Anxiety disorders are among the most prevalent psychiatric disorders in the general population, found nearly twice as often in women, and estimated to affect 26.9 million individuals in the United States alone. Anxiety disorders are associated with considerable chronicity, morbidity, and disability. Treatment of anxiety disorders includes pharmacologic and nonpharmacologic approaches. The first-line pharmacologic treatments currently include the use of serotonin reuptake inhibitors and selective serotonin reuptake inhibitors. However, despite the general success of the available treatments, no single anxiolytic appears to be effective for all patients suffering from anxiety. Low recovery rates have been reported in all anxiety disorders, underscoring the need for optimizing treatment for these disabling disorders. In recent years, there is increasing interest in the use of atypical neuroleptics in the treatment of anxiety disorders patients. This article discusses the emerging data on the use of these agents in the treatment of anxiety with a focus on treatment-refractory patients and on the implications for the treatment of women suffering from anxiety disorders.

Patients with schizophrenia have increased mortality due to higher rates of suicide. However, natural causes of death, such as cardiovascular disease, also contribute greatly to excess mortality. Significant sources of cardiovascular risk in this patient population include high smoking prevalence, inactive lifestyles, poor dietary habits, and the metabolic effects of atypical antipsychotics. These sources of risk interact with underrecognition of common medical conditions by mental health providers, limited access to primary care services, and undertreatment of health conditions in the general medical setting. For many patient with severe mental illness, the mental health setting represents the sole source of medical care, making the psychiatrist the de facto primary care provider for these individuals. With the recent focus on medical consequences of antipsychotic treatment, psychiatrist have an obligation to minimize these adverse effects by choosing antipsychotics with lower risk for metabolic side effects, and becoming familiar with the screening and management of common medical conditions.

Management strategies for treatment-resistant depression and anxiety disorders have evolved over the last decade. Our understanding of the factors that impair recovery from an episode of major depression has increased, leading to the development of more precise diagnostic methodology that highlight the presence of comorbid conditions. New medications, creative uses of existing medications, increased empirical data about augmentation strategies, and the development of innovative nonpharmacologic interventions are responsible for a marked expansion in treatment options. Traditionally, augmentations with lithium, thyroid hormones, or electroconvulsive therapy have demonstrated effectiveness in some patients with treatment-resistant mood disorders. Among the promising treatments in both depression and anxiety is augmentation using low-dose antipsychotics medications, combining antidepressants of different classes, and the addition of psychotherapy. Nonpharmacologic interventions that may have potential include transcranial magnetic stimulation, deep-brain stimulation, and vagus-nerve stimulation. This article provides a brief review of the available data summarizing existing and new treatment strategies in depression and anxiety disorders.

A major challenge in the management of Alzheimer's disease (AD) is accurate diagnosis of the condition. Aging itself is associated with cognitive change, and physicians must first distinguish between age-associated complaints and true memory impairment as in AD before optimal management can begin. This article reviews tools used to assess and diagnose AD patients in both the primary care and clinical trial setting. AD assessment instruments commonly used in research may be too cumbersome for use in primary care. Tools specifically designed to meet the needs of busy practitioners that can accurately assess function, cognition, and global change will be reviewed. The issues of cognitive screening in old age and age-associated memory impairment will be discussed. Similarly, the pitfalls and advantages of routine cognitive screening in daily practice will be addressed.

Individuals with mental illness and addiction comprise at least half of the patients in most mental health treatment systems. This combination results in increased risk for frequent psychiatric relapses, poor medication compliance, violence, suicide, legal problems, and high utilization of the emergency room or inpatient services. Traditional mental health and addiction treatments have not adequately addressed these co-occurring disorders due to clinical interventions, programs, and system flaws that have not addressed the individual's needs. Integrated treatment requires both an understanding of mental illness and addiction and the means to integrate and modify the traditional treatment approaches in both the mental health and addiction treatment fields. There is strong evidence to support the efficacy and effectiveness of integrated treatment in this population. All mental health clinicians should become experienced and skilled in the core psychotherapy approaches to treating substance use disorders, including motivational enhancement therapy, relapse prevention (cognitive-behavioral therapy), and 12-step facilitation. In addition, integrated treatment includes integrating medications for both addiction and mental illness with the behavioral therapies and other psychosocial interventions. This article reviews the clinical intervention, program, and system components of integrated treatment and specific clinical interventions for this population.

