Bipolar disorder (BD) is among the most impairing psychiatric disorders affecting children and adolescents, despite our best psychopharmacological and psychotherapeutic treatments. Cognitive remediation, defined as a behavioral intervention designed to improve cognitive functions so as to reduce psychiatric illness, is an emerging brain-based treatment approach that has thus far not been studied in pediatric BD. The present article reviews the basic principles of cognitive remediation, describes what is known about cognitive remediation in psychiatric disorders, and delineates potential brain/behavior alterations implicated in pediatric BD that might be targets for cognitive remediation. Emerging data show that cognitive remediation may be useful in children and adults with schizophrenia, ADHD, and anxiety disorders, and in adults with BD. Potential targets for cognitive remediation in pediatric BD include face processing, response inhibition, frustration, and cognitive flexibility. Further study is warranted to determine if cognitive remediation for these targets, or others, may serve as a novel, brain-based treatment for pediatric BD.

A growing number of common traumatic events involve both physical and emotional injuries. In contrast to previously held beliefs, the rapidly growing body of literature shows quite convincingly that physical injury, over and above exposure to the traumatic event itself, increases rather than decreases the risk for posttraumatic stress disorder (PTSD). A pertinent question becomes how bodily injury contributes to the risk of developing PTSD. In this article, we review contemporary findings regarding the neurobiological and psychological mechanisms by which bodily injury may augment or independently contribute to chronic posttraumatic stress. In addition, we propose three theoretical pathways through which physical injury can increase the risk for PTSD. These pathways are: additive, unique, and recovery impeding. Finally, we highlight unresolved issues pertaining to each one of these pathways and propose directions for future research to address them.

Background: Clinical trials of aripiprazole, a recentl Food and Drug Administration-approved atypical antipsychotic, included elderly patients, but more data are needed on the effects of aripiprazole in this population, especially those with comorbid medical illnesses.

Objective: To assess the response and safety of aripiprazole treatment in elderly patients with phrenia or schizoaffective disorder.

Method: Data was obtained by retrospective review of medical records. Aripiprazole was used to treat 10 elderly hospitalized patients between 62 and 85 years of age who manifested signs of psychosis related to schizophrenia or schizoaffective disorder. All patients had been treated previously with atypical and classic antipsychotics. Response was assessed by clinical observation of patients' behavior and Clinical Global Impression Scale assigned retrospectively.

Results: Seven patients responded to treatment, two did not respond, and one had a partial response. The mean Clinical Global Impression Scale scores improved from 6 (severely ill) at baseline to 2.3 (much improved) at discharge. Treatment was discontinued in the two patients who did not respond. Of the seven patients who responded, four presented with positive symptoms and showed significant improvement while three presented with positive and negative symptoms and both symptoms improved significantly. Four patients had preexisting extrapyramidal symptoms (EPS) and these symptoms decreased in three patients. In addition, two patients were able to discontinue antiparkinson medications. One patient who had severe tardive dyskinesia showed significant improvement in the dyskinetic symptoms. Four patients showed postural hypotension (without clinical symptoms) which resolved over time without treatment. Six patients showed a mean weight loss of 5.2 lbs. No adverse consequences occurred when divalproex sodium, carbamazepine, clonazepam or citalopram were given concurrently.

Conclusion: The reduction of both positive and negative symptoms of schizophrenia and the lack of significant EPS, tardive dyskinesia, sedation, weight gain, anticholinergic effects, and QTc prolongation gives preliminary indication that aripiprazole may be a safe and effective medication for elderly patients with schizophrenia or schizoaffective disorder.

