Lobe In Schizophrenia Research Articles

Facial emotion perception abilities are related to grey matter volume in the culmen of cerebellum anterior lobe in drug-naïve patients with first-episode schizophrenia.

Impaired capability for understanding and interpreting the expressions on other people's faces manifests itself as a core feature of schizophrenia, contributing to social dysfunction. With the purpose of better understanding of the neurobiological basis of facial emotion perception deficits in schizophrenia, we investigated facial emotion perception abilities and regional structural brain abnormalities in drug-naïve patients with first-episode schizophrenia, and then examined the correlation between them. Fifty-two drug-naive patients with first-episode schizophrenia and 29 group-matched healthy controls were examined for facial emotion perception abilities assessed with the Facial Emotion Categorization and performed magnetic resonance imaging. The Facial Emotion Categorization data were inserted into a logistic function model so as to calculate shift point and slope as outcome measurements. Voxel-based morphometry was applied to investigate regional grey matter volume (GMV) alterations. The relationship between facial emotion perception and GMV was explored in patients using voxel-wise correlation analysis within brain regions that showed a significant GMV alterations in patients compared with controls. The schizophrenic patients performed differently on Facial Emotion Categorization tasks from the controls and presented a higher shift point and a steeper slope. Relative to the controls, patients showed GMV reductions in the superior temporal gyrus, middle occipital gyrus, parahippocampa gyrus, posterior cingulate, the culmen of cerebellum anterior lobe, cerebellar tonsil, and the declive of cerebellum posterior lobe. Importantly, abnormal performance on Facial Emotion Categorization was found correlated with GMV alterations in the culmen of cerebellum anterior lobe in schizophrenia. This study suggests that reduced GMV in the culmen of cerebellum anterior lobe occurs in first-episode schizophrenia, constituting a potential neuropathological basis for the impaired facial emotion perception in schizophrenia.

The Correlation of P100 Latency and P100 Amplitude in Patients with Schizophrenia and Migraine Headache Using Visual Evoked Potentials (VEPS)

Background: The VEPs provide an objective measure of brain function, analyzing integrity of visual processing. With patients affected with schizophrenia, the changes with the implementation of VEP are evident, such as symmetrical deceleration of the impulse (reduction of the amplitude) and the continuance of latency, which points to a degenerative illness, suggesting the presence of optical neuritis or hemianopsia conjoined with mentioned intracranial illness. Objective: The aim of the study was to determine the correlation of l P100 latency and P100 amplitude (µV) between patients with schizophrenia and patients with migraine headache. Visual evoked potentials (VEPs) were applied. Methods: The sample included 80 subjects: a) S group- 40 patients with schizophrenia (21 males; 19 females), b) H group-40 healthy subjects with migraine headache (10 males; 30 females). The study was conducted at the Department of Psychiatry, Neurology and Radiology, University Clinical Center Sarajevo. Results: Our research revealed positive correlations were registered in P100 latency in left view field of both eyes and in P100 amplitude in the region of right eye (p=0.01) in comparison with left eye region (p=0.05) in patients with schizophrenia. Conclusion: Results imply that the cognitive impairment seen in schizophrenia is not just due to deficits in higher order aspects of cognition but also encompasses significant deficits in early sensory processing. Our study is useful to initiate new questions and recommendations for further studies, specifically on changes in the occipital lobe in the schizophrenic patient’s brain. Changes in the volume in the occipital lobe are quite evident and further studies are required to better understand how the progressive brain changes affect the structural, functional, and metabolic activities of the occipital lobe in schizophrenia.

Abnormal prediction error processing in schizophrenia and depression

To make adaptive decisions under uncertainty, individuals need to actively monitor the discrepancy between expected outcomes and actual outcomes, known as prediction errors. Reward‐based learning deficits have been shown in both depression and schizophrenia patients. For this study, we compiled studies that investigated prediction error processing in depression and schizophrenia patients and performed a series of meta‐analyses. In both groups, positive t‐maps of prediction error tend to yield striatum activity across studies. The analysis of negative t‐maps of prediction error revealed two large clusters within the right superior and inferior frontal lobes in schizophrenia and the medial prefrontal cortex and bilateral insula in depression. The concordant posterior cingulate activity was observed in both patient groups, more prominent in the depression group and absent in the healthy control group. These findings suggest a possible role in dopamine‐rich areas associated with the encoding of prediction errors in depression and schizophrenia.

