Impacts of a Self-directed Social Resources Study Program on Negative Symptoms and Quality of Life in Schizophrenia Outpatients: A Randomized Controlled Trial.

To clarify whether a self-directed study program on social resources improves negative symptoms, quality of life (QOL), and social participation among outpatients with schizophrenia. Eighty-six participants were randomly divided into intervention and control groups. In addition to the usual day programs, the intervention group participated in a self-directed study program on social resources once a week for eight weeks. The control group participated only in the usual day programs. Negative symptoms and QOL were assessed at baseline and post-intervention using the Positive and Negative Syndrome Scale (PANSS) and the WHO Quality of Life-BREF (WHOQOL-BREF), respectively. Social participation was also assessed. After the intervention, there were no significant differences in the PANSS negative symptoms and WHOQOL-BREF total scores between the two groups. Within-group, PANSS negative symptom scores significantly improved in the intervention group (p < 0.05), but not in the control group. The WHOQOL-BREF physical health subscale scores improved significantly only in the intervention group (p < 0.05). Social participation remained unchanged between the intervention and control groups. The results suggest that a self-directed study program on social resources may be useful for improving negative symptoms and physical QOL in outpatients with schizophrenia. The findings highlight the potential of such interventions to bridge the existing gap in psychosocial rehabilitation strategies for this population.

Longitudinal assessment of ventricular volume trajectories in early-stage schizophrenia: evidence of both enlargement and shrinkage.

BACKGROUND: Lateral ventricular enlargement represents a canonical morphometric finding in chronic patients with schizophrenia; however, longitudinal studies elucidating complex dynamic trajectories of ventricular volume change during critical early disease stages are sparse. METHODS: We measured lateral ventricular volumes in 113 first-episode schizophrenia patients (FES) at baseline visit (11.7 months after illness onset, SD = 12.3) and 128 age- and sex-matched healthy controls (HC) using 3T MRI. MRI was then repeated in both FES and HC one year later. RESULTS: Compared to controls, ventricular enlargement was identified in 18.6% of patients with FES (14.1% annual ventricular volume (VV) increase; 95%CI: 5.4; 33.1). The ventricular expansion correlated with the severity of PANSS-negative symptoms at one-year follow-up (p = 0.0078). Nevertheless, 16.8% of FES showed an opposite pattern of statistically significant ventricular shrinkage during ≈ one-year follow-up (-9.5% annual VV decrease; 95%CI: -23.7; -2.4). There were no differences in sex, illness duration, age of onset, duration of untreated psychosis, body mass index, the incidence of Schneiderian symptoms, or cumulative antipsychotic dose among the patient groups exhibiting ventricular enlargement, shrinkage, or no change in VV. CONCLUSION: Both enlargement and ventricular shrinkage are equally present in the early stages of schizophrenia. The newly discovered early reduction of VV in a subgroup of patients emphasizes the need for further research to understand its mechanisms.

Differences in fractional amplitude of low-frequency fluctuations (fALFF) and cognitive function between untreated major depressive disorder and schizophrenia with depressive mood patients.

BACKGROUND: Distinguishing untreated major depressive disorder without medication (MDD) from schizophrenia with depressed mood (SZDM) poses a clinical challenge. This study aims to investigate differences in fractional amplitude of low-frequency fluctuations (fALFF) and cognition in untreated MDD and SZDM patients. METHODS: The study included 42 untreated MDD cases, 30 SZDM patients, and 46 healthy controls (HC). Cognitive assessment utilized the Repeatable Battery for the Assessment of Neuropsychological Status (RBANS). Resting-state functional magnetic resonance imaging (rs-fMRI) scans were conducted, and data were processed using fALFF in slow-4 and slow-5 bands. RESULTS: Significant fALFF changes were observed in four brain regions across MDD, SZDM, and HC groups for both slow-4 and slow-5 fALFF. Compared to SZDM, the MDD group showed increased slow-5 fALFF in the right gyrus rectus (RGR). Relative to HC, SZDM exhibited decreased slow-5 fALFF in the left gyrus rectus (LGR) and increased slow-5 fALFF in the right putamen. Changes in slow-5 fALFF in both RGR and LGR were negatively correlated with RBANS scores. No significant correlations were found between remaining fALFF (slow-4 and slow-5 bands) and RBANS scores in MDD or SZDM groups. CONCLUSIONS: Alterations in slow-5 fALFF in RGR may serve as potential biomarkers for distinguishing MDD from SZDM, providing preliminary insights into the neural mechanisms of cognitive function in schizophrenia.

