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Background: Speech disturbances are a recognised aspect of schizophrenia that may have potential utility as a diagnostic indicator. Recent advances in quantitative speech assessment methods have led to more reproducible and precise metrics making this possible. The current study sought firstly to characterise the speech profile of schizophrenia patients using quantitative speech measures, then examine the diagnostic utility of these measures and explore their relationship to symptoms., Methods: Speech recordings from 43 schizophrenia/schizoaffective disorder (SZ) patients and 46 healthy controls (HC) were obtained and transcribed. Cognitive and symptom measures were also administered., Results: Compared to HCs, SZ patients had higher incidences of aberrance across five types of quantitative speech variables: utterances, single words, time/speaking rate, turns and formulation errors, but not pauses. Based on two machine learning algorithms, 21 speech variables across the same five speech variable types (again not including pauses) were identified as significant classifiers for a schizophrenia diagnosis with 90-100% specificity and 80-90% sensitivity for both models. Selective relationships were also observed between these speech variables and only positive, disorganisation, excitement and formal thought disorder symptoms., Conclusions: The findings support pervasive speech impairments in schizophrenia patients relative to HCs, and the potential diagnostic utility of these speech disturbances. Continued work is needed to build the evidence base for quantitative speech assessment as a future objective diagnostic tool for schizophrenia. It holds the promise of improved diagnostic accuracy leading to increased treatment efficacy and better patient outcomes., (Copyright © 2021 Elsevier B.V. All rights reserved.)

Objectives: Despite known overlaps in the pattern of cognitive impairments in individuals with bipolar disorder (BD), schizophrenia (SZ) and schizoaffective disorder (SZA), few studies have examined the extent to which cognitive performance validates traditional diagnostic boundaries in these groups., Method: Individuals with SZ (n=49), schizoaffective disorder (n=33) and BD (n=35) completed a battery of cognitive tests measuring the domains of processing speed, immediate memory, semantic memory, learning, working memory, executive function and sustained attention., Results: A discriminant functions analysis revealed a significant function comprising semantic memory, immediate memory and processing speed that maximally separated patients with SZ from those with BD. Initial classification scores on the basis of this function showed modest diagnostic accuracy, owing in part to the misclassification of SZA patients as having SZ. When SZA patients were removed from the model, a second cross-validated classifier yielded slightly improved diagnostic accuracy and a single function solution, of which semantic memory loaded most heavily., Conclusions: A cluster of non-executive cognitive processes appears to have some validity in mapping onto traditional nosological boundaries. However, since semantic memory performance was the primary driver of the discrimination between BD and SZ, it is possible that performance differences between the disorders in this cognitive domain in particular, index separate underlying aetiologies., (Copyright © 2015 Elsevier B.V. All rights reserved.)

Aberrant semantic processing has been linked to the etiology of formal thought disorder (TD) symptoms in schizophrenia. In this cross-sectional study, two prominent theories, overactivation and disorganized structure of semantic memory (SM), were examined in relation to TD symptoms using the continuum approach across two established semantic tasks (direct/indirect semantic priming and categorical fluency). The aim was to examine the validity of the two TD theories in relation to TD symptoms in schizophrenia. Greater direct and indirect priming, fluency productivity and category errors were expected if the data supported the overactivation theory. Reduced fluency productivity and increased category errors would be characteristic of disorganized storage. Fifty-seven schizophrenia/schizoaffective disorder patients and 48 controls completed a clinical assessment and the semantic tasks. There was significantly reduced direct priming in patients compared to controls (p<.05), while indirect priming was not significantly different; there was no association between TD and degree of priming. Patients produced more category-inappropriate words (p<.005) than controls, which was related to increasing severity of circumstantiality. The pattern of results was more indicative of a disorganized SM storage problem in this sample. This phenomenon may underlie some TD symptoms in general schizophrenia. The findings strengthen the relationship between SM deficits and TD symptoms, though this appears to differ between individual symptoms. The authors discuss the value of the continuum approach in addressing research questions in TD etiology. Given low levels of TD in this study, replication of these findings in a sample with greater TD is desirable.

Executive functioning (EF) impairments are common in schizophrenia. There are two propositions regarding the causes of these impairments: (1) executive impairments are the result of the compounding effects of deficits in lower order cognitive skills (e.g. processing speed, attention) or (2) EF impairments exist in their own right regardless of lower order skills. It is difficult to examine the separable effects of lower order cognitive skills on EF given the overlap required to complete most neuropsychological measures. One battery designed to parcel out the contributions of lower order skills from EF is the Delis-Kaplan Executive Function System (D-KEFS). Inhibition and switching specifically were examined using the D-KEFS versions of the Stroop and Trails task. No group differences in task performance after controlling for lower level skills would provide evidence for a generalised cognitive deficit. Group differences remaining after controlling for these influences would suggest a disproportionate deficit. Results supported both propositions. On both tasks, group differences reflecting slowed reaction time in the schizophrenia group disappeared when lower order skills were controlled for. Differences between groups performance in errors were only evident on the most complex versions of each task with more errors made by the schizophrenia group. These results suggest that (1) both RT and error data are needed to provide a full picture of performance and (2) the relationship between lower order and EF is too complex to provide support for one or the other proposal., (© 2013.)

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.

