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This study investigated the dosing patterns for aripiprazole augmentation for major depressive disorder (MDD) in a naturalistic treatment setting. Between 1 January 2009 and 31 March 2012, patients with a diagnosis of MDD who were receiving aripiprazole augmentation in conjunction with an ongoing antidepressant were recruited for this study. The electronic medical records and clinical data for a total of 276 patients were reviewed up to a year. The mean duration of aripiprazole augmentation was ∼5 months; the mean time to the first increase of aripiprazole was about 3 weeks; and the mean initial, first up-titrated, maximal, and maintenance doses were 3.4, 4.2, 4.7, and 4.4 mg/day, respectively. The most frequent adverse events were insomnia, followed by anxiety and sedation. The current results indicate that the actual doses of aripiprazole augmentation with ongoing antidepressant for MDD should be lower than the doses used in placebo-controlled clinical trials and those recommended by the US Food and Drug Administration. Adequately powered and well-controlled prospective studies are needed to better understand the exact role of low doses of aripiprazole augmentation in the treatment of MDD, particularly in routine practice.

Schizophrenia is a serious, chronic, and devastating mental illness with a substantial impact on psychological, physical, social, and economical areas of an individual and society. To treat such critical mental illness, a number of first-generation (typical) and second-generation (atypical) antipsychotics are currently available in the market. Despite such treatment options, most of patients with schizophrenia have a poor treatment outcome and become treatment resistant, causing continual deterioration on positive, negative, and cognitive symptoms, resulting in impairment of socio-occupational functioning. Hence, additional novel antipsychotics with better efficacy, safety, and tolerability profiles are needed to enable clinicians to diversify treatment options to improve treatment of schizophrenia. Recently, the 3 antipsychotics, including iloperidone (2009), asenapine (2009), and lurasidone (2010), have been approved by the US Food and Drug Administration. Two other atypical antipsychotics, including sertindole and blonanserin, are approved and used outside the United States for treatment of schizophrenia. Sertindole, after it has been voluntarily suspended by the manufacturer in 1998 due to its potential risk in causing cardiovascular-related death, was relaunched to the European market in 2005. More recently, blonanserin was approved in Japan (2008) and in Korea (2009) for the management of schizophrenia. Individual antipsychotic may have differential pros and cons compared with other antipsychotic in terms of efficacy, safety, tolerability, restoration of functional capacity, and economic aspect reflecting relapse prevention. The purpose of this review was to provide distinctive clinical characteristics and up-to-date of clinical trial data of the 5 novel atypical antipsychotics for the management of schizophrenia, which may deliver clinicians better understanding in the use of such atypical antipsychotics for the treatment of schizophrenia in clinical practice.

Milnacipran is a serotonin and norepinephrine reuptake inhibitor (SNRI) with negligible effects on any presynaptic or postsynaptic receptors. Milnacipran has unique pharmacokinetic and pharmacodynamic characteristics that distinguish it from the other marketed serotonin and norepinephrine reuptake inhibitors, venlafaxine, desvenlafaxine, and duloxetine such as equipotent serotonin and norepinephrine reuptake inhibition and a linear dose-concentration trend at therapeutic doses. The half-life of milnacipran is approximately 8 hours. In addition, milnacipran does not inhibit the cytochrome P 450 system, indicating minimal propensity for drug-drug interactions. The antidepressant efficacy of milnacipran has been clearly established in a number of randomized, double-blind, placebo-controlled clinical trials, and it has been widely used for treating major depressive disorder. Moreover, evidence suggests that milnacipran is effective and tolerable in the treatment of fibromyalgia and may have usefulness for fatigue and anxiety symptoms. The current paper reviews researches conducted to date that is relevant to the efficacy, tolerability, and mechanism of action of milnacipran in the treatment of depression, fibromyalgia, and other psychiatric syndromes. Future directions of research are also identified.

There are limited data to indicate effective treatment strategies for antidepressant-related sexual dysfunction, in particular for patients with treatment-resistant major depression. We subanalyzed our published data whether augmentation with methylphenidate extended release (OROS MPH) improved sexual dysfunction associated with antidepressants in patients with treatment-resistant major depression. The primary efficacy measure was the change in Arizona Sexual Experiences Survey (ASEX) from baseline to end of treatment in an intent-to-treat analysis with last observation carried forward approach. There were no significant differences between the 2 groups in terms of changes in ASEX scores over time (F1,35 = 1.14; P = 0.32), although the numerical decrease in ASEX score was greater in OROS MPH (mean change, -4.5; 20.1% decrease) than in the placebo group (mean change, -0.6; 2.6% decrease). Augmentation with OROS MPH showed no statistically significant benefit in antidepressant-related sexual dysfunction, although addition of OROS MPH to antidepressants did not worsen preexisting sexual dysfunction. Adequately powered controlled trials are needed to fully evaluate the efficacy of OROS MPH in this area.

PURPOSE OF REVIEW Economic evaluation is becoming more and more important as a means to assist policy makers in choosing the best intervention or treatment against a pervasive scarcity of resources relative to the demands. Health service provision and the practice of geriatric psychiatry are closely associated with costs and outcomes of health economics. Recently published literature raising unanswered questions in these areas is reviewed. RECENT FINDINGS Some studies on the costs, outcomes, and cost-effectiveness of certain interventions or treatments (e.g. respite care, home-visiting community service) compared with usual strategies show that these are not optimal in terms of health economics. The updated guidance by the National Institute for Health and Clinical Excellence that cholinesterase inhibitors should be used only for moderate severity dementia on the grounds of cost-effectiveness has been heavily criticized. Mental health provision for older people varies across 'developed' and 'developing' countries. SUMMARY Updated findings provide better understanding of recent progress and issues on mental health economics, health service provision, and the practice of geriatric psychiatry. The application of health economics to the field of mental health should make complicated issues simple and explicit. Constructive criticisms and scientific debates will hasten the development of better tools or methodologies to evaluate the cost-effectiveness of current and new interventions or treatments.

The serotonergic neurotransmitter system has been implicated in major depressive disorder (MDD) and appears to be the target of a variety of antidepressants. Tryptophan hydroxylase (TPH) is the rate-limiting enzyme in serotonin biosynthesis, and selective serotonin re-uptake inhibitors exert their activity enhancing the general serotonergic tone. The goal of this study was to investigate whether the A218C polymorphism of the TPH gene is associated with MDD or antidepressant response. All patients were evaluated at the start and in the eighth week of using the 21-item Hamilton Depression Rating Scale. Genotyping was analyzed with polymerase chain reaction. There were no significant differences in genotypes and allele frequencies between the MDD patients (n = 93) and the control group (n = 127) and in the antidepressant response among TPH gene variants. Results suggest that the A218C polymorphism of the TPH gene does not play a major role in pathogenesis in MDD and does not serve as a modulator of antidepressant activity.