With more long-acting injectable (LAI) antipsychotics available for treating schizophrenia, each with variable durations of action (2 weeks to 3 months), it is important to have clear management strategies for patients developing breakthrough psychotic symptoms or experiencing symptomatic worsening on LAIs. However, no treatment guidelines or clinical practice pathways exist; health-care providers must rely on their own clinical judgment to manage these patients. This article provides practical recommendations—based on a framework of clinical, pharmacokinetic, and dosing considerations—to guide clinicians’ decisions regarding management of breakthrough psychotic symptoms. Management options include ruling out/addressing medical illness or substance abuse/misuse as a contributing factor, addressing stressors, optimizing nonpharmacologic treatments, treating medical/psychiatric comorbidities, ensuring proper LAI administration technique, addressing missed LAI doses or lack of steady-state attainment, and increasing LAI dose directly or indirectly by shortening the injection interval (off-label). If these strategies do not work sufficiently with frequent monitoring, the LAI could be supplemented with a low dose of the corresponding oral formulation for fast symptom control (off-label). However, caution should be exercised with this strategy, because data on the safety of concomitant use of LAI and oral antipsychotics (OAPs) are limited, especially over extended periods. If symptoms abate, therapy optimization could be continued and slow discontinuation of the OAP could be considered. For persistent/worsening symptoms, the OAP should be increased to optimum effective dose while intensifying the initial steps used before it was added. If this fails, switching the OAP or LAI could be considered. We believe that these strategies will help clinicians manage breakthrough psychotic symptoms during LAI treatment and improve overall outcomes among those who can benefit from LAIs.

Somnambulism, a previously unreported side effect of quetiapine, is described in two cases. Both cases involved individuals who had no prior or family history of somnambulism and had attention-deficit/hyperactivity disorder. The possible significance of this will also be discussed. Somnambulism is a common parasomnia that reflects an impairment in the normal mechanisms of arousal from sleep in which motor behaviors are activated without full consciousness. Motor behaviors are initiated during deep non-rapid eye movement or slow-wave sleep (stages 3-4), and may be limited to relatively simple manifestations, such as sitting up, fumbling with objects or bedclothes, or mumbling.

Long-acting injectable (LAI) antipsychotics can have considerable advantages over oral medications for the management of patients with schizophrenia. Despite the high prevalence of treatment nonadherence with oral pharmacotherapy, LAI antipsychotics are significantly underutilized in this patient population. The availability of newer LAI antipsychotic preparations combined with a resurgent interest in the use of typical antipsychotics has rekindled awareness of the value of LAI medications. This article is intended to provide a visual understanding of the various kinetic profiles of LAI antipsychotics to facilitate initiation and greater use of these agents.

Despite its heterogeneous symptomatology, obsessive-compulsive disorder (OCD) is currently conceptualized as a unitary diagnostic entity. Recent factor-analytic studies have identified several OCD symptom dimensions that are associated with different demographic variables, comorbidity, patterns of genetic transmission, and treatment response. Functional abnormalities in neural systems important for emotion perception, including the orbitofrontal cortex, lateral prefrontal cortex, anterior cingulate gyrus, and limbic regions, have been reported in OCD. In this review, we discuss the extent to which neurobiological markers may distinguish these different symptom dimensions and whether specific symptom dimensions, such as contamination/washing, are associated with abnormalities in emotion and, in particular, disgust, perception in OCD. Also discussed are findings that indicate that anxiety can be induced in healthy volunteers in response to OCD symptom-related material, and that associated increases in activity within neural systems important for emotion perception occur to washing- and hoarding-related material in particular in these subjects. Further examination of neural responses during provocation of different symptom dimensions in OCD patients will help determine the extent to which specific abnormalities in neural systems underlying emotion perception are associated with different symptom dimensions and predict treatment response in OCD.

Depression is a common psychiatric condition characterized by affective, cognitive, psychomotor, and neurovegetative symptoms that interfere with a person's ability to work, study, deal with interpersonal relationships, and enjoy once-pleasurable activities. After the serendipitous discovery of the first antidepressants, for years the only pharmacodynamic mechanisms explored in the search of novel antidepressants were those related to the 3 main monoamines: serotonin, norepinephrine, and dopamine. New-generation monoaminergic antidepressants, such as selective-serotonin and dual-acting serotonin/norepinephrine reuptake inhibitors, improved treatment and quality of life of depressed patients. Nevertheless, there are still important clinical limitations: the long latency of onset of the antidepressant action; side effects, which can lead to early discontinuation; low rate of response; and high rate of relapse/recurrence. Therefore, in the last several years, the focus of research has moved from monoamines toward other molecular mechanisms, including glutamatergic (Glu) neurotransmission. This review provides a comprehensive overview of the current knowledge on the Glu system and on its relationships with mood disorders. Up to now, N-methyl-D-aspartate (NMDA) receptor antagonists, in particular ketamine, provided the most promising results in preclinical studies and produced a consistent and rapid, although transient, antidepressant effect with a good tolerability profile in humans. Although data are encouraging, more double-blind, randomized, placebo-controlled trials are needed to clarify the real potentiality of ketamine, and of the other Glu modulators, in the treatment of unipolar and bipolar depression.

