Interactions In Schizophrenia Research Articles

Schizophrenia in Bilingual Immigrants: is Verbal Fluency Preserved in Second Language Acquisition?

Objectives Language disturbances are the core symptoms of schizophrenia [Crow,2000]. Considering the influence of migration on the symptoms of schizophrenia [Bhugra, Gupta,2011] and few studies on the interaction of schizophrenia and bilingualism [Bersudsky, et al.,2005], we hope to clarify the linguistic profile of disorder and emphasize the role of language in schizophrenia research. Aim To examine the linguistic features of schizophrenia in the first (L1) and the second (L2) languages, particularly in fluency as the ability to cope with native and nonnative pragmatics. Methods Among sixty Russian immigrants to Israel diagnosed with schizophrenia, ten Russian-Hebrew fluent bilinguals met criteria for inclusion in the study (age: M=33.8,s.d.=11.0; length of residence: M=14.6,s.d.=6.8; time of immigration to diagnosis:M=5.3,s.d=3.9; PANSS Total score: M = 94.9,s.d = 9.8). Interviews were analyzed using clinical, linguistic and fluency speech markers. Statistical evaluation included t-test for dependent samples, two-way ANOVA(Fisher LSD post-hoc test). Results The mean length of language samples demonstrated more productivity in L1 (Table1). Clinical speech markers associated with thought disorders were similarly represented in both languages. Linguistic markers of schizophrenia occurred more often in L2. Discourse markers, as bilingual phenomenona, reflected more dysfluency in L1. Download : Download full-size image Conclusions 1) The higher frequency of linguistic schizophrenia markers in L2 shows more impairments in the syntax/semantic components of language, where different neural representations may underlay the two languages in a bilingual brain damaged by schizophrenia. 2) The higher frequency of fluency markers in L1 reflects attempts to maintain verbal fluency, evidenced by the use of L2 lexical items, which afford a compensatory resource for communicative discourse in schizophrenia.

Psychiatric genetics, neurogenetics, and neurodegeneration.

Psychiatric genetics, neurogenetics, and neurodegeneration.

Remediation of context-processing deficits in schizophrenia: preliminary data with ambiguous sentences.

BackgroundProcessing of contextual information is essential for the establishment of good interpersonal relations and communicational interactions. Nevertheless, it is known that schizophrenic patients present impairments in the processing of contextual information. The aim of this study is to explore the influence of the remediation of context processing in schizophrenic patients.MethodsThirty-one schizophrenic patients and 28 matched healthy participants were included in this study. All participants were assessed on verbal knowledge (Mill-Hill test) and depression intensity (Beck Depression Scale 21 items). Schizophrenic patients were also assessed on thought, language, and communication disorders (Thought, Language and Communication scale). All participants completed a disambiguation task with two different levels of contextualization (high or low context) and a context-processing remediation task containing social scenarios that included ambiguous words and were presented with two different types of instruction: with or without context explanation.ResultsFor the disambiguation task, results showed no effect of group, but a main effect of context, with better performances in the high-context than the low-context condition. For the context-processing remediation task, results showed a main effect of group: The performance of schizophrenic patients who had received explanations differed from that both of healthy participants and of schizophrenic patients who had not received explanations.ConclusionThis study revealed that for all participants, the structuring of context had a positive effect on the contextual integration of ambiguous words. Concerning the remediation task, explanations about the strategies that could be used to take context into account improved the schizophrenic patients’ performances. This allows us to consider new methods of remediation that could improve social interaction in schizophrenia.

Risk and protective effects of the complexin-2 gene and gene-environment interactions in schizophrenia.

