The Experts below are selected from a list of 297 Experts worldwide ranked by ideXlab platform
Tsung-ming Shih - One of the best experts on this subject based on the ideXlab platform.
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Neuropharmacological Mechanisms of Nerve Agent-induced Seizure and Neuropathology
Neuroscience and biobehavioral reviews, 1997Co-Authors: John H. Mcdonough, Tsung-ming ShihAbstract:This paper proposes a three phase "model" of the neuropharmacological processes responsible for the seizures and Neuropathology produced by nerve agent intoxication. Initiation and early expression of the seizures are cholinergic phenomenon; anticholinergics readily terminate seizures at this stage and no Neuropathology is evident. However, if not checked, a transition phase occurs during which the neuronal excitation of the seizure per se perturbs other neurotransmitter systems: excitatory amino acid (EAA) levels increase reinforcing the seizure activity; control with anticholinergics becomes less effective; mild Neuropathology is occasionally observed. With prolonged epileptiform activity the seizure enters a predominantly non-cholinergic phase: it becomes refractory to some anticholinergics; benzodiazepines and N-methyl-D-aspartate (NMDA) antagonists remain effective as anticonvulsants, but require anticholinergic co-administration; mild Neuropathology is evident in multiple brain regions. Excessive influx of calcium due to repeated seizure-induced depolarization and prolonged stimulation of NMDA receptors is proposed as the ultimate cause of Neuropathology. The model and data indicate that rapid and aggressive management of seizures is essential to prevent Neuropathology from nerve agent exposure.
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Protection against nerve agent-induced Neuropathology, but not cardiac pathology, is associated with the anticonvulsant action of drug treatment.
Neurotoxicology, 1995Co-Authors: John H. Mcdonough, L. W. Dochterman, C. D. Smith, Tsung-ming ShihAbstract:Protection Against Nerve Agent-Induced Neuropathology, But Not Cardiac Pathology, is Associated with the Anticonvulsant Action of Drug Treatment. Neurotoxicology16(1): 123-132, 1995. Brain and cardiac tissue was examined for pathological changes from rats that survived 24 hrs following exposure to a convulsant dose of the nerve agent soman. The animals had been treated following varying durations of seizure activity (2.5 - 40 min) with a number of different compounds that did or did not terminate the seizure. Moderate to severe Neuropathology was evident in virtually all animals (98 %) in which drug treatment did not terminate seizures. All animals that experienced up to 10 min of seizure activity before drug treatment successfully terminated the seizure were free of Neuropathology. There was an increasing frequency in the incidence of Neuropathology in animals that experienced 20 (10 %) or 40 min (79 %) of seizure activity before drug treatment terminated the seizure, but the degree of Neuropathology in these groups was significantly less than that observed in animals where seizure activity was not terminated. Cardiac lesions occurred at a much higher frequency (88 %) than neuropathological changes (57 %) and were not consistently associated with the anticonvulsant effectiveness. Early treatment (≤ 10 min) with anticholinergic drugs, however, was associated with protection from cardiac damage. The results strongly support the hypothesis that nerve agent-induced brain damage is linked to epileptiform activity. The minimal amount of seizure activity necessary for irreversible neural damage to become evident under these conditions is - 20 min, and the process accelerates greatly after this minimal time has elapsed. Successful termination of seizure activity, regardless of the type of drug used, protected either totally or relatively against brain damage depending upon how long the seizure had progressed. The mechanisms responsible for cardiac lesion formation occur more rapidly and may have a cholinergic component
Heinz-joachim Meencke - One of the best experts on this subject based on the ideXlab platform.
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Clinical Neuropathology of the epilepsies in the 100 years of the ILAE (1909-2009).
Epilepsia, 2009Co-Authors: Heinz-joachim MeenckeAbstract:The paper describes the history of the clinical Neuropathology of the epilepsies in the last hundred years from microscopy to molecular Neuropathology. The main focus is on the concepts of hippocampal sclerosis and its discussion of causative lesion or consequence of seizures, and the concept of developmental disturbances in respect to general epileptogenicity. Clinical Neuropathology remains an important discipline in the future of epileptology and brain research especially in the area of molecular genetics. Neuropathology will help to understand the stages of epileptogenesis and the factors responsible for the progressive nature of the disease.
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Clinical Neuropathology of the epilepsies in the 100 years of the ILAE (1909–2009)
Epilepsia, 2009Co-Authors: Heinz-joachim MeenckeAbstract:The paper describes the history of the clinical Neuropathology of the epilepsies in the last hundred years from microscopy to molecular Neuropathology. The main focus is on the concepts of hippocampal sclerosis and its discussion of causative lesion or consequence of seizures, and the concept of developmental disturbances in respect to general epileptogenicity. Clinical Neuropathology remains an important discipline in the future of epileptology and brain research especially in the area of molecular genetics. Neuropathology will help to understand the stages of epileptogenesis and the factors responsible for the progressive nature of the disease.
Mario F Mendez - One of the best experts on this subject based on the ideXlab platform.
