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Introduction: Major Depressive Disorder (MDD) is associated with a high burden of disease and notable economic costs. Standard treatments (e.g. medication or cognitive therapy) have been shown to be effective, but some patients remain unresponsive. With the knowledge that MDD patients have been shown to display an attentional cognitive bias towards negative stimuli, Cognitive Bias Modification (CBM)-training to focus attention on positive information is thought to improve emotional processing and depressive symptoms. Some studies imply reduced duration and occurrence of microstate D in MDD compared to healthy controls. However, the effect of CBM on microstates is still unclear. Objectives: (1) To replicate previous findings that duration and occurrence of microstate D is reduced in patients with MDD compared to healthy controls in an independent sample and (2) to investigate the effect of an active CBM-training versus a control-training on microstates and its association with symptom improvements. Methods: Thirty patients receiving outpatient treatment with MDD according to DSM V (aged 18-60) will be recruited in Essen and Aachen. The control group will consist of 30 healthy age-and-sex-matched participants. Psychological testing will be administered and all participants will be randomized to either an active or a control training. During the next visit, resting state EEG and a GoNoGo Task with positive, neutral and negative pictures will be measured. The participants will take a tablet home to undergo 10 sessions of CBM within 14 days. The training will be consisted of a dot-probe-task. In the active condition the probe will be more likely to appear behind a positive versus a neutral picture, while appearing randomly in the control condition. After 14 days, a second EEG will be recorded. Results: Differences in duration and occurrence of microstate D between patients and healthy controls will be analyzed by conducting ANCOVAs with age and sex as covariates. ANCOVAs for repeated measurements will be calculated to study effects of time (pre- vs. post-training) and group (patients vs. healthy controls in active training; patients in active vs. patients in control-training), on duration and occurrence of microstate D. Conclusions: CBM-training is proposed to be an effective treatment option for MDD patients, reflected in a reduced topographical bias of microstate D in EEG. Disclosure of Interest: None Declared [ABSTRACT FROM AUTHOR]

Introduction: Dysfunctional changes in the glutamatergic system play an important role in the pathophysiology of depression. Glutamate regulates various neuronal function, such as nerve migration, excitability, plasticity, as well as long-term potentiation and long-term synaptic depression. Failures in this process might cause emotional/cognitive changes associated with stress-induced depressive symptoms, a part of our current understanding of the pathophysiology of depression. These changes might be related to deviations in biochemical blood parameters, but also to volatile organic compounds (VOCs) measured in breath. Objectives: 1) To replicate our previous finding that concentration of volatile organic compounds in expiratory breath gas and metabolites derived from MR spectroscopy distinguish unmedicated depressed patients from healthy participants, (2) to determine whether the amount of these VOCs is associated with severity of depression and anxiety, and (3) to correlate breath-VOC-content with glutamatergic neurotransmission and energy metabolism derived from MR spectroscopy. Methods: 25 antidepressant-free patients with major depression according to DSM V (18-65 years of age) are recruited from our out- and inpatient clinics. The controls will consist of 25 healthy age-and-sex-matched participants. Breath gas analyses will be carried out at awakening, and 30 and 60 minutes thereafter, and at 5pm using PTR-TOF-MS with direct on time measurement through a special sampler. A 7 Tesla Siemens Terra MRI scanner will be used to undertake spectroscopic measurements. Concentrations of glutamate and β-hydroxybutyrate levels in the pregenual and dorsal anterior cingulate gyrus will subsequently be assessed. Results: Statistical analysis for differences between groups corrected for multiple measurements will be carried out. Concentration of VOCs will be correlated with brain metabolism and severity of symptoms. Conclusions: VOCs in breath are proposed to be an efficient and non-invasive marker for depression-related biochemical changes related to disease severity, and eventually useful for personalized treatment planning. Disclosure of Interest: None Declared [ABSTRACT FROM AUTHOR]

Introduction: Despite the fact, that symptomtriggered alcohol withdrawal treatment is recommended by German guidelines on alcoholism, many hospitals continue to use fixed-schedule protocols, as they have been successfully applied for many years. Methods: This retrospective study compared all patients' records of alcohol withdrawal treatment from October 2010 to November 2011 at Magdeburg's University Department of Psychiatry (n = 120). A symptom-triggered protocol with clomethiazole (AESB, n = 46) was used in parallel with the existing fixed-schedule protocol with diazepam (n = 74). Results: The symptom-triggered group showed less need of pharmacological treatment duration (p < 0.001) and cumulative dosage of medication compared to the fixed-schedule protocol (p < 0.006). No difference was observed regarding the need of clonidine or haloperidol (to treat blood pressure derailment or delirium) and the incidence of epileptic seizures. Discussion: Based on the shorter treatment duration and a similar rate of complications our department has switched to the symptom-triggered protocol to improve the quality of patient care. [ABSTRACT FROM AUTHOR]