Processing speed in first episode of psychosis and first-degree relatives: A candidate endophenotype of spectrum schizophrenia disorders.

OBJECTIVE: The processing speed (PS) is highly impacted in individuals experiencing their first episode of psychosis (FEP). Conducting family studies can help to determine whether PS can serve as an endophenotype of schizophrenia spectrum disorders (SSDs), offering valuable insights into the prevention and diagnosis of SSDs. METHOD: A comprehensive cognitive battery, encompassing tests for PS, verbal memory, visual memory, working memory, executive functions, motor dexterity, and attention, was administered to a sample consisting of 133 FEP patients, 146 parents, 98 siblings, and 202 healthy controls (HCs). Univariate analyses (analysis of covariance [ANCOVA]) were conducted to compare the different cognitive domains between groups, utilizing sex, age, and years of education as covariates and Bonferroni corrections. Effect sizes (ESs) were calculated for estimating the magnitude of differences between groups. RESULTS: Group comparisons revealed significant differences in all cognitive domains. PS was the most impaired function in patients. Parents and siblings had intermediate PS performance between FEP patients and HC. Large ES were observed in PS between FEP versus siblings, FEP versus controls, parents versus controls, and parents versus siblings. CONCLUSIONS: Despite not meeting all the necessary criteria, the PS observed in FEP patients and their first-degree relatives suggests its potential as a promising endophenotype of SSDs. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

Detecting schizophrenia with 3D structural brain MRI using deep learning.

Schizophrenia is a chronic neuropsychiatric disorder that causes distinct structural alterations within the brain. We hypothesize that deep learning applied to a structural neuroimaging dataset could detect disease-related alteration and improve classification and diagnostic accuracy. We tested this hypothesis using a single, widely available, and conventional T1-weighted MRI scan, from which we extracted the 3D whole-brain structure using standard post-processing methods. A deep learning model was then developed, optimized, and evaluated on three open datasets with T1-weighted MRI scans of patients with schizophrenia. Our proposed model outperformed the benchmark model, which was also trained with structural MR images using a 3D CNN architecture. Our model is capable of almost perfectly (area under the ROC curve = 0.987) distinguishing schizophrenia patients from healthy controls on unseen structural MRI scans. Regional analysis localized subcortical regions and ventricles as the most predictive brain regions. Subcortical structures serve a pivotal role in cognitive, affective, and social functions in humans, and structural abnormalities of these regions have been associated with schizophrenia. Our finding corroborates that schizophrenia is associated with widespread alterations in subcortical brain structure and the subcortical structural information provides prominent features in diagnostic classification. Together, these results further demonstrate the potential of deep learning to improve schizophrenia diagnosis and identify its structural neuroimaging signatures from a single, standard T1-weighted brain MRI.

