The study presented was conducted to analyze the effects of obsessive-compulsive symptoms on patients' quality of life and the costs incurred by patients and society for the treatment of obsessive-compulsive disorder (OCD). To accomplish this, a detailed 410-item questionnaire of psychosocial function and economic cost was sent to every fourth member of the Obsessive Compulsive Foundation. Of the 2,670 members who received the survey, 701 (26.9%) returned it.

Outcome measures included symptomatology, course of illness, impact of illness on psychosocial and other functioning, effects of diagnosis and treatment, and economic consequences. The demographics of this group were similar to those in smaller treatment-seeking clinical samples, but not necessarily to OCD sufferers within the US population as a whole. More than half of the patients reported moderate to severe interference in family relationships, socializing, and ability to study or work, secondary to OCD symptoms. A 10.2-year gap was observed between the onset of symptoms and the first attempt to seek professional help, and a 17.2-year gap was observed between the onset of symptoms and receipt of effective treatment. Specific treatments, such as serotonin reuptake inhibitors and behavior therapy showed greater symptom improvement, and significantly reduced the total annual fees incurred by OCD patients when compared with nonspecific treatments.

Our study results indicate that OCD has a profound effect on psychosocial functioning and quality of life. Large direct costs for OCD, and even larger indirect costs due to lost wages and underemployment were found. Greater awareness of OCD among practitioners may result in earlier diagnosis and more appropriate and cost-effective treatments.

Brexpiprazole is a new therapeutic agent that was recently approved for the treatment of schizophrenia and for the adjunctive treatment of major depressive disorder. Brexpiprazole has features that both overlap and contrast with a related molecule, aripiprazole, and these features are discussed here.

Stimulants are a highly efficacious and safe treatment for attention-deficit/hyperactivity disorder (ADHD), with 75% to 90% of patients responding well if two different stimulants (amphetamine and methylphenidate) are used. Nonetheless, a subset of ADHD patients will either fail to respond to stimulants or have side effects that preclude their use (tics, severe loss of appetite, marked insomnia). For such patients, there are a number of non-stimulant agents that serve as second-line treatments. Tricyclic antidepressants (TCAs) are the most studied of these drugs. They are superior to placebo in the treatment of ADHD and may reduce abnormal movements in patients with ADHD/tic disorder. TCAs often produce side effects of sedation, dry mouth, and constipation. Bupropion is superior to placebo in the treatment of ADHD and has a more favorable side-effect profile than the TCAs. A new selective norepinephrine reuptake inhibitor, atomoxetine, has been shown to be efficacious in the treatment of ADHD and has recently received an approvable letter from the Food and Drug Administration. The α-agonists clonidine and guanfacine have also been used as alternative agents in ADHD, though the controlled data are more limited. A recent controlled clinical trial suggests a combination of methylphenidate and clonidine has advantages in the treatment of comorbid ADHD and tics over either medication alone. Clinical guidelines for each of these agents, as well as their use in combination with stimulants in comorbid conditions, will be discussed.

Transcranial magnetic stimulation (TMS) is unique among the current brain stimulation techniques because it is relatively non-invasive. TMS markedly differs from vagus nerve stimulation, deep brain stimulation and magnetic seizure therapy, all of which require either an implanted prosthesis or general anesthesia, or both. Since its rebirth in its modern form in 1985, TMS has already shown potential usefulness in at least three important domains—as a basic neuroscience research instrument, as a potential clinical diagnostic tool, and as a therapy for several different neuropsychiatric conditions. The TMS scientific literature has now expanded beyond what a single summary article can adequately cover. This review highlights several new developments in combining TMS with functional brain imaging, using TMS as a psychiatric therapy, potentially using TMS to enhance performance, and finally recent advances in the core technology of TMS. TMS' ability to non-invasively and focally stimulate the brain of an awake human is proving to be a most important development for neuroscience in general, and neuropsychiatry in particular.

Introduction: High frequency repetitive transcranial magnetic stimulation (HF-rTMS) of the left dorsolateral prefrontal cortex (DLPFC) might be a promising strategy to treat depression, but not all patients show a positive outcome.

Objective: In this open study, we evaluate whether a favorable HF-rTMS treatment outcome could be predicted by baseline prefrontal brain glucose metabolism (CMRglc), measured by 18fluorodeoxyglucose positron emission tomography (18FDG-PET).

