P.0592 Investigating the relationships of N100-P3b with symptom dimensions and cognitive impairments in subjects with chronic schizophrenia

2021 ◽  
Vol 53 ◽  
pp. S432-S433
Author(s):  
G.M. Giordano ◽  
A. Perrottelli ◽  
A. Mucci ◽  
G. Di Lorenzo ◽  
F. Ferrentino ◽  
...  
2010 ◽  
Vol 117 (2-3) ◽  
pp. 216
Author(s):  
Lena A. Schmid ◽  
Marc M. Lässer ◽  
Christina J. Herold ◽  
Ulrich Seidl ◽  
Johannes Schröder

2011 ◽  
Vol 26 (S2) ◽  
pp. 1421-1421
Author(s):  
D. Kontis ◽  
E. Theochari ◽  
S. Kleisas ◽  
I. Makris ◽  
S. Kalogerakou ◽  
...  

IntroductionAlthough it is well established that patients with schizophrenia demonstrate cognitive impairments, little is known about their complaints concerning their cognition. We investigate the association of these complaints with clinical symptoms, global functioning and cognitive performance.Method93 patients with chronic schizophrenia (mean age = 42,59 years, SD = 9,83; mean illness duration = 18,43 years, SD = 11,84) were recruited from one psychiatric department. Their cognitive complaints (Subjective Scale to Investigate Cognition in Schizophrenia-SSTICS), clinical symptoms (Calgary depression scale-CDS, PANSS, GAF), and neuropsychological performance (7 non-verbal CANTAB tests involving psychomotor speed, attention, memory, and executive function and WAIS-III) were assessed at a time that they were able to cooperate with neuropsychological testing. Correlation analyses were performed between SSTICS scores and measures of symptoms, functioning or cognition, using the SPSS.ResultsSSTICS total score positively correlated with CDS total score (Spearman's rho = 0.311, p = 0.03). Positive correlations were also found between the SSTICS items and CDS total score. Similarly, SSTICS total score positively correlated with PANSS total score (Pearson r = 0,294, p = 0.04). PANSS negative and general psychopathology scores (r = 0,219, p = 0.035 and r = 0.333, p = 0.01, respectively), but not PANSS positive scores accounted for this relationship. SSTICS total score negatively correlated with GAF (rho = −0.251, p = 0.017). No significant associations were revealed between SSTICS total scores and PANSS insight item, PANSS cognitive score, CANTAB or WAIS scores.ConclusionsThe complaints of patients with schizophrenia about their cognitive impairments are mostly related to their depressive, negative, general psychopathological symptoms and global functioning, rather than their actual cognitive deficits.


2012 ◽  
Vol 18 (4) ◽  
pp. 459-465 ◽  
Author(s):  
O. D. Howes ◽  
P. Fusar-Poli ◽  
M. Bloomfield ◽  
S. Selvaraj ◽  
P. McGuire

2009 ◽  
Vol 24 (S1) ◽  
pp. 1-1
Author(s):  
C. Tintila ◽  
I.V. Miclutia ◽  
C. Popescu ◽  
I. Barsan

Aims:The aims of the current study are:•To examine the clinical symptoms and functional capacity of the patients.•To evaluate the cognitive dysfunctions and to see how they develop in 6 month.•To examine the relationship between clinical and functional capacity and the cognitive dysfunctions of the chronic schizophrenia patients.Method:24 people with chronic schizophrenia were followed up 6 month along with a control group of 50 individuals free from schizophrenia. Patients were diagnosed using DSM-IV criteria, assessed with the PANSS, GAF, to evaluate psychiatric symptoms, respectively functionality. Rey Memory Test, Trail Making, Spatial Recognition Memory (SRM),Spatial Working Memory (SWM), Paired Associated Learning (PAL), Spatial Spam (SSP) and Stoking of Cambridge (SOC) from the CANTAB were applied to all patients at the start point of the study and after 6 month, in order to evaluate the cognitive functions.Results:The overall performance of chronic schizophrenia patients was significantly lower compared to healthy individuals on all cognitive tasks. the cognitive dysfunction is independent of age and intellectual level, but does correlate with global functioning and remain stable. CANTAB is a useful tool to detect and estimate the cognitive impairments.Conclusions:The current study reveals that cognitive impairments are a central feature of schizophrenia and a major cause of poor functioning of the patients. the chronic schizophrenia patients perform worse on all investigated cognitive domains (memory, attention and executive function). the reviewed studies show different opinions about the development of these impairments. Further longitudinal studies are required in order to settle if they remain stable or progress in time.