This systematic review aimed to examine whether neurobiological methods, or other methods independent of clinical judgment, have been investigated to assist decision making in forensic mental health services and, if so, whether this may be a useful strategy for predicting outcomes. OVID-Medline, Embase, and PsychInfo (inception–January 2015) were searched, limiting to English and human studies, using terms relating to “predict,” “outcome,” “psychiatry,” and “forensic” to identify primary research articles reporting on predictors of outcome in forensic mental health services not reliant on clinical judgment/self-report. Fifty studies investigating demographic, neuropsychological/neurophysiological, and biological predictors were identified, reporting on 3 broad outcomes: (i) inpatient violence, (ii) length of stay, (iii) reoffending. Factors associated positively, negatively, and showing no relationship with each outcome were extracted and compiled across studies. Of various demographic predictors examined, the most consistent associations were between previous psychiatric admissions and inpatient violence; a more “severe” offense and a longer length of stay; and young age and reoffending. Poor performance on tests of cognitive control and social cognition predicted inpatient violence while a neurophysiological measure of impulsivity showed utility predicting reoffending. Serum cholesterol and creatine kinase emerged as biological factors with potential to predict future inpatient violence. Research in this field is in its infancy, but investigations conducted to date indicate that using objective markers is a promising strategy to predict clinically significant outcomes.

Depersonalization disorder is a poorly understood and treatment-resistant condition. This report describes a patient with depersonalization disorder who underwent six sessions of repetitive transcranial magnetic stimulation on the left dorsolateral prefrontal cortex. Repetitive transcranial magnetic stimulation produced a 28% reduction on depersonalization scores.

Accurate identification of individuals in the earliest symptomatic stages of psychosis offers new hope for developing more effective treatment strategies. Recently, research clinics have been set up to identify and possibly treat individuals who are seen as being at ultra-high risk of developing a psychotic disorder. This article reviews and describes measures that are currently being used and further developed in order to determine both the diagnostic criteria for the prodromal state and the severity of these putatively prodromal symptoms.

Oxytocin and vasopressin are highly conserved neuropeptides that play a key role in social attachment and affiliation, including parental care and pair-bonding. Oxytocin attenuates neural responses to aversive pictures and has been associated with reduced coupling of amygdala to brainstem regions involved in the fear response. Differential activation of the amygdala has been found to be associated with different genetic variants of the vasopressin receptor. There is growing evidence that oxytocin and vasopressin receptor variants are associated with individual differences in prosocial behavior. It is humbling that differences in complex human behaviors may be partially explicable on the basis of relatively simple neuropeptide systems. Nevertheless, such findings potentially allow for targeted interventions for a range of psychiatric disorders in which such systems play a role.

Computer-based measures to evaluate cognition have been used with growing frequency in recent years. These batteries are shown to be useful for identifying mild cognitive impairment (MCI) and dementia. There are few requirements to administer these tests. All that is typically needed is a computer, a response pad for patients to input their answers, and an examiner. In many cases, the examiner does not need to be a trained neuropsychologist. These computer-based assessments should yield a score report detailing the patient’s cognitive profile.

An important advantage of computerized assessments over standard paper-and-pencil testing is that they can provide precise measurement at the millisecond level. This can be a more sensitive measure of cognitive impairment, especially in high-functioning older adults and in patients with milder levels of cognitive deficit. Computer tests also have a shorter assessment time. Many batteries take <1 hour to administer, whereas many standard neuropsychological batteries require >4 hours to complete. The presentation of items in some batteries can be adapted to patients’ performance levels to avoid floor effects (the test restricts how low a patients’ scores can be) and ceiling effects (the test restricts how high scores can be). Computer tests have increased standardization; they are administered the same way every time. Scoring is automatic, meaning the results are available immediately and human scoring error is reduced. Examiner effects are reduced, which is an important advantage because clinicians may differ in how they administer standard tests, which may impact patients’ responses. In addition, the batteries are easily transported, and multiple tasks can be made available on a single computer.

In spite of their prevalence and persistence, why are behavioral and psychological symptoms of dementia difficult for clinicians to assess and manage? This paper provides an overview of the methodological challenges encountered in measuring behavioral disturbances of dementia. Specifically, conceptual constructs of behavioral and psychological symptoms of dementia, the strengths and weaknesses of the currently existing rating instruments, analytic methodologies, and the utility of technological devices are outlined in the service of formulating future directions in behavioral and psychological symptoms of dementia assessment research.

Background: Exposure-based therapy for anxiety disorders is believed to operate on the basis of fear extinction. Studies have shown acute administration of D-cycloserine (DCS) enhances fear extinction in animals and facilitates exposure therapy in humans, but the neural mechanisms are not completely understood. To date, no study has examined neural effects of acute DCS in anxiety-disordered populations.

Methods: Two hours prior to functional magnetic resonance imaging scanning, 23 spider-phobic and 23 non-phobic participants were randomized to receive DCS 100 mg or placebo. During scanning, participants viewed spider, butterfly, and Gaussian-blurred baseline images in a block-design paradigm. Diagnostic and treatment groups were compared regarding differential activations to spider versus butterfly stimuli.

Results: In the phobic group, DCS enhanced prefrontal (PFC), dorsal anterior cingulate (ACC), and insula activations. For controls, DCS enhanced ventral ACC and caudate activations. There was a positive correlation between lateral PFC and amygdala activation for the placebo-phobic group. Reported distress during symptom provocation was correlated with amygdala activation in the placebo-phobic group and orbitofrontal cortex activation in the DCS-phobic group.

Conclusions: Results suggest that during initial phobic symptom provocation DCS enhances activation in regions involved in cognitive control and interoceptive integration, including the PFC, ACC, and insular cortices for phobic participants.