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Steven Guich

Bio: Steven Guich is an academic researcher from University of California, Irvine. The author has contributed to research in topics: Positron emission tomography & Electroencephalography. The author has an hindex of 9, co-authored 11 publications receiving 599 citations.

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TL;DR: Patients with schizophrenia showed both absolutely and relatively reduced metabolic rates in the frontal cortex and in the temporoparietal regions compared with normal controls.
Abstract: Local cerebral uptake of glucose labelled with fluorine-18 was measured by positron emission tomography in 13 patients with schizophrenia and 37 right-handed volunteers. Patients received no medication for a minimum of 31 days and a mean of 30 weeks. The subjects were administered the labelled deoxyglucose just after the beginning of a 32-minute sequence of blurred numbers as visual stimuli for the Continuous Performance Test. In normal controls, task performance was associated with increases in glucose metabolic rate in the right frontal and right temporoparietal regions; occipital rates were unchanged. Patients with schizophrenia showed both absolutely and relatively reduced metabolic rates in the frontal cortex and in the temporoparietal regions compared with normal controls.

335 citations

Journal ArticleDOI
TL;DR: Increased delta activity in the frontal region of patients with schizophrenia in comparison to normal controls is confirmed, and a significant correlation between increased frontal delta and relative reduction in frontal lobe metabolism among patients with psychosis is found.

60 citations

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TL;DR: Functional relationships between cortical areas were assessed by calculating the coherences between different scalp electroencephalogram signals recorded from 13 unmedicated male patients with schizophrenia and 9 normal male subjects, suggesting that "cortical circuits" extending beyond prefrontal areas may be disrupted in schizophrenia.
Abstract: Multiple studies have demonstrated prefrontal dysfunction among schizophrenics. The prefrontal cortex does not function in isolation, but instead relies on extensive connections with other brain areas. Functional relationships between cortical areas were assessed by calculating the coherences between different scalp electroencephalogram (EEG) signals recorded from 13 unmedicated male patients with schizophrenia and 9 normal male subjects. Alpha-band coherences linked to prefrontal areas in schizophrenic patients were about the same as those of normal controls when subjects were cognitively "at rest," but they were reduced for certain electrode pairs in the former group when performing the degraded-stimulus continuous performance test. Most of these findings were not accounted for by changes in alpha power, suggesting that "cortical circuits" extending beyond prefrontal areas may be disrupted in schizophrenia.

60 citations

Journal ArticleDOI
TL;DR: In this paper, EEG epochs recorded from 12 neuroleptic-free schizophrenic patients and 11 normal control subjects were Laplacian-filtered to highlight activity specific to prefrontal and parietal areas.
Abstract: Dimensional complexity reflects the number of independent variables contributing to a dynamic process. EEG epochs recorded from 12 neuroleptic-free schizophrenic patients and 11 normal control subjects were Laplacian-filtered to highlight activity specific to prefrontal and parietal areas, and dimensional complexity measures of the resulting signals were then derived. Complexity of EEG waveforms generated by schizophrenic patients was depressed relative to that of normal subjects, especially in left frontal and right parietal regions. These data suggest that complexity of underlying is also reduced.

53 citations

Journal ArticleDOI
TL;DR: Both EEG delta in microvolts and metabolic rate had similar diagnostic sensitivity, but PET had fewer false positives among normals and the left amygdala had the highest sensitivity and percent correct diagnosis of any brain area.
Abstract: Quantitative scalp EEG from 32 channels and the cerebral glucose metabolic rate from the 32 underlying cortical positions as assessed by positron emission tomography (PET) with 18F-2-deoxyg

36 citations


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TL;DR: The results indicate that schizophrenia is characterized by a broadly based cognitive impairment, with varying degrees of deficit in all ability domains measured by standard clinical tests.
Abstract: The neurocognitive literature on test performance in schizophrenia is reviewed quantitatively. The authors report 22 mean effect sizes from 204 studies to index schizophrenia versus control differences in global and selective verbal memory, nonverbal memory, bilateral and unilateral motor performance, visual and auditory attention, general intelligence, spatial ability, executive function, language, and interhemispheric tactile-transfer test performance. Moderate to large raw effect sizes (d > .60) were obtained for all 22 neurocognitive test variables, and none of the associated confidence intervals included zero. The results indicate that schizophrenia is characterized by a broadly based cognitive impairment, with varying degrees of deficit in all ability domains measured by standard clinical tests.

