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Query: UMLS:C0036341 (schizophrenia)
 60,220 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Transcranial magnetic stimulation (TMS) is a very popular tool used within neuroscience. This and other associated techniques allow the in vivo investigation of cortical excitability, cortical connectivity and cortical plasticity. Schizophrenia is a brain disorder and various theories other than the dopamine hypothesis have been developed to describe its underlying neurobiology. Supported by animal and post mortem studies, findings from TMS studies indicate that schizophrenia is a disease of reduced cortical inhibition and impaired intra- and intercortical connectivity. Further studies using repetitive TMS and other plasticity-inducing techniques have shown that cortical plasticity is altered in schizophrenia patients, supporting the recently discussed plasticity deficiency theory of schizophrenia. This review gives an introduction to the most frequently applied techniques, describes findings in schizophrenia patients and discusses these findings with regard to the neurotransmitters and associated receptors involved. In summary, there is emerging evidence of an important pathophysiological interplay between reduced inhibition, impaired connectivity and reduced plasticity in schizophrenia patients. Gamma-aminobutyric-acid-receptors and glutamtergic N-Methyl-D-aspartic-acid-receptors are most likely to be involved in this complex interplay, which may reflect a disturbed signal-to-noise ratio in schizophrenia patients. This review will discuss this issue with regard to the available treatment options and will give implications for future research and therapeutic strategies regarding disinhibition and neuroplasticity in schizophrenia.
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PMID:Transcranial brain stimulation in schizophrenia: targeting cortical excitability, connectivity and plasticity. 2315 33

Huntington's disease (HD) is an autosomal dominant degenerative brain disorder that is characterized by motor, cognitive and affective symptoms. Previous research has shown that patients with HD, similar to patients with schizophrenia, are impaired in their ability to appreciate the mental states of others. Functional brain imaging studies have shown that patients with schizophrenia underactivate the neural network involved in mentalizing, and that deviant patterns of brain activation are also present in individuals at high risk of developing a psychotic disorder. Accordingly, the present study sought to examine the brain activation in premanifest mutation carriers for HD. Thirty premanifest mutation carriers (13 males) defined by a positive gene test and absence of unequivocal HD symptoms ("pre-HD") performed a cartoon mentalizing task during functional brain imaging. For comparison, a group of 26 healthy controls took part in the study. BOLD responses revealed that pre-HD subjects activated the mentalizing network comprising prefrontal, temporoparietal and parietal brain regions during task performance. A comparison between pre-HD patients and healthy controls revealed no significant activation differences. Premanifest mutation carriers of HD activated the neural network involved in mentalizing similar to healthy control subjects. This suggests that impaired mentalizing emerges with the clinical manifestation of the disease, but is not necessarily part of the pre-manifest stage.
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PMID:Mentalizing in preclinical Huntington's disease: an fMRI study using cartoon picture stories. 2317 63

Schizophrenia is a chronic, severe and recurrent brain disorder that requires continuous, long-term treatment with antipsychotic medication to minimize relapse and provide clinical benefit to patients. For patients with schizophrenia, non-adherence to medication is a major risk factor for relapse and re-hospitalization. Long-acting injectable formulations of second-generation antipsychotics (SGAs-LAIs) provide constant medication delivery and the potential for improved adherence. Currently, three drugs are available for the treatment of schizophrenia, risperidone longacting injectable, olanzapine pamoate and paliperidone palmitate. Several studies have also demonstrated efficacy and safety of such drugs in patients with acute schizophrenia. In the present paper the literature on LAI atypical antipsychotics will be reviewed and practical advice will be given concerning the use of these drugs in the clinical practice.
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PMID:Efficacy and safety of long acting injectable atypical antipsychotics: a review. 2334 45

