scholarly journals Increased Homotopic Connectivity in the Prefrontal Cortex Modulated by Olanzapine Predicts Therapeutic Efficacy in Patients with Schizophrenia

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Xiaoxiao Shan ◽  
Rongyuan Liao ◽  
Yangpan Ou ◽  
Yudan Ding ◽  
Feng Liu ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Support Vector ◽  
Individual Treatment ◽  
Antipsychotic Treatment ◽  
Individual Response ◽  
Healthy Controls ◽  
Imaging Data ◽  
Antipsychotic Therapy ◽  
Olanzapine Treatment ◽  
Schizophrenic Patients

Background. Previous studies have revealed the abnormalities in homotopic connectivity in schizophrenia. However, the relationship of these deficits to antipsychotic treatment in schizophrenia remains unclear. This study explored the effects of antipsychotic therapy on brain homotopic connectivity and whether the homotopic connectivity of these regions might predict individual treatment response in schizophrenic patients. Methods. A total of 21 schizophrenic patients and 20 healthy controls were scanned by the resting-state functional magnetic resonance imaging. The patients received olanzapine treatment and were scanned at two time points. Voxel-mirrored homotopic connectivity (VMHC) and pattern classification techniques were applied to analyze the imaging data. Results. Schizophrenic patients presented significantly decreased VMHC in the temporal and inferior frontal gyri, medial prefrontal cortex (MPFC), and motor and low-level sensory processing regions (including the fusiform gyrus and cerebellum lobule VI) relative to healthy controls. The VMHC in the superior/middle MPFC was significantly increased in the patients after eight weeks of treatment. Support vector regression (SVR) analyses revealed that VMHC in the superior/middle MPFC at baseline can predict the symptomatic improvement of the positive and negative syndrome scale after eight weeks of treatment. Conclusions. This study demonstrated that olanzapine treatment may normalize decreased homotopic connectivity in the superior/middle MPFC in schizophrenic patients. The VMHC in the superior/middle MPFC may predict individual response for antipsychotic therapy. The findings of this study conduce to the comprehension of the therapy effects of antipsychotic medications on homotopic connectivity in schizophrenia.

scholarly journals Serum Cortisol and DHEA-S Levels in Schizophrenic Patients with Different Response to Antipsychotic Therapy: Association with Psychopathology / Серумски Концентрации На Кортизол И DHEA-S Кал Пациенти Со Шизофренша Со Различен Одговор На Антипсихотичната Терапша Асоци.1Аци.1А Со Психопатологшата

PRILOZI ◽  
2015 ◽  
Vol 36 (1) ◽  
pp. 175-182 ◽  
Author(s):  
Zoja Babinkostova ◽  
Branislav Stefanovski ◽  
Danijela Janicevic-Ivanovska ◽  
Valentina Samardziska ◽  
Lila Stojanovska
Keyword(s):  
Elevated Serum ◽  
Serum Cortisol ◽  
Control Group ◽  
Antipsychotic Treatment ◽  
Healthy Controls ◽  
Symptom Scale ◽  
Antipsychotic Therapy ◽  
Schizophrenic Patients ◽  
Different Response ◽  
Age And Sex

Abstract Background: Previous studies suggested that alterations in serum cortisol and DHEA-S levels may play a role in the pathophysiology of schizophrenia. Imbalance in serum cortisol and DHEA-S levels may be related to responsivity to antipsychotic treatment. Aim: To compare serum cortisol and DHEA-S levels between patients with schizophrenia and healthy controls and to evaluate their association with psychopathology in schizophrenic patients with different response to antipsychotic treatment. Material and Methods: This clinical prospective study included 60 patients with schizophrenia and 40 healthy age and sex matched controls. All patients experienced an acute exacerbation of the illness (PANSS: P1 and P3 ≥ 4). Clinical evaluation of patients was performed using the Positive and Negative Symptom Scale. A questionnaire for socio-demographic and clinical data collection was used. For the purposes of the study, the examined group was divided in two subgroups: responders and nonresponders. Serum cortisol and DHEA-S levels were measuredat baseline in all participants and after 3 and 6 weeks of the antipsychotic treatment in patients with schizophrenia. Results: Patients with schizophrenia had significantly higher serum cortisol and DHEA-S levels comparedwith control group. Responders had significantly higher serum cortisol and DHEA-S levels compared with nonresponders. Responders group had significant correlation between serum cortisol and PANSS positive scale score as well as between hostility and serum DHEA-S. Conclusion: Elevated serum cortisol and DHEA-S levels may play a role in the pathophysiology of schizophrenia. Serum cortisol and DHEA-S are associated with psychopathology in schizophrenic patients with different response to antipsychotic therapy.