Depressive episodes or symptoms occur frequently in patients with schizophrenia and may have far-reaching consequences. Despite the high prevalence rate and clinical relevance of this comorbidity, knowledge about treatment options is still limited. The aim of this review is to provide an overview of the literature concerning treatment options for depressive episodes or symptoms in schizophrenia. Based on the current evidence, we present a stepwise treatment approach. The first step is to evaluate the current antipsychotic treatment of psychotic symptoms and consider lowering the dosage, since increased blockade of the dopamine D2 receptors may be associated with a worse subjective sense of well-being and dysphoria. A second step is to consider switching antipsychotics, since there are indications that some antipsychotics (including sulpiride, clozapine, olanzapine, aripiprazole, quetiapine, lurasidone, or amisulpride) are slightly more effective in reducing depressive symptoms compared to other antipsychotics or placebo. In the case of a persistent depressive episode, additional therapeutic interventions are indicated. However, the evidence is indecisive regarding the treatment of choice: either starting cognitive-behavioral therapy or adding an antidepressant. A limited number of studies examined the use of antidepressants in depressed patients with schizophrenia showing modest effectiveness. Overall, additional research is needed to determine the most effective treatment approach for patients with schizophrenia and depressive episodes.

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.

The obsessive-compulsive disorders spectrum concept has grown in recent years because of the common clinical features, such as obsessive thinking and compulsive rituals, biological markers, presumed etiology, and treatment response, that these disorders may share with obsessive-compulsive disorder (OCD). This concept has important implications in regard to diagnosis, nosology, neurobiology, and treatment of a wide group of diverse disorders affecting up to 10% of the population. New insights in central nervous system (CNS) mechanisms that drive the repetitive behaviors of the obsessive-compulsive spectrum disorders have heightened interest in the spectrum in researchers, clinicians, and those involved in drug development.

An important approach in neuropsychiatry centers on employing a dimensional classification of psychopathology. Psychiatric phenomena often fall on a continuum. A dimensional approach allows for the classification of patients who fall at the border of classical entities or who are otherwise atypical. Diagnostic categories are considered along a spectrum if there is considerable overlap in symptoms and in etiology, as demonstrated by familial linkage biological markers, and pharmacological dissection. Categorical and dimensional approaches to the OCD spectrum could have significant implications for diagnosis, nosology, neurobiology, and treatment of a wide group of disorders affecting a sizable percentage of the population.

Recent interest has focused on spectrums in movement disorders, affective disorders, schizophrenia, epileptic and impulsive disorders, and obsessive-compulsive disorders (which we will examine here); in addition, there has been interest in the overlap between these spectrums. Viewing disorders in terms of overlapping spectrums provides researchers and clinicians a framework with which to better understand and treat these disorders.

This chart review examined the effects of effort on neuropsychological assessment and test performance patterns among genuine and exaggerating patients, with and without neurological findings, as aids to diagnosing symptom exaggeration. The sample consisted of 561 consecutive patients involved in compensation claims. With a flexible neuropsychological test (NPT) battery, the claims were assessed over 2 days. The sample included 303 patients evaluated for traumatic brain injury, 55 patients with neurological disease, and 203 patients assessed for other conditions (eg, depression or chronic pain). An average of 38 ability measures per patient were used to generate an overall NPT domain score. Composite scores were also computed for symptom validity tests, self-report measures of psychiatric symptoms, and memory complaint inventory. Seven NPT cognitive subdomain scores were multiply regressed onto the symptom validity test composite, accounting for 45% of its total variance. Patients were also assigned to Genuine or Exaggerator groups based on symptom validity test performance. The NPT for Exaggerating patients averaged 1.43 standard deviations below that of Genuine patients, suggesting that NPT scores for most Exaggerating patients are underestimates of their true ability. Factor analysis results differed between these groups. As a result, clinicians might avoid falsely identifying genuine patients as exaggerating by incorporating their self-reports of psychiatric symptoms and memory complaints into the diagnostic process.