Background. The neurobiological underpinnings of attention deficit hyperactivity disorder (ADHD) are inconclusive. Activation abnormalities across brain regions in ADHD compared with healthy controls highlighted in task-based functional magnetic resonance imaging (fMRI) studies are heterogeneous. To identify a consistent pattern of neural dysfunction in ADHD, a meta-analysis of fMRI studies using Go/no-go, Stop and N-back tasks was undertaken. Method. Several databases were searched using the key words: 'ADHD and fMRI' and 'ADHD and fMRI task'. In all, 20 studies met inclusion criteria comprising 334 patients with ADHD and 372 healthy controls and were split into N-back, Stop task and Go/no-go case-control groups. Using Signed Differential Mapping each batch was meta-analysed individually and meta-regression analyses were used to examine the effects of exposure to methylphenidate (MPH), length of MPH wash-out period, ADHD subtype, age and intelligence quotient (IQ) differences upon neural dysfunction in ADHD. Results. Across all tasks less activity in frontal lobe regions compared with controls was detected. Less exposure to treatment and lengthier wash-out times resulted in less left medial frontal cortex activation in N-back and Go/no-go studies. Higher percentage of combined-type ADHD resulted in less superior and inferior frontal gyrus activation. Different IQ scores between groups were linked to reduced right caudate activity in ADHD. Conclusions. Consistent frontal deficits imply homogeneous cognitive strategies involved in ADHD behavioural control. Our findings suggest a link between fMRI results and the potentially normalizing effect of treatment and signify a need for segregated examination and contrast of differences in sample characteristics in future studies. [ABSTRACT FROM AUTHOR]

The aim of this dual-isotope SPECT imaging study was to evaluate striatal dopamine transporter (DAT) and D2 receptor availability in first-episode never-treated and haloperidol-treated schizophrenic patients and whether the availability is associated with psychopathology. Twenty-four inpatients with a first acute schizophrenic episode were enrolled in the study; 12 of these patients were treated with haloperidol for 2 weeks before dual-isotope SPECT was performed, whereas the other 12 patients underwent the SPECT evaluation directly after enrollment. Twelve healthy control persons were also recruited and evaluated with the dual-isotope SPECT protocol. Psychopathology was assessed by the Positive and Negative Syndrome Scale and other scales. D2-radioligand binding did not differ between drug-naïve patients and the control group but was significantly lower in the haloperidol-treated group. DAT availability was also significantly lower in the haloperidol patients than in the other two groups and differed significantly between drug-naïve, positive-syndrome-type patients and healthy controls. The data obtained with the new dual-isotope SPECT technique reveal a direct effect of haloperidol at the D2 and DAT receptor level. [ABSTRACT FROM AUTHOR]

Frodl T, Skokauskas N. Meta-analysis of structural MRI studies in children and adults with attention deficit hyperactivity disorder indicates treatment effects. Objective: About 50-80% of ADHD cases have been found to persist into adulthood, but ADHD symptoms change with age. The aim of this study was to perform a meta-analysis of MRI voxel-based morphometry (VBM) and manual tracing studies to identify the differences between adults and children with ADHD as well as between treated and untreated individuals. Method: Several databases were searched using keywords 'attention-deficit and MRI', 'ADHD and MRI'. Gray matter volumes from VBM studies and caudate volumes from tracing studies of patients and controls were analyzed using signed differential mapping. Results: Meta-analyses detected reduced right globus pallidus and putamen volumes in VBM studies as well as decreased caudate volumes in manual tracing studies in children with ADHD. Adult patients with ADHD showed volume reduction in the anterior cingulate cortex (ACC). A higher percentage of treated participants were associated with less changes. Conclusion: Basal ganglia regions like the right globus pallidus, the right putamen, and the nucleus caudatus are structurally affected in children with ADHD. These changes and alterations in limbic regions like ACC and amygdala are more pronounced in non-treated populations and seem to diminish over time from child to adulthood. Treatment seems to have positive effects on brain structure. [ABSTRACT FROM AUTHOR]