scholarly journals Individualized prediction of illness course at the first psychotic episode: a support vector machine MRI study

2011 ◽  
Vol 42 (5) ◽  
pp. 1037-1047 ◽  
Author(s):  
J. Mourao-Miranda ◽  
A. A. T. S. Reinders ◽  
V. Rocha-Rego ◽  
J. Lappin ◽  
J. Rondina ◽  
...  
Keyword(s):  
Support Vector Machine ◽  
Support Vector ◽  
Psychotic Episode ◽  
Svm Classifier ◽  
Healthy Controls ◽  
Imaging Data ◽  
Healthy Individuals ◽  
First Psychotic Episode ◽  
Episodic Course ◽  
Individualized Prediction

BackgroundTo date, magnetic resonance imaging (MRI) has made little impact on the diagnosis and monitoring of psychoses in individual patients. In this study, we used a support vector machine (SVM) whole-brain classification approach to predict future illness course at the individual level from MRI data obtained at the first psychotic episode.MethodOne hundred patients at their first psychotic episode and 91 healthy controls had an MRI scan. Patients were re-evaluated 6.2 years (s.d.=2.3) later, and were classified as having a continuous, episodic or intermediate illness course. Twenty-eight subjects with a continuous course were compared with 28 patients with an episodic course and with 28 healthy controls. We trained each SVM classifier independently for the following contrasts: continuous versus episodic, continuous versus healthy controls, and episodic versus healthy controls.ResultsAt baseline, patients with a continuous course were already distinguishable, with significance above chance level, from both patients with an episodic course (p=0.004, sensitivity=71, specificity=68) and healthy individuals (p=0.01, sensitivity=71, specificity=61). Patients with an episodic course could not be distinguished from healthy individuals. When patients with an intermediate outcome were classified according to the discriminating pattern episodic versus continuous, 74% of those who did not develop other episodes were classified as episodic, and 65% of those who did develop further episodes were classified as continuous (p=0.035).ConclusionsWe provide preliminary evidence of MRI application in the individualized prediction of future illness course, using a simple and automated SVM pipeline. When replicated and validated in larger groups, this could enable targeted clinical decisions based on imaging data.

scholarly journals T10. BIOMARKERS IN TREATMENT-RESISTANT SCHIZOPHRENIA; THE BITS STUDY (A STUDY PROTOCOL)

2020 ◽  
Vol 46 (Supplement_1) ◽  
pp. S234-S235
Author(s):  
Rikke Hilker ◽  
Jimmi Nielsen ◽  
Mette Ødegaard Nielsen
Keyword(s):  
Structural Changes ◽  
Genetic Material ◽  
Antipsychotic Treatment ◽  
Imaging Data ◽  
Treatment Resistant ◽  
Neuronal Structure ◽  
Antipsychotic Therapy ◽  
Longitudinal Outcome ◽  
Bbb Permeability ◽  
And Function

Abstract Background Approximately 30% of patients diagnosed with schizophrenia do not respond to conventional antipsychotic therapy, however, around 30% of these patients will respond to treatment with clozapine. The remaining clozapine non-respondent patients can be defined as ultra-treatment resistant. Special characteristics (biomarkers) may be found in this subgroup of ultra-treatment resistant patients. Recent evidence points to a central role of altered immunological and anti-inflammatory response in schizophrenia. Studies have found that antipsychotic medication affect the immune system and alter levels of different cytokines, but no clear relation between the effect on cytokine levels and improvement in symptoms has been documented. Also increased permeability of the blood brain barrier (BBB) have been linked to psychosis, and a dysfunctional BBB may lead to structural changes in the white matter and neurochemical changes (glutamatergic abnormalities) in CNS. The longitudinal course of BBB alterations in psychosis and how this may influence changes in neuronal structure and function and relate to fluctuation in symptoms have not been examined. The aim of this study is to establish a database with the purpose of identifying biomarkers for treatment resistant schizophrenia (TRS), containing measures of psychopathology and function, treatment variables, brain imaging data, immunological markers from blood and cerebrospinal fluid, BBB-permeability and genetic material. The database will consist of a group of ultra-treatment resistant patients and a group of patients responding to clozapine matched on sex, age and duration of illness (±3 years). Specific aims: Hypothesis Methods The study is a naturalistic longitudinal study including patients with TRS. We plan a thorough examination twice with a three months interval and ultra-treatment resistant patients will be compared with patients stable on clozapine. Between examinations there will be no planned interference with the antipsychotic treatment, but antipsychotic treatment may be changed during the period in the intention to improve symptoms. The primary longitudinal outcome is comparing changes in BBB-permeability along with symptom-fluctuations. This will be done by comparing changes in qAlb, which is the gold standard technique measuring the CSF:serum albumin ratio (QAlb). Results The study has been approved by the regional ethical committee and data collection will begin in 2020. Discussion We expect the obtained results will contribute to a better pathophysiological understanding about illness markers and their progression over time and in relation to functional outcome.