Structural and Functional Alterations of the Temporal lobe in Schizophrenia: A Literature Review.

Schizophrenia is a severe chronic mental illness leading to social and occupational dysfunction. Our primary focus in this review article was to analyze further the structural and functional alterations of the temporal lobe in patients with schizophrenia, which might contribute to the associated manifestations we often see in this illness. Our goal was to see if there was any correlation between temporal lobe abnormalities, more specifically, alterations in brain volume and specific symptoms such as auditory and language processing, etc. There is a positive correlation between volume alterations and thoughts disorders in the temporal lobe in the majority of studies. However, superior temporal gyrus volume has also been correlated negatively with the severity of hallucinations and thought disorders in some studies. We utilized Medical Subject Heading (MeSH) search strategy via PubMed database in our articles search yielding 241 papers. After the application of specific inclusion and exclusion criteria, a final number of 30 was reviewed. The involvement of the temporal lobe and its gray and white matter volume alterations in schizophrenia is quite apparent from our research; however, the exact mechanism of the underlying biological process is not thoroughly studied yet. Therefore, further research on larger cohorts combining different imaging modalities including volumetry, diffusion tensor, and functional imaging is required to explain how the progressive brain changes affect the various structural, functional, and metabolic activities of the temporal lobe in schizophrenia.

Covarying structural alterations in laterality of the temporal lobe in schizophrenia: A case for source-based laterality.

The human brain is asymmetrically lateralized for certain functions (such as language processing) to regions in one hemisphere relative to the other. Asymmetries are measured with a laterality index (LI). However, traditional LI measures are limited by a lack of consensus on metrics used for its calculation. To address this limitation, source-based laterality (SBL) leverages an independent component analysis for the identification of laterality-specific alterations, identifying covarying components between hemispheres across subjects. SBL is successfully implemented with simulated data with inherent differences in laterality. SBL is then compared with a voxel-wise analysis utilizing structural data from a sample of patients with schizophrenia and controls without schizophrenia. SBL group comparisons identified three distinct temporal regions and one cerebellar region with significantly altered laterality in patients with schizophrenia relative to controls. Previous work highlights reductions in laterality (ie, reduced left gray matter volume) in patients with schizophrenia compared with controls without schizophrenia. Results from this pilot SBL project are the first, to our knowledge, to identify covarying laterality differences within discrete temporal brain regions. The authors argue SBL provides a unique focus to detect covarying laterality differences in patients with schizophrenia, facilitating the discovery of laterality aspects undetected in previous work.

Molecular alterations in the medial temporal lobe in schizophrenia

The medial temporal lobe (MTL) and its individual structures have been extensively implicated in schizophrenia pathophysiology, with considerable efforts aimed at identifying structural and functional differences in this brain region. The major structures of the MTL for which prominent differences have been revealed include the hippocampus, the amygdala and the superior temporal gyrus (STG). The different functions of each of these regions have been comprehensively characterized, and likely contribute differently to schizophrenia. While neuroimaging studies provide an essential framework for understanding the role of these MTL structures in various aspects of the disease, ongoing efforts have sought to employ molecular measurements in order to elucidate the biology underlying these macroscopic differences. This review provides a summary of the molecular findings in three major MTL structures, and discusses convergent findings in cellular architecture and inter-and intra-cellular networks. The findings of this effort have uncovered cell-type, network and gene-level specificity largely unique to each brain region, indicating distinct molecular origins of disease etiology. Future studies should test the functional implications of these molecular changes at the circuit level, and leverage new advances in sequencing technology to further refine our understanding of the differential contribution of MTL structures to schizophrenia.

Choline Compounds of the Frontal Lobe and Temporal Glutamatergic System in Bipolar and Schizophrenia Proton Magnetic Resonance Spectroscopy Study.