Schizophrenia is a chronic brain disorder comprising a range of clinical features, including positive and negative symptoms, cognitive dysfunction and mood symptoms (particularly depression and anxiety). The management of schizophrenia requires effective short- and long-term treatment with antipsychotic medication that is effective across these symptom domains, while being well tolerated over the long term. Asenapine is the first tetracyclic atypical antipsychotic to be licensed in the USA and several other countries outside Europe for the acute and maintenance treatment of schizophrenia in adults. It has a unique receptor-binding profile and a broad range of therapeutic effects. Since clinical trials are conducted under strict conditions in tightly defined patient populations, evidence of an agent's efficacy and tolerability under 'real-world' clinical practice conditions is also required. As in clinical trials, real-life case reports demonstrate that asenapine is effective in treating the positive symptoms of schizophrenia, both in the acute setting and for relapse prevention. It is also effective in treating negative symptoms and shows promise in the treatment of depressive symptoms associated with schizophrenia. Asenapine has a favourable tolerability profile, having a minimal impact on weight and metabolic parameters. As such, asenapine is valuable option for the treatment of schizophrenia in adults.
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PMID:Management of schizophrenia: clinical experience with asenapine. 2353 51

Schizophrenia is a chronic debilitating brain disorder characterized by a complex set of perceptual and behavioural symptoms that severely disrupt and undermine the patient's psychological well-being and quality of life. Since the exact disease mechanisms remain essentially unknown, holistic animal models are indispensable tools for any serious investigation into the neurobiology of schizophrenia, including the search for remedies, prevention of the disease and possible biological markers. This review provides some practical advice to those confronted with the task of evaluating their animal models for relevance to schizophrenia, a task that inevitably involves behavioural tests with animals. To a novice, this challenge not only is a technical one but also entails attention to interpretative issues concerning validity and translational power. Here, we attempt to offer some guidance to help overcome these obstacles by drawing on our experience of diverse animal models of schizophrenia based on genetics, strain difference, brain lesions, pharmacological induction and early life developmental manipulations. The review pays equal emphasis to the general (theoretical) considerations of experimental design and the illustration of the problems related to critical test parameters and the data analysis of selected exemplar behavioural tests. Finally, the individual differences of behavioural expression in relevant tests observed in wild-type animals might offer an alternative approach in order to explore the mechanism of schizophrenia-related behavioural dysfunction at the molecular, cellular and structural levels, all of which are of more immediate relevance to cell and tissue research.
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PMID:A conceptual and practical guide to the behavioural evaluation of animal models of the symptomatology and therapy of schizophrenia. 2357 53

Neuroimaging data support the idea that schizophrenia is a brain disorder with altered brain structure and function. New resting-state functional connectivity techniques allow us to highlight synchronization of large-scale networks, such as the default-mode network (DMN) and salience network (SN). A large body of work suggests that disruption of these networks could give rise to specific schizophrenia symptoms. We examined the intra-network connectivity strength and gray matter content (GMC) of DMN and SN in 26 schizophrenia patients using resting-state functional magnetic resonance imaging and voxel-based morphometry. Resting-state data were analyzed with independent component analysis and dual-regression techniques. We reported reduced functional connectivity within both DMN and SN in patients with schizophrenia. Concerning the DMN, patients showed weaker connectivity in a cluster located in the right paracingulate cortex. Moreover, patients showed decreased GMC in this cluster. With regard to the SN, patients showed reduced connectivity in the left and right striatum. Decreased connectivity in the paracingulate cortex was correlated with difficulties in abstract thinking. The connectivity decrease in the left striatum was correlated with delusion and depression scores. Correlation between the connectivity of DMN frontal regions and difficulties in abstract thinking emphasizes the link between negative symptoms and the likely alteration of the frontal medial cortex in schizophrenia. Correlation between the connectivity of SN striatal regions and delusions supports the aberrant salience hypothesis. This work provides new insights into dysfunctional brain organization in schizophrenia and its contribution to specific schizophrenia symptoms.
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PMID:Links among resting-state default-mode network, salience network, and symptomatology in schizophrenia. 2372 17