scholarly journals Altered Structural Covariance of Insula, Cerebellum and Prefrontal Cortex Is Associated with Somatic Symptom Levels in Irritable Bowel Syndrome (IBS)

2021 ◽  
Vol 11 (12) ◽  
pp. 1580
Author(s):  
Cecilia Grinsvall ◽  
Lukas Van Oudenhove ◽  
Patrick Dupont ◽  
Hyo Jin Ryu ◽  
Maria Ljungberg ◽  
...  
Keyword(s):  
Irritable Bowel Syndrome ◽  
Prefrontal Cortex ◽  
Gray Matter ◽  
Brain Regions ◽  
Anterior Insula ◽  
Healthy Controls ◽  
Imaging Data ◽  
Structural Covariance ◽  
Sensitization Process ◽  
Irritable Bowel

Somatization, defined as the presence of multiple somatic symptoms, frequently occurs in irritable bowel syndrome (IBS) and may constitute the clinical manifestation of a neurobiological sensitization process. Brain imaging data was acquired with T1 weighted 3 tesla MRI, and gray matter morphometry were analyzed using FreeSurfer. We investigated differences in networks of structural covariance, based on graph analysis, between regional gray matter volumes in IBS-related brain regions between IBS patients with high and low somatization levels, and compared them to healthy controls (HCs). When comparing IBS low somatization (N = 31), IBS high somatization (N = 35), and HCs (N = 31), we found: (1) higher centrality and neighbourhood connectivity of prefrontal cortex subregions in IBS high somatization compared to healthy controls; (2) higher centrality of left cerebellum in IBS low somatization compared to both IBS high somatization and healthy controls; (3) higher centrality of the anterior insula in healthy controls compared to both IBS groups, and in IBS low compared to IBS high somatization. The altered structural covariance of prefrontal cortex and anterior insula in IBS high somatization implicates that prefrontal processes may be more important than insular in the neurobiological sensitization process associated with IBS high somatization.

Findings of Spectrum Funcional MRI (SF-MRI) in Schizophrenia

2011 ◽  
Vol 26 (S2) ◽  
pp. 942-942
Author(s):  
R. Martínez de Velasco Soriano ◽  
F. Pando Velasco ◽  
M. Serrano Díaz de Otálora ◽  
J. Gómez-Arnau Ramírez ◽  
C. Riaza Bermudo-Soriano
Keyword(s):  
Prefrontal Cortex ◽  
Psychotic Episode ◽  
Healthy Controls ◽  
Gamma Aminobutyric Acid ◽  
Measure Concentration ◽  
First Psychotic Episode ◽  
Neuronal Membranes ◽  
Schizophrenic Patients ◽  
Glutamine Synthesis ◽  
Indirect Indicator

