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

Research findings are increasingly reporting evidence of physiological abnormalities in dyslexia and sites for dyslexia have been identified on three chromosomes. It has been suggested that genetic inheritance may cause phospholipid abnormalities in dyslexia somewhat similar to those found in schizophrenia. A key enzyme in phospholipid metabolism, Type IV, or cytosolic, phospholipase A2 (cPLA2), releases arachidonic acid (AA), a 20-carbon fatty acid, which is the major source of production of prostaglandins and leukotrienes. An entirely new assay, which for the first time has enabled determination of the amount of the enzyme rather than its activity, was used to measure cPLA2 in dyslexic-type adults and controls and the two groups were found to differ significantly, the dyslexic-types having more of the enzyme. A report elsewhere of schizophrenics having even greater amounts of the enzyme suggests that dyslexia may be on a continuum with schizophrenia, as may be other neurodevelopmental disorders - which have also been described as phospholipid spectrum disorders.
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PMID:Increased levels of cytosolic phospholipase A2 in dyslexics. 1097 Jul 11

The success of diffusion magnetic resonance imaging (MRI) is deeply rooted in the powerful concept that during their random, diffusion-driven displacements molecules probe tissue structure at a microscopic scale well beyond the usual image resolution. As diffusion is truly a three-dimensional process, molecular mobility in tissues may be anisotropic, as in brain white matter. With diffusion tensor imaging (DTI), diffusion anisotropy effects can be fully extracted, characterized, and exploited, providing even more exquisite details on tissue microstructure. The most advanced application is certainly that of fiber tracking in the brain, which, in combination with functional MRI, might open a window on the important issue of connectivity. DTI has also been used to demonstrate subtle abnormalities in a variety of diseases (including stroke, multiple sclerosis, dyslexia, and schizophrenia) and is currently becoming part of many routine clinical protocols. The aim of this article is to review the concepts behind DTI and to present potential applications.
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PMID:Diffusion tensor imaging: concepts and applications. 1127 97

GABA (gamma-aminobutyric acid) is the principal inhibitory neurotransmitter in the brain. The human GABA(B) receptor (GABBR1) maps to the human leukocyte antigen (HLA) region of chromosome 6. Its function and location in a susceptibility region for schizophrenia, epilepsy, and dyslexia make GABBR1 a candidate gene for neurobehavioral disorders. We report the characterization of GABBR1 gene mutations in 100 chromosomes from a mixed American population. Eleven distinct mutations were found, including two previously reported missense mutations (A20V and G489S) and a previously reported silent 1977 T>C transition. Here, we report four novel silent substitutions (39C>T, 1473T>C, 1476T>C, 1545T>C) and four novel intron variants. These DNA variants may be useful in association and linkage studies of neurobehavioral disorders, and in pharmacogenetic studies of drugs targeting GABBR1.
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PMID:Human GABA(B) receptor 1 gene: eight novel sequence variants. 1129 33

BACKGROUND: Psychoacoustics is a fascinating developing field concerned with the evaluation of the hearing sensation as an outcome of a sound or speech stimulus. Neuroaudiology with electrophysiologic testing, records the electrical activity of the auditory pathways, extending from the 8th cranial nerve up to the cortical auditory centers as a result of external auditory stimuli. Central Auditory Processing Disorders may co-exist with mental disorders and complicate diagnosis and outcome. DESIGN: A MEDLINE search was conducted to search for papers concerning the association between Central Auditory Processing Disorders and mental disorders. The research focused on the diagnostic methods providing the inter-connection of various mental disorders and central auditory deficits. MEASUREMENTS AND MAIN RESULTS: The medline research revealed 564 papers when using the keywords 'auditory deficits' and 'mental disorders'. 79 papers were referring specifically to Central Auditory Processing Disorders in connection with mental disorders. 175 papers were related to Schizophrenia, 126 to learning disabilities, 29 to Parkinson's disease, 88 to dyslexia and 39 to Alzheimer's disease. Assessment of the Central Auditory System is carried out through a great variety of tests that fall into two main categories: psychoacoustic and electrophysiologic testing. Different specialties are involved in the diagnosis and management of Central Auditory Processing Disorders as well as the mental disorders that may co-exist with them. As a result it is essential that they are all aware of the possibilities in diagnostic procedures. CONCLUSIONS: Considerable evidence exists that mental disorders may correlate with CAPD and this correlation could be revealed through psychoacoustics and neuroaudiology. Mental disorders that relate to Central Auditory Processing Disorders are: Schizophrenia, attention deficit disorders, Alzheimer's disease, learning disabilities, dyslexia, depression, auditory hallucinations, Parkinson's disease, alcoholism, anorexia and childhood mental retardation. Clinical awareness should be high in order for doctors of the two specialties, psychiatry and otorhinolaryngology-audiology to collaborate.
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PMID:Contribution of psychoacoustics and neuroaudiology in revealing correlation of mental disorders with central auditory processing disorders. 1279 8

