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

Reduced auditory P300 amplitude generally has been considered to be a trait marker of schizophrenia, independent of antipsychotic treatment and clinical symptoms. However, several seemingly well-conducted studies have found P300 amplitude to be a state marker correlated with clinical symptoms. Recent research on atypical antipsychotics indicate that these medications may alter P300 amplitude as well as having beneficial clinical effects. The objective of the present study was to further elucidate the effects of schizophrenia, symptom severity, and medication status on the P300. The baseline auditory P300 was assessed in unmedicated schizophrenic patients who then were treated with olanzapine for 6 weeks and reassessed. Healthy control subjects were assessed at baseline and again at 6 weeks. Compared to healthy controls, the unmedicated patients' P300s were attenuated and delayed prior to treatment. Subsequent antipsychotic treatment increased the patients' P300 amplitudes without affecting latency. Frontal P300 amplitude was normalized, but parietal P300 amplitude remained below that of healthy controls. Although olanzapine was effective in reducing the patients' symptoms, there were no correlations between symptoms and P300 amplitude or latency either before or after treatment. The results of the present study lend support to the view that P300 amplitude behaves as a trait marker. No evidence is found of a P300 clinical state marker.
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PMID:Effects of olanzapine on auditory P300 in schizophrenia. 1255 41

Schizophrenia patients often exhibit impairments in executive functioning on formal testing and exhibit behaviors consistent with executive/frontal impairment in daily life. The Frontal Systems Behavior Scale (FrSBe) assesses behaviors associated with frontal lobe damage including executive dysfunction, apathy and disinhibition. We examined the reliability and validity of the FrSBe in 131 schizophrenia outpatients. Subjects were rated on the FrSBe and received symptom, cognitive and functional assessments. Statistical tests were corrected for multiple comparisons. The FrSBe was found to have good internal consistency and test-retest reliability. All three dimensions of the FrSBe (i.e. executive dysfunction, apathy and disinhibition) were significantly correlated with poor adaptive functioning as measured by the Social and Occupational Functioning Scale and the Functional Needs Assessment. In addition, differential relationships were found for apathy and disinhibition with symptoms as rated from the Brief Psychiatric Rating Scale and with cognitive variables including Trails B and verbal fluency scores. A multivariate analysis of variance examined differences on the FrSBe between patients and a group of 51 education-matched controls. Patients had significantly greater impairment on the FrSBe than controls. These differences were found for all FrSBe subscales. Results support the use of the FrSBe to characterize goal-directed behavior in schizophrenia patients.
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PMID:Frontal Systems Behavior Scale in schizophrenia: relationships with psychiatric symptomatology, cognition and adaptive function. 1255 79

Structural prefrontal deficits have been reported in patients with schizophrenia, but it is unclear if they are also found in patients with schizophrenia spectrum personality disorders. The hypothesis that a spectrum group will be characterized by prefrontal structural deficits was tested by assessing prefrontal gray and white volumes using magnetic resonance imaging in a community sample of 16 individuals with schizotypal/paranoid personality disorder, 27 comparisons, and 26 psychiatric controls. Frontal neurocognitive functioning was also assessed using the Wisconsin Card Sorting Test and the Continuous Performance Test. The spectrum group showed reduced prefrontal gray volumes and poorer frontal functioning compared to both other groups. Structural deficits were independent of functional deficits and together correctly classified 84.2 percent of subjects. Structural but not functional deficits were abolished after a strict control for antisocial personality was made. Results support the notion that frontal deficits may be centrally involved in the etiology of schizophrenia but also suggest that comorbid antisocial behavior may be one factor accounting for differences in prefrontal structural findings across studies.
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PMID:Prefrontal structural and functional deficits in schizotypal personality disorder. 1264 81

Magnetic resonance imaging (MRI) and positron emission tomography (PET) studies of the frontal and temporal lobes in schizophrenia patients and healthy controls have proliferated over the past 2 decades, but there have been relatively few attempts to quantify the evidence. In this meta-analytic review, 155 studies on frontal and temporal lobe neurobiology were synthesized, reflecting results from 4043 schizophrenia patients and 3977 normal controls. Cohen's d was used to quantify case-control differences, and moderator variable analysis indexed the relation of sample and imaging characteristics to the magnitude of these differences. Frontal metabolic and blood flow deficiencies in conjunction with cognitive activation tasks ("hypofrontality") emerged as the strongest body of evidence, demonstrating abnormalities that distinguish approximately half of schizophrenia patients from healthy people. Most case-control comparisons with structural and functional imaging yield small and in many cases unstable findings. Technical scanning parameters like slice thickness and magnet strength did not vary with case-control differences consistently across the meta-analyses. However, patient sample characteristics including sample size, handedness and gender composition emerged frequently as moderators of brain-imaging effect sizes.
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PMID:Quantification of frontal and temporal lobe brain-imaging findings in schizophrenia: a meta-analysis. 1271 72

