Most antidepressants and other psychotropics in clinical use are available as generic formulations (Table). The availability of lower-priced, generic drugs can benefit patients and third-party payers, but it should not be assumed that all generic drugs are equally beneficial. There are numerous reports in the literature of unexpected and untoward consequences that occur when a generic drug is substituted for the original brand-name drug. A previously stable clinical response may suddenly deteriorate, or the patient may experience new or more severe adverse events (AEs). The United States Food and Drug Administration requires that manufacturers of generic drugs demonstrate that their formulation has pharmacokinetic properties similar (or bioequivalent) to the brand-name drug. Bioequivalency studies are conducted in healthy volunteers, not in patients who would be treated with that drug. Moreover, bioequivalency studies are conducted on a current lot of the branded drug and do not account for variability between lots of the generic formulation. The manufacturer is only required to submit bioequivalency data that support the Abbreviated New Drug Application (ANDA); the FDA does not require disclosure of failed bioequivalence studies. Unlike brand-name drugs, lengthy and costly clinical studies are not required to show that the generic drug is effective and safe.

Although the FDA has taken the position that bioequivalence and therapeutic equivalence are equal, many questions related to the use of generic drugs remain unanswered. The following question-and-answer session is an excerpt of an interview with Pierre Blier, MD, PhD, conducted by Diane Sloan, PharmD, which addresses the issue of generic substitution of psychotropic drugs.

Attention-deficit/hyperactivity disorder (ADHD) is highly co-morbid across the life span. However, co-morbidity is not uniform across time; individual co-morbid conditions tend to occur at different times developmentally, with rates often reflecting lifetime occurrence (Slide 1). In addition to changes in the rates of co-morbidity, the nature of co-morbidity may also differ in late adolescence/adulthood, when co-morbid conditions can be especially impairing (eg, antisocial disorder, substance use disorder [SUD], more severe mood disorders).

Anxiety disorders are highly prevalent, are increasing in incidence, affect individuals early in life, and significantly impact health care and quality of life. As such, they are serious public health problems that deserve attention now and in the future. Over the last 10–20 years, there has been marked improvement in pharmacologic and psychosocial interventions for anxiety. Due to their broad spectrum of efficacy against common comorbidities and lack of association with abuse and dependence, serotonergic and mixed serotonergic noradrenergic antidepressants are first-line therapies for anxiety disorders. Benzodiazepines are still widely used in clinical practice because they are well tolerated and work quickly and effectively. Other medications that are emerging as potentially useful for selected populations with anxiety include atypical neuroleptics and anticonvulsants. Cognitive-behavioral therapy (CBT) is at least as effective as medication for many patients with anxiety disorders and facilitates maintenance of benefit over the long term. Resilience, the capacity to bounce back from adversity, can be reliably measured with a psychometrically valid scale, the Connor-Davidson Resilience Scale. Compared with the general population, individuals with anxiety disorders exhibit decreased resilience. Studies have shown that pharmacologic treatment combined with CBT may increase resilience within 2–3 months. Emerging neurobiologic research indicates that noradrenergic pathways and 5-HT2 transporter efficiency may mediate effects on resiliency.

Recent reviews have questioned whether the serotonin-norepinephrine reuptake inhibitor (SNRI) desvenlafaxine succinate offers any practical clinical advantages over existing SNRIs. The following case is one instance where it appears that this SNRI offers unique safety and benefit. Presented is a case report of a patient with Gilbert's syndrome, longstanding social phobia, and more recent depressive disorder not otherwise specified, who was found to have elevated liver transaminases when prescribed both duloxetine and venlafaxine. The patient subsequently responded to desvenlafaxine but without liver abnormalities. In this patient with Gilbert's Syndrome, desvenlafaxine's lack of metabolism through the cytochrome P450 (CYP) 2D6 pathway may explain the avoidance of these abnormalities and thus suggests a possible therapeutic role for this SNRI in similarly susceptible patients.

Secure settings are not queer because lesbian, gay, bisexual, transgender, queer, questioning, Two Spirit, and asexual (LGBTQ+) people populate them, and neither are LGBTQ+ people inherently criminal because they are found in those spaces. Queer people bear disproportionate health, mental health, and social inequities that have had, historically and currently, the effect to criminalize them. This review discusses effective language and ideologies when working with LGBTQ+ people in secure settings. Major health, mental health, and social inequities are reviewed, along with the applied framework of minority stress. Then, the process of criminalization is diagrammed across the phases of predetainment, being in the system, and through re-entering the community. Finally, multilevel strategies are offered to decriminalize LGBTQ+ people ideologically and in practice.

Evidence-based guidelines for the pharmacologic management of patients with generalized anxiety disorder (GAD) recommend initial treatment with either a selective serotonin reuptake inhibitor (SSRI) or a serotonin-norepinephrine reuptake inhibitor (SNRI). However, response rates to initial treatment with an SSRI or SNRI can be disappointing, and it remains impossible to predict reliably which patients will respond positively or negatively to treatment. Due to the dearth of longitudinal studies of outcome in GAD and the relatively small number of placebo-controlled relapse prevention studies, the optimal duration of treatment after a satisfactory response to acute treatment is still uncertain. Furthermore, there have been few studies on the management of patients who do not respond to initial treatment. Also, there is a clear need for further randomized controlled trials of augmentation treatment in patients who do not respond to SSRI, SNRI, or other initial pharmacologic approaches. Future guidelines will be influenced by emerging data with both established and novel drug treatments, and through better identification of patient groups that are likely to respond preferentially to particular interventions.