Schizophrenia (SCZ) is a multifactorial chronic and disabling mental disease. The specific genetic variants contributing to disease complex phenotype are largely unknown. Growing amount of evidence suggested that aberrant synaptic connectivity contributes to SCZ pathogenesis. From this point of view, complexin-2, a presynaptic regulatory protein, represents here a special interest, since it has been recently shown that genetic variants of the CPLX2 gene may affect current cognitive performance in patients with SCZ. A specific objective of this study was to evaluate if tagging single nucleotide polymorphisms (rs3892909, rs1366116) of gene encoding complexin-2 protein (CPLX2) linked to SCZ and to examine their relationships with complexin-2 blood levels. DNA samples of 260 patients with SCZ and 260 sex- and age-matched healthy controls were genotyped for the selected polymorphisms by application of polymerase chain reaction with sequence-specific primers, and concentration of complexin-2 in the blood plasma was determined using the enzymelinked immunosorbent assay. All study subjects were unrelated Armenians. According to the obtained results, in the patients group both the frequency distribution and carriage rate of the CPLX2 rs1366116*T minor allele were higher than in controls. On the contrary, the frequency distribution and carriage rate of the CPLX2 rs3892909*T minor allele in control group were higher than in patients. This data suggested that the presence of the CPLX2 rs1366116*T allele increases susceptibility to SCZ, whereas the rs3892909*T allele of the CPLX2 decreases the risk of SCZ. Furthermore, we found that CPLX2 rs1366116*T heterozygosity is associated with earlier disease onset. No difference between complexin-2 plasma levels in patients and controls and no significant interaction between complexin-2 plasma levels and CPLX2 genotypes in both groups were observed. In summary, we concluded that the CPLX2 rs1366116*T variant represents a risk factor of SCZ, and that, at the same time, the CPLX2 rs3892909*T variant is protective against SCZ.

Lateral interactions in schizophrenia: What is the role of spatial frequency?

Lateral interactions in schizophrenia: What is the role of spatial frequency?

From Tones in Tinnitus to Sensed Social Interaction in Schizophrenia: How Understanding Cortical Organization Can Inform the Study of Hallucinations and Psychosis

The content, modality, and perceptual attributes of hallucinations and other psychotic symptoms may be related to neural representation at a single cell and population level in the cerebral cortex. A brief survey of some principles and examples of cortical representation and organization will be presented together with evidence for a correspondence between the neurobiology of brain areas activated at the time of a hallucination and the content of the corresponding hallucinatory and psychotic experiences. Contrasting the hallucinations of schizophrenia with other conditions, we highlight phenomenological aspects of hallucinations that are ignored in clinical practice but carry potentially important information about the brain regions and dysfunctions underlying them. Knowledge of cortical representation and organization are being used to develop animal models of hallucination and to test treatments that are now beginning to translate to the clinical domain.

Identification of gene ontologies linked to prefrontal-hippocampal functional coupling in the human brain.

Functional interactions between the dorsolateral prefrontal cortex and hippocampus during working memory have been studied extensively as an intermediate phenotype for schizophrenia. Coupling abnormalities have been found in patients, their unaffected siblings, and carriers of common genetic variants associated with schizophrenia, but the global genetic architecture of this imaging phenotype is unclear. To achieve genome-wide hypothesis-free identification of genes and pathways associated with prefrontal-hippocampal interactions, we combined gene set enrichment analysis with whole-genome genotyping and functional magnetic resonance imaging data from 269 healthy German volunteers. We found significant enrichment of the synapse organization and biogenesis gene set. This gene set included known schizophrenia risk genes, such as neural cell adhesion molecule (NRCAM) and calcium channel, voltage-dependent, beta 2 subunit (CACNB2), as well as genes with well-defined roles in neurodevelopmental and plasticity processes that are dysfunctional in schizophrenia and have mechanistic links to prefrontal-hippocampal functional interactions. Our results demonstrate a readily generalizable approach that can be used to identify the neurogenetic basis of systems-level phenotypes. Moreover, our findings identify gene sets in which genetic variation may contribute to disease risk through altered prefrontal-hippocampal functional interactions and suggest a link to both ongoing and developmental synaptic plasticity.

Identifying gene-environment interactions in schizophrenia: contemporary challenges for integrated, large-scale investigations.

Recent years have seen considerable progress in epidemiological and molecular genetic research into environmental and genetic factors in schizophrenia, but methodological uncertainties remain with regard to validating environmental exposures, and the population risk conferred by individual molecular genetic variants is small. There are now also a limited number of studies that have investigated molecular genetic candidate gene-environment interactions (G × E), however, so far, thorough replication of findings is rare and G × E research still faces several conceptual and methodological challenges. In this article, we aim to review these recent developments and illustrate how integrated, large-scale investigations may overcome contemporary challenges in G × E research, drawing on the example of a large, international, multi-center study into the identification and translational application of G × E in schizophrenia. While such investigations are now well underway, new challenges emerge for G × E research from late-breaking evidence that genetic variation and environmental exposures are, to a significant degree, shared across a range of psychiatric disorders, with potential overlap in phenotype.