Frodl T, Stauber J, Schaaff N, Koutsouleris N, Scheuerecker J, Ewers M, Omerovic M, Opgen-Rhein M, Hampel H, Reiser M, Möller H.-J, Meisenzahl E. Amygdala reduction in patients with ADHD compared with major depression and healthy volunteers. Objective: Results in adult attention deficit hyperactivity disorder (ADHD) on structural brain changes and the clinical relevance are contradictory. The aim of this study was to investigate whether in adult patients with ADHD hippocampal or amygdala volumes differs from that in healthy controls and patients with major depression (MD). Method: Twenty patients with ADHD, 20 matched patients with MD and 20 healthy controls were studied with high resolution magnetic resonance imaging. Results: Amygdala volumes in patients with ADHD were bilaterally smaller than in patients with MD and healthy controls. In ADHD, more hyperactivity and less inattention were associated with smaller right amygdala volumes, and more symptoms of depression with larger amygdala volumes. Conclusion: This study supports findings that the amygdala plays an important role in the systemic brain pathophysiology of ADHD. Whether patients with ADHD and larger amygdala volumes are more vulnerable to affective disorders needs further investigation. [ABSTRACT FROM AUTHOR]

The serotonergic system is involved in the pathophysiology of major depression as well as in the early central nervous system development and adult neuroplasticity. The aim of the study was to examine in 77 patients with major depression and 77 healthy controls the association between the triallelic polymorphism in the promoter region of the serotonin transporter gene (5-HTTLPR) and gray matter (GM) brain volumes measured with 1.5 T magnetic resonance imaging. Voxel-based morphometry were estimated on magnetic resonance images and genotyping was performed. We found that healthy controls have a strong association between the 5-HTTLPR and GM volumes of the dorsolateral prefrontal cortex, left anterior gyrus cinguli, left amygdala as well as right hippocampus, whereas there is no such association in patients with major depression. Healthy subjects carrying the S- or LG-allele have smaller GM volumes than those with the LA-allele, indicating that 5-HTTLPR contributes to the development of brain structures. Patients with depression show reduced GM volumes, particularly when they are homozygous for the LA-allele, suggesting that these patients are more vulnerable for morphological changes during depressive episodes.Molecular Psychiatry (2008) 13, 1093–1101; doi:10.1038/mp.2008.62; published online 1 July 2008 [ABSTRACT FROM AUTHOR]

Objective: Stress-related changes in the hippocampus are influenced by genetic factors. To enhance our understanding of both the interaction between the brain, behaviour and genetics and of biological mechanisms in mood disorders neuroimaging genetics provide a good opportunity. Method: A MEDLINE search was conducted to identify articles on neuroimaging genetics in major depression (MD). Results: Hippocampal volumes were found to be associated with polymorphisms in the promotor region of the serotonin transporter (5-HTTLPR) in patients with MD. Met-allele carriers of the BDNF (val66met) polymorphism had smaller hippocampal volumes in both patients and healthy controls when compared with homozygous val-allele carriers. Polymorphisms of the serotonin transporter (5-HTTLPR) and 5-HT1a receptor are associated with increased amygdala activation investigated with functional MRI in patients with MD. Conclusion: Genetic variants seem to modulate the effects of stress on hippocampal volumes as well as amygdala activity as well as the development of the brain. [ABSTRACT FROM AUTHOR]

OBJECTIVE: According to the stress-toxicity hypothesis of depression, hippocampal volumes may diminish as the disease progresses. We sought to examine the changes in hippocampal and amygdala volumes at baseline and at 3 years after an acute depressive episode, and the impact of reduced hippocampal volumes on the outcome. METHODS: In a prospective, longitudinal study, we examined the hippocampus and amygdala of 30 inpatients with major depression from the Department of Psychiatry and Psychotherapy and 30 healthy participants from the community (control group) using high-resolution magnetic resonance images at baseline and after 3 years. Psychopathology was assessed at baseline, weekly during the inpatient phase and then after 1, 2 and 3 years. RESULTS: During the 3-year follow-up period, neither hippocampal nor amygdala volumes changed significantly among patients or participants in the control group. However, in the subgroup of patients who took antidepressants over the full 3 years, the left hippocampal volumes increased significantly. Patients with small hippocampal volumes and previous depressive episodes had a worse clinical outcome compared with patients with large hippocampal volumes and previous depressive episodes. CONCLUSION: Overall, our results suggest that a relatively small hippocampal volume may be a vulnerability factor for a bad treatment response in major depression. Subtle changes in hippocampal volumes may be detectable during continuous antidepressant therapy. Such changes may be the result of neuroplastic processes. [ABSTRACT FROM AUTHOR]