Schizophrenia is associated with severe consequences / Asociación de la esquizofrenia con consecuencias graves

Schizophrenia is an illness that affects millions of individuals. It is typically accompanied by positive, negative and cognitive symptoms. These symptoms are typically associated with the onset and progression of schizophrenia. However, aside from these known symptoms, there are consequences of having schizophrenia. In particular, metabolic syndrome, early death and suicide, diseases, lowered pain perception, sexual dysfunction, aggressive behavior/victimization, stigma, and cognitive deficit are all consequences of having schizophrenia. In this paper, we review the various consequences of having schizophrenia. These consequences should be monitored for, much like the typical symptoms, but are usually omitted from treatment. (AU)

La esquizofrenia es una enfermedad que afecta a millones de individuos, y que normalmente se acompaña de síntomas positivos, negativos y cognitivos. Dichos síntomas están normalmente asociados al inicio y progresión de la esquizofrenia. Sin embargo, aparte de estos síntomas conocidos, existen consecuencias de padecer esquizofrenia. En particular, el síndrome metabólico, la muerte prematura y el suicidio, las enfermedades, la disminución de la percepción del dolor, la disfunción sexual, el comportamiento agresivo/victimización, el estigma, y el déficit cognitivo son consecuencias de padecer esquizofrenia. En este documento, revisamos las diversas consecuencias del padecimiento de esquizofrenia. Deberán supervisarse dichas consecuencias, al igual que los síntomas típicos, aunque normalmente se omiten del tratamiento de la enfermedad. (AU)

Early life stress, low-grade systemic inflammation and weaker suppression of the default mode network (DMN) during face processing in Schizophrenia.

Childhood trauma (CT) is associated with lower cognitive and social cognitive function in schizophrenia. Recent evidence suggests that the relationship between CT and cognition is mediated by both low-grade systemic inflammation and reduced connectivity of the default mode network (DMN) during resting state. This study sought to test whether the same pattern of associations was observed for DMN connectivity during task based activity. Fifty-three individuals with schizophrenia (SZ) or schizoaffective disorder (SZA) and one hundred and seventy six healthy participants were recruited from the Immune Response and Social Cognition (iRELATE) project. A panel of pro-inflammatory markers that included IL-6, IL-8, IL-10, tumour necrosis factor-alpha (TNFa), and C-reactive protein (CRP), were measured in plasma using ELISA. DMN connectivity was measured during an fMRI social cognitive face processing task. Patients showed evidence of low grade systemic inflammation and significantly increased connectivity between the left lateral parietal (LLP) cortex-cerebellum and LLP-left angular gyrus compared to healthy participants. Across the entire sample, IL-6 predicted increased connectivity between LLP-cerebellum, LLP-precuneus, and mPFC-bilateral-precentral-gyri and left postcentral gyrus. In turn, and again in the entire sample, IL-6 (but no other inflammatory marker) mediated the relationship between childhood physical neglect and LLP-cerebellum. Physical neglect scores also significantly predicted the positive association between IL-6 and LLP-precuneus connectivity. This is to our knowledge the first study that provides evidence that higher plasma IL-6 mediates the association between higher childhood neglect and increased DMN connectivity during task based activity. Consistent with our hypothesis, exposure to trauma is associated with weaker suppression of the DMN during a face processing task, and this association was mediated via increased inflammatory response. The findings may represent part of the biological mechanism by which CT and cognitive performance are related.

Review of Major Social Determinants of Health in Schizophrenia-Spectrum Psychotic Disorders: III. Biology.

BACKGROUND: Social determinants of health (SDoHs) are nonmedical factors that significantly impact health and longevity. We found no published reviews on the biology of SDoHs in schizophrenia-spectrum psychotic disorders (SSPD). STUDY DESIGN: We present an overview of pathophysiological mechanisms and neurobiological processes plausibly involved in the effects of major SDoHs on clinical outcomes in SSPD. STUDY RESULTS: This review of the biology of SDoHs focuses on early-life adversities, poverty, social disconnection, discrimination including racism, migration, disadvantaged neighborhoods, and food insecurity. These factors interact with psychological and biological factors to increase the risk and worsen the course and prognosis of schizophrenia. Published studies on the topic are limited by cross-sectional design, variable clinical and biomarker assessments, heterogeneous methods, and a lack of control for confounding variables. Drawing on preclinical and clinical studies, we propose a biological framework to consider the likely pathogenesis. Putative systemic pathophysiological processes include epigenetics, allostatic load, accelerated aging with inflammation (inflammaging), and the microbiome. These processes affect neural structures, brain function, neurochemistry, and neuroplasticity, impacting the development of psychosis, quality of life, cognitive impairment, physical comorbidities, and premature mortality. Our model provides a framework for research that could lead to developing specific strategies for prevention and treatment of the risk factors and biological processes, thereby improving the quality of life and increasing the longevity of people with SSPD. CONCLUSIONS: Biology of SDoHs in SSPD is an exciting area of research that points to innovative multidisciplinary team science for improving the course and prognosis of these serious psychiatric disorders.