Methods: A sample of 21 antidepressant-free, treatment-resistant depression (TRD) patients of the melancholic subtype received 10 sessions of HF-rTMS delivered on the left DLPFC. Patients underwent a static 18FDG-PET before and after HF-rTMS treatment.

Results: Forty-three percent of the patients showed a reduction of at least 50% on their Hamilton Rating Scale for Depression scores. Higher baseline metabolic activities in the DLPFC and the anterior cingulate cortex (ACC) were associated with better clinical outcome. Successful HF-rTMS treatment was related to metabolic changes in subdivisions of the ACC (Brodmann areas 24 and 32).

Conclusion: This biological impact of HF-rTMS on regional brain CMRglc explains to some extent how HF-rTMS may improve moods in TRD patients. Larger sham-controlled HF-rTMS treatment studies are needed to confirm these results.

Understanding common pharmacologic and clinical “class” actions associated with atypical antipsychotics certainly reveals how these agents are alike, but what about unique differences from one agent to another? Atypical antipsychotics are also a heterogeneous group of agents that have complex pharmacologic entities, acting upon multiple dopamine receptors (D2, D1 (D3, and D4) and multiple serotonin receptors (5-HT2A, 5-HT2C, 5-HT1A, and 5-HT1D, among others). Atypical antipsychotics also interact with noradrenergic (α1- and α2-adrenergic receptor blockade), histaminergic (H1-receptor blockade), and cholinergic (muscarinic M1 blockade) neurotransmitter systems as well as with monoamine (D, 5-HT, and norepinephrine reuptake blockade) transporters. However, no two atypical antipsychotics possess the same portfolio of actions upon all of these additional neurotransmitter systems.

Antidepressants are currently the treatment of choice for major depressive disorder (MDD). Nevertheless, a high percentage of patients do not respond to a first-line antidepressant drug, and combination treatments and augmentation strategies increase the risk of side effects. Moreover, a significant proportion of patients are treatment-resistant. In the last 30 years, a number of studies have sought to establish whether exercise could be regarded as an alternative to antidepressants, but so far no specific analysis has examined the efficacy of exercise as an adjunctive treatment in combination with antidepressants. We carried out a systematic review to evaluate the effectiveness of exercise as an adjunctive treatment with antidepressants on depression.

A search of relevant papers was carried out in PubMed/Medline, Google Scholar, and Scopus with the following keywords: “exercise,” “physical activity,” “physical fitness,” “depressive disorder,” “depression,” “depressive symptoms,” “add-on,” “augmentation,” “adjunction,” and “combined therapy.” Twenty-two full-text articles were retrieved by the search. Among the 13 papers that fulfilled our inclusion criteria, we found methodological weaknesses in the majority. However, the included studies showed a strong effectiveness of exercise combined with antidepressants.

Further analyses and higher quality studies are needed; nevertheless, as we have focused on a particular intervention (exercise in adjunction to antidepressants) that better reflects clinical practice, we can hypothesize that this strategy could be appropriately and safely translated into real-world practice.

Numerous “antihistamines” as well as various psychotropic medications with antihistamine properties are widely utilized to treat insomnia. Over-the-counter sleep aids usually contain an antihistamine and various antidepressants and antipsychotics with antihistamine properties have sedative-hypnotic actions. Although widely used for the treatment of insomnia, many agents that block the histamine H1 receptor are also widely considered to have therapeutic limitations, including the development of next-day carryover sedation, as well as problems with chronic use, such as the development of tolerance to sedative-hypnotic actions and weight gain. Although these clinical actions are classically attributed to blockade of the H1 receptor, recent findings with H1 selective agents and H1 selective dosing of older agents are challenging these notions and suggest that some of the clinical limitations of current H1-blocking agents at their currently utilized doses could be attributable to other properties of these drugs, especially to their simultaneous actions on muscarinic, cholinergic, and adrenergic receptors. Selective H1 antagonism is emerging as a novel approach to the treatment of insomnia, without tolerance, weight gain, or the need for the restrictive prescription scheduling required of other hypnotics.

Introduction: Psychogenic disorders, also referred to as somatoform, conversion, somatization, hysteria, and medically unexplained symptoms, are among the most challenging disorders to diagnose and treat. Psychogenic movement disorders are increasingly encountered in specialized clinics, and represent ~15% of all patients evaluated in the Baylor College of Medicine Movement Disorders Clinic.

Objective: To characterize psychogenic tremor and provide data on prognosis and long-term outcome in a large group of patients with psychogenic tremor followed in a movement disorders clinic.