Purpose Modern neuroimaging techniques allow investigating brain structures and substances involved in the pathophysiology of mental disorders, trying to find new markers of these disorders. To better understanding of the pathophysiology and differential diagnosis of schizophrenia and bipolar disorder, this study was conducted to assess the neurochemical alterations in the frontal and temporal lobes in hospitalized patients with schizophrenia and bipolar disorder. Methods Twenty-one subjects with schizophrenia (paranoid and differentiated types), 16 subjects with bipolar I disorder (manic, depressive, and mixed episode), and 20 healthy subjects were studied. Magnetic resonance (MR) imaging and proton resonance magnetic spectroscopy (1H MRS) were performed on a 1.5 T scanner. Voxels of 8 cm3 were positioned in the left frontal and left temporal lobes. Results Glx/H2O (GABA, glutamine, and glutamate/nonsuppressed water signal) ratios were significantly increased in the left temporal lobe in schizophrenia, but not in bipolar disorder, compared with controls. Cho/H2O (choline/nonsuppressed water signal) ratios in the left frontal lobe had a tendency to increase in bipolar disorder and schizophrenia, relative to controls. A lower temporal lobe NAA/H2O ratio in mixed than in manic and depressive episode of bipolar patients was also found. No other significant differences were found among three studied groups as regards NAA, Cr, and mI ratios. Conclusions Our results partially confirm the role of a glutamatergic system in schizophrenia, however, only in a temporal lobe. We also point to the importance of the choline-containing compounds (marker of cellular density) in the frontal lobe of patients suffering from bipolar disorder and schizophrenia. We also found the deleterious effect of mixed bipolar episode on the integrity and functioning of the temporal lobe. Glutamatergic left temporal spectroscopic changes may potentially help in differential diagnosis of schizophrenia from bipolar disorder.

F146. S-KETAMINE-INDUCED NMDA RECEPTOR BLOCKADE DURING NATURAL SPEECH PRODUCTION AND ITS IMPLICATIONS FOR FORMAL THOUGHT DISORDER IN SCHIZOPHRENIA: A PHARMACO-FMRI STUDY

BackgroundFTD is a dimensional, phenomenologically defined construct, which can clinically be subdivided into positive (pFTD) versus negative (nFTD) as well as objective versus subjective symptom clusters. Structural and functional changes in the lateral temporal language areas have been related to formal thought disorder (FTD) in schizophrenia. Continuous, natural speech production activates the right lateral temporal lobe in schizophrenia, as opposed to the left in healthy subjects. Positive and negative FTD can be elicited in healthy subjects by glutamatergic NMDA blockade with ketamine. It is unclear, whether the glutamate system is related to the reversed hemispheric lateralization during speaking in patients.MethodsIn a double-blind, cross over, placebo-controlled study, 15 healthy, male, right-handed volunteers overtly described 7 pictures for 3 minutes each, while BOLD signal changes were acquired with fMRI. As a measure of linguistic demand, the number of words within 20-second epochs was correlated with BOLD responses.ResultsParticipants developed S-ketamine-induced psychotic symptoms, particularly positive FTD. Ketamine vs. placebo was associated with enhanced neural responses in the right middle and inferior temporal gyri.DiscussionSimilar to a previous fMRI study in schizophrenia patients vs. healthy controls applying the same design, S-ketamine reversed functional lateralization during speech production in healthy subjects. Results demonstrate an association between glutamatergic imbalance, dysactivations in lateral temporal brain areas, and FTD symptom formation. Left superior temporal gyrus (STG) cortical volume is decreased in schizophrenia patients (SZ) with pFTD in structural magnetic resonance imaging (sMRI) studies and shows reversed activation in functional MRI (fMRI) experiments during speech production. pFTDs are related to synaptic rarefication in the glutamate system of the superior and middle lateral temporal cortices.

Sulcal Depth-based Cortical Shape Analysis in Normal Healthy Control and Schizophrenia Groups.

