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.

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.

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.

In this study, we attempt to demonstrate an association between low platelet monoamine oxidase (MAO) activity, as assessed by isotopic methods, and the stable behavioral pattern of sensation- and risk-seeking of professional bull-fighters. Sixteen professional bullfighters were studied and compared with a control group of 46 healthy control subjects who did not engage in risky jobs or activities. The group of bullfighters had significantly reduced platelet MAO activity compared with the control group (P<0.05). Bullfighters were shown to be significantly more extroverted and sensation-seeking than controls on various temperament scales. A predisposition to engage in risky activities (eg, bullfighting) and sensation-seeking could be partly conditioned by the presence of biological components of personality manifested by a significantly decreased platelet MAO activity.

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.

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.

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.

For decades clinicians and researchers have been thinking and writing about the spectrum of schizophrenia disorders. Indeed both Kraepelin and Bleuler believed in schizophrenia as a spectrum, both in a clinical (individual) and hereditary (family) continuum, from just some exquisite personality traits to unquestionable chronic and debilitating psychosis. Other authors would put the schizophrenia spectrum disorders on different levels of continuum: developmental, psychofunctional, existential, and genetic. Here, we would like to present an historical chronology for the schizophrenia–schizoaffective–bipolar spectra plus a tridimensional model for these spectra: the first axis for categories (affective versus nonaffective psychoses), the second axis for dimensions (personality versus full blown psychosis), and a third axis for biomarkers (remission versus relapse). We believe that without the schizophrenia–schizoaffective–bipolar spectra concept in our minds all our efforts will keep failing one the hardest quest: searching for biomarkers in schizophrenia and related disorders.

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.

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.

Comorbid chronic pain is common in depressed patients. It is predictive of a poor prognosis for depression and is a major risk factor for suicidal behavior. Depression and chronic pain may result from a common neurobiological dysfunction of monoamine cell bodies in the basal ganglia. Amitriptyline, which inhibits both serotonin and norepinephrine reuptake, is a preferred treatment of chronic pain although it is not officially indicated for this condition. Chronic pain can be modeled in animals where amitriptyline has been shown to be highly effective. Similar effects are obtained with the serotonin norepinephrine reuptake inhibitors milnacipran, duloxetine, and venlafaxine, whereas selective serotonin reuptake inhibitors (SSRIs) are only weakly active. Both animal and clinical studies of chronic pain show that dual-acting reuptake inhibitors are more active than selective norepinephrine reuptake inhibitors, which are, in turn, more active than SSRIs. A meta-analysis of placebo-controlled studies confirmed that dual-action antidepressants, but not SSRIs, were effective in reducing chronic lower-back pain. Milnacipran, duloxetine, and venlafaxine, have all been reported to be effective in a number of chronic pain conditions, including the treatment of fibromyalgia where their analgesic effects are independent of comorbid depression.

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.

Obsessive-compulsive disorder (OCD) is now recognized as a frequent and disabling disorder among children and adolescents. The phenomenology is similar to adult OCD, but several reports have indicated that compulsions are more prominent in children and that children are more inclined than adults to include their family surroundings in ritualistic behavior. It is also clear that young children engage in a significant amount of repetitive, ritualistic compulsive activity that appears to be a normal part of their behavioral repertoire.

Although the cause of childhood-onset OCD is unknown, many factors are likely to contribute to the heterogenous clinical phenotypes, including both genetic and environmental factors. The neurobiological circuitry involved in childhood-onset OCD is likely to involve alterations to the same cortico-striatothalamic circuitry implicated in adult OCD, but the develop-mental differences have yet to be fully delineated. The treatment response patterns of adults and children are generally inconsis-tent with each other, and specific OCD subtypes may also respond differentially.

Phenotypic characterization can be undertaken either categorically, as seen with traditional diagnostic categories, or dimensionally. Extended phenotypes can be defined in terms of symptoms and course of the illness, or neuroimaging and neurobiologic study findings, or treatment responses. Phenotypic characterization must also reflect an understanding of the rituals and repetitive behaviors that are associated with normal development. (A proposed categorization of OCD subtypes appears in the “Table library.”)

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.

This case report illustrates the relationship between stress and obsessive-compulsive disorder (OCD) by describing an unusual case of OCD sequelae following a suicide attempt. The patient is a 29-year-old married woman who suffered a major depressive episode without OCD and tried to commit suicide by drinking household cleaner. Following the attempt, violent obsessive thoughts of harming herself and others emerged along with avoidance behavior. After exposure therapy, there was a decrease in her obsessive thoughts, less anxiety, and no avoidance behavior. This report highlights not only the existence of “posttraumatic obsession” but also the importance of accurate interpretation of suicidal preoccupation, leading to the diagnosis of OCD rather then suicidal ideation secondary to depression.

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.