Methods: Patients evaluated at the Baylor College of Medicine Movement Disorders Clinic in Houston, Texas, between 1990 and 2003 with the diagnosis of psychogenic movement disorder (PMD), who consented to be interviewed, were administered a structured questionnaire designed to assess current motor and psychological function.

Results: psychogenic tremor is the most common PMD, accounting for 4.1 % of all patients evaluated in our clinic. We were able to obtain clinical information on a total of 228 of 517 (44.1%) patients with PMD, followed for a mean of 3.4±2.8 years. Among the 127 patients diagnosed with psychogenic tremor, 92 (72.4%) were female, the mean age at initial evaluation was 43.7±14.1 years, and the mean duration of symptoms was 4.6±7.6 years. The following clinical features were considered to be characteristic of psychogenic tremor: abrupt onset (78.7%), distractibility (72.4%), variable amplitude and frequency (62.2%), intermittent occurrence (35.4%), inconsistent movement (29.9%), and variable direction (17.3%). Assessment of long-term outcome showed that 56.6% of patients reported improvement in their tremor. Factors predictable of a favorable outcome were elimination of stressors and patient's perception of effective treatment by the physician.

Conclusion: This largest longitudinal study of patients with psychogenic tremor provides data on the clinical characteristics and natural history of this most common PMD. The accurate diagnosis of psychogenic tremor is based not only on exclusion of other causes but is also dependent on positive clinical criteria, the presence of which should avoid unnecessary investigation. The prognosis of psychogenic tremor may be improved with appropriate behavioral and pharmacologic management.

There is growing recognition that substance use is associated with the emergence of psychosis.Elements of post-modernity dominate contemporary social contexts and operate as existential background factors that contribute to the emergence of substance-related psychotic phenomena, particularly use of potent and highly rewarding novel psychoactive substances (NPS). About 25% of first-episode psychoses are substance-induced (SIP). DSM-5 SIP diagnosis is based on the assumption that symptoms are transient and disappear after sustained abstinence. This narrowed definition does not consider the issue of persistent SIP. There is a clear need for a new diagnostic framework that provides reliable, unambiguous clinical criteria to differentiate between comorbid conditions (i.e., schizophrenia patients with a substance use disorder) and substance-related psychoses. In the present contribution, we aim to outline a novel and separate clinical entity: substancerelated exogenous psychosis (SREP). Within this diagnostic category, we refer to both transientand persistent psychoses associated with substance use. SREP is conceived as a distinct psychoticdisorder with psychopathological specificities that clearly differentiate it from schizophrenia. We address differences in terms of clinical presentation, epidemiology, etiological models and treatment response. SREP is characterized by altered states of consciousness, persecutory delusions, visual and cenesthetic hallucinations, impulsivity and psychomotor agitation, affectiveand negative symptoms, a pervasive feeling of unreality and intact insight. Delusions are typically secondary to abnormal perception resulting from a characteristic “sensorialization” of the world. Longitudinal studies are warranted to substantiate our hypothesis of a novel diagnostic categoryand support the clinical validity of SREP. This may have important implications in terms of early differential diagnosis and staging (i.e., between comorbid conditions, persistent and transientsubstance-related psychotic states) as well as choice of treatment interventions.

Mental imagery refers to the experience of perception in the absence of external sensory input. Deficits in the ability to generate mental imagery or to distinguish it from actual sensory perception are linked to neurocognitive conditions such as dementia and schizophrenia, respectively. However, the importance of mental imagery to psychiatry extends beyond neurocognitive impairment. Mental imagery has a stronger link to emotion than verbal-linguistic cognition, serving to maintain and amplify emotional states, with downstream impacts on motivation and behavior. As a result, anomalies in the occurrence of emotion-laden mental imagery has transdiagnostic significance for emotion, motivation, and behavioral dysfunction across mental disorders. This review aims to demonstrate the conceptual and clinical significance of mental imagery in psychiatry through examples of mood and anxiety disorders, self-harm and suicidality, and addiction. We contend that focusing on mental imagery assessment in research and clinical practice can increase our understanding of the cognitive basis of psychopathology in mental disorders, with the potential to drive the development of algorithms to aid treatment decision-making and inform transdiagnostic treatment innovation.

Drugs for psychosis and mood that bind dopamine D2 receptors can be classified not only by whether they also block serotonin 2A receptors, but by whether they also bind D3 or D1 receptors.