Sulcal depth is an important marker of brain anatomy in neuroscience/neurological function. Previously, sulcal depth has been explored at the region-of-interest (ROI) level to increase statistical sensitivity to group differences. In this paper, we present a fully automated method that enables inferences of ROI properties from a sulcal region-focused perspective consisting of two main components: 1) sulcal depth computation and 2) sulcal curve-based refined ROIs. In conventional statistical analysis, the average sulcal depth measurements are employed in several ROIs of the cortical surface. However, taking the average sulcal depth over the full ROI blurs overall sulcal depth measurements which may result in reduced sensitivity to detect sulcal depth changes in neurological and psychiatric disorders. To overcome such a blurring effect, we focus on sulcal fundic regions in each ROI by filtering out other gyral regions. Consequently, the proposed method results in more sensitive to group differences than a traditional ROI approach. In the experiment, we focused on a cortical morphological analysis to sulcal depth reduction in schizophrenia with a comparison to the normal healthy control group. We show that the proposed method is more sensitivity to abnormalities of sulcal depth in schizophrenia; sulcal depth is significantly smaller in most cortical lobes in schizophrenia compared to healthy controls (p < 0.05).

S-Ketamine-Induced NMDA Receptor Blockade during Natural Speech Production and Its Implications for Formal Thought Disorder in Schizophrenia: A Pharmaco-fMRI Study

Structural and functional changes in the lateral temporal language areas have been related to formal thought disorder (FTD) in schizophrenia. Continuous, natural speech production activates the right lateral temporal lobe in schizophrenia, as opposed to the left in healthy subjects. Positive and negative FTD can be elicited in healthy subjects by glutamatergic NMDA blockade with ketamine. It is unclear whether the glutamate system is related to the reversed hemispheric lateralization during speaking in patients. In a double-blind, crossover, placebo-controlled study, 15 healthy, male, right-handed volunteers overtly described 7 pictures for 3 min each while BOLD signal changes were acquired with fMRI. As a measure of linguistic demand, the number of words within 20 s epochs was correlated with BOLD responses. Participants developed S-ketamine-induced psychotic symptoms, particularly positive FTD. Ketamine vs placebo was associated with enhanced neural responses in the right middle and inferior temporal gyri. Similar to a previous fMRI study in schizophrenia patients vs healthy controls applying the same design, S-ketamine reversed functional lateralization during speech production in healthy subjects. Results demonstrate an association between glutamatergic imbalance, dysactivations in lateral temporal brain areas, and FTD symptom formation.

Transdiagnostic commonalities and differences in resting state functional connectivity of the default mode network in schizophrenia and major depression.

Schizophrenia and depression are prevalent psychiatric disorders, but their underlying neural bases remains poorly understood. Neuroimaging evidence has pointed towards the relevance of functional connectivity aberrations in default mode network (DMN) hubs, dorso-medial prefrontal cortex and precuneus, in both disorders, but commonalities and differences in resting state functional connectivity of those two regions across disorders has not been formally assessed. Here, we took a transdiagnostic approach to investigate resting state functional connectivity of those two regions in 75 patients with schizophrenia and 82 controls from 4 scanning sites and 102 patients with depression and 106 controls from 3 sites. Our results demonstrate common dysconnectivity patterns as indexed by a significant reduction of functional connectivity between precuneus and bilateral superior parietal lobe in schizophrenia and depression. Furthermore, our findings highlight diagnosis-specific connectivity reductions of the parietal operculum in schizophrenia relative to depression. In light of evidence that points towards the importance of the DMN for social cognitive abilities and well documented impairments of social interaction in both patient groups, it is conceivable that the observed transdiagnostic connectivity alterations may contribute to interpersonal difficulties, but this could not be assessed directly in our study as measures of social behavior were not available. Given the operculum's role in somatosensory integration, diagnosis-specific connectivity reductions may indicate a pathophysiological mechanism for basic self-disturbances that is characteristic of schizophrenia, but not depression.

Alterations of the occipital lobe in schizophrenia.

The relationship of the occipital lobe of the brain with schizophrenia is not commonly studied; however, this topic is considered an essential subject matter among clinicians and scientists. We conducted this systematic review to elaborate the relationship in depth. We found that most schizophrenic patients show normal occipital anatomy and physiology, a minority showed dwindled values, and some demonstrated augmented function and structure. The findings are laborious to incorporate within single disease models that present the involvement of the occipital lobe in schizophrenia. Schizophrenia progresses clinically in the mid-twenties and thirties and its prognosis is inadequate. Changes in the volume, the gray matter, and the white matter in the occipital lobe are quite evident; however, the mechanism behind this involvement is not yet fully understood. Therefore, we recommend further research to explore the occipital lobe functions and volumes across the different stages of schizophrenia.

