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Objective: Multiple sectional studies indicate that the cognitive functions of bipolar disorder (BD) patients in remission are damaged. These studies also suggest that cognitive functions get worse over time. Although the results are inconsistent, there are limited follow-up studies that reveal any contradictory results. Interestingly, there have been major difficulties in the interpretation related to this subject. In particular, scarcity of longitudinal studies and not eliminating the role of multidrug side effects on cognitive functions are just a few. Due to these aforementioned limitations, the longitudinal course of cognitive functions and their sectional differences were investigated in BD patients that underwent remission with monotherapy in this study. Methods: In this study, the cognitive functions (premorbid IQ, attention, executive functions, memory, visual-spatial skills, and psychomotor speed) of BD patients (n=27) in remission and on monotherapy for at least 1 month were assessed at baseline and at an 18 (6-77) month follow-up period and compared to healthy controls (n=35). Results: The BD group's performance was worse than those of the control group on tests that evaluated attention, executive functions including concept formation, mental flexibility, response inhibition, set shifting, and reasoning, verbal memory, and psychomotor speed. On the other hand, the BD group showed no significant differences at baseline and follow-up examinations. Conclusion: All cognitive functions of BD patients on monotherapy remained stable during the follow-up. This suggests that this group might be a sub-group of BD with good prognosis, and monotherapy may not be harmful on cognitive functions. On the other hand, it needs longer time to detect cognitive dysfunctions. [ABSTRACT FROM AUTHOR]

Introduction: Bipolar disorder is associated with cognitive dysfunction in several domains. Medication effect is a potential confounder that can only be statistically controlled in many studies. The cognitive profile in bipolar disorder during remission on maintenance antipsychotics or mood stabilizers medication has not been compared before. Methods: We compared the cognitive profile of bipolar disorder patients euthymic for 2 month or more on monotherapy with novel antipsychotics (AP) (n=16), lithium carbonate (Li) (n=25) or valproic acid (VPA; n=26). Forty-two individuals were assessed as controls. The cognitive battery included Wechsler Adult Intelligence Scale-Revised (WAIS-R) subtests, the Wechsler Memory Scale (WMS), and Wisconsin Card Sorting Test (WCST). Results: All three patient groups compared to controls performed poorly on the working memory and verbal memory tasks (F=3.59, df=3, p=0.02 for WAIS-R Arithmetic and F=123.64, df=3, p<0.01 for WMS Logical Memory). The differences remained significant after controlling for age. Across patients, the only significant difference was between the Li and AP groups in terms of working memory. The Li group performed better (F=3.59, df=2, p=0.02) and the difference survived correction for age and clinical features. Conclusions: The findings of this study suggest that working memory impairment in bipolar patients on monotherapy with atypical AP, whereas verbal memory impairment might be related to bipolar disorder itself. Working memory might be a state marker, whereas verbal memory could be a trait marker of bipolar disorder. Atypical AP might have an adverse effect on cognition in bipolar disorder. These findings cannot be generalized to all bipolar patients, particularly the poor responders to monotherapy. [ABSTRACT FROM AUTHOR]

Copyright of Archives of Neuropsychiatry / Nöropsikiyatri Arşivi is the property of Turkish Association of Neuropsychiatry and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Archives of Neuropsychiatry / Nöropsikiyatri Arşivi is the property of Turkish Association of Neuropsychiatry and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

The aim of this study was to determine the brain regions associated with suppressing the image of an object. We used functional magnetic resonance imaging (fMRI) during five mental tasks (imagining, suppressing, erasing, free thinking and resting) performed by the subjects. The analysis showed that the suppressing, erasing and imagining conditions all activated the parietal and prefrontal regions to a different extent. These results suggest that the regions associated with cognitive control were also activated while a simple mental process was performed. Additionally, the results showed that the parietal lobe is the key region for the suppression of a mental image. [ABSTRACT FROM AUTHOR]

