects climateric depression throughout a direct effect on neural activity and on the modulation of adrenergic and serotoninergic tones and may modulate the decrease in cognitive efficiency observed in climaterium. The identification of the brain as a de novo source of neurosteroids, suggests that the modifications in mood and cognitive performances occurring in postmenopausal women may also be related to a change in the levels of neurosteroids. These findings open new perspectives in the study of the effects of sex steroids on the central nervous system and on the possible use of alternative and/or auxiliary HRT.

This review addresses the methodologic issues relevant to the study of comorbidity and provides a broad overview of the medical and psychiatric conditions associated with migraine. Since the body of literature examining the comorbidity of migraine is enormous, the scope of this review will largely focus on community and case-control studies. Among the selected comorbid medical conditions, including disorders of the cardiovascular, respiratory, neurologic, gastrointestinal and immunologic systems, stroke, asthma, and allergies appear to be most strongly associated with migraine. Among the psychiatric illnesses, mood and anxiety disorders have been shown to be most strongly associated with migraine in the general population. Further research is indicated and necessary to elucidate the precise mechanism of migraine comorbidity.

Parkinson's disease is a neurodegenerative disorder characterized by bradykinesia, rigidity, postural instability, and resting tremor. Increasingly, Parkinson's disease has been associated with a broad spectrum of non-motor symptoms, such as olfactory loss, sleep disorders, autonomic dysfunction, cognitive impairment, psychosis, depression, anxiety, and apathy. In addition, a minority of Parkinson's disease patients develop compulsive behaviors while receiving dopamine-replacement therapy, including medication hoarding, pathological gambling, binge eating, hyperlibidinous behavior, compulsive shopping, and punding. These behaviors may result in psychosocial impairment for patients and therapeutic challenges for clinicians. This article reviews the anatomic substrates, behavioral spectrum, associated factors, and potential treatments for dopamine-replacement therapy-related compulsions in Parkinson's disease.

Biobehavioral features associated with binge-eating disorder (BED) have been investigated; however, few systematic reviews to date have described neuroimaging findings from studies of BED. Emerging functional and structural studies support BED as having unique and overlapping neural features as compared with other disorders. Neuroimaging studies provide evidence linking heightened responses to palatable food cues with prefrontal areas, particularly the orbitofrontal cortex (OFC), with specific relationships to hunger and reward-sensitivity measures. While few studies to date have investigated non-food-cue responses; these suggest a generalized hypofunctioning in frontostriatal areas during reward and inhibitory control processes. Early studies applying neuroimaging to treatment efforts suggest that targeting neural function underlying motivational processes may prove important in the treatment of BED.

Folate deficiency may increase the risk of depression and reduce the action of antidepressants. Individuals with an inherited polymorphism that reduces the efficiency of folate formation may be at high risk for folate deficiency and for major depression. Antidepressant effects have been reported when antidepressants are augmented with folic acid, folinic acid, or the centrally active L-methylfolate (known formally as (6(S)-5-methyltetrahydrofolate [MTHF]), particularly in depressed patients with folate deficiency whose major depressive episodes have failed to respond to antidepressants. The putative mechanism of action of MTHF as an augmenting agent to antidepressants is that it acts as a trimonoamine modulator (TMM), enhancing the synthesis of the three monoamines: dopamine (DA), norepinephrine (NE), and serotonin (5-HT), resulting in a boost to the efficacy of antidepressants.

Children and their parents who are exposed to medical life-threat due to illness or injury are at risk for developing symptoms of posttraumatic stress. However, the prevention, detection, and treatment needed are often not available in the acute care settings of the hospital. The National Child Traumatic Stress Network and the Substance Abuse and Mental Health Services Administration have created a set of materials for use by hospital health providers and families that is available for download free from the National Child Traumatic Stress Network website, www.nctsn.org.

Obsessive-compulsive (OC) symptoms and schizophrenia may present, as intertwined phenomena whose relationship remains poorly understood. The purpose of this paper is to provide a detailed phenomenological description of OC symptoms in schizophrenia.