Alterations of amygdala structure and function have been repeatedly described in patients with borderline personality disorder (BPD). The aim of our study was to determine whether a functional polymorphism of the 5-hydroxytryptamine1A receptor (5-HTR1A) gene C −1019 G (identity number: rs6295 G/C) is associated with structural changes of the amygdala in patients with BPD. Twenty-five right-handed female inpatients with BPD according to DSM IV and 25 healthy controls matched for age, sex, handedness and educational status were enrolled. Brain volumetry of the amygdala was performed with a 1.5-T Magnetom Vision apparatus (Siemens, Erlangen, Germany) and analyzed by the software program ‘brains’. Patients who have the 5-HTR1A gene G allele had significantly smaller amygdala volumes than C/C genotype carriers ( P = 0.02). While no difference of allelic distribution between patients and controls was detected, the described effect of 5-HTR1A genotype on amygdala volume was found for the whole group of patients, as well as in the subgroup of patients with comorbid major depression ( P = 0.004) but not in controls. In contrast to these subgroups of BPD patients who had significant amygdala volume differences, the mean amygdala volume of the whole group of BPD patients was not significantly different from that of controls. In summary, our study provides first evidence that 5-HTR1A gene C −1019 G polymorphism is associated with structural changes in the limbic system of BPD patients, a finding that might be disease related and might contribute to explanation of previous discrepant results regarding amygdala volume changes in BPD. Future research is recommended to clarify possible interactions between this functional polymorphism and symptoms, course and treatment responses in this disorder. [ABSTRACT FROM AUTHOR]

The processing of emotional facial expression is a major part of social communication and understanding. In addition to explicit processing, facial expressions are also processed rapidly and automatically in the absence of explicit awareness. We investigated 12 healthy subjects by presenting them with an implicit and explicit emotional paradigm. The subjects reacted significantly faster in implicit than in explicit trials but did not differ in their error ratio. For the implicit condition increased signals were observed in particular in the thalami, the hippocampi, the frontal inferior gyri and the right middle temporal region. The analysis of the explicit condition showed increased blood-oxygen-level-dependent signals especially in the caudate nucleus, the cingulum and the right prefrontal cortex. The direct comparison of these 2 different processes revealed increased activity for explicit trials in the inferior, superior and middle frontal gyri, the middle cingulum and left parietal regions. Additional signal increases were detected in occipital regions, the cerebellum, and the right angular and lingual gyrus. Our data partially confirm the hypothesis of different neural substrates for the processing of implicit and explicit emotional stimuli. Copyright © 2007 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Working memory as a part of higher-order executive functions is defined by the parallel storage and processing of information. Recent functional fMRI studies have revealed a functional, interregional disintegration of a neuronal network connecting cortical, subcortical and cerebellar regions in schizophrenic patients (SZ). Cognitive impairment in working memory is a core psychopathological correlate of schizophrenic symptoms. Atypical neuroleptics such as quetiapine have shown good efficacy in treating positive and negative symptoms. The presented study evaluated the impact of a neuroleptic steady state treatment with quetiapine on the altered working memory activation patterns in schizophrenia. Patients were examined by fMRI at baseline and after 12 weeks of steady state treatment with quetiapine. Matched healthy controls (HC) underwent baseline examination. In the scanner, stimuli were presented in a 2-back and 0-back condition of a working memory (wm) paradigm, whereby a degraded and a non-degraded version were used each time. Additionally, behavioural responses (reaction time to target stimuli and error ratio) were measured. At baseline, healthy controls revealed increased activity in the frontal lobe, especially in regions of the prefrontal cortex. Compared to HC, SZ showed hypoactivation in the right dorsolateral prefrontal cortex (DLPFC) and the ventrolateral prefrontal cortex (VLPFC) bilaterally for the 2-back condition. In the 2-back degraded condition there was a hypoactivation in both, the right DLPFC and the VLPFC. Additionally, patients showed bilaterally decreased activation in the basalganglia in the 2-back and in the right caudatus in the 2-back degraded condition compared to healthy controls. After treatment with quetiapine, patients activations patterns were increased. The pre–post comparison of the 2-back condition revealed a significant increase of activation in the left VLPFC at a significance level of 0.001 (uncorrected). The 2-back degraded condition led to a significant activation pattern in the lingual gyrus and the right precuneus. In both wm conditions, at baseline there were no differences in reaction time but only a worse performance in SZ. After treatment, behavioural measurement of responses, including reaction time and performance, showed slight improvements in SZ, although these did not reach statistical significance. The neuronal networks underlying working memory are clearly altered in schizophrenia. After 12 weeks of treatment with quetiapine monotherapy, patients showed significant clinical improvement and revealed increased BOLD activity in the VLPFC during a working memory task, although there was no improvement of cognitive performance. [ABSTRACT FROM AUTHOR]