Schizophrenia is a frequent and highly heritable brain disorder that typically manifests around or after puberty and has a fluctuating course. Multiple lines of evidence point to a neurodevelopmental origin of the illness and suggest that its (post) pubertal manifestation is related to genetic and environmental risk factors that interfere with the structural and functional reorganization of neural networks at this time. Longitudinal structural neuroimaging studies point to a progressive reduction in gray matter volume in many brain regions in schizophrenia. It has been proposed that these neuroimaging observations reflect an enduring disturbance of experience-dependent synaptic plasticity arising from developmental abnormalities in key neural circuits implicated in schizophrenia, including dorsolateral prefrontal cortex and hippocampal formation. Recent work has identified genetic variants linked to neural plasticity that are associated with changes in these circuits. Furthermore, non-invasive interventions such as transcranial magnetic stimulation have been shown to impact some of these systems-level intermediate phenotypes, suggesting a modifiability of these core pathophysiological processes of schizophrenia that may be exploited by therapy.
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PMID:Neuroimaging and plasticity in schizophrenia. 2390 83

Schizophrenia is a highly polygenic brain disorder. The main hypothesis for disease etiology in schizophrenia primarily focuses on the role of dysfunctional synaptic transmission. Previous studies have therefore directed their investigations toward the role of neuronal dysfunction. However, recent studies have shown that apart from neurons, glial cells also play a major role in synaptic transmission. Therefore, we investigated the potential causal involvement of the 3 principle glial cell lineages in risk to schizophrenia. We performed a functional gene set analysis to test for the combined effects of genetic variants in glial type-specific genes for association with schizophrenia. We used genome-wide association data from the largest schizophrenia sample to date, including 13 689 cases and 18 226 healthy controls. Our results show that astrocyte and oligodendrocyte gene sets, but not microglia gene sets, are associated with an increased risk for schizophrenia. The astrocyte and oligodendrocyte findings are related to astrocyte signaling at the synapse, myelin membrane integrity, glial development, and epigenetic control. Together, these results show that genetic alterations underlying specific glial cell type functions increase susceptibility to schizophrenia and provide evidence that the neuronal hypothesis of schizophrenia should be extended to include the role of glia.
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PMID:Specific glial functions contribute to schizophrenia susceptibility. 2395 19

Altered topological properties of brain connectivity networks have emerged as important features of schizophrenia. The aim of this study was to investigate how the state-related modulations to graph measures of functional integration and functional segregation brain networks are disrupted in schizophrenia. Firstly, resting state and auditory oddball discrimination (AOD) fMRI data of healthy controls (HCs) and schizophrenia patients (SZs) were decomposed into spatially independent components (ICs) by group independent component analysis (ICA). Then, weighted positive and negative functional integration (inter-component networks) and functional segregation (intra-component networks) brain networks were built in each subject. Subsequently, connectivity strength, clustering coefficient, and global efficiency of all brain networks were statistically compared between groups (HCs and SZs) in each state and between states (rest and AOD) within group. We found that graph measures of negative functional integration brain network and several positive functional segregation brain networks were altered in schizophrenia during AOD task. The metrics of positive functional integration brain network and one positive functional segregation brain network were higher during the resting state than during the AOD task only in HCs. These findings imply that state-related characteristics of both functional integration and functional segregation brain networks are impaired in schizophrenia which provides new insight into the altered brain performance in this brain disorder.
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PMID:State-related functional integration and functional segregation brain networks in schizophrenia. 2409 82

From 1980 to mid-1990 fifty-one gamblers were evaluated and treated at the psychiatric university hospital of Homburg/Saar in Germany. All were men with a mean age of 33.7 years. Gambling had lasted 5.2 years on average. Most patients were motivated to undergo therapy by members of their family. The majority of them had been in psychotherapeutic treatment before. Thirty-six of the 51 patients had committed punishable acts including fraud and embezzlement and, in 7 cases, robbery. The sample could be divided into three clinical subgroups. The first group consisted of patients with severe psychiatric diseases such as schizophrenia, manic-depressive illness or organic brain disorder. Patients of the second group suffered from serious personality disorders. Those of the third group showed deep-rooted problems in their current relationships.
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PMID:Diagnosis and therapy of male gamblers in a university psychiatric hospital. 2424 80


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