Extended-release formulations of antidepressants have been marketed as a strategy to increase patient adherence. Changes in the formulation of drugs, however, could be related to changes in efficacy and tolerability. Among second-generation antidepressants, bupropion, fluoxetine, mirtazapine, paroxetine, and venlafaxine are available in immediate- and extended-release formulations.

To compare the efficacy, tolerability, and adherence of immediate- versus extended-release formulations of second-generation antidepressants for the treatment of major depressive disorder (MDD) in adults.

To provide an evidence base for clinicians when choosing immediate- or extended-release formulations of antidepressants for the treatment of MDD.

We conducted a comparative effectiveness review for the U.S. Agency for Healthcare Research and Quality searching PubMed, EMBASE, The Cochrane Library, and the International Pharmaceutical Abstracts up to May 2010. Two people independently reviewed the literature, abstracted data, and rated the risk of bias.

Six RCTs and one observational study provided evidence about the comparative efficacy, tolerability, and adherence of bupropion SR (sustained release) versus bupropion XL (extended release), fluoxetine daily vs. fluoxetine weekly, paroxetine IR (immediate release) versus paroxetine CR (continuous release), and venlafaxine IR versus venlafaxine XR (extended release). Overall, no substantial differences in efficacy and safety could be detected. Open-label and observational evidence indicated better adherence for bupropion XL and fluoxetine weekly than for immediate-release medications. No differences in adherence could be detected between paroxetine IR and paroxetine CR.

Our findings indicate similar efficacy and tolerability between immediate- and extended-release formulations. Whether extended-release formulations lead to better adherence remains unclear.

Valproate is used in psychiatry as a mood-stabilizer and has efficacy in controlling impulsivity, therefore it seems to be a useful pharmacologic agent in pathologic gambling.

To assess the efficacy of valproate in the treatment of pathologic gambling.

A group of 13 patients, 9 male and 4 female, mean age 32.6, diagnosed with pathologic gambling, according to the DSM-IV-TR criteria, received treatment with flexible dose of valproate (600–1400 mg/day, mean dose 850 mg/day) and 2 times/week cognitive therapy sessions. Patients with other axis I and II conditions were excluded. Also, none of these patients received valproate or structured cognitive therapy prior to this trial. Patients were monitored for 3 months using monthly administered Gambling Symptoms Assessment Scale (G-SAS), Clinical Global Impressions (CGI) and 10 points self-evaluated Visual Analogue Scale (VAS).

Valproate was associated with a mean decrease of 10.5 points on G-SAS at week 12, compared to baseline (p < 0.05), while the CGI decreased with only 1.3 points (p = 0.122) and the VAS improved with 2.3 points (p < 0.05). The combined treatment was associated with good tolerability profile, since no drop-out was recorded in the study group due to side events and only 7 reports of mild and medium adverse events were recorded.

Valproate treatment associated with cognitive therapy could be a useful strategy in the management of pathologic gambling. Valproate's tolerability profile is good and the cognitive therapy offer an opportunity to ventilate the negative automatic thoughts, emotional distress and low impulse control strategies.

Selective serotonin reuptake inhibitors (SSRIs) are frequently used for irritable bowel syndrome, while duloxetine was evaluated in other similar psycho-somatic syndromes.

This prospective, single-blind trial intends to compare the efficacy of SSRIs and duloxetine in the treatment of irritable bowel syndrome.

A group of 22 patients, 15 female and 7 male, mean age 50.2, diagnosed with irritable bowel syndrome according to the Rome II Diagnostic Criteria (1992) were treated with either an SSRI (escitalopram 20 mg/day, n = 6 or fluoxetine 40 mg/day, n = 6) or duloxetine (90 mg/day, n = 10). Patients were evaluated initially and every 4 weeks, for 6 months, using Hamilton Anxiety Rating Scale (HAMA), Hamilton Depression Rating Scale 17 items version (HAMD), Clinical Global Impressions -Severity/Improvement (CGI-I/S) and a 7-points Likert scale (LS) for self-evaluated severity.