Therapy ◽  
2005 ◽  
Vol 2 (3) ◽  
pp. 399-406
Author(s):  
Shahin Akhondzadeh ◽  
K Mackinejad ◽  
SA Ahmadi-Abhari ◽  
ZM Alem

Author(s):  
Michael Maes ◽  
Sunee Sirivichayakul ◽  
Andressa Keiko Matsumoto ◽  
Annabel Maes ◽  
Ana Paula Michelin ◽  
...  

Accumulating evidence suggests that TNF-α-mediated immune-neurotoxicity contributes to cognitive impairments and the overall severity of schizophrenia (OSOS). There are no data whether peripheral IL-6 and IL-4 may affect the phenome of schizophrenia above and beyond the effects of TNF-α and whether those cytokines are regulated by lowered natural IgM to malondialdehyde (MDA) and paraoxonase 1 enzyme activity. We assessed the aforementioned biomarkers in schizophrenia patients with (n=40) and without (n=40) deficit schizophrenia and 40 healthy controls. Deficit schizophrenia was best predicted by a combination of increased IL-6 and PON1 status (QQ genotype and lowered CMPAase activity) and lowered IgM to MDA. Partial Least Squares bootstrapping shows that 41.0% of the variance in negative symptoms, psychosis, hostility, excitation, mannerism, psychomotor retardation, and formal thought disorders was explained by increased TNF-α and PON1 status (QQ genotype and lowered CMPAase activity), lowered IL-4 and IgM to MDA as well as male sex and lowered education. We found that 47.9% of the variance in verbal fluency, word list memory, true recall, Mini-Mental State Examination, and executive functions was predicted by increased TNF-α and lowered IL-4, IgM to MDA and education. In addition, both TNF-α and IL-4 levels were significantly associated with lowered IgM to MDA, while TNF-α was correlated with PON1 status. These data provide evidence that the symptomatic (both the deficit subtype and OSOS) and cognitive impairments in schizophrenia are to a large extent mediated by the effects of immune-mediated neurotoxicity as well as lowered regulation by the innate immune system.


2020 ◽  
Vol 46 (Supplement_1) ◽  
pp. S200-S201
Author(s):  
Matthias Kirschner ◽  
Golia Shafiei ◽  
Ross D Markello ◽  
Carolina Markowsky ◽  
Alexandra Talpalaru ◽  
...  

Abstract Background Although widespread structural brain abnormalities have been consistently reported in schizophrenia, their relation to the heterogeneous clinical manifestations is not well understood. Multivariate methods are needed to uncover covariance patterns between multiple symptom dimensions and system-wide brain imaging data. Methods This cross-sectional study used structural magnetic resonance imaging and neuropsychological data from 133 patients with chronic schizophrenia (48 female, 34.8±13.2 years) from the Northwestern University Schizophrenia Data and Software Tool (NUSDAST). We estimate disease-related voxel-wise tissue volume loss using deformation-based morphometry (DBM) of T1 weighted images. In patients with schizophrenia, multiple clinical dimensions including positive/negative symptoms and cognitive deficits, demographic data as well as individual tissue volume loss (DBM) were included in the multivariate model. Clinical-anatomical phenotypes were identified using partial least squares analysis. Results Multivariate analysis revealed three distinct clinical-anatomical phenotypes accounting for 27.5%, 15%, and 13% of the shared covariance between clinical-behavioural data and tissue volume loss (total of 55.5%). The first clinical-anatomical phenotype encompassed cognitive impairments, severity of negative symptoms and tissue volume loss within the default mode network and visual network. The second clinical-anatomical phenotype was associated with additional cognitive impairments and tissue volume loss within the frontoparietal and ventral attention network, while the third clinical-anatomical phenotype encompassed a mixed positive and negative symptoms phenotype and tissue volume loss within the dorsal attention network. Critically, the pattern of volume loss within the first most prevalent clinical-anatomical phenotype mediated (a*b) the effect of socioeconomic status on clinical outcome (cognitive performance and negative symptoms) (a*b=-0.033(0.008); P<1.0×〖10〗^(-4); 95% CI [-0.049, -0.018]). Finally, we partly replicated the first clinical-anatomical phenotype in an independent sample of patients with schizophrenia (n=108). Discussion The heterogeneous clinical manifestation of schizophrenia can be significantly explained by three clinical-anatomical phenotypes. Despite their distributed topography, each phenotype is centered on a specific, well-defined set of intrinsic networks.


Sign in / Sign up

Export Citation Format

Share Document