Early electrophysiological and histologic changes after global cerebral ischemia in rats.
Identifieur interne : 000256 ( Ncbi/Checkpoint ); précédent : 000255; suivant : 000257Early electrophysiological and histologic changes after global cerebral ischemia in rats.
Auteurs : R G Geocadin [États-Unis] ; J. Muthuswamy ; D L Sherman ; N V Thakor ; D F HanleySource :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 2000.
English descriptors
- KwdEn :
- Animals, Brain Ischemia (pathology), Brain Ischemia (physiopathology), Brain Mapping, Cerebral Cortex (pathology), Cerebral Cortex (physiopathology), Electroencephalography, Epilepsies, Myoclonic (pathology), Epilepsies, Myoclonic (physiopathology), Evoked Potentials, Somatosensory (physiology), Hypoxia, Brain (pathology), Hypoxia, Brain (physiopathology), Male, Myoclonus (pathology), Myoclonus (physiopathology), Neurons (pathology), Neurons (physiology), Rats, Rats, Wistar, Ventral Thalamic Nuclei (pathology), Ventral Thalamic Nuclei (physiopathology).
- MESH :
- pathology : Brain Ischemia, Cerebral Cortex, Epilepsies, Myoclonic, Hypoxia, Brain, Myoclonus, Neurons, Ventral Thalamic Nuclei.
- physiology : Evoked Potentials, Somatosensory, Neurons.
- physiopathology : Brain Ischemia, Cerebral Cortex, Epilepsies, Myoclonic, Hypoxia, Brain, Myoclonus, Ventral Thalamic Nuclei.
- Animals, Brain Mapping, Electroencephalography, Male, Rats, Rats, Wistar.
Abstract
Cerebral anoxia is fundamental to morbidity and mortality after resuscitation from cardiac arrest. With no proven effective primary therapy for post-anoxic brain injury, the goal of neurologic care are supportive, to provide prognosis and prevention of further complications. With the multifaceted approach using electroencephalography (EEG), somatosensory evoked potentials (SEP), multiunit recordings, behavioral and histologic assessment, we investigated the hyperacute recovery period after resuscitation from cardiac arrest in a rat model to define the value of EEG and SEP in assessing neurologic injury.
PubMed: 10755267
Affiliations:
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pubmed:10755267Le document en format XML
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<affiliation wicri:level="1"><nlm:affiliation>Department of Neurology, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, USA.</nlm:affiliation>
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<author><name sortKey="Sherman, D L" sort="Sherman, D L" uniqKey="Sherman D" first="D L" last="Sherman">D L Sherman</name>
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<series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title>
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<term>Cerebral Cortex (physiopathology)</term>
<term>Electroencephalography</term>
<term>Epilepsies, Myoclonic (pathology)</term>
<term>Epilepsies, Myoclonic (physiopathology)</term>
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<term>Ventral Thalamic Nuclei (physiopathology)</term>
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<front><div type="abstract" xml:lang="en">Cerebral anoxia is fundamental to morbidity and mortality after resuscitation from cardiac arrest. With no proven effective primary therapy for post-anoxic brain injury, the goal of neurologic care are supportive, to provide prognosis and prevention of further complications. With the multifaceted approach using electroencephalography (EEG), somatosensory evoked potentials (SEP), multiunit recordings, behavioral and histologic assessment, we investigated the hyperacute recovery period after resuscitation from cardiac arrest in a rat model to define the value of EEG and SEP in assessing neurologic injury.</div>
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<name sortKey="Sherman, D L" sort="Sherman, D L" uniqKey="Sherman D" first="D L" last="Sherman">D L Sherman</name>
<name sortKey="Thakor, N V" sort="Thakor, N V" uniqKey="Thakor N" first="N V" last="Thakor">N V Thakor</name>
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