Duloxetine improved anxiety and depressive symptoms, as reflected by the significant decrease of HAMA (−17.6 points, p < 0.05) and HAMD scores (−18.2 points, p < 0.05) at week 12. SSRIs also reduced the affective symptoms, significantly to baseline (p < 0.05), but less than duloxetine (−14.3, −15.2) at week 12, with no significant difference at week 24 (p = 0.120). The CGI-I results paralleled the decrease of HAMD and HAMA, while the LS evaluation of gastrointestinal symptoms improved similarly in both groups, with no significant difference (p = 0.09).

Duloxetine is an efficient agent in the treatment of irritable bowel syndrome, because it decreases the mood symptoms more rapidly than SSRIs. The overall efficacy of SSRIs and duloxetine at 6 months is nevertheless similar.

Efficacy differences between antidepressants have only been detected exceptionally (Bauer et al., 2009). Due to the fact that escitalopram is the enantiomer of the racemate citalopram the question arose whether this compound possesses besides pharmacodynamic differences (e.g. Sánchez, 2006) also clinical relevant advantages.

In order to investigate this issue thoroughly the relevant studies of evidence level Ia (systematic surveys of randomized controlled studies) and Ib (randomized controlled trials) were summarized regarding three main outcome parameters: response (decrease of the depressive symptomatology of at least 50% on a depression scale), remission (reduction of the depressive symptomatology below a certain threshold on a depression scale) and change in depression symptomatology (point difference on a depression scale during the treatment period).

Overall, approximately 20% more patients responded under escitalopram than under Citalopram. Regarding remission, this difference is approximately 30%. The point difference on the Montgomery-Åsberg depression scale was between 1 and 2 (statistically significant). In a subanalysis it was found that the superiority of escitalopram increased with increasing initial depression severity.

These very robust data are discussed regarding their clinical implications.

Gynecomastia and hypogonadism can occur during treatment with a range of antidopaminergic drugs and is most likely to a medication induced increase in serum prolactin levels. However there is little evidence for an association between antidepressants and hypogonadism.

We report the case of a 23 year old male with a 3 year history of bulimia nervosa and recurring depression who had been treated with duloxetine for a period of 6 months during which he developed pronounced bilateral gynocomastia. Since serum prolactine and serum testosterone levels were normal and duloxetin was initially not considered causative, the drug was continued and bilateral gynecomastia was performed. 4 months later the patient again experienced tension and swelling in the breast.

The endocrinologic exams revealed reduced serum testosterone levels and reduced testicular volume. Body weight was 63 kg, height 176 cm and a neurological exam, including olfactory testing and MR brain imaging was normal. Hypogonadotropic hypogonadism was diagnosed.

Increased prolactin levels under antipsychotic medications are not uncommon. Some rare instances of gynecomastia have been reported under fluoxetine and venlafaxine, always associated with increased serum prolactin levels. In the present case the close tempral relationship between initiation of duloxetine and the development of gynecomastia and the recurrence under continued medication and resolution after termination of the medication suggests a possible causal relationship. The normal prolactin levels argue against anvolvement of prolactin in the pathogenesis. We suspect a prolactine independent mechanism.

Treatment with antypsychotics is associated with cardiovascular side effects. This results from mechanism of action of antypsychotics. Arrhythmias are the serious side effects. Treatment with antipsychotics may prolong QTc and increase the risk of dangerous supraventricular and ventricular arrhythmias.

The main aims of the research are the following: If Any antypsychotics agents may prolong QT interval? If monotherapy with olanzapine, zyprasidone, arypiprazole and politherapy with perphenazine and olanzapine may induce any arrhythmias?

Data for this study were collected from 65 patients hospitalized in the Department of Adult Psychiatry and treated with olanzapine and perphenazine (n = 10) and with olanzapine (n = 20), aripiprazole (n = 20), ziprasidone (n = 15). All patients had 12 leads ECG two times: before admitting the drugs and during the treatment. All ECG were assessed on the presence of any abnormalities and QTc was calculated manually by using Bazzet formula.

Among treated patients no QTc prolongation was observed. There was no prolonged QTc over 450 ms in Male and 470 ms in female patients treated with antypsychotics in mono and politherapy. Potassium level in all patients was within the norm. Bradykardia (< 50/min) and tachykardia (>100/min) was not observed among participants.

