The Experts below are selected from a list of 4218 Experts worldwide ranked by ideXlab platform
Neil R. Cashman - One of the best experts on this subject based on the ideXlab platform.
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Temporal lobe epilepsy caused by domoic acid intoxication: Evidence for glutamate receptor–mediated excitotoxicity in humans
Annals of neurology, 1995Co-Authors: Fernando Cendes, Frcp Frederick Andermann, Stirling Carpenter, Robert J. Zatorre, Neil R. CashmanAbstract:We describe the development of temporal lobe epilepsy in an 84-year-old man who had suffered domoic acid intoxication. Following intoxication he had nausea, vomiting, confusion, and coma. Generalized convulsions and complex partial status epilepticus progressively developed. After 3 weeks he improved and was seizure free with severe residual memory deficit. Electroencephalograms initially showed periodic epileptiform discharges, later evolving to epileptic abnormalities over frontotemporal regions with diffuse slow waves. Eight months after the intoxication the electroencephalogram was normal. One year after the acute episode, complex partial seizures developed. Electroencephalograms showed epileptic discharges independently over both temporal lobes, with left-sided predominance. Magnetic resonance imaging revealed a hyperintense T2-weighted signal and atrophy of both hippocampi; a positron emission tomographic scan showed bitemporal decreased glucose metabolism. Pneumonia developed and the patient died 3 1/4 years after the intoxication. Autopsy disclosed severe bilateral hippocampal sclerosis. The seizures following acute domoic acid intoxication, the Postmortem Pathology, and the fact that temporal lobe epilepsy developed 1 year after intoxication indicate that the human hippocampus is also vulnerable to kainate receptor excitotoxicity, and provide strong evidence supporting the role of excitotoxic injury in epileptogenesis. This report provides a unique human parallel to, and validates the animal model of, kainate-induced epilepsy as an important tool for studying temporal lobe epilepsy.
Brian Dean - One of the best experts on this subject based on the ideXlab platform.
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neurochemistry of schizophrenia the contribution of neuroimaging Postmortem Pathology and neurochemistry in schizophrenia
Current Topics in Medicinal Chemistry, 2012Co-Authors: Brian DeanAbstract:: The advent of molecular neuroimaging has greatly impacted on understanding the neurochemical changes occurring in the CNS from subjects with psychiatric disorders, especially schizophrenia. This review focuses on the outcomes from studies using positron emission tomography and single photon emission computer tomography that have measure levels of neurotransmitter receptors and transporters in the CNS from subjects with schizophrenia. One outcome from such studies is the confirmation of a number of findings using Postmortem tissue, but in the case of neuroimaging, using drug na�ve and drug free subjects. These findings add weight to the argument that findings from Postmortem studies are not an artifact of tissue processing or a simple drug effect. However, there are some important unique findings from studies using neuroimaging studies. These include evidence to suggest that in schizophrenia there are alterations in dopamine synthesis and release, which are not accompanied by an appropriate down-regulation of dopamine D2 receptors. There are also data that would support the notion that decreased levels of serotonin 2A receptors may be an early marker of the onset of schizophrenia. Whilst there is a clear need for on-going development of neuroimaging ligands to expand the number of targets that can be studied and to increase cohort sizes in neuroimaging studies to give power to the analyses of the resulting data, current studies show that existing neuroimaging studies have already extended our understanding of the underlying pathophysiology of psychiatric disorders such as schizophrenia.
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Recent advances in Postmortem Pathology and neurochemistry in schizophrenia.
Current opinion in psychiatry, 2009Co-Authors: Brian Dean, Simone Boer, Andrew Gibbons, T. T. Money, Elizabeth ScarrAbstract:Purpose of reviewThis is a review examining recent data from the study of the Postmortem central nervous system (CNS) of patients with schizophrenia.Recent findingsStudies on the human CNS transcriptome suggest changes in pro-inflammatory pathways and myelination in schizophrenia, whereas changes in
Fernando Cendes - One of the best experts on this subject based on the ideXlab platform.
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Temporal lobe epilepsy caused by domoic acid intoxication: Evidence for glutamate receptor–mediated excitotoxicity in humans
Annals of neurology, 1995Co-Authors: Fernando Cendes, Frcp Frederick Andermann, Stirling Carpenter, Robert J. Zatorre, Neil R. CashmanAbstract:We describe the development of temporal lobe epilepsy in an 84-year-old man who had suffered domoic acid intoxication. Following intoxication he had nausea, vomiting, confusion, and coma. Generalized convulsions and complex partial status epilepticus progressively developed. After 3 weeks he improved and was seizure free with severe residual memory deficit. Electroencephalograms initially showed periodic epileptiform discharges, later evolving to epileptic abnormalities over frontotemporal regions with diffuse slow waves. Eight months after the intoxication the electroencephalogram was normal. One year after the acute episode, complex partial seizures developed. Electroencephalograms showed epileptic discharges independently over both temporal lobes, with left-sided predominance. Magnetic resonance imaging revealed a hyperintense T2-weighted signal and atrophy of both hippocampi; a positron emission tomographic scan showed bitemporal decreased glucose metabolism. Pneumonia developed and the patient died 3 1/4 years after the intoxication. Autopsy disclosed severe bilateral hippocampal sclerosis. The seizures following acute domoic acid intoxication, the Postmortem Pathology, and the fact that temporal lobe epilepsy developed 1 year after intoxication indicate that the human hippocampus is also vulnerable to kainate receptor excitotoxicity, and provide strong evidence supporting the role of excitotoxic injury in epileptogenesis. This report provides a unique human parallel to, and validates the animal model of, kainate-induced epilepsy as an important tool for studying temporal lobe epilepsy.
