Depression is increasingly recognized as a highly recurrent and potentially chronic illness that imposes a substantial burden on individuals, families, and society. Evidence indicates that the risks of depressive recurrence, treatment resistance, and chronicity increase as the illness becomes more highly recurrent. Up to 1 year of continuation phase therapy is now recommended for virtually all depressed patients who respond to antidepressants, with a longer course of maintenance phase pharmacotherapy recommended for those who have experienced multiple episodes. Antidepressants, when effective during the acute phase of therapy, reduce the risk of depressive relapse (continuation phase) and recurrence (maintenance phase) by at least 50%. Longer-term antidepressant pharmacotherapy is most effective when the full dose of medication effective during acute-phase treatment is continued. As combined treatment with antidepressants and psychotherapy may improve shorter-term outcomes for patients with more severe recurrent depression, ongoing combined therapy may be indicated, especially for patients at particularly high risk. Approximately 5% to 10% of patients maintained on antidepressants relapse yearly, leading some to implicate tachyphylaxis. However, before attributing relapse or recurrence to diminished responsiveness to antidepressant medication at the neurochemical level, clinicians should ensure that the patient has been adherent to therapy as prescribed and consider other explanations.

Depression is an important public health problem affecting about 15% of the general population; however, little is known about possible changes in the brain that might underlie the disorder. Neuroimaging has been a powerful tool to map actual changes in the brain structure of depressed patients that might be directly related to their symptoms of depression. Some imaging studies of brain structure have shown smaller hippocampal volume with the chronicity of depression correlating to a reduction in volume. Although the meaning of these findings is unclear, other studies have shown increased amygdala volume. Studies have found reductions in volume of the frontal cortex, with some studies showing specific reductions in subregions of the frontal cortex, including the orbitofrontal cortex. Findings of an increase in white matter lesions in elderly patients with depression have been replicated and correlated with late-onset depression, as well as impairments in social and cognitive function. These findings point to alterations in a circuit of brain regions hypothesized to include the frontal cortex, hippocampus, amygdala, striatum, and thalamus, that underlie symptoms of depression.

Rats treated chronically with the D2/D3, dopamine receptor agonist quinpirole show a pattern of behavior that meets a set of ethologically derived criteria of compulsive behavior in obsessive-compulsive disorder (OCD). Moreover, in both quinpirole-treated rats and OCD patients, the structure of compulsive rituals appear similar in being composed of relatively few motor acts that are organized in a flexible yet recurrent manner. In addition, the development of compulsive behavior in quinpirole-treated rats is attenuated by the OCD pharmacotherapeutic drug clomipramine. These similarities support the validity of quinpirole-treated rats as a psychostimulant-induced animal model of OCD. Considering that the induction of compulsive behavior in the rat model involves chronic hyperstimulation of dopamine receptors, this raises the possibility that dopaminergic mechanisms may play a role in OCD, at least in some subtypes of this disorder.

Balancing efficacy with tolerability and safety of prescribed treatments is critical to optimizing antipsychotic treatment outcomes in the mentally ill. Symptom control, symptom remission, and functional recovery are only realistic goals when treatments are both effective and well tolerated. The consideration of predictable differences in antipsychotic adverse-effect profiles is central to successful illness management. Minimizing adverse effects on alertness, motivation, cognition, sexual/reproductive functioning, and physical health enhancesmental health outcomes, partly through improving treatment adherence. Neuroendocrine and metabolic side effects of antipsychotics for cardiovascular morbidity and mortality need to be addressed proactively and aggressively. In view of the widespread lack of primary care engagement and the adverse effects of psychotropic medications on cardiovascular health, psychiatric care providers should function as key facilitators of an integrated mental and physical health management approach. In addition to psychoeducation and healthy lifestyle counseling, clinicians can improve psychiatric and physical health by selecting medications carefully, routinely screening and monitoring for reversible cardiovascular risk factors, and playing an active role in the prevention and interdisciplinary management of cardiovascular risk factors and medical illness in the vulnerable mentally ill.