Atypical antypsychotics such as olanzapine, arypiprazole, zyiprasidon are cardiovascular safe drugs. They did not induce dangerous for life arrhythmias especially ventricular arrhythmia (known as torsades de pointes), which can progress to ventricular fibrillation and sudden death. Politherapy with olanzapine and first generation agents perphenazine is a safe combination and did not induce any cardiovascular side effects.

To evaluate the efficacy of galantamine in patients with Mild Cognitive Impairment. So there is a possible benefit in the deficit in executive and cognitive cerebral function (cholinergic system) with treatment with Galantamine.

Galantamine is a reversible, competitive cholinesterasa inhibitor that also allosterically modulates nicotine acetylcholine receptors. Inhibition of acetylcholinesterase, the enzyme responsible for hydrolisis of acetylcholine at the cholinergic cognitive impairment. To evaluate the efficacy, safety and tolerability of galantamine in long-term in Mild Cognitive Disorder.

A multicenter, open label, prospective, observational study enrolled 1028 patients, more 55 years old with Mild Neurocognitive Disorder (DSM IV criteria), during 30 months of treatment with galantamine 16 mg./day. Assessments included the MMSE, CDR, ADAS-GOG, FAQ, GCI, Trail making test, Global Deterioration Scale, and UKU scale of Adverse Effects.

A total 1028 outpatients were treated with 16 mg./day galantamine during 30 months, the therapeutic response evaluated with CDR, MMSE and the tests and scales of function cognitive measuring, GCI and UKU scale of adverse effects, comparing the baseline to final scores.

Mild Cognitive Disorder is being examined, so there aren’t enought treatment for this. A long-term treatment (30 months) galantamine improves cognition and global function, behavioural symptoms and the general state well being of patients with MCD. With incidence of adverse effects not significant and a very good profile of safety, the final results of the study suggest that galantamine may be particularly appropiate in the Mild Cognitive Disorder.

To evaluate the efficacy of galantamine-paroxetine association in patients with Mild Cognitive Disorder and Depression. So there is a possible relation between the deficit in executive and cognitive cerebral function and depression or relation between the serotonin system and cholinergic system in relation with disease comorbidity cognitive-depression.

To evaluate the therapeutic response in patients with comorbility between Mild Cognitive Disorder and Depression in treatment with Galantamine (acetylcholinesterase inhibitor) with Escitalopram (Selective serotonin reuptake inhibitors) and the two drugs associated.

A group of 705 patients with symptoms of Mild Cognitive Disorder and Depression (DSM IV-TR criteria) were separated in 3 groups of 235 patients. Each group received different treatment in an 12 months period:

• Group 1: Galantamine 16 mg/day.

• Group 2: Escitalopram 10 mg/day.

• Group 3: both drugs, same dose.

The therapeutic response evaluated in Hamilton Scale for Depression (HAM-D), Montgomery and Äsberg Depression Rating Scale (M.A.D.R.S.), Mini Mental State Examination (M.M.S.E.) and Global Clinical Impression (G.C.I.) scores during 12 months. In the third group who received the two drugs associated, had much better response than the others and “brain enhancer”.

The group who received the association of the cholinergic agent Galantamine with antidepressant (SSRIs) Escitalopram had a relevant satisfactory therapeutic response: the best result, so there is a possible relation between the deficit in cholinergic systems and depression. Could be cerebral cholinergic systems deficit a generator of Depressive Disorder?

Metabolic syndrome and cardiovascular diseases are important causes of morbidity and mortality among patients with mental illness. Atypical antipsychotics are more associated with obesity, metabolic syndrome, abnormal glucose and lipid metabolism than first generation antipsychotics.

To identify risk factors related to glucose metabolism in short, medium and long time treatment and find out which are related to neuroleptic therapy and which depends on genetic background and lifestyle. To follow up clinical and self-rated variations of the psychiatric symptoms.

We included psychotic or bipolar patients in treatment with only one typical (haloperidol) or atypical (clozapine, olanzapine, risperidon, aripiprazole, paliperidon) neuroleptic, drug-naïve or after a wash-out from previous therapy. Patients will be evaluated five times (at baseline and after 1, 3, 6, 12 months) with a blood sample (haemocrome, glucose, insulin, Hb A1C, thyroid hormones, liver and pancreatic function), BMI, Basal Metabolic Rate (BMR), OGTT, HOMA index, familiar and pharmacological history, SIDE and CGI.