OBJECTIVE: Dysfunction of neuronal plasticity or remodelling seems to contribute to the pathopysiology of major depression and may cause the well-documented hippocampal changes in depression. We aimed to investigate whether reduced hippocampal volumes correlate with executive dysfunctioning or memory dysfunctioning or with depression severity. METHODS: We recruited 34 inpatients with a previous or current episode of major depression from the department of psychiatry at the Ludwig-Maximilians University of Munich, Germany. We examined the 34 patients and 34 healthy control subjects with structural high resolution MRI. We assessed cognitive functions with the Wisconsin Card Sorting Test (WCST) and the Rey Auditory Verbal Learning Test (RAVLT) and severity of depression with the Hamilton Depression Rating Scale. RESULTS: Hippocampal volumes and frontal lobe volumes were significantly smaller in patients, compared with healthy control subjects. Furthermore, lower hippocampal volumes were correlated with poorer performance in the WCST. No significant correlations were found between hippocampal volumes and RAVLT performance or severity of depression. CONCLUSIONS: The present findings emphasize that patients with reduced hippocampal volumes show more executive dysfunctions than their counterparts. Thus, the mechanisms resulting in reduced hippocampal volumes seem to be related to the development of major depression. [ABSTRACT FROM AUTHOR]

Discusses data which supports evidence that differences in presynaptic dopaminergic activity in schizophrenic patients are associated with the extend of the acute psychotic syndrome. Role being played by the membrane bound presynaptic dopamine transporter in regulating the dopamine content in the synaptic cleft; Dopamine transporter imaging in schizophrenia; Difference between striatal dopamine transporter availability of the whole group of never treated patients and age-matched healthy controls.

Following the current hypothesis that acute schizophrenic psychotic illness is associated with a striatal 'hyperdopaminergic state', presynaptic integrity and dopamine transporter (DAT) density in first-episode, neuroleptic-naive schizophrenic patients was measured by single-photon-emission-tomography (SPECT) and compared with that in healthy control subjects. A new SPECT-ligand for assessment of the striatal DAT, the Technetium-99m-labelled tropane TRODAT-1 ([99mTc]TRODAT-1), was used. Ten inpatients suffering from a first acute schizophrenic episode and 10 age- and sex-matched healthy control subjects underwent SPECT with [99mTc]TRODAT-1. On the day of SPECT, psychopathological ratings were performed with the Brief Psychiatric Rating Scale (BPRS), the Positive and Negative Syndrome Scale (PANSS) and Schedule for Assessment of Negative Symptoms (SANS). Patients had not previously received any neuroleptic or antidepressant medication. Mean specific TRODAT-1 binding in the striatum did not differ significantly between the patient and the age- and sex-matched control group (1.25 vs. 1.28). Variance was significantly higher in the patient group. The data obtained with the new ligand in first-episode, drug-naive schizophrenic patients are in line with the PET results from the group of Laakso et al. in a comparable patient sample. [99mTc]TRODAT-1 seems to be a valuable new SPECT-ligand in the evaluation of the presynaptic site of the striatal dopaminergic synapse in schizophrenia. [ABSTRACT FROM AUTHOR]

The aim of this investigation was to compare the degree of striatal dopamine-(D2) receptor blockade by two atypical antipsychotic drugs, risperidone and olanzapine. The percentage of D2 receptor occupancy during treatment was calculated by comparing the results of 123I-iodobenzamide SPECT with those from healthy control subjects. Twenty inpatients suffering from schizophrenia or schizoaffective psychosis according to DSM IV/ICD-10 criteria were treated with clinically recommended doses of risperidone and compared with 13 inpatients treated with up to 20 mg olanzapine. Neuroleptic dose and D2 receptor blockade correlated strongly for both risperidone (Pearson r = -0.86, p = 0.0001) and olanzapine (Pearson r = -0.77, p = 0.002). There was no significant difference between the D2 receptor occupancy of the two substances when given in the clinically recommended dose range (unpaired t-test, t = -0.112, p = 0.911). [ABSTRACT FROM AUTHOR]