Gene-sex interactions in schizophrenia: focus on dopamine neurotransmission

Schizophrenia is a severe mental disorder, with a highly complex and heterogenous clinical presentation. Our current perspectives posit that the pathogenic mechanisms of this illness lie in complex arrays of gene × environment interactions. Furthermore, several findings indicate that males have a higher susceptibility for schizophrenia, with earlier age of onset and overall poorer clinical prognosis. Based on these premises, several authors have recently begun exploring the possibility that the greater schizophrenia vulnerability in males may reflect specific gene × sex (G×S) interactions. Our knowledge on such G×S interactions in schizophrenia is still rudimentary; nevertheless, the bulk of preclinical evidence suggests that the molecular mechanisms for such interactions are likely contributed by the neurobiological effects of sex steroids on dopamine (DA) neurotransmission. Accordingly, several recent studies suggest a gender-specific association of certain DAergic genes with schizophrenia. These G×S interactions have been particularly documented for catechol-O-methyltransferase (COMT) and monoamine oxidase (MAO), the main enzymes catalyzing DA metabolism. In the present review, we will outline the current evidence on the interactions of DA-related genes and sex-related factors, and discuss the potential molecular substrates that may mediate their cooperative actions in schizophrenia pathogenesis.

Reduced susceptibility to confirmation bias in schizophrenia

Patients with schizophrenia (SZ) show cognitive impairments on a wide range of tasks, with clear deficiencies in tasks reliant on prefrontal cortex function and less consistently observed impairments in tasks recruiting the striatum. This study leverages tasks hypothesized to differentially recruit these neural structures to assess relative deficiencies of each. Forty-eight patients and 38 controls completed two reinforcement learning tasks hypothesized to interrogate prefrontal and striatal functions and their interaction. In each task, participants learned reward discriminations by trial and error and were tested on novel stimulus combinations to assess learned values. In the task putatively assessing fronto-striatal interaction, participants were (inaccurately) instructed that one of the stimuli was valuable. Consistent with prior reports and a model of confirmation bias, this manipulation resulted in overvaluation of the instructed stimulus after its true value had been experienced. Patients showed less susceptibility to this confirmation bias effect than did controls. In the choice bias task hypothesized to more purely assess striatal function, biases in endogenously and exogenously chosen actions were assessed. No group differences were observed. In the subset of participants who showed learning in both tasks, larger group differences were observed in the confirmation bias task than in the choice bias task. In the confirmation bias task, patients also showed impairment in the task conditions with no prior instruction. This deficit was most readily observed on the most deterministic discriminations. Taken together, these results suggest impairments in fronto-striatal interaction in SZ, rather than in striatal function per se.

Pathophysiology of Schizophrenia Based on Impaired Glial-Neuronal Interactions

The model of impaired glial-neuronal interactions in schizophrenia is based on the core hypothesis that non-functional astrocyte receptors may cause an unconstrained synaptic information flux such that glia lose their modulatory function in tripartite synapses. This may lead to a generalization of information processing in the neuronal networks responsible for delusions and hallucinations on the behavioral level. In this acute paranoid stage of schizophrenia, non-functional astrocytic receptors or their loss decompose the astrocyte domain organization with the effect that a gap between the neuronal and the glial networks arises. If the illness progresses the permanent synaptic neurotransmitter flux may additionally impair the oligodendrocyte-axonic interactions, accompanied by a “creeping” decay of oligodendroglia, axons and glial gap junctions responsible for severe cognitive impairment. Here we may deal with after-effects caused by the basic fault of information processing in tripartite synapses. The gaps between the neuronal and glial networks prohibit the neuronal reality testing of intentional programs presumably generated in the glial networks, called schizophrenic dysintentionality. In non-schizophrenic delusions glia may not be disturbed, but exhausted extrasynaptic information processing may cause an unconstrained synaptic flux responsible for delusions.

Nonverbal Behavior During Face-to-face Social Interaction in Schizophrenia

Patients with a diagnosis of schizophrenia display social cognitive deficits. However, little is known about patients' nonverbal communication during their social encounters with others. This review identified 17 studies investigating nonverbal communication in patients' unscripted face-to-face interactions, addressing a) nonverbal differences between patients and others, b) nonverbal behavior of the patients' partners, c) the association between nonverbal behavior and symptoms, and d) the association between nonverbal behavior and social outcomes. Patients displayed fewer nonverbal behaviors inviting interaction, with negative symptoms exacerbating this pattern. Positive symptoms were associated with heightened nonverbal behavior. Patients' partners changed their own nonverbal behavior in response to the patient. Reduced prosocial behaviors, inviting interaction, were associated with poorer social outcomes. The evidence suggests that patients' nonverbal behavior, during face-to-face interaction, is influenced by patients symptoms and impacts the success of their social interactions.