From blood exams and OGTT we will obtain data regarding variations of glucose metabolism and the possible relationship with neuroleptic medications. From SIDE questionnaire we will assess the impact of side-effects by the patient's perspective and with CGI the variations of symptom severity.

Our study will allow us to identify risk factors concerning glucose metabolism alterations related to antipsychotic medications.

Numerous results from investigations including children with ADHD show associations between a diminished serotonin synthesis and memory impairments as well as higher aggression scores. The aim of the present study was the investigation of the association between a diminished serotonin synthesis, logical memory and impulsive aggression in male adult patients with ADHD.

Twenty male adult patients with ADHD and twenty healthy controls were recruited for this double-blind within subjects crossover study. Subjects completed the Rapid Tryptophan Depletion (RTD) Test or a placebo condition (balanced amino acid load) on either one of two examination days. Clinical variables and general intellectual functioning were assessed. The neuropsychological test battery included the subtest logical memory from the Wechsler Memory Scale (WMS-R), self-assessment of aggression as well as the Point Subtraction Aggression Game (PSAG).

Statistical analysis revealed significant memory impairments of ADHD patients, which were associated with severity of symptoms in early childhood as well as subjective aggression scores. Effects of the tryptophan depletion were not found, neither for the logical memory subtest nor performance in the PSAG.

In contrast to previous studies, these findings suggest that the serotonergic system as reflected by the RTD Test has no effect on memory performance or impulsive aggression. However, these results may be due to possible interactions of other catecholamine systems with the serotonergic system that were not controlled in this study. Therefore an additional study is needed to further explore the catecholamine systems and their effects on memory and impulsive aggression.

Anxiety is a core symptom of schizophrenia which elicits significant subjective burden of disease and contributes to treatment resistance in schizophrenia. Anxious syndromes might be attributed to incompletely remitted delusions, the negative syndrome, depressive episodes, panic attacks, social phobia, avoidance after hospitalization and down-tapering of benzodiazepine medication. Previous treatment attempts involved several strategies of combination and augmentation.

Pregabalin, an antagonist at the α2δ-subunit of voltage-gated Ca2+-channels, modulates several neurotransmitter systems and was found able to alleviate anxiety in depression and other mental disorders.

In schizophrenia, this treatment option has not been evaluated before.

Here, we report a case series of 11 schizophrenic patients who suffered from treatment-resistant anxiety and received augmentation with pregabalin.

This observational investigation reveals that augmentation with pregabalin was able to significantly reduce scores on the Hamilton anxiety scale; furthermore, we observed improvements of psychotic positive and negative symptoms and mood as assessed by PANSS, SANS and CDSS. After augmentation, both a complete discontinuation of concomitant benzodiazepine (BZD) treatment as well as a dose reduction of antipsychotics could be achieved. We did not observe pharmacokinetic interactions or adverse events.

These observations suggest that treating anxious syndromes in schizophrenia with pregabalin can be effective and tolerable. Further investigations should differentiate schizophrenic sub-syndromes of anxiety and evaluate benefits and risks of pregabalin in comparison to placebo and active competitors.

To estimate efficacy of risperidone and olanzapine in treatment of DD.

135 patients with DD were divided into Haloperidol-control (41), Risperidone (49) and Olanzapine group (45 patients). Patients were observed for 6 months according to protocol, which included PANSS Scale and CGI1-4 Scale. Control group was treated with haloperidol 5–30 mg/24 h. Experimental groups were treated with risperidone 2–6 mg/24 h and olanzapine 10–20 mg/24 h.

Pretrial PANSS score was 57.28 in risperidone(R), 60.47 in olanzapine(O) and 58.45 in control(H) group. PANSS score after 180 days was 34.32 in R, 35.58 in O and 37.97 in H group. There was no statistical difference in pretrial scores for PANSS (p = 0.691), CGI1 (p = 0.733), CGI2 (p = 1.000), and CGI3 (p = 1.000) scores. There was statistical significance in PANSS and CGI1-4 score reduction after 180 days in all groups (p = 0.000). There was no statistical difference in PANSS score reduction between R and H (p = 0.114) and O and H group (p = 0.136). CGI1-4 scores reduction: CGI1, Rvs.H, p = 0.019 and Ovs.H, p = 0.032 with high statistical significance; CGI2, Rvs.H, p = 0.153 and Ovs.H, p = 0.179 with no statistical significance; CGI3, Rvs.H, p = 0.183 and Ovs.H, p = 0.161 with no statistical significance; CGI4, Rvs.H, p = 0.000 and Ovs.H, p = 0.000 with high statistical significance. Adverse effects were significantly lower in Risperidone (21.42%) and Olanzapine (21.81%) than in Haloperidol (57.5%) group.