Catatonia and neuroleptic malignant syndrome (NMS) are uncommon disorders that can be life-threatening. Many researchers consider them as clinically divergent entities; however, they share similar and overlapping literature on causative agents, phenomenology, and treatment response. This hypothesis considers both disorders as a single entity that result from variable combinations of the following: 1) γ-aminobutyric acid (GABA) hypoactivity at the GABAA receptor; 2) dopamine hypoactivity at the D2 receptor; 3) serotonin hyperactivity at the 5-HT1A receptor and hypoactivity at the 5-HT2A receptor; and 4) glutamate hypoactivity at the N-methyl-D-aspartate (NDMA) receptor. In this paper, evidence to support this hypothesis is limited to retrospective human studies of catatonia and NMS. The four components of the hypothesis are: 1) GABAA agonists have been shown to alleviate catatonia and NMS; 2) D2 antagonism is proportional to the relative likelihood of NMS and catatonia; 3) 5-HT1A agonism with 5-HT2A antagonism is implicated in catatonia and NMS; 4) NMDA receptor antagonists, such as phencyclidine and ketamine, reduce glutamate transmission. This hypothesis proposes that it is the interaction of these systems that prediposes, initiates, and maintains the twin syndromes of catatonia and NMS.

Background: Assertive community treatment (ACT) is an intensive and comprehensive treatment for clients with severe mental illness (SMI) who do not readily benefit from clinic-based services. Monitoring the implementation of such programs is critical, because better-implemented programs have been found to be effective in improving client outcomes.

Objective: We tested the hypothesis that fidelity to the ACT model would be positively correlated with improved client outcomes, as measured by reduction in psychiatric hospital use.

Methods: A scale measuring fidelity of program implementation, the Dartmouth ACT Scale, was examined in 10 newly formed ACT teams. Using the team as the unit of measure, the mean reduction in state hospital days for a 1-year period before and after program admission was calculated. Mean effect size in reduction in hospital days was used as the outcome measure in a correlational design.

Results: Pre/post comparisons showed a 43% reduction in hospital days for 317 clients (t=8.61, P<.001). The Pearson correlation between DACTS fidelity and reduction of state hospitaldays was .49, P=.08, one-tailed.

Conclusion: Several possible reasons are offered for why the study hypothesis was not confirmed. However, even if predictive validity of the Dartmouth ACT Scale is limited, it continues to be a useful tool for program monitoring and for providing corrective feedback.

The current tools used to define and diagnose mental disorders, including the Diagnostic and Statistical Manual of Mental Disorders and the International Classification of Diseases, have added specificity to the psychiatric nomenclature. However, their stereotypic rigidity in classification has resulted in the failure to identify the full range of potentially debilitating psychiatric symptoms with which patients may present. A spectrum model of psychopathology is more adept at recognizing the subclinical or threshold symptomatology that may occur concomitantly with core psychiatric disorders. The authors discuss the development of a spectrum approach to the diagnosis of mental disorders, which offers the potential to improve treatment selection and therapeutic outcomes.

Compulsive sexual behavior (CSB) is characterized by inappropriate or excessive sexual behaviors or cognitions that lead to subjective distress or impaired functioning. Both abnormal (paraphilic) and conventional (nonparaphilic) forms of sexual behavior are usually included in the definition. CSB is reported to affect 3% to 6% of the general population in the United States, occurring more frequently in men. It typically begins in the late teens or early twenties and is chronic or intermittent. The disorder has been described as a progression through four stages: preoccupation, ritualization, gratification, and despair. Men with CSB typically focus on physical sexual gratification; women focus on romantic or emotional aspects of sexuality. Psychiatric comorbidity is common, particularly substance use, mood, anxiety, and personality disorders. CSB can lead to medical complications. Risk factors are thought to include family history and childhood abuse.

Postpartum psychiatric changes can range from maternity blues to psychosis. Causality is still undetermined, but explanations for these disturbances often focus on hormonal changes and dysregulation. Researchers have begun the process of delineating what neurobiological factors may be associated with depressive disorders in pregnancy and the postpartum. This article reviews the current literature on the roles of gonadal and pituitary hormones in the psychopathophysiology of postpartum mood disorders. Other biological factors, such as biogenic amines, neuroactive steroids, cholesterol, and fatty acids, are also discussed. The potential benefits of neuroimaging to aid in understanding neuropsychiatric changes that occur in the context of postpartum depression are also considered.

