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.

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.

There is growing basic-science interest in the mechanisms underpinning the positive effects of exercise on brain function and cognitive-affective performance. There is also increasing clinical evidence that exercise may prevent and treat various neuropsychiatric disorders. At the same time, there is growing awareness that athletic performance is mediated in crucial ways by central nervous system mechanisms. The relevant mechanisms in all these cases requires further exploration, but likely includes neurotrophic, neuroendocrine, and neurotransmitter systems, which in turn are crucial mediators of psychopathology and resilience. The hypothesis that Homo sapiens evolved as a specialist endurance runner provides an intriguing context against which to research the proximal mechanisms relevant to a cognitive-affective neuroscience of exercise.

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.

Moving from a behavioral-based to a biological-based classification of mental disorders is a crucial step toward a precision-medicine approach in psychiatry. In the last decade, a big effort has been made in order to stratify genetic, immunological, neurobiological, cognitive, and clinical profiles of patients. Making the case of obsessive–compulsive disorder (OCD), a lot have been made in this direction. Indeed, while the Diagnostic and Statistical Manual of Mental Disorders (DSM) diagnosis of OCD aimed to delineate a homogeneous group of patients, it is now clear that OCD is instead an heterogeneous disorders both in terms of neural networks, immunological, genetic, and clinical profiles. In this view, a convergent amount of literature, in the last years, indicated that OCD patients with an early age at onset seem to have a specific clinical and biological profile, suggesting it as a neurodevelopmental disorder. Also, these patients tend to have a worse outcome respect to adult-onset patients and there is growing evidence that early-interventions could potentially improve their prognosis. Therefore, the aim of the present paper is to review the current available genetic, immunological, neurobiological, cognitive, and clinical data in favor of a more biologically precise subtype of OCD: the early-onset subtype. We also briefly resume current available recommendations for the clinical management of this specific population.

Migraine varies in its frequency, severity, and impact; treatment should consider these variations and the patient’s needs and goals. Migraine pharmacologic treatment may be acute (abortive) or preventive (prophylactic), and patients often require both. New medication devices are available or in development, including an intracutaneous, microneedle system of zolmitriptan and sumatriptan, and breath-powered powder sumatriptan intranasal treatment. Lasmiditan, a 5-HT1F receptor agonist, is in development for acute treatment, as are small molecule calcitonin gene-related peptide (CGRP) receptor antagonists (Gepants) for acute and preventive treatment. Antibodies to CGRP and its receptor are being developed for migraine prevention. All 4 treatments are effective and have, as of yet, no safety concerns.

Criminal conduct is not always violent, and violence does not always lead to criminal charges. Moreover, crime and violence have multifaceted etiologies. Most violence in society is not attributable to mental illness. Where there is a small relationship between violence and mental illness, the risk of violence increases for individuals with substance use histories. Underlying trauma can also play a role. Antisocial attitudes, behaviors, and peer groups further increase the risk that individuals, including those with mental illness, will find themselves at risk of criminal recidivism. Criminal histories among public mental health populations, and mental health and substance use disorders among criminal populations are each higher than general population comparisons. Care within behavioral health settings should therefore target decreased criminal recidivism and decreased violence as part of recovery for those individuals at risk, using trauma-informed approaches and peer supports. Interventions that show promise bring criminal justice and behavioral health systems together, and include police-based diversion, specialty courts, court-based alternatives to incarceration, and coordinated re-entry programs. This article reviews these options along with specific risk management strategies, such as using risk, needs, and responsivity factors as a means of improving overall outcomes for persons with mental illness, while minimizing their risk of further criminalization and victimization.

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.

Despite significant progress in the development of antidepressant therapies, tolerability remains an important factor associated with the selection of appropriate antidepressant treatment. Side effects commonly reported by depressed patients taking antidepressants include weight gain, sexual dysfunction, and gastrointestinal effects. Tolerability issues associated with antidepressants can negatively impact treatment outcomes for patients with major depressive disorder. In addition, a drug's tolerability profile substantially influences a physician's choice of specific antidepressant therapy. Despite the availability of many antidepressants, empirical clinical evidence to guide physicians in making the best choice is limited and not always clear. Thus, it is key for clinicians to understand the short- and long-term outcomes and side effect profiles of the available antidepressants.

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.

Substance use disorder is the most frequent and clinically significant comorbidity among schizophrenia patients today. All schizophrenia patients should be assessed and monitored carefully regarding their substance use. Those with any regular use of alcohol or other drugs should be considered at risk for multiple adverse effects. As therapies for co-occurring substance use disorders have evolved over the past 20 years, medication management, psychosocial interventions, and rehabilitation models have increasingly emphasized the integration of mental health and substance abuse treatments, attention to group and residential interventions, matching interventions to stage of treatment, comprehensiveness, and long-term perspectives on recovery. Clinicians should understand the implications of each of these principles of care.

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.