The hypothesis that normal brain torque (i.e. rightward frontal and leftward occipital asymmetry) is anomalous in schizophrenia (Crow, 1997. Trends in Neuroscience, 20, 339-343) was tested by application of a novel image analysis technique on three-dimensional magnetic resonance images obtained in 26 adult patients with chronic schizophrenia (18 males, 8 females) and 24 controls (14 males, 10 females). Right and left cerebral hemisphere tissue was extracted via non-linear co-registration with a mask image, and maps were computed of inter-hemispheric differences in tissue volume in an array of columns of voxels orthogonal to the mid-plane (2D), and profiles of coronal slice volumes (1D). Furthermore, integration of two-dimensional column maps gave approximate lobar asymmetries, and occipital and frontal asymmetries were combined to give a volumetric measure of brain torque. Significant brain torque was revealed in male and female control and patient groups, and did not correlate with brain size. Frontal and occipital asymmetries were significantly correlated in all groups. Both frontal and occipital components of torque were significantly increased in males than females. Patients tended to have reduced torque, particularly the leftward occipital component. Furthermore, 3/26 patients (but no controls) had reversed torque (leftward frontal and rightward occipital asymmetry). Contrary to Crow's hypothesis, brain torque was not significantly reduced in patients with schizophrenia relative to controls, although reversal of torque was found in three cases. Future studies with larger sample sizes should consider sexual dimorphism and specific symptoms in relation to asymmetry.
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PMID:Application of a new image analysis technique to study brain asymmetry in schizophrenia. 1451 93

This study investigated the morphology of the frontal lobe and the caudate nucleus in velocardiofacial syndrome, a neurogenetic disorder caused by a microdeletion at chromosome 22q11.2 and frequently associated with severe psychiatric disturbances. Volumes of the caudate nucleus and subregions of the frontal lobe were compared on magnetic resonance images of 10 children with velocardiofacial syndrome and 10 age- and gender-matched controls. Frontal deep white matter was reduced significantly (by about 23%) in subjects with velocardiofacial syndrome relative to controls. Frontal and prefrontal volumes were also reduced in subjects with velocardiofacial syndrome, although not disproportionately to whole brain volume. The volume of the right caudate nucleus was increased in children with velocardiofacial syndrome. Associations between right caudate and right frontal regions were noted in controls but not in children with velocardiofacial syndrome. These findings suggest frontostriatal dysfunction in children with velocardiofacial syndrome. Insofar as up to 30% of adults with velocardiofacial syndrome (also known as chromosome 22q11 deletion syndrome) develop schizophrenia and frontostriatal dysfunction has been noted in schizophrenia, the findings support the hypothesis that velocardiofacial syndrome might represent a neurodevelopmental model of schizophrenia.
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PMID:Frontal and caudate alterations in velocardiofacial syndrome (deletion at chromosome 22q11.2). 1522 7

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

The objective of this study was to delineate further the nature of diffusion anisotropy abnormalities in frontal white matter previously observed in schizophrenic patients using a high-field magnetic resonance imaging (MRI) system. Six schizophrenia patients and six healthy control subjects were examined using a highfield MRI (3.0T) system. In order to confirm previously reported abnormalities in anisotropy, data were first analyzed to determine fractional anisotropy (FA), a frequently utilized general index of anisotropy. Subsequently, the identical data set was subjected to lambda chart analysis (LCA), a newly developed algorithm for diffusion tensor analysis (DTA) that more effectively provides eigenvalue information. Frontal white matter FA was found to be significantly reduced in schizophrenic patients compared to control subjects, confirming previously reported findings. LCA revealed that the decline in FA was due to a disproportionate increase in small eigenvalue components, and not due to a decline in principal eigenvalue components.
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PMID:Diffusion tensor analysis in chronic schizophrenia. A preliminary study on a high-field (3.0T) system. 1564 57

This review presents data showing that apathy is common across a number of disorders. Apathy is not only common, but is also associated with significant problems: reduced functional level, decreased response to treatment, poor illness outcome, caregiver distress, and chronicity. Preliminary evidence of treatment efficacy exists for dopaminergic drugs and for amphetamines. Strong evidence of efficacy exists for acetylcholinesterase inhibitors in Alzheimer's disease, and for atypical antipsychotics in schizophrenia. Frontal-subcortical system(s) dysfunction is implicated in the causation of apathy; apathy subtypes based on the various frontal-subcortical loops may thus exist. Further research involving diagnosis, pathophysiology, and treatment is suggested.
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PMID:Apathy: why care? 1574 78

Several studies have shown that schizophrenia is characterized by impaired frontal lobe functions, functions that are responsible, for example, for the management of rules, strategic reasoning, and selective attention. Using event-related potentials (ERP), we assessed the brain's electrical activity in a group of patients with schizophrenia (n=11) and a healthy control group (n=14) during a reaction time task requiring the use of a rule. ERP waves were compared with those elicited in a similar task based on a direct sensory association. In the control group, ERP analyses showed a negative wave moving from the posterior to the anterior regions of the scalp in a latency range of 250-400 ms. Then, the negativity remained at the frontal scalp region in a latency range of 400-800 ms. In this group, the amplitude was higher during the rule operation than during the sensory association task. In schizophrenic patients, the anteroposterior component of the negative wave was totally absent in both tasks, and we did not find a modulation of the ERP by the task. Frontal scalp negativity was observed, but its latency was longer and its amplitude lower than in the control group. We discuss these findings in terms of the frontoposterior disconnection hypothesis.
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PMID:Event-related potentials during rule processing in schizophrenia. 1580 90


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