Abnormal expression of glutamate transporters in temporal lobe areas in elderly patients with schizophrenia

Glutamate transporters facilitate the buffering, clearance and cycling of glutamate and play an important role in maintaining synaptic and extrasynaptic glutamate levels. Alterations in glutamate transporter expression may lead to abnormal glutamate neurotransmission contributing to the pathophysiology of schizophrenia. In addition, alterations in the architecture of the superior temporal gyrus and hippocampus have been implicated in this illness, suggesting that synapses in these regions may be remodeled from a lifetime of severe mental illness and antipsychotic treatment. Thus, we hypothesize that glutamate neurotransmission may be abnormal in the superior temporal gyrus and hippocampus in schizophrenia. To test this hypothesis, we examined protein expression of excitatory amino acid transporter 1–3 and vesicular glutamate transporter 1 and 2 in subjects with schizophrenia (n=23) and a comparison group (n=27). We found decreased expression of EAAT1 and EAAT2 protein in the superior temporal gyrus, and decreased EAAT2 protein in the hippocampus in schizophrenia. We didn't find any changes in expression of the neuronal transporter EAAT3 or the presynaptic vesicular glutamate transporters VGLUT1-2. In addition, we did not detect an effect of antipsychotic medication on expression of EAAT1 and EAAT2 proteins in the temporal association cortex or hippocampus in rats treated with haloperidol for 9months. Our findings suggest that buffering and reuptake, but not presynaptic release, of glutamate is altered in glutamate synapses in the temporal lobe in schizophrenia.

Changes in cortical thickness in the frontal lobes in schizophrenia are a result of thinning of pyramidal cell layers

Decreased cortical thickness and reduced activity as measured by fMRI in the grey matter of the subgenual cingulate cortex have been reported in schizophrenia and bipolar disorder, and cortical grey matter loss has been reliably reported in the frontal and temporal lobes in schizophrenia. The aim of this study was to examine the thickness of each of the six cortical layers in the subgenual cingulate cortex, five frontal lobe and four temporal lobe gyri. We examined two separate cohorts. Cohort 1 examines the subgenual cingulate cortex (SCC) in schizophrenia (n = 10), bipolar disorder (n = 15) and major depressive disorder (n = 20) against control subjects (n = 19). Cohort two examines frontal and temporal gyri in schizophrenia (n = 16), major depressive disorder (n = 6) against matched controls (n = 32). The cohorts were selected with identical clinical criteria, but underwent different tissue processing to contrast the effect of chemical treatment on tissue shrinkage. Measurements of layer I-VI thickness were taken from cresyl-violet- and haematoxylin-stained sections in cohort one and from cresyl-violet- and H&E-stained sections in cohort two. SCC cortical thickness decreased in male subjects with bipolar disorder (p = 0.048), and male schizophrenia cases showed a specific decrease in the absolute thickness of layer V (p = 0.003). Compared to controls, the relative thickness of layer V in the crown of the SCC decreased in schizophrenia (p < 0.001). A significant decrease in total cortical thickness was observed across the frontal lobe in schizophrenia (p < 0.0001), with specific pyramidal layer thinning in layers III (p = 0.0001) and V (p = 0.005). There was no effect of lateralization. No changes were noted in temporal lobe cortical thickness. This study demonstrates diminished pyramidal layer thickness resulting in decreased frontal lobe thickness in schizophrenia.

Cortical thickness, neuron density and size in the inferior parietal lobe in schizophrenia

The inferior parietal lobe (IPL) is a center of multisensory integration, and both functional and structural MRI studies have found evidence that pathology in this region may contribute to disrupted sensory perception in schizophrenia. To further define this pathology, we used postmortem samples from the left and right IPL, to compare the thickness and volume of the upper (I–III) and lower (IV–VI) cortical layers. The samples were divided into supramarginal and angular gyri, and neuron density and size were measured in the supramarginal gyrus. The laminar thickness and volume measurements did not demonstrate significant changes in schizophrenia, but did show that the angular gyrus was thinner than the supramarginal gyrus, due to a difference mainly in the lower layers. Measurements of cortical thickness, neuron size and neuron density all showed some evidence of previously reported normal hemispheric differences. These asymmetries were reduced in schizophrenia, but the small changes were at the threshold of detection, and are discussed in the context of the sensitivity of the methods applied.