Long-range inhibition synchronizes and updates prefrontal task activity.

Changes in patterns of activity within the medial prefrontal cortex enable rodents, non-human primates and humans to update their behaviour to adapt to changes in the environment-for example, during cognitive tasks1-5. Parvalbumin-expressing inhibitory neurons in the medial prefrontal cortex are important for learning new strategies during a rule-shift task6-8, but the circuit interactions that switch prefrontal network dynamics from maintaining to updating task-related patterns of activity remain unknown. Here we describe a mechanism that links parvalbumin-expressing neurons, a new callosal inhibitory connection, and changes in task representations. Whereas nonspecifically inhibiting all callosal projections does not prevent mice from learning rule shifts or disrupt the evolution of activity patterns, selectively inhibiting only callosal projections of parvalbumin-expressing neurons impairs rule-shift learning, desynchronizes the gamma-frequency activity that is necessary for learning8 and suppresses the reorganization of prefrontal activity patterns that normally accompanies rule-shift learning. This dissociation reveals how callosal parvalbumin-expressing projections switch the operating mode of prefrontal circuits from maintenance to updating by transmitting gamma synchrony and gating the ability of other callosal inputs to maintain previously established neural representations. Thus, callosal projections originating from parvalbumin-expressing neurons represent a key circuit locus for understanding and correcting the deficits in behavioural flexibility and gamma synchrony that have been implicated in schizophrenia and related conditions9,10.

Impaired emotion perception in schizophrenia shows sex differences with channel- and category-specific effects: A pilot study.

Individuals with schizophrenia reportedly demonstrate deficits in emotion perception. Relevant studies on the effects of decoder's sex, communication channels and emotion categories have produced mixed findings and seldom explored the interactions among these three key factors. The present pilot study examined how male and female individuals with schizophrenia and healthy controls perceived emotional (e.g., angry, happy, and sad) and neutral expressions from verbal semantic and nonverbal prosodic and facial channels. Twenty-eight (11 females) individuals with schizophrenia and 30 healthy controls (13 females) were asked to recognize emotional facial expressions, emotional prosody, and emotional semantics. Both accuracy and response time showed subpar performance for all communication channels and emotional categories in the schizophrenia group. More severe emotion perception deficits were found with the nonverbal (not the verbal) materials. There was also a reduced level of impairment with anger perception, especially in the female individuals with schizophrenia while biased perception towards emotional semantics was more pronounced in male individuals with schizophrenia. These findings, although preliminary, indicate the channel- and category-specific nature of emotion perception with potential sex differences among people with schizophrenia, which has important theoretical and practical implications.

Discrimination of auditory verbal hallucination in schizophrenia based on EEG brain networks.

Auditory verbal hallucinations (AVH) are a core positive symptom of schizophrenia and are regarded as a consequence of the functional breakdown in the related sensory process. Yet, the potential mechanism of AVH is still lacking. In the present study, we explored the difference between AVHs (n = 23) and non-AVHs (n = 19) in schizophrenia and healthy controls (n = 29) by using multidimensional electroencephalograms data during an auditory oddball task. Compared to healthy controls, both AVH and non-AVH groups showed reduced P300 amplitudes. Additionally, the results from brain networks analysis revealed that AVH patients showed reduced left frontal to posterior parietal/temporal connectivity compared to non-AVH patients. Moreover, using the fused network properties of both delta and theta bands as features for in-depth learning made it possible to identify the AVH from non-AVH patients at an accuracy of 80.95%. The left frontal-parietal/temporal networks seen in the auditory oddball paradigm might be underlying biomarkers of AVH in schizophrenia. This study demonstrated for the first time the functional breakdown of the auditory processing pathway in the AVH patients, leading to a better understanding of the atypical brain network of the AVH patients.