There is a growing interest towards the nature of autism spectrum disorder (ASD) in adults in the social cognition literature to gain further insights about the nature of language and cognition. Joint attention, which constitutes the basis of any social encounter, is one of the important predictors of language development and social learning. Referring expressions are linguistic resources that speakers use to achieve joint attention by identifying and referring to the objects relevant to the ongoing interaction. Reference production and understanding involve the ability to think of and represent objects, to direct others' attention to relevant objects, and to identify what other speakers are talking about when they use such expressions. People with ASD exhibit difficulties for using such references since their competent use requires an understanding of the partner's cognitive status and what information might be available/accessible from the partner's perspective. Existing studies have produced conflicting characterizations since they tend to use simulated scenarios at the individual level of analysis. New experimental paradigms are needed that include both sides of naturalistic social interaction where eye movements and linguistic structures can be analyzed together. This study aims to address this need by employing a dual eye-tracking paradigm where linguistic structures are analyzed in relation to gaze correlates of joint attention. 21 ASD adults and 21 age/education-matched controls participated in the study. During the experiment, participants interacted through a computerized tangram puzzle. Participants assumed two interchanging roles; the presenter had access to the target shape and the workspace but could not move the tangram pieces, whereas the operator could only see the workspace and had control of the mouse. Our initial findings suggest that controls exhibited significantly higher level of gaze coordination than the ASD group, and there is a significant difference between gaze coordination levels observed for presenters and operators. [ABSTRACT FROM AUTHOR]

Background: There is evidence that environmental and genetic risk factors for schizophrenia spectrum disorders are transdiagnostic and mediated in part through a generic pathway of affective dysregulation., Methods: We analysed to what degree the impact of schizophrenia polygenic risk (PRS-SZ) and childhood adversity (CA) on psychosis outcomes was contingent on co-presence of affective dysregulation, defined as significant depressive symptoms, in (i) NEMESIS-2 ( n = 6646), a representative general population sample, interviewed four times over nine years and (ii) EUGEI ( n = 4068) a sample of patients with schizophrenia spectrum disorder, the siblings of these patients and controls., Results: The impact of PRS-SZ on psychosis showed significant dependence on co-presence of affective dysregulation in NEMESIS-2 [relative excess risk due to interaction (RERI): 1.01, p = 0.037] and in EUGEI (RERI = 3.39, p = 0.048). This was particularly evident for delusional ideation (NEMESIS-2: RERI = 1.74, p = 0.003; EUGEI: RERI = 4.16, p = 0.019) and not for hallucinatory experiences (NEMESIS-2: RERI = 0.65, p = 0.284; EUGEI: -0.37, p = 0.547). A similar and stronger pattern of results was evident for CA (RERI delusions and hallucinations: NEMESIS-2: 3.02, p < 0.001; EUGEI: 6.44, p < 0.001; RERI delusional ideation: NEMESIS-2: 3.79, p < 0.001; EUGEI: 5.43, p = 0.001; RERI hallucinatory experiences: NEMESIS-2: 2.46, p < 0.001; EUGEI: 0.54, p = 0.465)., Conclusions: The results, and internal replication, suggest that the effects of known genetic and non-genetic risk factors for psychosis are mediated in part through an affective pathway, from which early states of delusional meaning may arise.

Background: This study attempted to replicate whether a bias in probabilistic reasoning, or 'jumping to conclusions'(JTC) bias is associated with being a sibling of a patient with schizophrenia spectrum disorder; and if so, whether this association is contingent on subthreshold delusional ideation., Methods: Data were derived from the EUGEI project, a 25-centre, 15-country effort to study psychosis spectrum disorder. The current analyses included 1261 patients with schizophrenia spectrum disorder, 1282 siblings of patients and 1525 healthy comparison subjects, recruited in Spain (five centres), Turkey (three centres) and Serbia (one centre). The beads task was used to assess JTC bias. Lifetime experience of delusional ideation and hallucinatory experiences was assessed using the Community Assessment of Psychic Experiences. General cognitive abilities were taken into account in the analyses., Results: JTC bias was positively associated not only with patient status but also with sibling status [adjusted relative risk (aRR) ratio : 4.23 CI 95% 3.46-5.17 for siblings and aRR: 5.07 CI 95% 4.13-6.23 for patients]. The association between JTC bias and sibling status was stronger in those with higher levels of delusional ideation (aRR interaction in siblings: 3.77 CI 95% 1.67-8.51, and in patients: 2.15 CI 95% 0.94-4.92). The association between JTC bias and sibling status was not stronger in those with higher levels of hallucinatory experiences., Conclusions: These findings replicate earlier findings that JTC bias is associated with familial liability for psychosis and that this is contingent on the degree of delusional ideation but not hallucinations.