2,372 citations

Journal ArticleDOI
TL;DR: A model that implicates connectivity among nodes located in prefrontal regions, the thalamic nuclei, and the cerebellum is developed that produces "cognitive dysmetria", difficulty in prioritizing, processing, coordinating, and responding to information in schizophrenia.
Abstract: Earlier efforts to localize the symptoms of schizophrenia in a single brain region have been replaced by models that postulate a disruption in parallel distributed or dynamic circuits. Based on empirical data derived from both magnetic resonance and positron emission tomography, we have developed a model that implicates connectivity among nodes located in prefrontal regions, the thalamic nuclei, and the cerebellum. A disruption in this circuitry produces "cognitive dysmetria," difficulty in prioritizing, processing, coordinating, and responding to information. This "poor mental coordination" is a fundamental cognitive deficit in schizophrenia and can account for its broad diversity of symptoms.

1,108 citations

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TL;DR: It is argued that this neurobiological mechanism can explain failures of self-monitoring, leading to a mechanistic explanation for first-rank symptoms as pathognomonic features of schizophrenia, and may provide a basis for future diagnostic classifications with physiologically defined patient subgroups.
Abstract: Over the last 2 decades, a large number of neurophysiological and neuroimaging studies of patients with schizophrenia have furnished in vivo evidence for dysconnectivity, ie, abnormal functional integration of brain processes. While the evidence for dysconnectivity in schizophrenia is strong, its etiology, pathophysiological mechanisms, and significance for clinical symptoms are unclear. First, dysconnectivity could result from aberrant wiring of connections during development, from aberrant synaptic plasticity, or from both. Second, it is not clear how schizophrenic symptoms can be understood mechanistically as a consequence of dysconnectivity. Third, if dysconnectivity is the primary pathophysiology, and not just an epiphenomenon, then it should provide a mechanistic explanation for known empirical facts about schizophrenia. This article addresses these 3 issues in the framework of the dysconnection hypothesis. This theory postulates that the core pathology in schizophrenia resides in aberrant N-methyl-D-aspartate receptor (NMDAR)-mediated synaptic plasticity due to abnormal regulation of NMDARs by neuromodulatory transmitters like dopamine, serotonin, or acetylcholine. We argue that this neurobiological mechanism can explain failures of self-monitoring, leading to a mechanistic explanation for first-rank symptoms as pathognomonic features of schizophrenia, and may provide a basis for future diagnostic classifications with physiologically defined patient subgroups. Finally, we test the explanatory power of our theory against a list of empirical facts about schizophrenia.

1,073 citations

Journal ArticleDOI
TL;DR: Abnormally high density in the cerebral cortices of schizophrenics suggests that neuronal atrophy is the anatomic substrate for deficient information processing in schizophrenia.
Abstract: Background: In the past two decades, gross morphologic changes have been uncovered in the schizophrenic brain, eg, increased ventricular width and decreased cortical volume; however, relatively little is known about the area-specific and laminar density of cells in the schizophrenic cortex, particularly in prefrontal areas. Method: A direct, three-dimensional counting method was used to determine cell density in 16 brains from patients with schizophrenia, 19 from normal subjects, six from patients with schizoaffective disorder, and nine from patients with advanced-stage Huntington's disease. Results: Increased neuronal density was found in prefrontal area 9 (17%) and occipital area 17 (10%) in the schizophrenic brains. In area 9, neuronal density was increased in layers III to VI; cell packing of pyramidal and nonpyramidal neurons was elevated. Cortical thickness in the schizophrenic brains was slightly but not significantly reduced in both areas, with a disproportionate reduction in layer V in area 9. In contrast, brains with Huntington's disease exhibited markedly higher glial density Abnormally high density in the cerebral cortices of schizophrenics suggests that neuronal atrophy is the anatomic substrate for deficient information processing in schizophrenia. Conclusion: Abnormally high density in the cerebral cortices of schizophrenics suggests that neuronal atrophy is the anatomic substrate for deficient information processing in schizophrenia.

874 citations