Current evidence from epidemiological, neuroimaging, pathological, pharmacotherapeutic, and clinical studies indicate an association of Alzheimer's disease with risk factors of vascular atherosclerotic disease either in isolation or in aggregate. “Metabolic syndrome” (MetS) is the name for a clustering of risk factors for cardiovascular disease and type 2 diabetes that are of metabolic origin. These include central obesity, elevated plasma glucose, high blood pressure, atherogenic dyslipidemia, a prothrombotic state, and a proinflammatory state. In this article, we provide an overview of the relevant literature with regard to the relationship of Alzheimer's disease with MetS. Accumulating evidence suggests a “vascular hypothesis” to be related to the pathology of Alzheimer's disease. In the light of this evidence, clinician may consider lifestyle interventions toward an early and effective cardiovascular risk-factor management to reduce the cardiometabolic and the cognitive decline risk, while further research of other preventive strategies may be warranted.

The study of social cognition in psychiatric disorders has become increasingly popular in recent years. This is due to the its proposed link to social functioning and the inability of general neurocognitive skills to explain the spectrum of impairments observed in patients. This article reviews research into two of the processes thought to underlie social cognition (emotion perception and theory of mind) in schizophrenia and autism. This is followed by a look at neuroimaging studies and their efforts to localize the neural correlates of emotion perception and theory of mind in the two disorders. We concluded that while a specific impairment in emotion perception and theory of mind skills cannot be generalized to all individuals with autism and schizophrenia, there are subpopulations that have lingering deficits of social cognition tasks. Neuroimaging work consistently points to the involvement of the fusiform gyrus and amygdala in emotion processing, while the medial prefrontal and frontal cortex are implicated in tasks invoking theory of mind. We propose that deficits of social cognition may benefit from cognitive remediation therapy and pharmacological cognitive enhancers.

Can psychological factors, such as depression, affect human immunodeficiency virus progession? HIV infection is viewed as a chronic illness in which those infected often confront a number of emotional challenges and physical health and disease-related issues. Over the past 20 years, there has been increasing evidence that depression and other mood-related disturbances are commonly observed among HIV-positive individuals. There is also mounting data showing that depressive symptoms might further impact upon specific elements of immune system functioning and influence quality of life and health status. This paper will highlight studies examining the prevalence of depression during HIV infection and review some of the evidence examining the impact of depressive symptoms on immune function and HIV disease progression.

It has been proposed that certain Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition Axis I disorders share overlapping clinical features, genetic contributions, and treatment response and fall within an “obsessive-compulsive” spectrum. Obsessive-compulsive personality disorder (OCPD) resembles obsessive-compulsive disorder (OCD) and other spectrum disorders in terms of phenomenology, comorbidity, neurocognition, and treatment response.This article critically examines the nosological profile of OCPD with special reference to OCD and related disorders. By viewing OCPD as a candidate member of the obsessive-compulsive spectrum, we gain a fresh approach to understanding its neurobiology, etiology, and potential treatments.

Binge eating disorder (BED) is the most common of eating disorders and is characterized by excessive, out-of-control, rapid food intake. This review focuses on cognitive impairments in BED, which represent an endophenotype that mediates brain function and behavior. Here we focus on reviewing impulsivity, compulsivity, attentional biases to food cues, and executive function. Behavioral regulation in BED appears to be influenced by the context of motivationally salient food cues and the degree of obesity. Deficits in delay discounting and risk taking under ambiguity are impaired in obesity irrespective of BED status. However, in BED subjects with milder obesity, greater risk seeking under explicit probabilistic risk is observed to monetary rewards, whereas this shifts to risk aversion and enhanced delay discounting in more severe obesity. Relative to non-BED obese subjects, BED is characterized by enhanced behavioral inflexibility or compulsivity across multiple domains, with subjects selecting the same choices despite change in relevance (set shifting), being no longer rewarding (habit formation), or irrespective of outcome (perseveration). The context of food cues was associated with multiple attentional and early and late inhibitory impairments and enhanced memory bias, although BED patients also have generalized cognitive interference in working memory. These findings may help explain the phenotype of binge eating. Motivationally salient food cues provoke attentional and memory biases along with impairing response inhibitory processes. Those with BED are also more susceptible to cognitive interference and have impaired decisional impulsivity, with the tendency to inflexibly stick with the same choices irrespective of changes in context. These findings suggest critical cognitive domains that may guide therapeutic interventions.