Reading impairment in schizophrenia: Dysconnectivity within the visual system

Patients with schizophrenia suffer from perceptual visual deficits. It remains unclear whether those deficits result from an isolated impairment of a localized brain process or from a more diffuse long-range dysconnectivity within the visual system. We aimed to explore, with a reading paradigm, the functioning of both ventral and dorsal visual pathways and their interaction in schizophrenia. Patients with schizophrenia and control subjects were studied using event-related functional MRI (fMRI) while reading words that were progressively degraded through word rotation or letter spacing. Reading intact or minimally degraded single words involves mainly the ventral visual pathway. Conversely, reading in non-optimal conditions involves both the ventral and the dorsal pathway. The reading paradigm thus allowed us to study the functioning of both pathways and their interaction.Behaviourally, patients with schizophrenia were selectively impaired at reading highly degraded words. While fMRI activation level was not different between patients and controls, functional connectivity between the ventral and dorsal visual pathways increased with word degradation in control subjects, but not in patients. Moreover, there was a negative correlation between the patients' behavioural sensitivity to stimulus degradation and dorso-ventral connectivity. This study suggests that perceptual visual deficits in schizophrenia could be related to dysconnectivity between dorsal and ventral visual pathways.

Schizophrenia Symptoms Relieved by CO-Induced Pallidal Lesion: A Case Report

Back to table of contents Previous article Next article LettersFull AccessSchizophrenia Symptoms Relieved by CO-Induced Pallidal Lesion: A Case ReportSalvatore Galati, M.D., Ph.D., and Claudio Städler, M.D.Salvatore GalatiSearch for more papers by this author, M.D., Ph.D., and Claudio StädlerSearch for more papers by this author, M.D.Published Online:1 Apr 2013https://doi.org/10.1176/appi.neuropsych.12060139AboutSectionsPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InEmail To the Editor: Although basal ganglia (BG) physiology is classically joined to motor function, increasing evidence has outlined its involvement also in cognitive and behavioral domains.1 Personality changes as well as clearly psychiatric traits can be recognized in BG syndromes like Parkinson’s disease, and BG alterations have been described in psychiatric disorders. In schizophrenia, changes in subcortical brain regions have been extensively observed.2 Herein, we describe a patient with schizophrenia who experienced a sustained remission after an occasional “selective” bilateral pallidal lesion induced by carbon monoxide (CO) intoxication.“Mrs. R” was a 50-year-old woman affected by a paranoid form of schizophrenia, with several hospitalizations for episodes of paranoia, complex auditory hallucinations, and delusional religious beliefs. During her life, she has been managed with several antipsychotic drugs, and the last therapy was based on haloperidol decanoate injections (200 mg every 4 weeks), with residual symptoms consisting of minor delusions and few episodes of auditory hallucinations.In December 2008, she was intoxicated with CO that caused an anoxic lesion of both pallidum structures, as shown in the MRI brain scan (Figure 1). During hospitalization, she was unexpectedly relating better, without paranoid or any delusion, and therefore no antipsychotic treatments were prescribed. Surprisingly, after the hospital discharge and in the following 2 years of visit appointments, she was completely stable, with full sustained psychiatric remission.FIGURE 1. Two Horizontal Sections of the MRI Scan Before and After CO IntoxicationRight: the two pallidal lesions.This unexpected clinical observation shines a further light on the intimate involvement of BG in schizophrenia. Although we cannot definitely demonstrate a causal relationship between the CO-mediated pallidal lesion and psychotic compensation, the temporal association is highly convincing. In one of the most fascinating patho-physiological theories, in schizophrenia, the pallidum is placed in overdrive by the hippocampus unbalancing the two distinct firing patterns of dopaminergic neurons of the ventral tegmental area.3 Particularly, the tonic component (responsible for the “background” dopamine) release is impaired, causing a lower threshold of the system sensitivity to short-term phasic increase of dopamine levels in response to behaviorally-relevant stimuli.3Thus, the present case could support this patho-physiological theory of schizophrenia, leading to a picture in the future of a neuro-surgical approach for this disorder as extensively proposed in other psychiatric conditions.4Neurocenter (EOC) of Southern Switzerland, SwitzerlandCorrespondence: Dr. Salvatore Galati, Neurocenter (EOC) of Southern Switzerland; e-mail: salvatore.[email protected]chReferences1 Afifi AK: The basal ganglia: a neural network with more than motor function. Semin Pediatr Neurol 2003; 10:3–10Crossref, Medline, Google Scholar2 Menon V, Anagnoson RT, Glover GH, et al.: Functional magnetic resonance imaging evidence for disrupted basal ganglia function in schizophrenia. Am J Psychiatry 2001; 158:646–649Crossref, Medline, Google Scholar3 Lisman JE, Coyle JT, Green RW, et al.: Circuit-based framework for understanding neurotransmitter and risk gene interactions in schizophrenia. Trends Neurosci 2008; 31:234–242Crossref, Medline, Google Scholar4 Schlaepfer TE, Bewernick B, Kayser S, et al.: Modulating affect, cognition, and behavior: prospects of deep brain stimulation for treatment-resistant psychiatric disorders. Front Integr Neurosci 2011; 5:29Crossref, Medline, Google Scholar FiguresReferencesCited byDetailsCited ByMutisme akinétique et lésion bipallidale après intoxication médicamenteuse à l’hydroxyzine. À propos d’un casL'Évolution Psychiatrique, Vol. 81, No. 1 Volume 25Issue 2 Spring 2013Pages E52-E53 Metrics PDF download History Published online 1 April 2013 Published in print 1 April 2013

