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.

Vortioxetine is an antidepressant with multiple pharmacologic modes of action at targets where serotonin neurons connect with other neurons. These actions modify the release of both glutamate and GABA (gamma amino butyric acid) within various brain circuits.

Akathisia is one of the most vexing problems in neuropsychiatry. Although it is one of the most common side effects of antipsychotic medications, it is often difficult to describe by patients, and is difficult to diagnose and treat by practitioners. Akathisia is usually grouped with extrapyramidal movement disorders (ie, movement disorders that originate outside the pyramidal or corticospinal tracts and generally involve the basal ganglia). Yet, it can present as a purely subjective clinical complaint, without overt movement abnormalities. It has been subtyped into acute, subacute, chronic, tardive, withdrawal-related, and “pseudo” forms, although the distinction between many of these is unclear. It is therefore not surprising that akathisia is generally either underdiagnosed or misdiagnosed, which is a serious problem because it can lead to such adverse outcomes as poor adherence to medications, exacerbation of psychiatric symptoms, and, in some cases, aggression, violence, and suicide. In this article, we will attempt to address some of the confusion surrounding the condition, its relationship to other disorders, and differential diagnosis, as well as treatment alternatives.

Impulsive violence may be the behavioral consequence of inefficient information processing within specific neuronal networks. Analogous to the hypothetical pathophysiology of addiction, maladaptations within reward pathways may shift goal-directed behaviors to impulsive reactions and then to compulsive habits, in order to create impulsive violence.

Vortioxetine is an antidepressant with multiple pharmacologic modes of action at targets where serotonin neurons connect with other neurons. 5HT3 receptor antagonism is one of these actions, and this leads to increased release of norepinephrine (NE), acetylcholine (ACh), and serotonin (5HT) within various brain circuits.

Vortioxetine is an antidepressant with multiple pharmacologic modes of action that enhance release of dopamine, norepinephrine, acetylcholine, and histamine.

Flibanserin is a novel multifunctional serotonin agonist and antagonist (MSAA) that improves sexual functioning in premenopausal women who suffer from reduced sexual interest and desire.

Treating to target in chronic diseases [e.g. Major Depressive Disorder (MDD)] fosters precision, consistency, and appropriateness of treatment selection and sequencing. Therapeutic target definitions/endpoints in MDD should satisfy patient-, provider-, and societal expectations. Functional recovery in depression and return to both physical and mental health are the overarching therapeutic objectives. Treating to target in MDD implies multidimensional symptomatic remission, with a particular emphasis on cognitive function and aspects of positive mental health. Several atypical antipsychotic agents (i.e. brexpiprazole, aripiprazole, quetiapine) are FDA-approved as augmentation agents in MDD. Vortioxetine, duloxetine, and psychostimulants have evidence of independent, direct, and robust effects on cognitive function in MDD. Vortioxetine is the only agent that demonstrates efficacy across multiple cognitive domains in MDD associated with functional recovery. Measurement-based care, health information technology/systems, and integrated care models (e.g. medical homes) provide requisite tools and health environments for optimal health outcomes in MDD. Achieving remission in MDD does not equate to health. Return to positive mental health as well as full functioning provide the impetus to pivot away from traditional provider-defined outcomes toward an inclusive perspective involving patient- and society-defined outcomes (i.e. optimization of human capital). As in other chronic diseases, treating to target (e.g. cognitive function) further increases the probability of achieving optimal health outcomes.

Early-life adversity is a well-established risk factor for the development of depression later in life. Here we discuss the relationship between early-life adversity and depression, focusing specifically on effects of early-life caregiver deprivation on alterations in the neural and behavioral substrates of reward-processing. We also examine vulnerability to depression within the context of sensitive periods of neural development and the timing of adverse exposure. We further review the development of the ventral striatum, a limbic structure implicated in reward processing, and its role in depressive outcomes following early-life adversity. Finally, we suggest a potential neurobiological mechanism linking early-life adversity and altered ventral striatal development. Together these findings may help provide further insight into the role of reward circuitry dysfunction in psychopathological outcomes in both clinical and developmental populations.

In addition to the well-known cognitive impairment following traumatic brain injury (TBI), neuropsychiatric sequelae are often reported as well. Although not the most common neuropsychiatric consequence of TBI, obsessive-compulsive disorder (OCD) has been associated with TBI. However, diagnosing new onset OCD secondary to TBI is complicated by the potential for cognitive impairment secondary to TBI masquerading as OCD. In particular, memory difficulties and executive dysfunction may be confused as representing obsessions and compulsions. Research in this area, which could guide clinical practice, remains limited. In addition to using Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-V) criteria, neuropsychological testing and collateral interviews may help clinicians when considering differential diagnoses in this complex area of neuropsychiatry.

This narrative review provides an overview of the epidemiology of binge eating disorder (BED), highlighting the medical history of this disorder and its entry as an independent condition in the Feeding and Eating Disorders section of the recently published Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition. Estimates of prevalence are provided, as well as recognition that the female to male ratio is lower in BED than in other eating disorders. Evidence is also provided of the most common comorbidities of BED, including mood and anxiety disorders and a range of addiction disorders. In addition, discussion of the viewpoint that BED itself may be an addiction — at least in severe cases — is presented. Although the genetic study of BED is still in its infancy, current research is reviewed with a focus on certain neurotransmitter genes that regulate brain reward mechanisms. To date, a focal point of this research has been on the dopamine and the μ-opioid receptor genes. Preliminary evidence suggests that a predisposing risk factor for BED may be a heightened sensitivity to reward, which could manifest as a strong dopamine signal in the brain’s striatal region. Caution is encouraged, however, in the interpretation of current findings, since samples are relatively small in much of the research. To date, no genome-wide association studies have focused exclusively on BED.

Many forensic psychiatric settings serve unique populations who have, in addition to traditional psychiatric symptoms, diverse legal and criminogenic needs. A lack of clear treatment standards that address all aspects of forensic care can lead to inefficient or inappropriate interventions and contribute to institutional violence.

Cognitive impairment in schizophrenia is present in almost all persons with the disorder and can be a substantial obstacle to efforts in the recovery process. In clinical research, cognition is assessed through neuropsychological testing as well as by different types of structured instruments focusing on function. Although nonpharmacological interventions such as cognitive remediation have been therapeutic, particularly in combination with vocational rehabilitation and supported employment, these modalities are not always easy to access. Pharmacological interventions are in development and have principally focused on the dopamine, glutamate, and acetylcholine neurotransmitter systems, aiming to target the dorsolateral prefrontal cortex and its interactions with other brain regions.

Anxiety and obsessive compulsive disorders are among the earliest occurring psychopathology and may derive from atypical maturation of neural networks for error processing. Psychological models have alternately suggested that over-detection of errors, excessive caring about errors, or failure of errors to elicit regulatory control could associate with the expression of anxiety. In this review article, the potential relevance of error processing for anxiety and obsessive compulsive disorders is described in the context of neurophysiological and functional magnetic resonance imaging (fMRI) research demonstrating altered brain response to errors in pediatric and adult patients. Finally, hypotheses about developmentally sensitive mechanisms of anxiety and obsessive compulsive disorders are drawn from the extant literature, and avenues for clinical translation are discussed.