De novo mutations disturb early brain development more frequently than common variants in schizophrenia.

Investigating functional, temporal, and cell-type expression features of mutations is important for understanding a complex disease. Here, we collected and analyzed common variants and de novo mutations (DNMs) in schizophrenia (SCZ). We collected 2,636 missense and loss-of-function (LoF) DNMs in 2,263 genes across 3,477 SCZ patients (SCZ-DNMs). We curated three gene lists: (a) SCZ-neuroGenes (159 genes), which are intolerant to LoF and missense DNMs and are neurologically important, (b) SCZ-moduleGenes (52 genes), which were derived from network analyses of SCZ-DNMs, and (c) SCZ-commonGenes (120 genes) from a recent GWAS as reference. To compare temporal gene expression, we used the BrainSpan dataset. We defined a fetal effect score (FES) to quantify the involvement of each gene in prenatal brain development. We further employed the specificity indexes (SIs) to evaluate cell-type expression specificity from single-cell expression data in cerebral cortices of humans and mice. Compared with SCZ-commonGenes, SCZ-neuroGenes and SCZ-moduleGenes were highly expressed in the prenatal stage, had higher FESs, and had higher SIs in fetal replicating cells and undifferentiated cell types. Our results suggested that gene expression patterns in specific cell types in early fetal stages might have impacts on the risk of SCZ during adulthood.

Shared and distinct structural brain alterations and cognitive features in drug-naïve schizophrenia and bipolar disorder.

Our study aimed to examine the shared and distinct structural brain alterations, including cortical thickness(CT) and local gyrification index(LGI), and cognitive impairments between the early course stage of drug-naïve schizophrenia(SZ) and bipolar disorder(BD) patients when compared to healthy controls(HCs), and to further explore the correlation between altered brain structure and cognitive impairments. We included 72 SZ patients, 35 BD patients and 43 HCs. The cognitive function was assessed using the MATRICS Consensus Cognitive Battery. Cerebral cortex analyses were performed with FreeSurfer. Furthermore, any structural aberrations related to cognition impairments were examined. Cognitive impairments existed in SZ and BD patients and were much more severe and widespread in SZ patients, compared to HCs. There were no significant differences in LGI among three groups. Compared to HCs, SZ had thicker cortex in left pars triangularis, and BD showed thinner CT in left postcentral gyrus. In addition, BD showed thinner cortex in left pars triangularis, left pars opercularis, left insula and right fusiform gyrus compared to SZ. Moreover, our results indicated that CT in many brain areas were significantly correlated with cognitive function in HCs, but only CT of left pars triangularis was correlated with impaired social cognition found in SZ. The findings suggest that changes of CT in the left pars triangularis and left postcentral gyrus may be potential pathophysiological mechanisms of the cognition impairments in SZ and BD, respectively, and the divergent CT of partly brain areas in BD vs. SZ may help distinguish them in early phases.

Neural responses to biological motion distinguish autistic and schizotypal traits.