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What progressive aphasia says about its Neuropathology
Neurology, 2009Co-Authors: Mario F MendezAbstract:The primary progressive aphasia (PPA) syndromes are heterogeneous neurodegenerative disorders. The 3 major PPA syndromes are not identical to the usual aphasia syndromes from strokes. Progressive nonfluent aphasia (PNFA) involves effortful speech with agrammatism and frequent apraxia of speech. The semantic variant or semantic dementia (SemD) involves fluent speech with loss of word and object meaning. Logopenic progressive aphasia (LPA), the third and most recently described PPA, involves word-finding pauses, moderate anomia, and impaired repetition of sentences. Each PPA syndrome correlates with a specific patterns of focal atrophy, but has a less robust relationship with the underlying Neuropathology. An important reason for clarifying the relationship between clinical syndrome and Neuropathology is that it facilitates clinical trials with disease-modifying therapies. In this issue of Neurology ®, Deramecourt et al.1 have decreased the gap between the clinical syndromes of PPA and their Neuropathology. This clinicopathologic study investigated 18 patients followed in the Lille Memory Clinic over a 15-year period. These patients presented with progressive …
P L Lantos - One of the best experts on this subject based on the ideXlab platform.
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The Neuropathology of Schizophrenia. Progress and Interpretation
Journal of Neurology Neurosurgery & Psychiatry, 2001Co-Authors: P L LantosAbstract:The Neuropathology of Schizophrenia. Progress and Interpretation . Edited by paul j harrison andgareth w roberts (Pp374, £65.00). Published by Oxford University Press, Oxford, 2000. ISBN 0-19-262907-7. The Neuropathology of schizophrenia has been for a long time perhaps one of the most controversial fields of biomedical research. In the middle decades of the last century there was an increased interest in the Neuropathology of psychosis based on the assumption that structural alterations in the brain would provide insight into the understanding of this complex and devastating disease. However, the results of these investigations have been contradictory and it has become a cliche to say that schizophrenia is the graveyard of neuropathologists. Indeed, the results of neuropathological investigations were confusing, and resulted from both clinical and pathological problems. The clinical definition of schizophrenia has been controversial and for a long time internationally accepted diagnostic criteria did not exist. Patients' cohorts …
John H. Mcdonough - One of the best experts on this subject based on the ideXlab platform.
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Neuropharmacological Mechanisms of Nerve Agent-induced Seizure and Neuropathology
Neuroscience and biobehavioral reviews, 1997Co-Authors: John H. Mcdonough, Tsung-ming ShihAbstract:This paper proposes a three phase "model" of the neuropharmacological processes responsible for the seizures and Neuropathology produced by nerve agent intoxication. Initiation and early expression of the seizures are cholinergic phenomenon; anticholinergics readily terminate seizures at this stage and no Neuropathology is evident. However, if not checked, a transition phase occurs during which the neuronal excitation of the seizure per se perturbs other neurotransmitter systems: excitatory amino acid (EAA) levels increase reinforcing the seizure activity; control with anticholinergics becomes less effective; mild Neuropathology is occasionally observed. With prolonged epileptiform activity the seizure enters a predominantly non-cholinergic phase: it becomes refractory to some anticholinergics; benzodiazepines and N-methyl-D-aspartate (NMDA) antagonists remain effective as anticonvulsants, but require anticholinergic co-administration; mild Neuropathology is evident in multiple brain regions. Excessive influx of calcium due to repeated seizure-induced depolarization and prolonged stimulation of NMDA receptors is proposed as the ultimate cause of Neuropathology. The model and data indicate that rapid and aggressive management of seizures is essential to prevent Neuropathology from nerve agent exposure.
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Protection against nerve agent-induced Neuropathology, but not cardiac pathology, is associated with the anticonvulsant action of drug treatment.
Neurotoxicology, 1995Co-Authors: John H. Mcdonough, L. W. Dochterman, C. D. Smith, Tsung-ming ShihAbstract:Protection Against Nerve Agent-Induced Neuropathology, But Not Cardiac Pathology, is Associated with the Anticonvulsant Action of Drug Treatment. Neurotoxicology16(1): 123-132, 1995. Brain and cardiac tissue was examined for pathological changes from rats that survived 24 hrs following exposure to a convulsant dose of the nerve agent soman. The animals had been treated following varying durations of seizure activity (2.5 - 40 min) with a number of different compounds that did or did not terminate the seizure. Moderate to severe Neuropathology was evident in virtually all animals (98 %) in which drug treatment did not terminate seizures. All animals that experienced up to 10 min of seizure activity before drug treatment successfully terminated the seizure were free of Neuropathology. There was an increasing frequency in the incidence of Neuropathology in animals that experienced 20 (10 %) or 40 min (79 %) of seizure activity before drug treatment terminated the seizure, but the degree of Neuropathology in these groups was significantly less than that observed in animals where seizure activity was not terminated. Cardiac lesions occurred at a much higher frequency (88 %) than neuropathological changes (57 %) and were not consistently associated with the anticonvulsant effectiveness. Early treatment (≤ 10 min) with anticholinergic drugs, however, was associated with protection from cardiac damage. The results strongly support the hypothesis that nerve agent-induced brain damage is linked to epileptiform activity. The minimal amount of seizure activity necessary for irreversible neural damage to become evident under these conditions is - 20 min, and the process accelerates greatly after this minimal time has elapsed. Successful termination of seizure activity, regardless of the type of drug used, protected either totally or relatively against brain damage depending upon how long the seizure had progressed. The mechanisms responsible for cardiac lesion formation occur more rapidly and may have a cholinergic component