Background: A cumulative environmental exposure score for schizophrenia (exposome score for schizophrenia [ES-SCZ]) may provide potential utility for risk stratification and outcome prediction. Here, we investigated whether ES-SCZ was associated with functioning in patients with schizophrenia spectrum disorder, unaffected siblings, and healthy controls., Methods: This cross-sectional sample consisted of 1,261 patients, 1,282 unaffected siblings, and 1,525 healthy controls. The Global Assessment of Functioning (GAF) scale was used to assess functioning. ES-SCZ was calculated based on our previously validated method. The association between ES-SCZ and the GAF dimensions (symptom and disability) was analyzed by applying regression models in each group (patients, siblings, and controls). Additional models included polygenic risk score for schizophrenia (PRS-SCZ) as a covariate., Results: ES-SCZ was associated with the GAF dimensions in patients (symptom: B = -1.53, p-value = 0.001; disability: B = -1.44, p-value = 0.001), siblings (symptom: B = -3.07, p-value < 0.001; disability: B = -2.52, p-value < 0.001), and healthy controls (symptom: B = -1.50, p-value < 0.001; disability: B = -1.31, p-value < 0.001). The results remained the same after adjusting for PRS-SCZ. The degree of associations of ES-SCZ with both symptom and disability dimensions were higher in unaffected siblings than in patients and controls. By analyzing an independent dataset (the Genetic Risk and Outcome of Psychosis study), we replicated the results observed in the patient group., Conclusions: Our findings suggest that ES-SCZ shows promise for enhancing risk prediction and stratification in research practice. From a clinical perspective, ES-SCZ may aid in efforts of clinical characterization, operationalizing transdiagnostic clinical staging models, and personalizing clinical management.

Background: First-degree relatives of patients with psychotic disorder have higher levels of polygenic risk (PRS) for schizophrenia and higher levels of intermediate phenotypes., Methods: We conducted, using two different samples for discovery (n = 336 controls and 649 siblings of patients with psychotic disorder) and replication (n = 1208 controls and 1106 siblings), an analysis of association between PRS on the one hand and psychopathological and cognitive intermediate phenotypes of schizophrenia on the other in a sample at average genetic risk (healthy controls) and a sample at higher than average risk (healthy siblings of patients). Two subthreshold psychosis phenotypes, as well as a standardised measure of cognitive ability, based on a short version of the WAIS-III short form, were used. In addition, a measure of jumping to conclusion bias (replication sample only) was tested for association with PRS., Results: In both discovery and replication sample, evidence for an association between PRS and subthreshold psychosis phenotypes was observed in the relatives of patients, whereas in the controls no association was observed. Jumping to conclusion bias was similarly only associated with PRS in the sibling group. Cognitive ability was weakly negatively and non-significantly associated with PRS in both the sibling and the control group., Conclusions: The degree of endophenotypic expression of schizophrenia polygenic risk depends on having a sibling with psychotic disorder, suggestive of underlying gene-environment interaction. Cognitive biases may better index genetic risk of disorder than traditional measures of neurocognition, which instead may reflect the population distribution of cognitive ability impacting the prognosis of psychotic disorder.