A combined study of genetic association and brain imaging on the DAOA gene in schizophrenia

While there has been no objective biomarker available for both diagnosis and prognosis of schizophrenia, compelling evidence suggests that the glutamatergic system may influence susceptibility to schizophrenia. To test genetic association of the glutamatergic system with schizophrenia and abnormal brain activities in resting-state patients with schizophrenia, a two-stage association study was performed in 454 patients and 480 controls, followed by regional homogeneity (ReHo) analysis of resting-state functional magnetic resonance imaging in 48 first-episode medication-free patients and 43 well-matched controls. The differences in ReHo between genotypes of interest were initially tested by the Student's t-test and the 2 × 2 (genotypes × disease status) ANOVA was then performed to identify the main effects of genotypes, disease status and their interactions in schizophrenia. The stage-1 study showed association of the DAOA and PSEN2 genes with schizophrenia in a small sample; the stage-2 study with an expanded sample confirmed the disease association for 2-SNP and 3-SNP haplotypes, and the cis-phase interactions between rs2391191 and some other SNPs in the DAOA gene. Four clusters with altered ReHo in the bilateral culmen, left putamen and left cuneus were associated with rs2391191. Main effects of rs2391191 genotypes were found in the left putamen. The left cuneus showed a genotype × disease status interaction. In conclusion, the DAOA gene may confer genetic risk of schizophrenia and associate with the altered ReHo in schizophrenia; genotype effect and its interaction with disease status may contribute to the altered ReHo, leading to specific ReHo in schizophrenic brain due to glutamatergic modulation.

Neuregulin 1: a prime candidate for research into gene-environment interactions in schizophrenia? Insights from genetic rodent models

Schizophrenia is a multi-factorial disease characterized by a high heritability and environmental risk factors. In recent years, an increasing number of researchers worldwide have started investigating the “two-hit hypothesis” of schizophrenia predicting that genetic and environmental risk factors (GxE) interactively cause the development of the disorder. This work is starting to produce valuable new animal models and reveal novel insights into the pathophysiology of schizophrenia. This mini review will focus on recent advancements in the field made by challenging mutant and transgenic rodent models for the schizophrenia candidate gene neuregulin 1 (NRG1) with particular environmental factors. It will outline results obtained from mouse and rat models for various Nrg1 isoforms/isoform types (e.g., transmembrane domain Nrg1, Type II Nrg1), which have been exposed to different forms of stress (acute versus chronic, restraint versus social) and housing conditions (standard laboratory versus minimally enriched housing). These studies suggest Nrg1 as a prime candidate for GxE interactions in schizophrenia rodent models and that the use of rodent models will enable a better understanding of GxE interactions and the underlying mechanisms.

