Current Psychiatry Reviews - Volume 2, Issue 4, 2006

Bipolar disorder remains a serious public health problem with a significant personal and economic burden. In line with the widespread recognition of the value of active patient involvement in their care, daily mood charting may increase the patient's understanding of their condition and improve adherence with complex medication regimes. Knowledge about the course and pattern of an individual's disorder may also allow earlier recognition of new episodes and help determine the optimal treatment strategy. Mood charting is also an essential tool for longitudinal studies of patient outcomes. Traditionally, patients have used paper-based tools for this daily self-assessment, but these forms are associated with problems of data quality, poor compliance, high costs for data entry, and only provide limited feedback for the patient and physician. As computer technology has gained acceptance by the public worldwide, new options are available to automate monitoring of patients with mood disorders. This article will review mood charting and describe our experience with the development, validation and use of ChronoRecord, an automated instrument for mood charting.

One central issue in schizophrenia research is to identify and characterize behavioral and biological markers that are intrinsic to the complex psychiatric disorder and that can serve as targets for detection, treatment, and prevention. A trait marker represents the properties of the behavioral and biological processes that play an antecedent, possibly causal, role in the pathophysiology of the psychiatric disorder, whereas a state marker reflects the status of clinical manifestations in patients. Certain visual functions, while deficient in schizophrenia, may be independent of psychosis. The question of what types of visual functions can serve as trait or state markers is beginning to be understood. Examining clinically unaffected relatives of schizophrenia patients and patients with bipolar disorder can provide information about the relationship between a schizophrenic disposition and visual response traits. In this effort, researchers found that motion integration is dysfunctional in schizophrenia patients but not in their relatives or bipolar patients, whereas motion discrimination is dysfunctional in schizophrenia patients and their relatives, but not in bipolar patients. By synthesizing these findings, this review suggests that distinguishing enduring trait markers from transient state markers for schizophrenia through visual processes is helpful for developing neurobiologically and psychologically based intervention strategies.

Many of the positive symptoms of schizophrenia, including hallucinations and passivity phenomena, have been related to dysfunction within association cortices. In addition, many of the cognitive deficits observed in patients with schizophrenia can also be characterised as impairments of higher level cognitions known to depend on these same association cortices. While most attention has been directed towards dysfunction of the frontal and temporal cortices, there is mounting evidence for impaired functioning of the parietal cortices as well. That is, there is a substantial body of research demonstrating impaired spatial and motor behaviours in patients with schizophrenia - behaviours known to depend on the parietal cortex. In this selective review we contrast some of these impairments with a neurological syndrome that commonly arises from damage to the right parietal cortex, known as unilateral neglect. Although the spatial impairments characteristic of neglect are far more severe than those observed in patients with schizophrenia, there are some important parallels that make the comparison worthwhile. We intend to outline those parallels and highlight ways in which they may inform models of schizophrenia.

The striatum and its dense dopaminergic innervation originating in the substantia nigra pars compacta and the ventral tegmental area compose the mesostriatal dopamine system. The nigrostriatal system is particularly involved in habit learning and in motor coordination; the dopaminergic projections from the ventral tegmental area to the ventral striatum are most well known for their role in shaping behaviors leading to reward. In close proximity to the very dense dopaminergic innervation, the stratum also receives more moderate serotonergic innervation. After vesicular release from their terminals, dopamine and serotonin (5-hydroxytryptamine, 5-HT) signals are controlled by transporter reuptake. Dopamine transporters (DATs) reuptake dopamine, and they are expressed at a very high density in the striatum. Serotonin transporters (SERTs) normally efficiently reuptake 5-HT, but DATs also display a low affinity for 5-HT. When selective serotonin reuptake inhibitors (SSRIs, e.g., antidepressants such as fluoxetine) elevate extracellular 5-HT, the dense striatal DATs uptake 5-HT into dopamine terminals. Subsequently, 5-HT enters dopaminergic synaptic vesicles, where it is coreleased with dopamine. Evidence indicates that the small 5-HT release accompanying the dopamine signal takes roughly a couple weeks to develop. Antidepressants that block serotonin transporters or other factors that elevate extracellular serotonin alter the temporal and spatial relationship between dopamine and serotonin signaling in the striatum.

Childhood-onset schizophrenia (COS; defined as onset by age 12) is rare, difficult to diagnose, and represents a severe and chronic phenotype of the adult illness. A study of childhood onset psychoses has been ongoing at the NIMH since 1990, where children with childhood onset schizophrenia (COS) and severe atypical psychoses (provisionally labeled “multidimensionally impaired” or MDI by the NIMH team) are studied. Familial risk factors, genetic analyses, neurocognitive functioning, and brain imaging data are obtained every two years on probands and all first degree relatives. Multiple analysis from the NIMH study have found that COS subjects have more severe premorbid neurodevelopmental abnormalities, a higher rate of genetic anomalies, and a robust cortical gray matter (GM) loss during adolescence, which proceeds in a ‘back to front wave like fashion’ and appears to be an exaggeration of the normal cortical gray matter developmental pattern. These cortical GM changes in COS are diagnostically specific and seemingly unrelated to the effects of medications, as they are not shared by medication matched MDI patients, or psychosis not otherwise specified (NOS) patients who have converted to bipolar I at follow up.

Studies have shown that hallucinations and delusions occur in a number of different populations including psychiatric and non-psychiatric patients and in non clinical (i.e. normal) individuals. However, the majority of these studies have included adult populations. The goal of the present article is to review the research on hallucinations and delusions in children and adolescents. The prevalence, characteristics and nature of hallucinations and delusions in both non clinical and clinical child and adolescent populations will be presented. In addition, a section on assessment strategies is included. Finally, the paper will conclude with a discussion of important issues and questions, including definitional issues, the predictive value of hallucinations and delusions, in addition to various clinical and theoretical implications.

Non-adherence to treatment of patients with psychotic disorders is related to higher rates of relapse, hospitalization, and suicide. Important predictors of non-adherence include poor social structure, cognitive deficits, negative medication attitude, side effects, depression, a sealing-over recovery style, feelings of stigmatization, denial of treatment need, and lack of insight. Attempts to improve adherence have shown that psychoeducation alone is not fully effective, and that motivational interviewing, behavioral strategies, and linking a patient' s personal goals to treatment may increase adherence. Based on the empirical data reviewed, we formed four clusters of possible causes of non-adherence, each of which can be targeted by a specific module of our developed Treatment Adherence Therapy (TAT). These four modules are: self-enhancement, motivational interviewing, medication dosage trials, and behavioral training. An individual patient may benefit from one or more of these modules; and thus the contents of TAT vary in accordance with individual causes of non-adherence. Basically, TAT aims to help patients work out what they want regarding treatment and then support them in following this through. TAT will be investigated in a multicenter randomized clinical trial in the Netherlands, starting March 2006.