Behavioral and psychological symptoms of dementia pose significant challenges in the management of patients with Alzheimer's disease. Neuropsychiatric symptoms are associated with cognitive decline, highly impaired activities of daily living, and frontal lobe pathology. Moreover, behavioral and psychological symptoms can diminish patient quality of life, increase caregiver distress, and accelerate nursing home placement. Although these symptoms are often associated with the later stages of Alzheimer's disease, a high percentage of individuals with mild cognitive impairment or mild Alzheimer's report symptoms as well. This article provides an overview of behavioral and neuropsychiatric symptoms associated with Alzheimer's disease and discusses nonpharmacologic and pharmacologic approaches to the management of such symptoms. For patients with severe behavioral and psychological symptoms of dementia, pychotropic agents may be warranted, whereas approved therapies for Alzheimer's, including cholinesterase inhibitors and the N-methyl-D-aspartate receptor antagonist memantine, may be appropriate in less severe cases.

There is clear overlap in the clinical symptoms of obsessive-compulsive disorder (OCD) and Tourette syndrome (TS). As a result, OCD (with or without tics) and TS (with or without obsessive-compulsive symptoms [OCS]) have been conceptualized to form a disorder spectrum—an overlapping set of phenotypes reflecting presumed commonality at the level of the underlying genetics and neuropathology. We identified the characteristics of a research sample of patients with OCD or TS, based on information obtained in semistructured clinical interviews, to examine the similarities and differences in the clinical symptoms across this spectrum. This sample conformed to known age-of-onset and sex distribution patterns for OCD and TS. Previously reported patterns of predominant aggressive and sexual obsessions and touching compulsions were observed in subjects with tic-related OCD, compared with non—tic-related OCD (ie, OCD alone). The majority of patients with tic-related OCD experienced horrifically violent obsessions that were less common in OCD alone and much less common in TS. Nonetheless, symptomatic and functional impairment in TS subjects was clearly related to the intensity of their OCS. The specific obsessions and compulsions associated with clinical impairment in TS differed from those associated with impairment in OCD. These results suggest that, despite the many overlapping dimensions of these disorders, the symptoms and associated impairment in “pure” OCD, tic-related OCD, and TS do not form a simple continuous spectrum.

Current measures for major depressive disorder focus primarily on the assessment of depressive symptoms, while often omitting other common features. However, the presence of comorbid features in the anxiety spectrum influences outcome and may effect treatment. More comprehensive measures of depression are needed that include the assessment of symptoms in the anxiety–depression spectrum. This study examines the reliability and validity of the Symptoms of Depression Questionnaire (SDQ), which assesses irritability, anger attacks, and anxiety symptoms together with the commonly considered symptoms of depression. Analysis of the factor structure of the SDQ identified 5 subscales, including one in the anxiety–depression spectrum, with adequate internal consistency and concurrent validity. The SDQ may be a valuable new tool to better characterize depression and identify and administer more targeted interventions.

Attention-deficit/hyperactivity disorder (ADHD) is a developmental disorder which effects an estimated 3% to 5% of children. Despite estimates that ADHD persists in 30% to 70% of adults having had the disorder in childhood, ADHD in adulthood remains controversial. This report summarizes current thinking in the diagnosis and etiology of adult ADHD. Most theories posit that ADHD is related to anomalies in frontal lobe function and dopaminergic transmission. However, there is debate as to whether ADHD is a unitary disorder with different manifestations, a syndrome, or multiple disorders. The Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, classifies ADHD into inattention, hyperactivity-impulsivity, and combined subtypes. Although problems with cognition are core ADHD symptoms, self reporting has not been a reliable predictor of neuropsychological test performance. Nevertheless, we suggest that a performance-based diagnosis, including empirically derived, age-sensitive neuropsychological tests, provides the best hope of dissociating ADHD from psychiatric disorders with similar symptoms. We also describe the promise of new neuroimaging technologies, such as functional magnetic resonance imaging, in elucidating the pathophysiology of ADHD and similar psychiatric disorders.