Risperidone and Olanzapine have slightly better efficacy in treatment of DD comparing to haloperidol, with statisticaly significant lower adverse effects rate.

Previous studies have shown that in comparison to healthy people, patients with social anxiety (SA) identify fewer emotions of happiness in vocal expressions.

1. (1) To repeat previous studies on emotion recognition in SA patients;

2. (2) To examine the effect of training on emotion recognition in SA patients.

1. (1) To examine the effect of training in emotion recognition of non-verbally vocal musical improvisations on the ability of SA patients to identify happiness in verbal vocal spoken language.

2. (2) To create a preliminary procedure for improving this ability in SA patients. Methods: 41 SA patients and 39 healthy controls aged 24–40, were examined. SA diagnosis was conducted according to the norms of the Liebowitz (1987) questionnaire. Half underwent an intervention that focused them on happiness recognition in non-verbally vocal musical improvisations, and half did not. The four groups were then compared on level of precision of emotion recognition (happiness, fear, anger, sadness and surprise) in spoken language sentences.

A Multivariate analysis of variance showed that SA patients significantly identified fewer emotions of happiness in vocal expressions than healthy controls. SA patients who were trained demonstrated a similar precision level of happiness recognition in woman spoken language sentences as healthy controls (ps < 0.05).

Our findings demonstrate that short exposure (20 min) to non-verbally vocal musical improvisations immediately improves the ability of SA patients to recognize happiness in spoken language. Future studies can refine our procedure and examine its impact on SA patients over longer time periods (e.g., months).

The study evaluates a central hypothesis of synergetic psychotherapy research according to which a marked instability in the psychotherapeutic process is associated with high response rates.

14 patients with obsessive-compulsive disorder (OCD) successfully completed an eight-week in-patient course of multi-modal behavior therapy with exposure exercises followed by response management. The instability during the course of the therapy was recorded by daily self-assessment by the patient using the Synergetic Navigation System (SNS), an Internet-based real-time monitoring procedure.

There was a negative correlation between the degree of the instability and the percentage reduction in the Yale-Brown Obsessive Compulsive Scale (Y-BOCS) (r = −0.395; P = 0.199), the “Global Severity Index” (GSI) of the symptom check-list (SCL-90-R) (r = −0.718; P = 0.013), the scale value for obsessive-compulsiveness in the SCL-90-R (r = −0.782; P = 0.004) and the remaining sub-scales of this data-gathering instrument.

An unstable progress of the psychotherapy causes a smaller reduction in symptoms than a stable one. The contradiction relative to the study hypothesis is possibly based on the special features of OCD, with a high level of patient insecurity when anticipating new, non-obsessive-compulsive ways of thought and behavior. The relationships between instability and reduction in symptoms appear to be diagnosis-specific.

Mental disease is faced during the past years as a result of various factors, such as the participation of the family which sometimes has a negative aspect in the course of the disease.

Through the study of 15 families of the patients who live in the Residential Unit of Aspropirgos, we present the role of the family environment in the appearance and process of the disease.

We observed the background of 15 patients of the Residential Unit. When they completed a month living in Aspropirgos, we completed their Personal and Social Performance Scale (PSP). At the same time, we accepted the patients’ families in four weekly sessions whose goal was to explore and cope effectively with the problems that led those patients to mental disease. Patients completed the same questionnaire in their 4th and 12th month of their stay in Aspropirgos while we continued to have monthly sessions with their families.

Patients presented a decrease of their functionality in their 4th month in the Residential Unit (around 30%), which was accompanied by the resistance of their families in the suggestions of the therapeutic group. When 4 months were completed we put more strict limits regarding the relationships of the patients with their families, we even forbidded their contact with members who provoked the most severe dysfunction in the patient. At the end of 12 months we concluded that there was an improvement of up to 50–60% compared to patients’ situation in the 4th month.