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. [ABSTRACT FROM AUTHOR]

Objective: The personality characteristics and symptoms observed in schizophrenia are postulated to lie on a continuum, with non-clinical manifestations referred to as schizotypy. High schizotypy behaviours are argued to correspond with the three main clusters of symptoms in schizophrenia: positive, negative and cognitive/disorganised symptoms, yet there is limited empirical evidence to support this. This study aimed to investigate whether schizotypy dimensions significantly correlate with their respective schizophrenia symptomatology in the largest sample to date. Methods: A total of 361 adults (103 patients with schizophrenia/schizoaffective disorder and 258 healthy controls) were assessed for schizotypy using the Oxford-Liverpool Inventory of Feelings and Experiences. The MATRICS Consensus Cognitive Battery supplemented by the Stroop task and Wisconsin Card Sorting Test was administered to all participants to obtain objective measurements of cognition. Schizophrenia symptomatology was assessed using the Positive and Negative Syndrome Scale in patients only. Results: The results demonstrated significant correlations between the Oxford-Liverpool Inventory of Feelings and Experiences positive and negative subscales and their respective Positive and Negative Syndrome Scale subscales only, indicating that positive and negative schizotypy dimensions across patients and controls accurately reflect the respective schizophrenia symptomatology observed in patients. Cognitive performance did not correlate with cognitive/disorganised symptom dimensions of the Oxford-Liverpool Inventory of Feelings and Experiences or the Positive and Negative Syndrome Scale, indicating that cognitive impairment is an independent symptom dimension that requires objective cognitive testing. Conclusion: Collectively, the findings provide empirical evidence for the continuum theory and support the use of schizotypy as a model for investigating schizophrenia. [ABSTRACT FROM AUTHOR]

IntroductionSchizotypy is a useful schizophrenia analogue that controls for confounding factors such as medication and general intellectual decline. In the current study this analogue approach was used to examine implicit/explicit and direct/indirect semantic memory function. This is the first study to examine both implicit and explicit semantic access in the same schizotypy sample. MethodsParticipants completed four semantic tasks: (1) implicit indirect priming, (2) implicit direct priming, (3) explicit object (indirect) task, and (4) explicit association (direct) task. The schizophrenia literature suggests that semantic impairments are associated with thought disorder. As such, participants were divided into low (n=18) and high (n=18) schizotypy groups based on their responses to a thought disorder subscale of the Oxford Liverpool Inventory of Feelings and Experiences (O-Life) scale. ResultsIn terms of implicit performance, the high schizotypy group demonstrated increased direct priming but nonsignificant indirect priming. The low schizotypy group demonstrated no significant difference in direct and indirect priming. Performance on the explicit tasks was equivalent between the two groups for direct stimuli. On the indirect explicit task, high schizotypy was associated with an increase in errors. ConclusionsIncreased direct priming in high schizotypy is equivalent to that seen in schizophrenia, which has been interpreted as increased spreading of activation. Abnormal performance using the indirect stimuli was found across implicit and explicit versions. The relevance of these findings to schizophrenia are discussed. [ABSTRACT FROM PUBLISHER]

Background It is believed that the personality characteristics and symptoms observed in schizophrenia lie on a continuum, with subclinical symptoms referred to as schizotypy. The continuum theory of schizophrenia recognises schizotypy as a suitable model for investigating schizophrenia: individuals with high levels of schizotypy demonstrate similar symptoms, cognitive profiles and neuroimaging findings to schizophrenia, albeit in a more subtle manner, without the potential confounding factors associated with schizophrenia. Both schizophrenia and schizotypy have been shown to be influenced by genetic factors. Neuregulin-1 (NRG1), involved in neuronal development, migration, myelination and synaptic plasticity, has been identified as a promising candidate gene for schizophrenia risk. Several NRG1 single nucleotide polymorphisms (SNPs) have been associated with schizophrenia and cognitive deficits, though only one SNP has been previously associated with schizotypy. The aim of this study was to examine the link between NRG1 and schizotypy across the schizotypy/schizophrenia continuum. Methods Participants were 200 adults (83 patients with schizophrenia and 117 healthy controls) who were assessed for schizotypy factors using the Oxford-Liverpool Inventory of Feelings and Experience (O-LIFE). The factors assessed were unusual experiences (UnEx), introvertive anhedonia (InAn) and cognitive disorganisation (CogDis), which are thought to reflect the positive, negative and cognitive symptoms of schizophrenia respectively. Participants were also genotyped for five NRG1 SNPs; rs10503929, rs3924999, rs2466058, rs35753505 and rs6994992. A MANOVA was conducted with schizotypy factors as dependent variables and participant group as independent variables to observe differences between patients and controls. Another MANOVA was conducted with schizotypy factors as dependent variables and NRG1 SNPs as independent variables to observe differences and interactions of the NRG1 SNPs on schizotypy across the continuum. Results Confirming previous findings, schizotypy scores were significantly higher in the patient group as compared to controls (p < 0.001). There were no significant differences in schizotypy scores for individual SNPs. However, significant interactions were observed between rs10503929 and rs3924999 (p = 0.006) and between rs10503929 and rs2466058 (p = 0.007) for combined schizotypy variables. Non-significant interaction trends were observed between rs10503929, rs3924999 and rs2466058 (p = 0.034) and between rs6994992, rs10503929 and rs2466058 (p = 0.11). Post-hoc analysis showed significant interaction between rs10503929 and rs3924999 for UnEx (p = 0.008) and non-significant interaction trends between rs10503929 and rs3924999 (p = 0.012) and rs10503929 and rs2466058 (p = 0.018) for CogDis. Discussion This is the first study to demonstrate an association between NRG1 and schizotypy across the continuum, in particular CogDis. From this, it can be inferred that genetic variation in NRG1 may be a contributing factor to cognitive deficits in the clinical population, consistent with previous findings. As individual SNPs were not significantly associated with schizotypy but significant interactions were observed, this study also demonstrates the heterogeneity of schizophrenia. This finding contributes to the literature associating NRG1 with cognitive deficits in schizophrenia and supports the use of schizotypy as a model for schizophrenia. [ABSTRACT FROM AUTHOR]