Proton magnetic resonance spectroscopy of lenticular nuclei in simple schizophrenia
ABSTRACT 1. The lenticula nuclei have been suggested to be the site of structural and functional abnormalities in schizophrenia. 2. Recently, several studies involving proton magnetic resonance spectroscopy (1H MRS) showed that the ratio of N-acetyl-aspartate (NAA) to choline-containing compounds (Cho) was significantly reduced in the basal ganglia region in patients with schizophrenia. 3. Simple schizophrenia is characterized by social withdrawal and affective flattening, but not by prominent catatonic, hebephrenic or paranoid features. 4. We studied, using 1H MRS, the lenticula nuclei of 10 patients with simple schizophrenia, and 10 age- and sex-matched healthy controls. 5. No differences between the patients and the controls were found in any of the measured ratios, i.e. Cho/Cr, NAA/Cr and NAA/Cho. 6. Our results suggest the normal viability of neuronal cells, as found on quantification of NAA, Cr and Cho, in the lenticular nuclei of patients with simple schizophrenia. 7. The pathophysiology of simple schizophrenia may be different from those of other types of schizophrenia.
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- " recent - onset FEP before treatment with anti - psychotic med - ication . Only one study found increased caudal NAA levels in drug - na€ ıve FEP with prodromal symptoms ( de la Fuente - Sandoval et al . 2011 ) . This contrasts with no metabolite alterations in childhood - onset patients ( O ' Neill et al . 2004 ) , simple schizophrenia patients ( Ohara et al . 2000 ) , schizo - phrenia patients with and without Gilbert ' s Syndrome ( Miyaoka et al . 2005 ) , medicated schizophreniform spec - trum patients ( Bertolino et al . 2003 ) , CSP ( Callicott et al . 1998 , 2000 ; Block et al . 2000 ; Bertolino et al . 2001 ; Ando et al . 2002 ; Tayoshi et al . 2009 , 2010 ) , schizophrenia patients with ta"
ABSTRACT: By reviewing the existing (1) H-magnetic resonance spectroscopy literature in schizophrenia, the relationship of different sample characteristics and applied methodologies with metabolite alterations is explored. Furthermore, we emphasize common pitfalls and discrepancies in the methodological framework of the reviewed studies that introduce unwanted variation in findings and complicate the comparison of studies. A total of 92 studies were reviewed. Articles were retrieved by searching the Pubmed database. Care was taken to note down reliability and validity measures of each included study. Despite many methodological differences and shortcomings, progressive NAA reductions could be seen in several brain regions implicated in the pathogenesis of schizophrenia. In terms of treatment effects, cross-sectional evidence implicates a normalizing role for atypical antipsychotic medication; however, longitudinal studies remain inconclusive on this issue. Choline, creatine and myo-inositol levels remain largely unchanged and a time-dependent role of glutamate finds confirmation in several spectroscopy studies. Other findings are less consistent and need further replication. Most studies lack power and methodological precision. Future studies should aim for standardization and for more distinguished study populations in order to gain more valid and reliable findings. This article is protected by copyright. All rights reserved.Journal of Neurochemistry 08/2013; 128(1). DOI:10.1111/jnc.12398 · 4.24 Impact Factor
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ABSTRACT: The Human Genome Project (HGP) provides researchers with the data of nearly all human genes and the challenge to use this information for elucidating the etiology of common disorders. A secondary Darwinian method was applied to HGP and other research data to approximate and possibly unravel the etiology of schizophrenia. The results indicate that genetic and epigenetic variants of genes involved in signal transduction, transcription and translation - converging at the protein-synthesis rate (PSR) as common final pathway - might be responsible for the genetic susceptibility to schizophrenia. Environmental (e.g. viruses)and/or genetic factors can lead to cerebral PSR (CPSR) deficiency. The CPSR hypothesis of schizophrenia and antipsychotic mechanism explains 96% of the major facts of schizophrenia, reveals links between previously unrelated facts, integrates many hypotheses, and implies that schizophrenia should be easily preventable and treatable, partly by immunization against neurotrophic viruses and partly by the development of new drugs which selectively increase CPSR. Part of the manuscript has been published in a modified form as "The glial growth factors deficiency and synaptic destabilization hypothesis of schizophrenia" in BMC Psychiatry available online at [http://www.biomedcentral.com/1471-244X/2/8/].