Objective: As part of this national project, we examined barriers and strategies to implementation of two evidence-based practices (EBPs) in Indiana.

Background: Despite many advances in the knowledge base regarding mental health treatment, the implementation of EBPs in real-world setting remains poorly understood. The National EBP Project is a multi-state study of factors influencing implementation of EBPs.

Methods: Over a 15-month period we observed eight assertive community treatment (ACT) programs and six integrated dual disorders treatment (IDDT) programs and noted pertinent actions taken by the state mental health agency influencing implementation. We created a database containing summaries of monthly visits to each program and interviews with key leaders. Using this database and clinical impressions, we rated barriers and strategies at each site on seven factors: Attitudes, Mastery, Leadership, Staffing, Policies, Workflow, and Program Monitoring.

Results: At the site level, the most frequently observed barriers were in the areas of leadership, staffing and policies for ACT, and mastery and leadership for IDDT. Overall, barriers were more evident for IDDT than for ACT. Strategies were less frequently noted but generally paralleled the areas noted for barriers. However, our central finding was that ACT was generally more successfully implemented than IDDT throughout the state, and that this difference could be traced in large part to state-level factors relating to historical preparation for the practice, establishment of standards, formation of a technical assistance center, and funding.

Conclusion: In this case study, both state-level and site-specific factors influenced success of implementation of EBPs. To address these factors, the field needs systematic strategies to anticipate and overcome these barriers if full implementation is to be realized.

Background: Attention-deficit/hyperactivity disorder (ADHD) occurs in as many as 4% of adults yet it is often not recognized in clinical settings because the presenting symptoms may resemble those seen in other disorders or because symptoms may be masked by commonly comorbid conditions such as anxiety and depression.

Objective: The purpose of this study was to examine the diagnostic utility of instruments commonly used in the assessment of adults presenting with symptoms of ADHD.

Methods: We reviewed several widely used self-report and laboratory measures and empirically examined the utility of the Brown Attention-Deficit Disorder Scale for Adults (Brown ADD Scale) and the Conners Continuous Performance Test (CPT) in differentially identifying adults with ADHD and those with other Axis I disorders.

Results:Ninety-three adults who self-referred to the ADHD program for adults at a university medical center participated in the study. Of these, 44 had ADHD combined subtype (ADHD-CB), and 26 had ADHD, predominantly inattentive subtype (ADHD-IA). Thirty-three non-ADHD adults diagnosed with Axis I mood or anxiety disorders comprised an “Other Psychiatric” group. Rates of comorbid disorders, including substance abuse, in the ADHD groups were typical of those reported in the adult ADHD literature. Data on the Brown ADD Scale and on the CPT were available for subsets of 61 and 46 participants, respectively. Analyses showed that the ADHD-CB, ADHD-IA, and Other Psychiatric groups all received mean scores in the clinical range on the Brown ADD Scale, with a trend toward even higher elevations in the two ADHD groups. Among 12 CPT variables assessed for the three groups, the mean scores on only two variables for the ADHD-IA group were clinically elevated. Neither the Brown ADD Scale nor CPT scores evinced sufficient sensitivity and specificity to qualify them to assist in differential diagnosis of ADHD vis-a-vis other, predominantly internalizing, psychiatric disorders.

Conclusion: The results indicate a need for closer examination of executive and adaptive functioning in adults with ADHD compared with those with internalizing disorders in order to identify features that could assist in differential diagnosis.