Current Psychiatry Reviews - Volume 7, Issue 1, 2011

The duration of untreated psychosis (DUP) construct is recognized as a predictor of early-course outcomes of individuals diagnosed with nonaffective psychotic disorders. Although a major area of early-psychosis research has been DUP as a predictor of outcomes, less is known about the potential determinants of DUP. Because the community-level median DUP may be modifiable, which is compelling evidence for the promotion of the early intervention paradigm, knowledge of determinants of DUP is critical. This review summarizes what is known of the multifaceted determinants of DUP. In general, these complex determinants can be categorized as demographic factors (e.g., ethnic minority status), premorbid and onset-related factors (such as mode of onset of psychosis), illness-related factors (exemplified by the levels of positive and negative symptoms), family-level factors (including family involvement in help-seeking and family functioning), societal factors (e.g., the beliefs and practices of one's social networks), and health services/system-level factors (including health insurance status and the efficiency of referring clinicians). Despite the great complexity, efforts to understand and conceptualize the multifaceted determinants of DUP may inform key components of early detection and intervention programs, such as mobile early detection teams and community-level informational campaigns.

Weight gain in schizophrenia patients is becoming a major concern as second generation antipsychotics (SGAs) have been associated with considerable increase in weight. The mechanisms by which they produce this side effect are not known. The orexins, are a family of hypothalamic neuropeptides that are selectively expressed in neurons of “feeding area” (lateral hypothalamus and perifornical area). They arise from the precursor peptide prepro-orexin by proteolytic processing and act through two closely related G-protein-coupled receptors, the orexin 1 (OX1R) and orexin 2 receptors (OX2R). Despite the small number of orexin cells, orexin axons are distributed throughout the brain. The orexins modulate feeding behavior, some metabolic processes and arousal. Fos expression is induced in orexin neurons by SGAs that cause significant weight gain but not by those SGAs with low weight gain liability. Moreover, in the same paradigm, amphetamine also activated orexin neurons. Clozapine markedly increased fos expression in orexin neurons that innervate the PFC whereas amphetamine had a weak effect. These findings suggest that it is likely that changes in the activity of afferents or hormonal signals to these orexin neurons determine the differential response. One study has pointed that the same effect on fos-induction by olanzapine was reversed by Zonisamide, an anti-epilepsy drug. It is suggested that the receptors targeted by SGAs may be present on orexin neurons or on their afferents and play a role in induction of weight gain.

In a recent paper, Andrews & Thomson (2009) presented the hypothesis that depression is a functional trait that was selected because it helps to solve complex problems and that it is related to high levels of serotonin in the brain. Notwithstanding the fact that the authors' main focus is on the first issue, the hypothesis ends up being much bolder in relation to the second one, as it challenges much about everything that is accepted by the scientific community in relation to the neurobiological basis of depression, as much as many of their own citations. As revealed in this paper, the studies cited by Andrews & Thomson (2009), in association with a compilation of the recent literature on the matter, suggest that serotonin levels vary from diminished to normal in the brain of non-medicated depressive patients without psychiatric or neurological comorbidities. Based on these studies, general lines of a new serotonergic hypothesis of depression (MDD) are introduced.

Despite great progress in basic schizophrenia research, the conclusive identification of specific etiological factors or a pathogenic process in the illness has remained elusive. The convergence of modern neuroscientific studies in molecular genetics, molecular neuropathology, neurophysiology, in vivo brain imaging, and psychopharmacology, however, indicates that we may be coming much closer to understanding the molecular basis of schizophrenia. Schizophrenia may be a neurodevelopmental and progressive disorder with multiple biochemical abnormalities involving the dopaminergic, serotonin, glutamate, and γ-aminobutyric acidergic systems. In the near future, biological markers for the illness may come from the combination of diverse assessment techniques. An understanding of the pathophysiology of schizophrenia will be essential to the discovery of preventive measures and therapeutic intervention. Rapidly advancing research into schizophrenia includes diverse etiological hypotheses, and offers directions for future research and treatments.