IntroductionN-acetil-aspartate (NAA) is located inside the soma and dendrites. Its believed to be an indirect indicator of the metabolic activity of these cells. Phosphomonoesters (PME) are involved in synthesis of neuronal membranes and phosphodiesters (PDE) in its degradation. Glutamine, an aminoacid produced by glial cells, is transported into the neurone for its transformation into glutamate and gamma aminobutyric acid.MethodsReview clinical trials performed on schizophrenic patients with SF-MRI, with 31P y 1H, to measure concentration of NAA, PME, PDE and glutamine.ObjectivesDetecting chemichal alterations that could be used as indicators in schizophrenia.ResultsNAA concentration in temporal and frontal cortex of schizophrenic patients, are significantly lower than in healthy controls. In other trials, differences in NAA concentration (measured in prefrontal cortex) have not been found, comparing patients during their first psychotic episode and healthy controls. Lowered concentrations of PME and increased ones of PDE in prefrontal cortex of schizophrenic patients have been found. Glutamine levels are increased in schizophrenic patients, being directely correlated with the duration of the process. These levels are reduced when antipsychotic drugs are used.ConclusionsThe decrease on NAA levels at schizophrenia onset and on healthy relatives remark its value as an endophenotypical indicator, but not as an illness indicator. Changes on PME and PDE concentrations cannot be used as illness indicators. The increase on glutamine synthesis could be due to glutamatergic hypofunction in schizophrenic patients, but there are other factors that may cause it, so it cannot be used as an indicator.

Antipsychotic-induced tardive dyskinesia: The role of glutamatergic system

2016 ◽  
Vol 33 (S1) ◽  
pp. S97-S97
Author(s):  
A. Boiko ◽  
S. Ivanova ◽  
A. Semke
Keyword(s):  
Tardive Dyskinesia ◽  
Glutamate Transporter ◽  
Antipsychotic Treatment ◽  
Nucleotide Polymorphisms ◽  
Antipsychotic Therapy ◽  
Drug Induced ◽  
Schizophrenic Patients ◽  
Competing Interest

Tardive dyskinesia (TD) occurs in 20–25% of patients with long-term antipsychotic therapy. Abnormalities in glutamatergic transmission are considered one of the key components of the pathogenesis of drug-induced side effects. Glutamate acts as excitotoxin under certain conditions and in excessive concentrations.Aim is to study the concentration of glutamate and analysis of single nucleotide polymorphisms (SNP) in genes coding the glutamate transporter and NMDA-receptors in schizophrenic patients with TD and without it.The study group included 156 patients with schizophrenia receiving long-term antipsychotic treatment. Patients were divided into two groups: 63 patients with TD and 93 patients without it. Glutamate was determined in serum by spectrophotometric method. Determination of allelic variants of gene SLC1A2 (rs4354668) and GRIN2A (rs2650427, rs1969060) was performed by polymerase chain reaction in real-time.We found a significant (P < 0.05) increase of the concentration of glutamate in patients with TD. Significant (P < 0.05) reduction in frequency of genotype GG of GRIN2A (rs1969060) and TT of SLC1A2 (rs4354668) were found in patients with TD in comparison to group without TD. In the study of glutamate concentration depending on the genotype GRIN2A (rs1969060) and genotype SLC1A2 (rs4354668) we observed a statistically significant change: elevated levels of glutamic acid identified with the heterozygous genotype in patients.It is possible to suggest that reduction in frequency of these genotypes increases the risk of movement disorders due to the protective effect of these genotypes.Disclosure of interestThe authors have not supplied their declaration of competing interest.

scholarly journals Large-scale Gradient Dysfunction of the Functional Connectome in Major Depression

2020 ◽  
Author(s):  
Mingrui Xia ◽  
Jin Liu ◽  
Xiaoyi Sun ◽  
Qing Ma ◽  
Xiaoqin Wang ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cognitive Processing ◽  
Sensory Processing ◽  
Large Scale ◽  
Support Vector ◽  
Ion Binding ◽  
Healthy Controls ◽  
Learning Approaches ◽  
Imaging Data ◽  
Shed Light

AbstractMajor depressive disorder (MDD) is associated with coexisting disturbances in low-level sensory processing and high-order cognitive functions. However, the neurobiological mechanism underlying these phenotype deficits remains poorly understood. Here, we collect large-sample, multisite resting-state functional magnetic resonance imaging data (1,150 patients with MDD and 1,084 healthy controls) and postmortem gene expression data. We show downgraded and contracted connectome gradients that are mainly involved in primary sensory and transmodal regions in patients with MDD relative to healthy controls, leveraging an association with gene expression enriched in transsynaptic signaling and calcium ion binding. Machine learning approaches based on support vector regression suggest that the alterations of connectome gradients in patients significantly predict depressive symptoms. These results shed light on gradient dysfunction of the large-scale functional connectomes in MDD and consolidate the spectrum deficits of sensory and cognitive processing in this disorder.

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