DISC1 mouse models as a tool to decipher gene-environment interactions in psychiatric disorders

DISC1 was discovered in a Scottish pedigree in which a chromosomal translocation that breaks this gene segregates with psychiatric disorders, mainly depression and schizophrenia. Linkage and association studies in diverse populations support DISC1 as a susceptibility gene to a variety of neuropsychiatric disorders. Many Disc1 mouse models have been generated to study its neuronal functions. These mouse models display variable phenotypes, some of them relevant to schizophrenia, others to depression. The Disc1 mouse models are popular genetic models for studying gene-environment interactions in schizophrenia. Five different Disc1 models have been combined with environmental factors. The environmental stressors employed can be classified as either early immune activation or later social paradigms. These studies cover major time points along the neurodevelopmental trajectory: prenatal, early postnatal, adolescence, and adulthood. Various combinations of molecular, anatomical and behavioral methods have been used to assess the outcomes. Additionally, three of the studies sought to rescue the resulting abnormalities. Here we provide background on the environmental paradigms used, summarize the results of these studies combining Disc1 mouse models with environmental stressors and discuss what we can learn and how to proceed. A major question is how the genetic and environmental factors determine which psychiatric disorder will be clinically manifested. To address this we can take advantage of the many Disc1 models available and expose them to the same environmental stressor. The complementary experiment would be to expose the same model to different environmental stressors. DISC1 is an ideal gene for this approach, since in the Scottish pedigree the same chromosomal translocation results in different psychiatric conditions.

Decanalization mediating gene-environment interactions in schizophrenia and other psychiatric disorders with neurodevelopmental etiology.

OPINION article Front. Behav. Neurosci., 13 November 2013Sec. Pathological Conditions Volume 7 - 2013 | https://doi.org/10.3389/fnbeh.2013.00157

Gene X Environment Interactions in Schizophrenia and Bipolar Disorder: Evidence from Neuroimaging

Introduction: Schizophrenia (SZ) and Bipolar disorder (BD) are considered as severe multifactorial diseases, stemming from genetic and environmental influences. Growing evidence supports gene x environment (GxE) interactions in these disorders and neuroimaging studies can help us to understand how those factors mechanistically interact. No reviews synthesized the existing data of neuroimaging studies in these issues.Methods: We conduct a systematic review on the neuroimaging studies exploring GxE interactions relative to SZ or BD in PubMed.Results: First results of the influence of genetic and environmental risks on brain structures came from monozygotic twin pairs concordant and discordant for SZ or BD. Few structural magnetic resonance imaging (sMRI) studies have explored the GxE interactions. No other imaging methods were found. Two main GxE interactions on brain volumes have arisen. First, an interaction between genetic liability to SZ and obstetric complications on gray matter, cerebrospinal fluid, and hippocampal volumes. Second, cannabis use and genetic liability interaction effects on cortical thickness and white matter volumes.Conclusion: Combining GxE interactions and neuroimaging domains is a promising approach. Genetic risk and environmental exposures such as cannabis or obstetrical complications seem to interact leading to specific neuroimaging cerebral alterations in SZ. They are suggestive of GxE interactions that confer phenotypic abnormalities in SZ and possibly BD. We need further, larger neuroimaging studies of GxE interactions for which we may propose a framework focusing on GxE interactions data already known to have a clinical effect such as infections, early stress, urbanicity, and substance abuse.

Cognition–emotion interactions in schizophrenia: Emerging evidence on working memory load and implicit facial-affective processing

Although much is known about working memory (WM) and emotion perception deficits in schizophrenia, little is known of how these deficits interact. We sought to address this gap by conducting a narrative review of relevant literatures and distilling core themes. First, people with schizophrenia have difficulty with high load and during initial phases of WM (e.g., encoding, early rehearsal), yet are able to activate WM-related prefrontal brain regions to the same maximal degree as comparison controls under certain circumstances. Second, people with schizophrenia have difficulty identifying and expressing facial emotions, yet demonstrate heightened automatic/implicit processing of facial emotions. Third, people with schizophrenia behaviourally demonstrate intact cognition–emotion interactions on laboratory tasks wherein emotional processing is automatic/implicit, yet demonstrate cognition–emotion disconnections in other levels of analysis. Insights are drawn from basic science showing interdependency between WM load and implicit emotion. Future research questions are raised regarding interactions between WM load and implicit facial-affective processing in schizophrenia.