Early identification and treatment of schizophrenia may alleviate the symptoms, delay the onset and improve the outcome of psychosis. Thus, detection of individuals at risk during the prodromal phase is an important task. Universal approaches to screen the general population or healthy subjects at risk have not proven possible to-date. However, clinical criteria for detecting ultra-high risk individuals have been developed for specialized settings, with their implementation in interventional studies. This article examines the rationale for early detection and intervention of psychosis, along with a review of some of the current studies. These target prevention using psychological and/or pharmacological intervention strategies have demonstrated promising results in high risk individuals. The German Research Network on Schizophrenia (GRNS) is conducting two multicenter early intervention studies; one with early psychological intervention in subjects who manifest early prodromal symptoms; with the second trial applying clinical management and pharmacological early intervention in subjects experiencing late prodromal symptoms (high risk subjects). Despite the promising results, many of the current studies have small sample sizes with study durations of a short period. The full benefits of early detection and intervention should be revealed once larger and longer studies are conducted.

As the phenomenology of pediatric bipolar disorder has become better delineated, clinicians are now able to more accurately assess and treat young people suffering from this condition. For pediatric patients with bipolar I disorder and symptoms of mania, medication monotherapy has been shown to lead to symptom amelioration. However, this treatment modality oftentimes does not lead to full symptom remission. In an attempt to address this observation, combination treatment strategies have recently been investigated. Recently, a maintenance study has shown that in youths who achieved remission on a combination of lithium and divalproate therapy, either of these agents alone was equally effective as a treatment strategy. In youths identified as being at genetic high risk for bipolarity who also had problematic affective symptomatology, treatment with divalproate was not found to be superior to placebo; however, those with the greatest degree of genetic risk for familial psychopathology remained in the trial longer than those with more modest amounts of familial psychopathology. These data suggest that intervention in youths with only one affected parent may not be a rational prevention strategy for pharmacological intervention in bipolar disorder, and that cohorts more genetically at risk may be a more appropriate group for preventative pharmacotherapy.

Persons with mental illness frequently encounter public stigma and may suffer from self-stigma. This review aims to clarify the concept of mental illness stigma and discuss consequences for individuals with mental illness. After a conceptual overview of stigma we discuss two leading concepts of mental illness stigma and consequences of stigma, focussing on self-stigma/empowerment and fear of stigma as a barrier to using health services. Finally, we discuss three main strategies to reduce stigma - protest, education, and contact – and give examples of current anti-stigma campaigns. Well-designed anti-stigma initiatives will help to diminish negative consequences of mental illness stigma.

Clinical guidelines for treatment and research of bipolar disorder greatly benefit from the synthesis of data from individual studies. The British Association for Psychopharmacology bases its guidelines on evidence from opinions (level D) to systematic reviews of primary trial data (level A). The report details conclusions of its 1-day consensus meeting to develop guidelines covering diagnosis, clinical management, pharmacotherapy for acute episodes, relapse prevention and treatment discontinuation. Monotherapy for long-term management is preferred, having reduced side-effects and drug interactions and improved compliance. Combination therapy is often preferred for acute episodes, using antipsychotics for mania or antidepressants for depression. Increased efficacy may be attributed to multiple mechanisms of action and potentially lower doses. In clinical practice, maintenance monotherapy has limited success for chronic episodes and polypharmacy is frequently used, though the best combination remains unclear. A new collaborative approach based on simple clinical trials is required to change current medical practice.

Diabetes mellitus is a complex metabolic disorder, caused by defects in insulin action and/or insulin production and is defined as afasting hyperglycaemia of >126 mg/dl, with normoglycaemia being ≥70 and ≤ 110 mg/dl. There are two main types of diabetes. Type 1 diabetes (around 10% of cases) is an autoimmune disease, usually of early onset, in which pancreatic islet beta cells that secrete insulin are destroyed. Type 2 diabetes (around 85% of cases) is characterised principally by insulin resistance and impaired insulin secretion. Heredity and obesity are major risk factors for Type 2 diabetes. Diabetes is associated with potentially life-threatening microvascular and macrovascular complications caused by elevated serum glucose levels. Treatment of diabetes aims at restoring glycaemic control. In Type 1 diabetes, this can be achieved by injecting insulin. Oral hypoglycaemic medications that stimulate insulin secretion and/or modify glucose metabolism can be used as a first-line treatment in Type 2 diabetes mellitus. However, insulin is usually necessary in later phases of the disease. Lifestyle changes, such as diet and exercise, are also important. Glycaemic control can be measured by fasting blood glucose levels and also by glycosylated haemoglobin levels. The latter measure gives an indication of glycaemic control over a period of three months, and a reduction in glycosylated haemoglobin is the most appropriate treatment goal in the management of diabetes.

The impact of acute and chronic stress on the hypothalamic-pituitary-adrenal (HPA) axis is reviewed and evidence presented that corticotrophin releasing factor (CRF) is the stress neurotransmitter which plays an important role in the activation of the central sympathetic and serotonergic systems. The activity of CRF is expressed through specific receptors (CRF 1 and 2) that are antagonistic in their actions and widely distributed in the limbic regions of the brain, as well as in the hypothalamus, and on immune cells.

The mechanism whereby chronic stress, via the CRF induced activation of the dorsal raphe nucleus, can induce a change in the serotonergic system, involves an increase in the 5HT2A and a decrease in the 5HT1A receptor mediated function. Such changes contribute to the onset of anxiety and depression. In addition, the hypersecretion of glucocorticoids that is associated with chronic stress and depression desensitises the central glucocorticoid receptors to the negative feedback inhibition of the HPA axis. This indirectly results in the further activation of the HPA axis.

The rise in pro-inflammatory cytokines that usually accompanies the chronic stress response results in a further stimulation of the HPA axis thereby adding to the stress response. While CRF would appear to play a pivotal role, evidence is provided that simultaneous changes in the serotonergic and noradrenergic systems, combined with the activation of peripheral and central macrophages that increase the pro-inflammatory cytokine concentrations in the brain and blood, also play a critical role in predisposing to anxiety and depression. Neurodegenerative changes in the brain that frequently occur in the elderly patient with major depression, could result from the activation of indoleaminedioxygenase (IDO), a widely distributed enzyme that converts tryptophan via the kynenine pathway to for the neurotoxic end product quinolinic acid.

In our opinion the best guide to prescribing antipsychotics is the clinician’s experience with his patients and in particular the patient being treated. If treatment works, stick with it. We feel it is also important for the clinician to consider the evidence from well-controlled double-blind random-assignment studies because in “evidence-based medicine,” biases both known and unknown are controlled by blinding and randomization. The purpose of this paper is to summarize and discuss the evidence on efficacy. Choice of antipsychotic, in our opinion, is probably the most important decision that the clinician makes for the psychotic patient. This involves the choice of drug, its dose, balancing efficacy, side-effects and cost.