Search

Objectives:Schizophrenia is a debilitating psychiatric illness associated with positive and negative symptoms as well as significant impairments in cognition. Current antipsychotic medications do not alleviate these cognitive deficits, and more effective therapeutic options are required. Increased oxidative stress and altered antioxidant levels, including glutathione (GSH) have been observed both in individuals with cognitive impairment and in people with schizophrenia. A GSH precursor, the antioxidant N-acetylcysteine (NAC) has been investigated as a novel treatment for the cognitive symptoms of schizophrenia, and recent research suggests that NAC may be a promising adjunctive treatment option. However, the current literature lacks integration as to why NAC may effectively improve cognition in schizophrenia. The present theoretical synthesis aimed to address this gap by examining the processes by which NAC may improve cognitive function in schizophrenia. Methods:The schizophrenia literature was reviewed in three key domains: cognitive impairment, the relationship between oxidative stress and cognition, and the efficacy of NAC as a novel treatment. This led to a theoretical analysis of the neurobiological processes by which NAC may improve cognition in schizophrenia. Results:This theoretical review concluded that improved cognition may result from a combination of factors, including decreased oxidative stress, neuroprotection of cognitive networks and an increase in glutamatergic modulation of the N-methyl-d-aspartate receptor system. Whilst a number of mechanisms by which NAC may improve cognition and symptoms in schizophrenia have been proposed, there is still limited understanding of the specific metabolic pathways involved and how they interrelate and modify specific symptomology. Discussion:Exploration of how NAC treatment may act to improve cognitive function could guide clinical trials by investigation of the specific neurotransmitter systems and processes involved, allowing for targeted neurological outcome measures. Future research would benefit from the investigation of both in vivo cortical GSH concentration and peripheral plasma GSH in a population of individuals with chronic schizophrenia.

Cannabinoids have an emerging evidence base as an effective treatment option in a number of medical conditions, including anorexia and intractable vomiting. It is well known that patients with schizophrenia are more likely to use cannabis; it has also been argued that this could be a way of self-treating adverse side effects (secondary to antipsychotics) in a group of people with schizophrenia. Therefore, studies have attempted to examine the use of cannabinoids in schizophrenia. Given the recent interest in the use of cannabinoids in general and the ensuing ethical debates, we systematically review the available literature on the use of four cannabinoids, namely delta-9-tetrahydrocannabinol, dronabinol, rimonabant, and cannabidiol, in the management of schizophrenia. We also offer suggestions for future research in this area. Cannabinoids have an emerging evidence base as an effective treatment option in a number of medical conditions, including anorexia and intractable vomiting. It is well known that patients with schizophrenia are more likely to use cannabis; it has also been argued that this could be a way of self-treating adverse side effects (secondary to antipsychotics) in a group of people with schizophrenia. Therefore, studies have attempted to examine the use of cannabinoids in schizophrenia. Given the recent interest in the use of cannabinoids in general and the ensuing ethical debates, we systematically review the available literature on the use of four cannabinoids, namely delta-9-tetrahydrocannabinol, dronabinol, rimonabant, and cannabidiol, in the management of schizophrenia. We also offer suggestions for future research in this area. [[Psychiatr Ann. 2018;48(5):214–223.]

This article describes the study design of Parenting Today in Victoria: a representative survey of contemporary parenting experiences, behaviours, concerns and needs of parents. The aims of the study, sample design, survey content development processes, including pilot survey administration, data collection procedures and demographic characteristics of the sample are described. The survey was administered via computer assisted telephone interviewing using random dialling of landline and mobile phone numbers in 2016 to parents of children aged 0–18 years who were living in Victoria, Australia. The response rate was 57% with 2600 parents surveyed (40% fathers). The sample was broadly representative of the Victorian population on major demographic characteristics when compared to data from the Australian Census of Population and Housing (Australian Bureau of Statistics, 2011). However, adjustments were made for over representation of younger parents (16–34 years), more highly educated parents and for those living outside major cities. This survey provides rigorously collected, accurate and up-to-date information about the experiences, preferences and concerns of a large and representative sample of parents. Findings will provide vital new insights to inform policy decision making, service planning and future research aimed at understanding parents’ attitudes and behaviours, and the psychology behind their help-seeking.

Ketamine can induce a transient psychosis via its influence on ionotropic N-methyl-d-aspartate receptors. Unlike dopamine agonists, which specifically mimic the positive symptoms seen in psychotic illnesses such as schizophrenia, ketamine may provide a better model because it is able to induce not only positive symptoms but also schizophrenia-like cognitive and negative symptoms. To test the veracity of the ketamine model further, research is attempting to replicate a range of cognitive deficits associated with schizophrenia in healthy controls under the influence of ketamine. Facial processing is one area that is impaired in schizophrenia. More specifically, research suggests that schizophrenia is associated with a reduced facial inversion effect reflecting abnormalities in configural face processing. The purpose of the current study was to determine whether ketamine would also reduce the facial inversion effect. This study was a double-blind, placebo-controlled repeated-measures design in which data are presented for 14 participants who received ketamine on one occasion and saline on another. The results supported the ketamine model, with the participants demonstrating an intact inversion effect in the placebo condition but no inversion effect under the influence of ketamine. Further, participants’ self-reported deficits in visual processing correlated with their inversion score and errors on the faces task. Future studies should examine a wider range of facial processing tasks with a larger sample to confirm the current results and to determine the specificity of ketamine’s ability to mimic schizophrenia facial processing deficits. The current study is supportive of the role of glutamate system in the processing of configural face information.

Semantic deficits constitute a core cognitive abnormality in schizophrenia. In the current study, the N-methyl-d-aspartate receptor antagonist ketamine was administered to healthy individuals acutely while they performed semantic processing tasks that included word pairs of differing degrees of semantic relatedness. Two dimensions of semantic processing were investigated (1) explicit versus implicit processing, that is, unconscious versus conscious processing of semantic relationships and (2) direct versus indirect processing, that is, word pairs that are closely (LION-TIGER) or distantly (LION-STRIPES) related. The immediate effects of ketamine (0.8 mg/kg per hour during 80 minutes with approximate target plasma levels of 200 ng/mL) were examined in a placebo-controlled double-blind repeated-measures group design with 19 participants. It was predicted that ketamine would disrupt access to semantic memory as evidenced in schizophrenia, especially the indirectly related word pairs. In addition, implicit processing and explicit processing were predicted to be differentially affected. Ketamine administration did result in an abnormal performance in the reaction time responses to implicitly presented indirectly related word pairs (ie, greater priming) and reduced accuracy for explicit pairs. Performance on the directly related word pair tasks (both implicit and explicit) was similar across ketamine and placebo conditions, except for the suggestion of abnormal semantic matching in the accuracy data in the implicit task. This study confirms that implicit indirect semantic processing is changed under the influences of ketamine akin to schizophrenia. Future research comparing a schizophrenia group and a ketamine group directly about these tasks is needed to determine the similarity of impairments.