Exposures constitute a dense network of the environment: exposome. Here, we argue for embracing the exposome paradigm to investigate the sum of nongenetic "risk" and show how predictive modeling approaches can be used to construct an exposome score (ES; an aggregated score of exposures) for schizophrenia. The training dataset consisted of patients with schizophrenia and controls, whereas the independent validation dataset consisted of patients, their unaffected siblings, and controls. Binary exposures were cannabis use, hearing impairment, winter birth, bullying, and emotional, physical, and sexual abuse along with physical and emotional neglect. We applied logistic regression (LR), Gaussian Naive Bayes (GNB), the least absolute shrinkage and selection operator (LASSO), and Ridge penalized classification models to the training dataset. ESs, the sum of weighted exposures based on coefficients from each model, were calculated in the validation dataset. In addition, we estimated ES based on meta-analyses and a simple sum score of exposures. Accuracy, sensitivity, specificity, area under the receiver operating characteristic, and Nagelkerke's R2 were compared. The ESMeta-analyses performed the worst, whereas the sum score and the ESGNB were worse than the ESLR that performed similar to the ESLASSO and ESRIDGE. The ESLR distinguished patients from controls (odds ratio [OR] = 1.94, P < .001), patients from siblings (OR = 1.58, P < .001), and siblings from controls (OR = 1.21, P = .001). An increase in ESLR was associated with a gradient increase of schizophrenia risk. In reference to the remaining fractions, the ESLR at top 30%, 20%, and 10% of the control distribution yielded ORs of 3.72, 3.74, and 4.77, respectively. Our findings demonstrate that predictive modeling approaches can be harnessed to evaluate the exposome., (© The Author(s) 2019. Published by Oxford University Press on behalf of the Maryland Psychiatric Research Center. All rights reserved. For permissions, please email: journals.permissions@oup.com.)

Objective: Multiple sectional studies indicate that the cognitive functions of bipolar disorder (BD) patients in remission are damaged. These studies also suggest that cognitive functions get worse over time. Although the results are inconsistent, there are limited follow-up studies that reveal any contradictory results. Interestingly, there have been major difficulties in the interpretation related to this subject. In particular, scarcity of longitudinal studies and not eliminating the role of multidrug side effects on cognitive functions are just a few. Due to these aforementioned limitations, the longitudinal course of cognitive functions and their sectional differences were investigated in BD patients that underwent remission with monotherapy in this study., Methods: In this study, the cognitive functions (premorbid IQ, attention, executive functions, memory, visual-spatial skills, and psychomotor speed) of BD patients (n=27) in remission and on monotherapy for at least 1 month were assessed at baseline and at an 18 (6-77) month follow-up period and compared to healthy controls (n=35)., Results: The BD group's performance was worse than those of the control group on tests that evaluated attention, executive functions including concept formation, mental flexibility, response inhibition, set shifting, and reasoning, verbal memory, and psychomotor speed. On the other hand, the BD group showed no significant differences at baseline and follow-up examinations., Conclusion: All cognitive functions of BD patients on monotherapy remained stable during the follow-up. This suggests that this group might be a sub-group of BD with good prognosis, and monotherapy may not be harmful on cognitive functions. On the other hand, it needs longer time to detect cognitive dysfunctions. Kewords: Bipolar disorder, neurocognition, euthymia, monotherapy, prospective design.

Introduction: Bipolar disorder is associated with cognitive dysfunction in several domains. Medication effect is a potential confounder that can only be statistically controlled in many studies. The cognitive profile in bipolar disorder during remission on maintenance antipsychotics or mood stabilizers medication has not been compared before., Methods: We compared the cognitive profile of bipolar disorder patients euthymic for 2 month or more on monotherapy with novel antipsychotics (AP) (n=16), lithium carbonate (Li) (n=25) or valproic acid (VPA; n=26). Forty-two individuals were assessed as controls. The cognitive battery included Wechsler Adult Intelligence Scale-Revised (WAIS-R) subtests, the Wechsler Memory Scale (WMS), and Wisconsin Card Sorting Test (WCST)., Results: All three patient groups compared to controls performed poorly on the working memory and verbal memory tasks (F=3.59, df=3, p=0.02 for WAIS-R Arithmetic and F=123.64, df=3, p<0.01 for WMS Logical Memory). The differences remained significant after controlling for age. Across patients, the only significant difference was between the Li and AP groups in terms of working memory. The Li group performed better (F=3.59, df=2, p=0.02) and the difference survived correction for age and clinical features., Conclusions: The findings of this study suggest that working memory impairment in bipolar patients on monotherapy with atypical AP, whereas verbal memory impairment might be related to bipolar disorder itself. Working memory might be a state marker, whereas verbal memory could be a trait marker of bipolar disorder. Atypical AP might have an adverse effect on cognition in bipolar disorder. These findings cannot be generalized to all bipolar patients, particularly the poor responders to monotherapy., Competing Interests: Conflict of Interest: No conflict of interest was declared by the authors.