Tolerability, safety and effectiveness of quetiapine in an in-patient group with a relapse of schizophrenia and the possible role of plasma amino acid concentrations, 5-HT parameters and HVA in the prediction of response to treatment were investigated in an open-label baseline-controlled trial of 14 weeks in 21 hospitalized schizophrenic patients. Responders were defined as those patients who exhibit at least a 40% reduction of BPRS total scores. Secondary efficacy measures were the PANSS, the Clinical Global Impression (CGI)-severity scale and the MADRS. Extrapyramidal side-effects were evaluated with the AIMS. Other side-effects were monitored at regular intervals. Amino acids and the derived tryptophan and tyrosine ratios, as well as monoaminergic parameters, were assessed in plasma at baseline and at weeks 3, 6 and 14.

Treatment with quetiapine resulted in the predefined treatment effect in 10 out of the 17 patients who completed at least 4 weeks of treatment. Effect in responders was observed on all efficacy parameters, including lower MADRS scores. No extrapyramidal side-effects emerged. Clinical and biochemical parameters did not predict response to treatment.

This study demonstrates the moderate antipsychotic efficacy of quetiapine on preferentially positive symptoms in a group of relatively young schizophrenics. Some observed changes in biochemical parameters are discussed.

To find out whether the neurodevelopmental disorders autism and childhood-onset schizophrenia have a common developmental pathway and whether the abnormalities detected are ‘disorder-specific’, by reviewing magnetic resonance imaging (MRI) studies.

As a result of a Medline search, we were able to access 28 studies on autism and 12 studies on childhood-onset schizophrenia, which focused on children and adolescents.

Larger lateral ventricles were found to be a common abnormality in both disorders. ‘Disorder-specific’ abnormalities in patients with autism were larger brains, a larger thalamic area, and a smaller right cingulate gyrus. Subjects with childhood-onset schizophrenia were found to have smaller brains, a smaller amygdalum and thalamus, and a larger nucleus caudatus. In subjects with childhood-onset schizophrenia, abnormalities appeared to progress over a limited period of time.

Because the study designs varied so much, the results should be interpreted cautiously. Before abnormalities found in the disorders can be designated as equal or ‘disorder-specific’, it will be essential to perform large longitudinal and cross-sectional follow-up studies.

The psychopharmacotherapy of somatoform disorders (SD; ICD-10: F45) has been less frequently investigated and is not as well established as in other (neurotic) disorders of ICD-10 section F4, i.e. generalized anxiety disorder (GAD; ICD-10: F41.1). The atypical compound opipramol is very often used to treat SD and GAD in clinical practice in Germany. However, state-of-the-art controlled clinical trials have not yet been performed.

Two clinical trials were performed with the aim of confirming the efficacy and tolerability of opipramol in SD and GAD.

Both trials were performed as randomized, double-blind, placebo-controlled, multicenter studies. While the GAD trial was a three-arm study with opipramol (200 mg/day) vs. placebo and alprazolam (2 mg/day) for 28 days, the SD trial was a placebo-controlled two-arm study with a treatment duration of 42 days. Each group consisted of about 100 patients.

Significant differences (alpha = 0.05) were found for the primary efficacy criteria (HAMA total score in GAD, HAMA somatic subscore in SD) and most of the secondary criteria in favor of the active drug therapies. Considerable differences between the psychopathology of SD and GAD were detected.

The well-tolerated anxiolytic opipramol is the first psychotropic drug with proven efficacy in somatoform disorders with effects on symptoms of somatization, anxiety, and depression. The compound is also effective and safe in GAD.

Recognition memory dysfunction has been frequently reported in schizophrenic populations, and has been linked with the development of delusions and thought disorder. A range of neuropsychological abnormalities have also been documented in the biological asymptomatic relatives of patients with schizophrenia; however, recognition memory has not been one of them.

This study was carried out in order to investigate: (i) verbal and facial recognition memory in terms of accuracy and false alarm rates; and (ii) contributions from the episodic and semantic memory systems to recognition memory, in the biological asymptomatic parents of a reported schizophrenic patient and a set of male and female psychotic controls.

Gender differences failed to emerge between the psychotic controls on any of the recognition measures (discrimination accuracy, response bias, hit and false alarm rates, ‘remember’ and ‘know’ recognition memory decisions). However, there was evidence of recognition dysfunction in the female relative, and to a lesser extent, in the male. Both parent's recognition memory performance profiles were marked by a pathologically elevated false alarm rate, and an increased dependence ‘remember’ judgements, i.e. input from the episodic memory system, to drive recognition memory decisions.