Difficulties in social interactions characterize both autism and schizophrenia and are correlated in the neurotypical population. It is unknown whether this represents a shared etiology or superficial phenotypic overlap. Both conditions exhibit atypical neural activity in response to the perception of social stimuli and decreased neural synchronization between individuals. This study investigated if neural activity and neural synchronization associated with biological motion perception are differentially associated with autistic and schizotypal traits in the neurotypical population. Participants viewed naturalistic social interactions while hemodynamic brain activity was measured with fMRI, which was modeled against a continuous measure of the extent of biological motion. General linear model analysis revealed that biological motion perception was associated with neural activity across the action observation network. However, intersubject phase synchronization analysis revealed neural activity to be synchronized between individuals in occipital and parietal areas but desynchronized in temporal and frontal regions. Autistic traits were associated with decreased neural activity (precuneus and middle cingulate gyrus), and schizotypal traits were associated with decreased neural synchronization (middle and inferior frontal gyri). Biological motion perception elicits divergent patterns of neural activity and synchronization, which dissociate autistic and schizotypal traits in the general population, suggesting that they originate from different neural mechanisms.

Decreased activation of parvalbumin interneurons in the medial prefrontal cortex in intact inbred Roman rats with schizophrenia-like reduced sensorimotor gating.

Prepulse inhibition (PPI) allows assessing schizophrenia-like sensorimotor gating deficits in rodents. Previous studies indicate that PPI is modulated by the medial prefrontal cortex (mPFC), which is in agreement with our findings showing that PPI differences in the Roman rats are associated with divergences in mPFC activity. Here, we explore whether differences in PPI and mPFC activity in male Roman rats can be explained by (i) differences in the activation (c-Fos) of inhibitory neurons (parvalbumin (PV) interneurons); and/or (ii) reduced excitatory drive (PSD-95) to PV interneurons. Our data show that low PPI in the Roman high-avoidance (RHA) rats is associated with reduced activation of PV interneurons. Moreover, the RHA rats exhibit decreased density of both PV interneurons and PSD-95 puncta on active PV interneurons. These findings point to reduced cortical inhibition as a candidate to explain the schizophrenia-like features observed in RHA rats and support the role of impaired cortical inhibition in schizophrenia.

Schizophrenia decreases guilt and increases self-disgust: Potential role of altered executive function.

Our knowledge of how the more complex self-conscious emotions (SCEs) are affected in schizophrenia is sparse. SCEs, unlike basic emotions, involve sophisticated frontal-lobe-related cognition, impairment of which characterizes the neurocognitive profile of schizophrenia. We investigated, in a cross-sectional study, whether SCEs (shame, guilt and self-disgust) are affected in schizophrenia, and the relationship between changes in SCEs and executive (dys)function. Twenty-nine Greek and thirty Arabic patients with schizophrenia were recruited alongside twenty-two Greek and thirty Arabic matched controls. Participants were administered the Self-Disgust Scale (TOSCA for shame and guilt was also administered to the Greek sample), and the Trail Making and Verbal Fluency Tests to measure executive function (EF). Trait levels of self-disgust and guilt were found to be higher and lower, respectively, in patients with schizophrenia relative to control participants; and poorer EF was related with higher trait levels of SD, but lower trait levels of guilt. The pattern of findings was largely unaffected when controlling for anxiety and depression. Given that altered levels of SCEs are closely related to poorer EF, we suggest that the link between EF and emotion regulation, widely established in basic emotions but under-studied in SCEs, may explain the current findings.

El gen del receptor cannabinoide tipo 2 se asocia con la comorbilidad entre esquizofrenia y dependencia de cannabis y el gen de la enzima amidohidrolasa de ácidos grasos se asocia con la dependencia de cannabis en población española / Cannabinoid receptor type 2 gene is associated with comorbidity of schizophrenia and cannabis dependence and fatty acid amide hydrolase gene is associated with cannabis dependence in the Spanish population