Combination treatments, especially combinations of antipsychotics, are used frequently for schizophrenia, despite a paucity of evidence regarding their safety and efficacy. Because the literature basis is weak and expert recommendations are largely lacking, providers should be vigilant in documenting improved outcomes for patients thought to benefit from combination treatments. Target symptoms that have been studied include psychosis, cognitive deficits, and negative symptoms. The strongest evidence is for augmentation of clozapine with another antipsychotic or with electroconvulsive therapy for persistent positive symptoms. Combination treatments for cognitive deficits and negative symptoms are being actively investigated, but current evidence is insufficient to recommend available agents for these components of schizophrenia. It is important that appropriate monotherapies be given adequate trials before resorting to combination therapies.

Objective: Few studies have used a combination of objective and self-report measures to examine neuropsychological and behavioral functioning in parents of children with attention-deficit/hyperactivity disorder (ADHD). This study examined attention and inhibitory control in the parents of preschool children who were rated as “at risk” for developing ADHD as compared with parents of controls.

Methods:Preschool children (N=53) were divided into at risk for ADHD and control groups based on parent and teacher ratings of Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition ADHD symptoms. One parent of each child was administered an identical pairs Continuous Performance Test (CPTIP), a Go/No-Go task, and the Brown Attention-Deficit Disorder Scale for Adults.

Results: Parents of preschoolers at risk for ADHD showed a pattern of responding on measures of vigilance characterized by slower reaction times and increased commission errors as compared with parents of controls. There were no significant group differences on self-report measures on the Brown Attention-Deficit Disorder Scale for Adults.

Conclusion: Parents of preschoolers at risk for ADHD appear to exhibit cognitive processing deficits that may not be evident using self-report measures. Further research is needed to more clearly identify the specific nature of these neuropsychological deficits and to determine whether they have a negative impact on their children.

In treating schizophrenia there has been a shift in focus, with more attention being paid to early intervention based on the notion that effective treatment at this point can improve outcome. Most of this work has centred on pharmacotherapeutic interventions during the first psychotic break. More recently, attention has turned to the potential value of intervening even earlier, that is during the so-called “prodrome” that has been identified as predating the first psychotic break by as much as 4–5 years. We now have a limited number of published reports addressing this topic and these are reviewed here.

The goal of psychopharmacohgic research in autism is to provide guidance to clinicians and families on the risks and benefits of specific interventions. Careful subject selection and subject characterization in clinical trials are necessary for replication, to inform clinicians about the sample, and to elucidate the type of patients who might benefit from, the treatment. At minimum, subject characterization includes demographic information, diagnosis (autism, Åsperger's syndrome, or pervasive developmental disorder-not otherwise specified), intellectual functioning, adaptive functioning, symptom severity, general behavioral profile, health status, pertinent clinical laboratory measures, height, weight, current treatments, and educational placements. Subject selection, sample size, and choice of the primary outcome measure are closely interrelated and linked to the study hypothesis. The magnitude of expected improvement on the primary outcome measure, which can be expressed by effect size, has direct implications for sample size. Large sample sizes are required to detect small effect sizes. To facilitate interpretation of study results, research reports should provide descriptive characteristics of the sample as well as the mean change and standard deviation on the primary outcome measure data to permit calculation of the effect size.

The consequences of epilepsy can be quite severe and include shortened lifespan, excessive bodily injury, neuropsychological and psychiatric impairment, and social disability. There is evidence that seizures cause brain injury, including neuronal death and physiological dysfunction. Mortality rates are 4—7 times higher in people with medically refractory seizures, and injury rates are substantial, ranging from one per 20 person-years to as much as one per 3 person-years. Quality of life is impaired in epilepsy, and relates to seizure control. Psychosocial disabilities, including lower social interaction with reduced marriage rates and reduced employment levels, are more common in people with refractory seizures. Complete seizure control is desirable, since seizures potentially constitute a serious threat to health and well-being. Therefore, satisfactory seizure control should be defined as having no seizures. Treatment should be directed to preventing seizures whenever possible and achieving control early in the course of illness. The risks of uncontrolled seizures outweigh the risks of aggressive medical or surgical therapy.