Treatment with the newer generation antidepressants is considered generally effective for most patients with major depressive disorder when taken in accordance with treatment guidelines. However, multiple clinical studies have demonstrated that rates of patient adherence to antidepressants are inadequate, specifically with regard to long-term maintenance treatment. Tolerability issues associated with antidepressants can increase the risk for patient nonadherence and result in subsequent relapse of depressive symptoms. Comorbid symptoms of anxiety also influence psychiatrists' choice of antidepressants for patients with depression. Physicians can improve long-term patient outcomes for patients with major depressive disorder by considering the possibility of drug-drug interactions before prescribing a specific antidepressant.

The author reviews both the epidemiology and the genetics of obsessive-compulsive disorder (OCD). A relatively common disorder, OCD has an onset in late adolescence or early adulthood. Its gender distribution is nearly equal, although women are slightly more likely to develop the disorder. Usually chronic, OCD fluctuates depending on factors including the presence of depressed mood or stressful life events. OCD is associated with substantial psychiatric comorbidity, it affects quality of life, and it affects health care utilization. Many questions remain unanswered, such as whether its natural history has changed with the advent of effective therapies, and to what extent patients with OCD are disabled.

There are no adoption studies of OCD, but reports of twins suggest greater monozygotic than dizygotic concordance. Family study results are not entirely consistent, probably because of differences in study methods, but tend to show that OCD is familial. They also show a genetic relationship to subclinical OCD and Tourette's syndrome. Molecular genetic studies are just getting under way. Important issues remain to be answered, including defining the extent of an OCD spectrum of disorders, and determining what constitutes an OCD phenotype.

The author concludes by recommending that further studies on OCD involve samples from the general population rather than clinic- or hospital-based samples, which are inherently biased for severity.

The past 15 years have been exciting for psychiatric researchers interested in the epidemiology and genetics of OCD. Combined with ongoing development of effective pharmacologic and behavioral treatments, new research in these areas has affected how physicians think about OCD, as well as how we clinically manage patients. More work needs to be done, as many important questions about both the epidemiology and genetics of OCD remain unanswered.

Obsessive-compulsive disorder (OCD) is a psychiatric disorder in which the patient suffers from recurrent intrusive ideas, impulses, thoughts (obsessions), and/or patterns of behavior (compulsions) that are ego-alien and produce anxiety if resisted. The ego-dystonic nature of OCD is one of the hallmarks of this disorder. OCD can be a disabling condition because the obsessions and compulsions are time-consuming and interfere with patients' everyday activities and their relationships with friends and family. In severe cases, OCD conflicts even with the simplest tasks of daily living.

Research interest in OCD has been growing steadily in the past decade. A search on MEDLINE reveals an over 300% increase in citations on OCD from 1986 to 1998. These range across the spectrum of research fields, from genetic studies, brain imaging, and neurobiological research examining the underlying pathogenesis of OCD to epidemiological studies evaluating the course of clinical symptoms, comorbidities, and outcomes. Each area represents an important piece in the complex jigsaw puzzle of OCD.

The two main diagnostic systems, the International Classification of Diseases (ICD) and the Diagnostic and Statistical Manual of Mental Disorders (DSM), have undergone a number of revisions since their first editions: whereas the fifth edition of the DSM has been published in 2013, the eleventh revision of the ICD is expected by 2018. Although the process of harmonization between the 2 systems is still a debated topic, the forthcoming revision of the ICD is seemingly converging toward the DSM approach in regard to the reclassification of a number of disorders. Nevertheless, the 2 systems still exhibit considerable differences, partly due to their different purposes, development and revision processes, and target audiences. Furthermore, while alternative and innovative classification approaches are emerging with the aim of integrating the latest findings from neuroscience and genomics, both the DSM and ICD still fail to incorporate core concepts such as the clinical staging of psychiatric disorders and “neuroprogression,” as well as an adequate consideration of endophenotypes.

Despite medical, technological, and humanitarian advances, the criminalization of those with serious mental illness continues. This is not an isolated phenomenon. The benefits of treatment reform and innovation are difficult to maintain or sometimes outright harmful. Across time and geography, the care of those with serious mental illness tends towards maltreatment, be it criminalization or other forms of harm. We present a social history of serious mental illness, along with the idea that the treatment of serious mental illness is a Sisyphean task—perpetually pushing a boulder up a hill, only for it to roll down and start again. The history is provided as a basis for deeper reflection of treatment, and treatment reform, of those with serious mental illnesses.

Neurocognition is one of the strongest predictors of clinical and functional outcomes across the spectrum of psychopathology, yet there remains a dearth of unified neurocognitive nosology and available neurocognition-targeted interventions. Neurocognitive deficits manifest in a transdiagnostic manner, with no psychiatric disorder uniquely affiliated with one specific deficit. In fact, recent research has identified that essentially all investigated disorders are comprised of 3–4 neurocognitive profiles. This within-disorder neurocognitive heterogeneity has hampered the development of novel, neurocognition-targeted interventions, as only a portion of patients with any given disorder possess neurocognitive deficits that would warrant neurocognitive intervention. The development of criteria and terminology to characterize these neurocognitive deficit syndromes would provide clinicians with the opportunity to more systematically identify and treat their patients and provide researchers the opportunity to develop neurocognition-targeted interventions for patients. This perspective will summarize recent work and discuss possible approaches for neurocognition-focused diagnosis and treatment in psychiatry.