Receptive language disorder in schizophrenia has been hypothesized to involve a fundamental deficit in the temporal (time-based) dynamics of brain function that includes disruptions to patterns of activation and synchronization. In this paper, candidate mechanisms and pathways that could account for this basic deficit are discussed. Parallels are identified between the patterns of language dysfunction observed for schizophrenia and dyslexia, two separate clinical disorders that may share a common abnormality in cell membrane phospholipids. A heuristic is proposed which details a trajectory involving an interaction of brain fatty acids and second-messenger function that modulates synaptic efficacy, and, in turn, influences language processing in schizophrenia patients. It is additionally hypothesized that a primary deficit of functional excitation originating in the cerebellum, in combination with a compensatory decrease of functional inhibition in the prefrontal cortex, influences receptive language dysfunction in schizophrenia.
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PMID:The relationship between membrane pathology and language disorder in schizophrenia. 1462 99

In the present review, we summarize the most recent findings and current views about the structural and functional basis of human brain lateralization in the auditory modality. Main emphasis is given to hemodynamic and electromagnetic data of healthy adult participants with regard to music- vs. speech-sound encoding. Moreover, a selective set of behavioral dichotic-listening (DL) results and clinical findings (e.g., schizophrenia, dyslexia) are included. It is shown that human brain has a strong predisposition to process speech sounds in the left and music sounds in the right auditory cortex in the temporal lobe. Up to great extent, an auditory area located at the posterior end of the temporal lobe (called planum temporale [PT]) underlies this functional asymmetry. However, the predisposition is not bound to informational sound content but to rapid temporal information more common in speech than in music sounds. Finally, we obtain evidence for the vulnerability of the functional specialization of sound processing. These altered forms of lateralization may be caused by top-down and bottom-up effects inter- and intraindividually In other words, relatively small changes in acoustic sound features or in their familiarity may modify the degree in which the left vs. right auditory areas contribute to sound encoding.
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PMID:Lateralization of auditory-cortex functions. 1462 26

Many studies have shown altered hemispheric asymmetry-particularly in perisylvian regions-in schizophrenia patients as well as in individuals with dyslexia. Here we explore the similarity of these findings comparing the localization of the magnetic auditory N100m to the German syllable [ba:] in schizophrenia patients, dyslexic adults, and healthy control subjects. Control subjects showed the typical finding of more anterior sources in the right than in the left perisylvian region. In contrast, both schizophrenia patients and dyslexic subjects displayed a symmetrical N100m source configuration. While in people with dyslexia the alteration appears to originate in the right hemisphere, left-hemispheric deviations might contribute to reduced asymmetry in schizophrenia patients. Our results indicate that an absence of lateralized auditory responses in the temporal lobes may reflect a common deviance present in dyslexia and schizophrenia. The nonspecific finding of reduced cerebral laterality may be accounted for by population-specific differences in the functional organization of perisylvian sites.
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PMID:Cerebral lateralization in schizophrenia and dyslexia: neuromagnetic responses to auditory stimuli. 1472 5