W. -d. Heiss - One of the best experts on this subject based on the ideXlab platform.
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Regional cerebral glucose metabolism and Postmortem Pathology in Alzheimer’s disease
Acta Neuropathologica, 1996Co-Authors: R. Mielke, R. Schröder, G. R. Fink, J. Kessler, K. Herholz, W. -d. HeissAbstract:In four patients with an antemortem diagnosis of probable Alzheimer’s disease (AD) regional cerebral glucose metabolism (rCMRGl) was studied prospectively by positron emission tomography (PET) and compared with Postmortem semiquantitative neuroPathology. The interval between the last PET study and autopsy was 1.3±0.8 years. In comparison with age-matched controls, the AD patients showed predominant temporoparietal hypometabolism spreading to other cortical and subcortical regions during serial PET scans. All patients had neuropathological findings typical for AD. There was a significant relationship between rCMRGl and density of senile plaques (SP) in one patient (τ = -0.86, P < 0.05). SP were distributed quite homogeneously in all regions examined. Neurofibrillary tangles (NFT) were concentrated focally in the hippocampus-amygdala-entorhinal complex. In the context of widespread developing cortical hypometabolism, the predilection of NFT for involvement in limbic areas suggests a disruption of projection neurons as the pathogenetic process of cortical dysfunction.
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Regional cerebral glucose metabolism and Postmortem Pathology in Alzheimer's disease.
Acta neuropathologica, 1996Co-Authors: R. Mielke, R. Schröder, G. R. Fink, J. Kessler, K. Herholz, W. -d. HeissAbstract:In four patients with an antemortem diagnosis of probable Alzheimer’s disease (AD) regional cerebral glucose metabolism (rCMRGl) was studied prospectively by positron emission tomography (PET) and compared with Postmortem semiquantitative neuroPathology. The interval between the last PET study and autopsy was 1.3±0.8 years. In comparison with age-matched controls, the AD patients showed predominant temporoparietal hypometabolism spreading to other cortical and subcortical regions during serial PET scans. All patients had neuropathological findings typical for AD. There was a significant relationship between rCMRGl and density of senile plaques (SP) in one patient (τ = -0.86, P < 0.05). SP were distributed quite homogeneously in all regions examined. Neurofibrillary tangles (NFT) were concentrated focally in the hippocampus-amygdala-entorhinal complex. In the context of widespread developing cortical hypometabolism, the predilection of NFT for involvement in limbic areas suggests a disruption of projection neurons as the pathogenetic process of cortical dysfunction.
Stirling Carpenter - One of the best experts on this subject based on the ideXlab platform.
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Temporal lobe epilepsy caused by domoic acid intoxication: Evidence for glutamate receptor–mediated excitotoxicity in humans
Annals of neurology, 1995Co-Authors: Fernando Cendes, Frcp Frederick Andermann, Stirling Carpenter, Robert J. Zatorre, Neil R. CashmanAbstract:We describe the development of temporal lobe epilepsy in an 84-year-old man who had suffered domoic acid intoxication. Following intoxication he had nausea, vomiting, confusion, and coma. Generalized convulsions and complex partial status epilepticus progressively developed. After 3 weeks he improved and was seizure free with severe residual memory deficit. Electroencephalograms initially showed periodic epileptiform discharges, later evolving to epileptic abnormalities over frontotemporal regions with diffuse slow waves. Eight months after the intoxication the electroencephalogram was normal. One year after the acute episode, complex partial seizures developed. Electroencephalograms showed epileptic discharges independently over both temporal lobes, with left-sided predominance. Magnetic resonance imaging revealed a hyperintense T2-weighted signal and atrophy of both hippocampi; a positron emission tomographic scan showed bitemporal decreased glucose metabolism. Pneumonia developed and the patient died 3 1/4 years after the intoxication. Autopsy disclosed severe bilateral hippocampal sclerosis. The seizures following acute domoic acid intoxication, the Postmortem Pathology, and the fact that temporal lobe epilepsy developed 1 year after intoxication indicate that the human hippocampus is also vulnerable to kainate receptor excitotoxicity, and provide strong evidence supporting the role of excitotoxic injury in epileptogenesis. This report provides a unique human parallel to, and validates the animal model of, kainate-induced epilepsy as an important tool for studying temporal lobe epilepsy.