These findings are discussed in the context of models of episodic and semantic memory impairment in schizophrenia.

The pathogenesis of atypical psychoses, in particularly those characterized by polymorphic psychopathology, is hypothesized to be related to disturbances in amino acid metabolism.

In the present study, the role of the amino acid serine was investigated in patients with acute transient polymorphic psychosis.

Patients were loaded with serine and with the amino acids glycine and alanine as controls and subsequently evaluated for the development of psychopathological symptoms. In addition, plasma levels of amino acids were measured.

In a subgroup of patients suffering from atypical psychoses, this biochemical challenge resulted in the reappearance of psychedelic symptoms in particular. Furthermore, significantly lower plasma concentrations of serine were found. In vitro experiments revealed a disturbance in the one-carbon metabolism. In another group of patients the loading provoked vegetative symptoms and fatigue.

Disturbances in amino acid metabolism may be involved in the emergence of certain psychotic disorders.

The United Nations, WHO and the World Bank have called the current prevalence rate of neuro-psychiatric disorder approaches of 1 in 4 individuals worldwide and ‘unheralded public health crisis’. Rates are driven by an early onset, high impairment and high chronicity of these disorders. Most importantly, detection and treatment rates are low, estimated at les than 10% worldwide resulting in 500 million people underserved. The related economic costs soared in 1999 to 120 billion dollars in Europe and North America, with over 60 billion dollars assigned to stress related disorders. Contributing factors are bio-psycho-social and include rapid social change as well as the time compression of modern life resulting in the experience of increased work-life stress that parallels a decade long intensification of activities in the workplace. Coping with the requirements of the new economy of mental performance has lagged behind at many individual and social levels as we cling to adjustments made during the industrial economy of the last century. A climate of transition, and more recently, terror and fear have stressed the landscape of mental health and work already ravaged by the destructive forces of stigma.

This presentation will examine the other side of prosperity from the point of view of stress in the workplace as two global problems converge at this time in history, the escalation of neuro-psychiatric disorders and the increasing dependence on the mental faculties of the world's citizens.

In this paper we also discuss how the international community can work together to help reduce the burden of mental disorders worldwide and sketch the implications for research and policy.

Ultimately the media will need to be enlisted to educate the public on the value of investments in mental health.

The intention of this study was to evaluate therapy outcome of a cognitive-behavioral group treatment program for functional gastrointestinal disorders. As a particular characteristic, gastrointestinal symptoms were investigated independently from diagnostic categories on a dimensional basis, considering the persistence of symptoms as well as the aspect of severity.

A total of 64 subjects participated in the 10-week treatment program, and 49 completed the study. Subjects underwent four assessments (baseline, pre-, post-treatment, 12-month follow-up), each comprising several self-rated questionnaires on gastrointestinal, somatoform, depressive, hypochondriacal and anxious symptoms, and health locus of control, as well as a diagnostic interview of functional gastrointestinal and mental disorders at the baseline assessment. Treatment effects were controlled by subjects' waiting list period before treatment.

Gastrointestinal symptoms, as well as comorbid psychopathology scores, decreased significantly during treatment and remained unchanged during the follow-up period, whereas no relevant changes were found in health locus of control. Largest effect sizes were found for gastrointestinal symptoms, which decreased by 30–50% of their initial number.

The group treatment investigated was effective and particularly successful with respect to functional gastrointestinal symptoms. However, the mechanisms of treatment outcome remain indistinct. Further studies comparing different setting conditions directly are required to clarify the question of whether group treatment is significantly superior or inferior to individual therapy.

The aim of the controlled therapy study was to evaluate the effect of a 6 session biofeedback intervention program on cognitive aspects of patients with somatoform disorders. The treatment consisted of psycho-physiological demonstrations how mental processes can influence biological functions. We expected this treatment to be of high credibility, to change maladaptive cognitions, to enhance acceptance of psychosocial causal attribution and to improve coping.

Patients were assessed using a structured interview to diagnose somatization syndrome (SSI-8) and comorbidity according to DSM-IV criteria. Fifty patients were recruited and randomly assigned to biofeedback treatment or control relaxation group. Participants completed a questionnaire battery assessing cognitive characteristics, causal attributions and controllability before and after intervention as well as evaluation protocols for each session.

The results suggest that biofeedback modified the patients' cognitive schemata: Patients with somatization syndrome of the biofeedback group showed a greater reduction of catastrophizing of somatic sensations and higher acceptance of psychosocial causal attributions than the control group. Both groups improved significantly in the conviction of self-efficacy.