The aim of this study was to compare the degree of striatal dopamine D2 receptor availability in patients treated with recommended (5-20 mg, mean dose 11.9 +/- 6.3 mg daily) and higher doses (25-40 mg, mean 32.1 +/- 5.6 mg daily) of the novel antipsychotic drug olanzapine by means of [123I] IBZM Single photon emission computed tomography (SPECT). The results were compared to those of a group of 10 untreated, healthy, age- and sex-matched controls. The degree of dopamine D2 receptor occupancy in the patient group was correlated with the presence of extrapyramidal symptoms (EPS). A total of 20 patients who met the DSM III R criteria for schizophrenia or schizoaffective disorder received a clinically effective antipsychotic monotherapy with olanzapine. The mean daily dose of olanzapine ranged from 0.05-0.6 mg/kg body weight. The dopamine D2 receptor binding was reduced in all patients treated with olanzapine. Specific IBZM binding expressed as the [STR-BKG]/BKG ratio ranged from 0.13-0.61 (healthy controls 0.95). The D2 receptor availability revealed an exponential dose-response relationship (r = - 0.85, p < 0.001). The frequency of EPS induced by olanzapine was considerably lower. Only one patient, treated with 40 mg olanzapine, suffered from severe EPS symptoms and had to be given biperiden. There were no significant differences in the presence of EPS symptoms between patients with recommended doses and those with higher doses of olanzapine. [ABSTRACT FROM AUTHOR]

The serotonergic neurotransmission was suggested to play an important role in the aetiology of alcoholism. This study explores the association between tryptophan hydroxylase (TPH)-alleles and Loudness Dependence of Auditory Evoked N1/P2 Potentials (LDAEP). The TPH is the rate-limiting biosynthetic enzyme in serotonergic pathway. The LDAEP is one of the best validated non-invasive indicators for serotonergic neurotransmission. A sample of 54 alcoholics was recruited. N1/P2 potentials were evoked by five different sound intensities. A dipole source analysis using BESA (brain electric signal topography) was performed and intensity dependence was computed. The TPH intron 7 polymorphism was determined by using PCR in DNA samples. There was a weak but significant association between low LDAEP and the L-TPH allele. No influence from an individual's history of alcohol dependence or a positive family history of alcohol dependence on LDAEP was found. The weak but significant relationship found between L-TPH-allele and high serotonergic neurotransmission may contribute to a more detailed neurobiological characterization of alcohol dependents using functional and genetic parameters. [ABSTRACT FROM AUTHOR]

Abstract Previous MRI studies have shown differences in corpus callosum size between schizophrenic patients and controls. The corpus callosum (CC), as the main interhemispheric fiber tract, plays an important role in interhemispheric integration and communication. Though MRI studies suggest smaller CC in schizophrenia, there are still conflicting findings. Using in vivo magnetic resonance imaging, it was investigated whether the mid-sagittal area of CC differs between twenty-three right-handed male schizophrenic patients and twenty-three matched controls. Total CC area, five subregions of CC, total brain volume, gray and white matter were measured. No differences between schizophrenic patients and controls were found regarding all CC measurements, total brain volume, and gray matter tissue. However, a significant reduction of white matter tissue in the patient group emerged. There was no correlation between CC morphology and clinical variables such as age of onset, length of illness or symptom severity. Interestingly, five schizophrenic patients with a positive family history of schizophrenia showed significant reduction of the subregion C3, associated with a reduced total brain and gray and white matter volume. Significant reduction in the CC and its subregions was not confirmed in this group of patients with schizophrenia. In the subgroup of schizophrenic patients with a positive family history of schizophrenia, a significant reduction of the subregion corresponding to a part of the trunk of the CC was found. [ABSTRACT FROM AUTHOR]

Abstract Event-related potentials (ERPs) can serve as markers for cognitive processing stages. Identification of those ERPs altered in schizophrenia offer information about cognitive dysfunction. Auditory evoked potentials (AEPs) were elicited within an oddball paradigm in 35 schizophrenic patients and compared with 35 healthy controls. N100 and P200, as well as N200, frontal P300 and parietal P300 subcomponents, were separated using dipole source analysis. The amplitudes of the N100 and the parietal P300 measured in schizophrenics were diminished. The input-related processing stages (N100 and P200) were not altered, whereas later, the deviant and task-related processes (N200, frontal P300, parietal P300 and reaction time) were significantly prolonged in schizophrenia. [ABSTRACT FROM AUTHOR]