Twenty years have passed from the International Classification of Diseases, Tenth Revision (ICD-10) to the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) and, in the meanwhile, a lot of research data about eating disorders has been published. This article reviews the main modifications to the classification of eating disorders reported in the “Feeding and Eating Disorders” chapter of the DSM-5, and compares them with the ICD-10 diagnostic guidelines. Particularly, we will show that DSM-5 criteria widened the diagnoses of anorexia and bulimia nervosa to less severe forms (so decreasing the frequency of Eating Disorders, Not Otherwise Specified (EDNOS) diagnoses), introduced the new category of Binge Eating Disorder, and incorporated several feeding disorders that were first diagnosed in infancy, childhood, or adolescence. On the whole, the DSM-5 revision should allow the clinician to make more reliable and timely diagnoses for eating disorders.

While impairments in cognitive emotional processing are key to the experience of mood disorders, little is understood of their shared and distinct features across major depressive disorder (MDD) and bipolar disorder (BD). In this review, we discuss the similarities and differences in abnormal emotional processing associated with mood disorders across the cognitive domains of perception, attention, memory, and reward processing, with a particular focus on how these impairments relate to the clinical profile of the disorders. We consider behavioral and neuroimaging evidence, especially that of the growing consensus surrounding mood-congruent biases in cognition, in combination with state- and trait-related characteristics in an attempt to provide a more comprehensive and translational overview of mood disorders. Special consideration is given to the shared phenomenon of mood instability and its role as a potential transdiagnostic marker across the prodrome and maintenance of mood disorders.

Intervention in the progression of schizophrenia is an effort not just to deter psychosis but also to protect the brain from physiologic deterioration. Neurodegeneration is believed to result from neurochemical dysregulation during the onset of schizophrenia. Deterioration accrued over recurring psychotic episodes causes cumulative loss of cell processes, loss of gray matter volume, and apoptosis. Neurodegeneration ultimately results in persistent symptomology and functional impairment. Functional decline occurs early in the course of schizophrenia, and the symptoms that emerge during the prodromal stage may derail the normal adolescent neurodevelopment. Both first-episode psychosis and the prodrome may be opportunities to forestall neurodegeneration. Unfortunately, people with schizophrenia often experience a long duration of untreated psychosis. Treatment of first-episode psychosis with antipsychotic agents shows robust response. However, early-stage patients have very high rates of medication noncompliance. Treatment in the prodrome may offer the best chance to delay the onset of illness, mitigate its severity after onset, or even prevent onset of symptoms entirely. Nonpharmacologic treatments during the prodrome, such as education, treatment for substance use, and cognitive-behavioral therapy, are low-risk interventions that are potentially beneficial. Pharmacologic interventions during the prodrome are also effective in delaying onset of illness, but carry the risk of adversely affecting patients who are false positives for prodromal schizophrenia.

In this Expert Roundtable Supplement, Jeffrey A. Lieberman, MD, provides an overview of the neurobiological basis of neurodegeneration and the concept of neuroprotection. Next, Peter F. Buckley, MD, reviews the importance of first-episode psychosis, including duration of untreated illness and medication adherence. Finally, Diana O. Perkins, MD, MPH, reviews treatment strategies for prodromal schizophrenia.

Parkinson's disease is predominantly a dopamine deficiency syndrome, which is produced in the brain by the loss of cells located in a small area in the ventral midbrain called the substantia nigra. Complete unilateral dopamine lesions, based on the administration of toxic substances (ie, 6-hydroxy-dopamine in rats and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine in mice and primates) have been extremely useful in testing strategies of replacement. For example, the functional and biochemical impact of the transplanted ventral mesencephalic dopaminergic progenitors has been characterized to a large extent, using the complete lesion model in rats. Over the last decade, however, studies addressing the ability of neurotrophic factors to protect injured dopamine cells prompted researchers to make available partial and progressive lesion models to allow a window of opportunity to interfere the disease progression. Recent findings relating a-synuclein with Parkinson's disease pathology have opened new possibilities to develop alternative models based on the overexpression of this protein using recombinant adeno-associated viral vectors, which is valuable not only for helping to better understand its involvement in the disease process, but also to more closely resemble the neurodegeneration found in Parkinson's disease.