El sistema cannabinoide se ha asociado con varios trastornos psiquiátricos como la esquizofrenia y las adicciones. Diversos estudios hanobservado que algunos polimorfismos del receptor cannabinoide tipo2 (CNR2), del receptor cannabinoide tipo 1 (CNR1) y del gen de la enzima amido hidrolasa de ácidos grasos (FAAH) pueden ser factores deriesgo de estos trastornos. Hemos analizado diversos polimorfismos delsistema cannabinoide en pacientes diagnosticados de esquizofrenia sintrastorno por uso de sustancias (n = 379), esquizofrenia con trastornopor uso de cannabis (n = 124), dependientes de cannabis sin psicosisasociada (n = 71) y un grupo de control (316) procedentes de diversoshospitales y centros de asistencia sanitaria españoles. Hemos encontrado una asociación entre los polimorfismos rs35761398 y rs12744386 delCNR2 con la presencia de esquizofrenia y trastorno por uso de cannabis comórbido y una pérdida de heterocigosidad en el polimorfismors324420 del gen FAAH con la dependencia de cannabis en poblaciónespañola. Los polimorfismos rs35761398 y rs12744386 en CNR2 son factores de riesgo para esquizofrenia en sujetos dependientes de cannabis.La pérdida de heterocigosidad en el polimorfismo rs324420 en el genFAAH es un factor de riesgo para la dependencia de cannabis. (AU)

The endocannabinoid system has been associated with various psychiatric disorders, such as schizophrenia or addictive disorders. Recent studies have found that some polymorphisms in the cannabinoid receptortype 2 (CNR2), cannabinoid receptor type 1 (CNR1) and fatty acid amide hydrolase (FAAH) genes could play an important role as risk factorsin the etiology of these diseases. We analysed different cannabinoidgene polimorphisms from non-substance using patients diagnosed withschizophrenia (n = 379), schizophrenic patients with cannabis use disorders (n = 124), cannabis users who did not have psychoses (n = 71),and 316 controls from various Spanish hospitals and health centres.We found a statistical association between polymorphisms rs35761398and rs12744386 in the CNR2 gene and comorbidity of schizophreniaand cannabis dependence, as well as an association between loss ofheterozygosity (overdominance) for polymorphism rs324420 in theFAAH gene and cannabis dependence in a Spanish population sample.The rs35761398 and rs12744386 polymorphisms in the CNR2 gene aregenetic risk factors for schizophrenia in cannabis-dependent subjects.Loss of heterozygosity for polymorphism rs324420 in the FAAH gene isa genetic risk factor for cannabis dependence in this population. (AU)

Altered brain connectivity during visual stimulation in schizophrenia.

Schizophrenia (SCZ) can be described as a functional dysconnectivity syndrome that affects brain connectivity and circuitry. However, little is known about how sensory stimulation modulates network parameters in schizophrenia, such as their small-worldness (SW) during visual processing. To address this question, we applied graph theory algorithms to multi-electrode EEG recordings obtained during visual stimulation with a checkerboard pattern-reversal stimulus. Twenty-six volunteers participated in the study, 13 diagnosed with schizophrenia (SCZ; mean age = 38.3 years; SD = 9.61 years) and 13 healthy controls (HC; mean age = 28.92 years; SD = 12.92 years). The visually evoked potential (VEP) showed a global amplitude decrease (p < 0.05) for SCZ patients as opposed to HC but no differences in latency (p > 0.05). As a signature of functional connectivity, graph measures were obtained from the Magnitude-Squared Coherence between signals from pairs of occipital electrodes, separately for the alpha (8-13 Hz) and low-gamma (36-55 Hz) bands. For the alpha band, there was a significant effect of the visual stimulus on all measures (p < 0.05) but no group interaction between SCZ and HZ (p > 0.05). For the low-gamma spectrum, both groups showed a decrease of Characteristic Path Length (L) during visual stimulation (p < 0.05), but, contrary to the HC group, only SCZ significantly lowered their small-world (SW) connectivity index during visual stimulation (SCZ p < 0.05; HC p > 0.05). This indicates dysconnectivity of the functional network in the low-gamma band of SCZ during stimulation, which might indirectly reflect an altered ability to react to new sensory input in patients. These results provide novel evidence about a possible electrophysiological signature of the global deficits revealed by the application of graph theory onto electroencephalography in schizophrenia.