Magnetic resonance spectroscopy is one of the most important tools for quantitative analysis of chemical composition and structure, and this non-invasive technique is now being applied in vivo to study biochemical processes in those neuropsychiatric disorders that are part of the phospholipid spectrum. Interpretation of a clinical magnetic resonance spectrum can provide information about membrane phospholipid turnover, cellular energetics, neuronal function, selected neurotransmitter activity and intracellular pH. Cerebral proton and phosphorus magnetic resonance spectroscopy findings are summarized in relation to schizophrenia, dyslexia and chronic fatigue syndrome.
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PMID:In vivo MR spectroscopy in diagnosis and research of neuropsychiatric disorders. 1504 Oct 27

Receptive language disorder in schizophrenia is hypothesized to represent a learning disorder that involves a neurodevelopmental etiology. It is argued that a preexisting developmental language disorder may characterize a subset of schizophrenia patients. A primary deficit in the temporal dynamics of brain function is assumed to cause receptive language disorder in schizophrenia. This hypothesized core deficit includes both disturbance in the processing of rapid, sequential information and disruptions to patterns of brain activation and synchronization. These timing deficits may alter the way associative connections are formed and/or accessed in semantic memory. It is suggested that abnormalities in second-messenger pathways of subcortical-cortical circuitry offer an etiological nexus for language dysfunction in schizophrenia and developmental dyslexia.
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PMID:Language disorder in schizophrenia as a developmental learning disorder. 1556 71

With optimal pregnancy conditions (natural, enriched diet which includes fish) African (Digo) infants are 3-4 weeks ahead of European/American infants in sensorimotor terms at birth, and during the first year. Infants of semi-aquatic sea-gypsies swim before they walk, and have superior visual acuity compared with us. With adverse pregnancy behaviour (fear of fat, a trend to dieting), neglecting the need for brain fat to secure normal brain development and function, we run a risk of dysfunction--death. Sudden Infant Death Syndrome victims have depressed birth weight, lower levels of marine fat in brainstem than controls, and >80 suffer multiple hypoxic episodes prior to death. Depressed birth weight (more than 10% below mean) is seen in learning and behaviour disorders, and a trend towards weights of less than 3kg is increasing, which supports a rise in antenatal sub optimality. Given marine fat deficiency in pregnancy and infancy, neurons starved for fuel could delay myelination and maturation in the latest developed Frontal Lobes. The phylogenetic oldest Lateral Frontal Lobe System (feed-back mechanism etc.) derived from olfactory bulb-amygdala, which crosses in Anterior Commisure is probably spared, while the Medial Frontal Lobe System derived from Hippocampus-Cingulum and crosses in Corpus Callosum (delayed response task) is most likely affected. The rise in infantile autism (intact vision and hearing) with deficit in delayed response task only, could suggest a deficit in the Medial Frontal Lobe System. The human species is unique; 70% of total energy to the foetus goes to development of the brain, which mainly consists of marine fat. It undergoes pervasive regressive events, before birth, in infancy and at puberty. Minimal retraction of neuronal arborisation is advantageous. Attributable to adverse pregnancy childrearing practice, excessive retraction is likely prenatally and in infancy. Pubertal age affects the fundamental property of nervous tissue, excitability: excessive excitatory drive is seen in early, and a deficiency in late puberty. It is postulated that with adequate marine fat, there is probably no risk of psychopathology at the extremes, whereas a deficiency could lead to paroxysmal (subcortical) dysfunction in early puberty, and breakdown of cortical circuitry and cognitive dysfunctions in late puberty. The post-pubertal psychoses, schizophrenia and manic-depressive psychosis at the extremes of the pubertal age continuum, with contrasting excitability and biological treatment, are probably the result of continuous dietary deficiency, which has inactivated the expression of genes for myelin development and oligodendrocyte-related genes in their production of myelin. The beneficial effect of marine fat in both disorders, in other CNS disorders as well as in developmental dyslexia (DD) and ADHD among others, supports our usual diet is persistently deficient. We have neglected the similarity of our great brain to other mammals, and our marine heritage. Given the amount of marine fat needed to secure normal brain development and function is not known, nor the present dietary level, it seems unduly conjectural to postulate that a dietary deficiency in marine fat is causing brain dysfunction and death. However, all observations point in the same direction: our diet focusing on protein mainly, is deficient, the deficiency is most pronounced in maternal nutrition and in infancy.
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PMID:From superior adaptation and function to brain dysfunction--the neglect of epigenetic factors. 1561 23


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