Despite the large number of depressed patients who do not respond to first-line antidepressants, the evidence base of alternate strategies is quite thin. In this article, a simple 5-stage system for categorizing treatment-resistant depression (TRD) is described and the evidence pertaining to the major strategies currently utilized is summarized using four grades, ranging from D (case reports only) to A (multiple positive placebo-controlled trials). It is concluded that the level of evidence supporting many of the contemporary strategies used for TRD (eg, combinations of antidepressants and augmentation with medications such as pindolol, buspirone, or modafinil) is scanty at best. Even the fundamental question concerning “to augment or to switch” is not answerable with available data. It is noted that the best-documented treatments (ie, lithium augmentation, switching to a monoamine oxidase inhibitor, and electroconvulsive therapy) are among the least utilized. This state of affairs will improve with completion of the studies of Systematic Treatment Alternatives to Relieve Depression, a large multicenter study of difficult-to-treat depression funded by the National Institute of Mental Health. There is a need for greater collaboration among academicians and organizations, such as the American Psychiatric Association, the National Institute of Mental Health, and the pharmaceutical industry, to ensure that sufficient research is conducted so that clinician's choices for patients with TRD can be guided by empirical evidence.

A growing body of evidence documents the value of structured psychotherapeutic interventions for the co-management of bipolar disorder in the context of ongoing medication treatment. This article reviews the rationale, elements, and outcomes for those psychosocial treatments for bipolar disorder that have been emmined in randomized trials. The available evidence suggests that interventions delivered in individual, group, or family settings, can provide significant benefit to patients undergoing pharmaco-theraby for bibolar disorder.

Hyperprolactinemia is increasingly prevalent in patients with common psychiatric disorders due to increasing prescriptions of antipsychotics, particularly newer atypical neuroleptics, in these patients. However, measurement of prolactin levels is indicated only in symptomatic patients. When hyperprolactinemia is diagnosed, work-up should include exclusion of other causes of hyperprolactinemia, particularly those that might require treatment. Once such causes have been ruled out, a minority of patients with antipsychotic medication-induced hyperprolactinemia, including those with clinically significant signs and symptoms, will require treatment. When treatment is indicated, specifically when hyperprolactinemia results in amenorrhea in women or testosterone deficiency in men, dopamine agonist therapy is generally not advisable. Hormone-replacement therapy, which involves estrogen/progestogen in women and testosterone in men, can often prevent modification and interruption of successful psychiatric medication regimens.

A review of the literature demonstrates that the incidence of new mental disorders and their prevalence during pregnancy is similar to the 12-month incidence of mental disorders in women during other periods of their lives. The prevalence of severe mood, behavior, and cognitive symptoms during pregnancy is rather high. Severe mental symptoms during pregnancy have been reported to be associated with an increased rate of complications during pregnancy and delivery, preterm deliveries, low birth weight, a higher rate of postpartum depression, and a longer-term impact on the offspring's development. Several pre-pregnancy risk factors to develop dysphoric symptoms have been reported, but their utility for primiparous women with no previous history of mental disorders is unclear. The association of mental symptoms with general symptoms and biological changes during pregnancy is also unclear. Given the short- and long-term impact of dysphoric symptoms and stress during pregnancy on mother and child, efficacious, efficient, and safe prevention and treatment modalities are essential and achievable. Clarification of the nature and phenotyping of mental and general symptoms during pregnancy is an important step for the development of effective interventions.

Substantial evidence suggests that alterations in noradrenergic function contribute to the cognitive impairments of schizophrenia. Activation of post-junctional α2a-adrenergic receptors in the prefrontal cortex by the α2a-selective agonist guanfacine has demonstrated some preliminary benefit in subjects with schizophrenia treated with atypical antipsychotics.α1-drenergic receptor activity may be less important in mediating the cognitive impairments of schizophrenia, β-adrenergic receptors may serve as another potential target for cognitive remediation in schizophrenia. However, the potential increase in memory consolidation in schizophrenia patients produced by β-adrenergic agonists may be outweighed by the impairment in cognitive flexibility and executive functioning produced by α-adrenergic agonists. Finally, norepinephrine reuptake inhibitors, such as atomoxetine, hold promise as potential cognitive enhancers in schizophrenia because of their ability to indirectly but selectively increase extracellular dopamine concentrations in the prefrontal cortex.