Depression is an important public health problem affecting about 15% of the general population; however, little is known about possible changes in the brain that might underlie the disorder. Neuroimaging has been a powerful tool to map actual changes in the brain structure of depressed patients that might be directly related to their symptoms of depression. Some imaging studies of brain structure have shown smaller hippocampal volume with the chronicity of depression correlating to a reduction in volume. Although the meaning of these findings is unclear, other studies have shown increased amygdala volume. Studies have found reductions in volume of the frontal cortex, with some studies showing specific reductions in subregions of the frontal cortex, including the orbitofrontal cortex. Findings of an increase in white matter lesions in elderly patients with depression have been replicated and correlated with late-onset depression, as well as impairments in social and cognitive function. These findings point to alterations in a circuit of brain regions hypothesized to include the frontal cortex, hippocampus, amygdala, striatum, and thalamus, that underlie symptoms of depression.

Family psychoeducation programs have emerged as a strongly supported evidence-based practice in the treatment of schizophrenia and bipolar disorder. Over 30 randomized clinical trials demonstrated that psychoeducation programs reduce relapse, improve symptomatic recovery, and enhance psychosocial and family outcomes. Recent work supports family psychoeducation strategies for other disorders, including major depression, obsessive-compulsive disorder, and borderline personality disorder. This review summarizes the research evidence supporting prominent models of family psychoeducation. Professional and peer-led family education programs are also reviewed and differentiated from family psychoeducation. Directions for future research studies to enhance the evidence base and inform treatment recommendations are proposed. Finally, strategies for implementation of family psychoeducation in routine clinical practice are discussed.

Rats treated chronically with the D2/D3, dopamine receptor agonist quinpirole show a pattern of behavior that meets a set of ethologically derived criteria of compulsive behavior in obsessive-compulsive disorder (OCD). Moreover, in both quinpirole-treated rats and OCD patients, the structure of compulsive rituals appear similar in being composed of relatively few motor acts that are organized in a flexible yet recurrent manner. In addition, the development of compulsive behavior in quinpirole-treated rats is attenuated by the OCD pharmacotherapeutic drug clomipramine. These similarities support the validity of quinpirole-treated rats as a psychostimulant-induced animal model of OCD. Considering that the induction of compulsive behavior in the rat model involves chronic hyperstimulation of dopamine receptors, this raises the possibility that dopaminergic mechanisms may play a role in OCD, at least in some subtypes of this disorder.

Depression is increasingly recognized as a highly recurrent and potentially chronic illness that imposes a substantial burden on individuals, families, and society. Evidence indicates that the risks of depressive recurrence, treatment resistance, and chronicity increase as the illness becomes more highly recurrent. Up to 1 year of continuation phase therapy is now recommended for virtually all depressed patients who respond to antidepressants, with a longer course of maintenance phase pharmacotherapy recommended for those who have experienced multiple episodes. Antidepressants, when effective during the acute phase of therapy, reduce the risk of depressive relapse (continuation phase) and recurrence (maintenance phase) by at least 50%. Longer-term antidepressant pharmacotherapy is most effective when the full dose of medication effective during acute-phase treatment is continued. As combined treatment with antidepressants and psychotherapy may improve shorter-term outcomes for patients with more severe recurrent depression, ongoing combined therapy may be indicated, especially for patients at particularly high risk. Approximately 5% to 10% of patients maintained on antidepressants relapse yearly, leading some to implicate tachyphylaxis. However, before attributing relapse or recurrence to diminished responsiveness to antidepressant medication at the neurochemical level, clinicians should ensure that the patient has been adherent to therapy as prescribed and consider other explanations.

Compulsive sexual behavior (CSB) is characterized by inappropriate or excessive sexual behaviors or cognitions that lead to subjective distress or impaired functioning. Both abnormal (paraphilic) and conventional (nonparaphilic) forms of sexual behavior are usually included in the definition. CSB is reported to affect 3% to 6% of the general population in the United States, occurring more frequently in men. It typically begins in the late teens or early twenties and is chronic or intermittent. The disorder has been described as a progression through four stages: preoccupation, ritualization, gratification, and despair. Men with CSB typically focus on physical sexual gratification; women focus on romantic or emotional aspects of sexuality. Psychiatric comorbidity is common, particularly substance use, mood, anxiety, and personality disorders. CSB can lead to medical complications. Risk factors are thought to include family history and childhood abuse.