Background: Medical guidelines claim to be evidence based, to report newest scientific information and to be transparent in respect to authorship. They want to optimize treatment, improve patient outcome, and reduce unnecessary costs. It must empirically be tested in randomized controlled trials to which degree these claims are fullfilled in day-to-day practice, and whether “guideline exposed physicians” treat their patients differently and, if so, have better or worse treatment results in comparison to “guideline naive physicians”. Method: Systematic review in the PubMed database of controlled clinical trials comparing “guideline exposed physicians” with “guideline naive physicians” in the area of depression, hypertension, and diabetes mellitus. Results: Two studies for hypertension, three for diabetes and nine for depression were found. In two studies there was an improvement in treatment outcome in the guideline exposed-group, in one a worsening in treatment outcome and in eleven no differences Conclusions: Effects of treatment guidelines can be tested in controlled clinical trials. Results of such studies for depression, diabetes and hypertension suggest, similar to conclusions from other authors, that guidelines do often not reach their goal but can even have negative consequences. This can be explained in reference to theoretical knowledge on medical decision making. The term “evidence based” should not be used for guidelines which are literature reviews only, but for guidelines which have been empirically tested by controlled trials.

There has been a global surge in the use of mobile phones over the past decade with subscription rates of devices in Europe now exceeding 100%. Mobile phones are popular, portable and affordable, and allow for easy communication. This provides an opportunity for their use in improving mental health related outcomes, especially through use of text message technology. Several studies have demonstrated the usefulness of text messages in improving various aspects of medical care, including attendance with primary care and outpatient clinic appointments, adherence with physical health medication, managing side effects of non-psychotropic medication and promoting smoking cessation. We review here the potential for using text message technology in psychiatry, specifically for improving adherence with scheduled outpatient appointments, increasing adherence with psychotropic medication, managing side effects of psychotropic medication and managing patients with addictive disorders and co-morbid mental health problems. We identify barriers to the potential use of text messaging technology in psychiatry and propose solutions to some of these barriers. We also propose the need for further research into the use of text messaging in psychiatry and how this might impact upon the therapeutic relationship with patients.

From an evolutionary perspective, psychiatric depression presents a paradox: despite disadvantages for survival and reproduction, depression has significant heritability and is remarkably prevalent. A potential explanation for this paradox is provided by the hypothesis that the immune system helps regulate mood to aid defense against infection. This “infection-defense” hypothesis proposes that immune vulnerability to infection elicits depressed mood, which in turn stimulates behaviors that help protect vulnerable individuals and their kin against infectious diseases. This paper examines evidence on predictions of the hypothesis that concern depression's relation to immune function and vulnerability to infection. A review finds support for several predictions: 1) depressed patients show elevated levels of key types of immune vulnerability; 2) in animal experiments, chronic conditions that increase vulnerability to infection also cause depressionlike behaviors; 3) there are adaptive mechanisms to fight infection that involve interactions of immune and neuroendocrine factors; 4) conditions associated with depression in humans are also associated with immune vulnerability and infection; and 5) somatic antidepressant treatments often enhance immune function and resistance to infection, with time courses of immune responses to different treatments often paralleling those for mood. 6) Finally, positive mood tends to be associated with enhanced resistance to infection. This review focuses on immune factors that are crucial for defense against infectious diseases and have been widely studied in relation to depressive symptoms and antidepressant therapies. The hypothesis has potential clinical implications for prevention and treatment of depression.

Background: The accommodation and support needs of former long-stay and “new” long-stay patients with severe mental illness are complex. These two groups with different histories but similar needs are referred to in this paper as long-term patients. The science of psychiatric rehabilitation has advanced, but residential instability, homelessness, forensic involvement and substance abuse contribute to the rehabilitation challenges for long-term patients. Methods: This paper reviews recent evidence concerning outcomes of community mental health care for long-term patients. It reviews models of residential rehabilitation and residential care and the application of recovery principles to them. Results: Long-term patients continue to experience unstable accommodation, isolation, poor quality of life and are vulnerable to reinstitutionalisation. Their varied needs can be met effectively, but are frequently not met in a sustained way. Positive outcomes are associated with provision of choices in small-scale accommodation services that are linked with assertive outreach from specialist mental health teams and integrated with existing community services. Conclusions: Providing the accommodation and care needed by long-term patients to support recovery and effective rehabilitation requires analysis of the determinants of outcomes for patients in residential and non-residential settings. Particular attention is needed to continuing enhanced community mental health care, treatment of concurrent substance use and access to a range of residential support services for as long as necessary. For a small but important minority of patients there is a need to continue these arrangements indefinitely. Research on the essential ingredients of effective models of care, including consumer perspectives, is required.