Fifty long-term patients with chronic schizophrenia or schizoaffective disorder from a continuing day-treatment program were assessed using the Structured Clinical Interview for DSM-IV and the Yale-Brown Obsessive-Compulsive Scale symptom checklist. Forty-six percent (n=23) reported clinically significant OC symptoms. Twenty-six percent (n=13) met criteria for OCD, from which three subgroups emerged: (1) patients whose OCD was unrelated to their psychotic symptoms, (2) patients whose OCD was related to, but not restricted to, their psychotic symptoms, and (3) patients whose OC symptoms existed on a continuum with their psychosis. The last group tended to incorporate their OC symptoms into delusional beliefs during the active phase of illness and shift to OCD during full or partial remissions. Eight percent met all inclusion criteria for OCD, but their OC symptoms were better accounted for by their psychosis.

We conclude that these findings support previous clinical constructs that OCD and schizophrenia are not always dichotomous disorders, but may be interconnected.

A review of the literature demonstrates that the incidence of new mental disorders and their prevalence during pregnancy is similar to the 12-month incidence of mental disorders in women during other periods of their lives. The prevalence of severe mood, behavior, and cognitive symptoms during pregnancy is rather high. Severe mental symptoms during pregnancy have been reported to be associated with an increased rate of complications during pregnancy and delivery, preterm deliveries, low birth weight, a higher rate of postpartum depression, and a longer-term impact on the offspring's development. Several pre-pregnancy risk factors to develop dysphoric symptoms have been reported, but their utility for primiparous women with no previous history of mental disorders is unclear. The association of mental symptoms with general symptoms and biological changes during pregnancy is also unclear. Given the short- and long-term impact of dysphoric symptoms and stress during pregnancy on mother and child, efficacious, efficient, and safe prevention and treatment modalities are essential and achievable. Clarification of the nature and phenotyping of mental and general symptoms during pregnancy is an important step for the development of effective interventions.

There is controversy about whether mindfulness-based approaches to psychotherapy represent a new wave of cognitive-behavioral therapy or a core process in all psychotherapies. One way of conceptualizing mindfulness is in terms of emotion regulation; mindfulness is a strategy aimed at opposing suppression and avoidance. Dispositional mindfulness has been associated with greater activation in prefrontal cortex and greater deactivation of amygdala during affect labeling. A number of rigorous studies of mindfulness-based cognitive therapy for depression have been positive. However, much remains to be discovered about the underlying mechanisms of and clinical indications for mindfulness-based approaches.

The duration of untreated illness (DUI), defined as the interval between the onset of a psychiatric disorder and the administration of the first pharmacological treatment, has been increasingly investigated in the last decade as a predictor of outcome across different psychiatric conditions including schizophrenia and psychotic disorders (duration of untreated psychosis), and mood and anxiety disorders. Converging evidence indicates that a prolonged DUI may be viewed as a negative prognostic factor in schizophrenia and increasing data point toward a similar conclusion in mood and anxiety disorders. Through a Medline search, the present article highlights the role of the DUI in this group of psychiatric disorders, focusing on social and psychopathological determinants of the DUI, as well as the clinical consequences related to a longer DUI in terms of outcome. Hypotheses on neurobiological mechanisms underpinning outcome differences in relation to a prolonged DUI are provided and methodological limitations related to the assessment of the DUI in published studies and clinical practice discussed. Finally, given that DUI is supposed to be a potentially modifiable prognostic factor, intervention programs aimed to reduce this variable are briefly considered and discussed.

A growing body of research has shown that two domains of cognition, neurocognition and social cognition, predict different domains of real-world outcomes in people with schizophrenia. Social cognition has been shown to predict social outcomes but not non-social outcomes (e.g. living independently), and neurocognition provides minimal prediction of social outcomes (e.g. interpersonal relationships). The differing predictive value of neurocognition and social cognition has led to an exploration of potential factors that interact with cognition to influence everyday outcomes. Functional skills, negative symptoms, and self-assessment have shown particularly promising relationships with cognitive ability. Several consensus studies have pinpointed valid performance-based assessments. High-contact informant ratings have additionally been shown to be highly accurate. The emerging understanding of divergent patterns of predicting outcomes and reliable assessments present an opportunity to improve treatment targets and real-world outcomes for individuals with schizophrenia. In particular, a recently defined component of metacognition has shown particular promise. Introspective accuracy (IA) addresses how well individuals evaluate their own abilities. Emerging research has found that IA of neurocognitive ability better predicts everyday functional deficits than scores on performance-based measures of neurocognitive skills and has found that IA of social cognition accounts unique variance in real world disability above social cognitive abilities. Intriguingly, IA of neurocognition appears to preferentially predict non-social outcomes while IA of social cognition predicts social outcomes.