Changes in cortical thickness in the frontal lobes in schizophrenia are a result of thinning of pyramidal cell layers

Decreased cortical thickness and reduced activity as measured by fMRI in the grey matter of the subgenual cingulate cortex have been reported in schizophrenia and bipolar disorder, and cortical grey matter loss has been reliably reported in the frontal and temporal lobes in schizophrenia. The aim of this study was to examine the thickness of each of the six cortical layers in the subgenual cingulate cortex, five frontal lobe and four temporal lobe gyri. We examined two separate cohorts. Cohort 1 examines the subgenual cingulate cortex (SCC) in schizophrenia (n = 10), bipolar disorder (n = 15) and major depressive disorder (n = 20) against control subjects (n = 19). Cohort two examines frontal and temporal gyri in schizophrenia (n = 16), major depressive disorder (n = 6) against matched controls (n = 32). The cohorts were selected with identical clinical criteria, but underwent different tissue processing to contrast the effect of chemical treatment on tissue shrinkage. Measurements of layer I-VI thickness were taken from cresyl-violet- and haematoxylin-stained sections in cohort one and from cresyl-violet- and H&E-stained sections in cohort two. SCC cortical thickness decreased in male subjects with bipolar disorder (p = 0.048), and male schizophrenia cases showed a specific decrease in the absolute thickness of layer V (p = 0.003). Compared to controls, the relative thickness of layer V in the crown of the SCC decreased in schizophrenia (p < 0.001). A significant decrease in total cortical thickness was observed across the frontal lobe in schizophrenia (p < 0.0001), with specific pyramidal layer thinning in layers III (p = 0.0001) and V (p = 0.005). There was no effect of lateralization. No changes were noted in temporal lobe cortical thickness. This study demonstrates diminished pyramidal layer thickness resulting in decreased frontal lobe thickness in schizophrenia.

Changes in cortical thickness in the frontal lobes in schizophrenia are a result of thinning of pyramidal cell layers

The 15th Biennial Winter Workshop in Psychoses, 15–18 November 2009, Barcelona, Spain: IMAGING AND NEUROPATHOLOGY

Joint Modeling of Anatomical and Functional Connectivity for Population Studies

We propose a novel probabilistic framework to merge information from diffusion weighted imaging tractography and resting-state functional magnetic resonance imaging correlations to identify connectivity patterns in the brain. In particular, we model the interaction between latent anatomical and functional connectivity and present an intuitive extension to population studies. We employ the EM algorithm to estimate the model parameters by maximizing the data likelihood. The method simultaneously infers the templates of latent connectivity for each population and the differences in connectivity between the groups. We demonstrate our method on a schizophrenia study. Our model identifies significant increases in functional connectivity between the parietal/posterior cingulate region and the frontal lobe and reduced functional connectivity between the parietal/posterior cingulate region and the temporal lobe in schizophrenia. We further establish that our model learns predictive differences between the control and clinical populations, and that combining the two modalities yields better results than considering each one in isolation.

Parietal Lobes in Schizophrenia: Do They Matter?

Objective. Despite observations that abnormal parietal lobe (PL) function is associated with psychotic-like experiences, our knowledge about the nature of PL involvement in schizophrenia is modest. The objective of this paper is to investigate the role of the PL in schizophrenia. Method. Medline databases were searched for English language publications using the following key words: parietal lobe, combined with schizophrenia, lesions, epilepsy, cognition, rare genetic disorders, MRI, fMRI, PET, and SPECT, respectively, followed by cross-checking of references. Results. Imaging studies in childhood onset schizophrenia suggest that grey matter abnormalities start in parietal and occipital lobes and proceed to frontal regions. Although, the findings are inconsistent, several studies with patients at risk to develop schizophrenia indicate early changes in the PL. Conclusions. We want to propose that in a proportion of individuals with emerging schizophrenia structural and functional alterations may start in the PL and progress to frontal regions.

The potential role of the parietal lobe in schizophrenia

Although the anatomy of the parietal lobe has been under-investigated in schizophrenia, some magnetic resonance imaging studies have shown decreased volumes, suggesting its possible implication for the pathophysiology of the disease.