Psychotherapy research shows that problems in emotion regulation are at the core of many different psychiatric disorders. Greenberg and colleagues distinguish between two categories of emotion regulation problems: emotional under- and overregulation. Whereas the first category is associated with diminished impulse control, the second is constituted of difficulties in perceiving and expressing emotions.

Is it possible to validate the clinical concept of emotional underregulation and overregulation?

Patients of a psychotherapy day clinic attended a specific group therapy program aimed at improving emotion regulation. The program included interventions to control impulses as well as interventions focussing on a more appropriate perception and expression of emotions.

The evaluation of the program was based on pre-post comparisons of standard questionnaires and on repeated assessments of therapy processes using session reports.

Results of about 50 patients attending the group therapy program will be presented. Different clusters depending on a patient's position on the two emotion regulation dimensions were found. Each cluster represented a unique pattern of emotion regulation.

It was possible to validate the clinical construct of emotional underregulation and overregulation. The results contribute to a transdiagnostic approach to emotion regulation.

Albert Ellis’ Rational Therapy, founded in 1955, evolved into Rational-Emotive Therapy (RET) in 1959; and finally as Rational-Emotive Behavior Therapy (REBT) in 1992. This evolution has showed, much more, its resemblance to Acceptance and Commitment Therapy (ACT) (Ellis, 2005). REBT highlights treatment of secondary disturbances (berating oneself for having symptoms), beyond primary ones (nosographical symptoms), because these are ways of control and experiential avoidance which foster suffering.

To treat primary anxiety in a patient reducing his secondary disturbance through TREC.

Participants: A 40-year-old man diagnosed with Panic Disorder who attended a Public Mental Health Service. He was being treated with Alprazolam y Lorazepam, which he has taken before psychotherapy.

Design, materials and procedure: It's implemented a single-subject AB design during 4 months (7 therapeutic sessions). It's applied a weekly self-report to record panic attack frequency and variations in anxiolytics-taken. C Young (p < 0.01) was used for statistical analysis of data and the method of least squares to obtain trend line. 16 measures were registered at a weekly interval.

Significant declining trends are observed in panic attack frequency (C = .750, Zo = 3.201, Zt = 2.240), and collaterally in anxiolytics-taking (Alprazolam: C = .811, Zo = 3.462, Zt = 2.240; Lorazepam: C = .801, Zo = 3.420, Zt = 2.240) from beginning of therapy.

Techniques targeting symptoms-extirpation induced intolerance and self condemnation feelings when patient didn’t achieve the wanted control (as way of destructive experiential avoidance -Luciano and Hayes, 2001). Treating these feelings (secondary disturbance), based on symptomatology acceptance (Ellis, 2005), decreased distress related to panic attacks and paroxysmal crisis frequency itself.

The exponential growth of evidence-based practice (EBP) interventions offers clinicians a growing number of empirically-supported psychosocial treatments for youth mental disorders. These interventions are likely to be ineffective with clients who drop out of treatment prematurely or who fail to adhere to the required intervention protocols. However, despite the critical role of client adherence, systematic evidence about strategies to support client adherence is lacking.

The primary aim of this present study is to establish an empirical base for developing adjunctive adherence promoters to enhance client participation in psychosocial interventions.

Mental health child and adolescent intervention researchers who published RCT on three psychosocial interventions (CBT, IPT. Psycho-ed) were surveyed on type, use, and efficacy of intervention adherence promoters.

Interventions included an average of 13.4 sessions (SD = 7.8) across 5 months. Most researchers reported using multiple adherence promoting interventions throughout their studies. On average, respondents reported using little more than one promoter per session and devoting approximately 12.4 minutes per session on all adherence promoters.

Results of this study will assist practitioners and researchers in improving adherence to psychiatric interventions for children and adolescents. Specifically, study results fill gaps in the literature on active efforts to sustain and increase client adherence to treatment for childhood and adolescent mental health disorders. Findings of this study support best practices for adherence promotion and open new avenues for research into the tailoring of adherence to EBP interventions for child and adolescent mental health problems.