Cariprazine is a new atypical antipsychotic drug (APD) with a unique pharmacodynamic profile, different from both typical and atypical APDs. Specifically, cariprazine acts as a partial agonist at the dopamine (DA) D2 and D3 receptors and serotonin 5-HT1A receptors, and as an antagonist at the 5-HT2B receptors. Moreover, it shows moderate affinities for adrenergic, histaminergic, and cholinergic receptors that are involved in mediating the side effects characteristic of typical APDs. In this review, we discuss the contribution of DA D3 receptors (D3Rs) in the etiology and pathophysiology of schizophrenia and the potential benefits that may be associated with a more selective targeting of D3R by APDs, as compared to other dopaminergic and non-dopaminergic receptor subtypes. Cariprazine, by acting on D3Rs, ameliorates anhedonia and cognitive deficits in animal models based on environmental or pharmacological manipulation. The reviewed results support the potential benefits of cariprazine in treating negative symptoms and cognitive deficits of schizophrenia, and therefore representing a promising approach in addressing the unmet clinical needs for the improved treatment of this serious neuropsychiatric disorder.

Individuals with mental illness and addiction comprise at least half of the patients in most mental health treatment systems. This combination results in increased risk for frequent psychiatric relapses, poor medication compliance, violence, suicide, legal problems, and high utilization of the emergency room or inpatient services. Traditional mental health and addiction treatments have not adequately addressed these co-occurring disorders due to clinical interventions, programs, and system flaws that have not addressed the individual's needs. Integrated treatment requires both an understanding of mental illness and addiction and the means to integrate and modify the traditional treatment approaches in both the mental health and addiction treatment fields. There is strong evidence to support the efficacy and effectiveness of integrated treatment in this population. All mental health clinicians should become experienced and skilled in the core psychotherapy approaches to treating substance use disorders, including motivational enhancement therapy, relapse prevention (cognitive-behavioral therapy), and 12-step facilitation. In addition, integrated treatment includes integrating medications for both addiction and mental illness with the behavioral therapies and other psychosocial interventions. This article reviews the clinical intervention, program, and system components of integrated treatment and specific clinical interventions for this population.

People with fibromyalgia syndrome (FMS) experi-ence unrefreshing sleep, aches, hypersensitivity, and cognitive and emotional difficulties. Although no specific causative factor or biological agent is known to account for all of the features of FMS and these related diagnoses, the generalized hypersensitivity of the body is considered to be affected by disturbances in cen-tral nervous system (CNS) functions. Such CNS dis-turbances are intrinsic to the sleeping-waking brain, where the common symptom elements in all these illnesses are poor quality of sleep, nonspecific pain, fatigue, and psychological distress in the absence of known disease pathology.

Vortioxetine is an antidepressant that targets multiple pharmacologic modes of action at sites—or nodes—where serotonergic neurons connect to various brain circuits. These multimodal pharmacologic actions of vortioxetine lead to enhanced release of various neurotransmitters, including serotonin, at various nodes within neuronal networks.

Until recently, body dysmorphic disorder (BDD) had been vastly ignored in the scientific literature. Despite a recent surge in interest, treatment studies are still surprisingly neglected. Reports from the 1970s–1990s discuss few case descriptions and suggest anecdotal treatment strategies. Since the 1990s, information about the treatment of BDD has increased slightly. The intent of this paper is to review the current state of knowledge regarding cognitive and behavior therapy, which so far has been found to be effective. The current literature suggests that there is no difference between the efficacy of one treatment strategy over another nor the combination of cognitive and behavior therapy over behavior therapy. However, more research is needed in this area before definitive conclusions can be made.