Early electrophysiological and histologic changes after global cerebral ischemia in rats.
Identifieur interne : 003F95 ( PubMed/Corpus ); précédent : 003F94; suivant : 003F96Early electrophysiological and histologic changes after global cerebral ischemia in rats.
Auteurs : R G Geocadin ; 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
Links to Exploration step
pubmed:10755267Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Early electrophysiological and histologic changes after global cerebral ischemia in rats.</title><author><name sortKey="Geocadin, R G" sort="Geocadin, R G" uniqKey="Geocadin R" first="R G" last="Geocadin">R G Geocadin</name><affiliation><nlm:affiliation>Department of Neurology, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Muthuswamy, J" sort="Muthuswamy, J" uniqKey="Muthuswamy J" first="J" last="Muthuswamy">J. Muthuswamy</name></author><author><name sortKey="Sherman, D L" sort="Sherman, D L" uniqKey="Sherman D" first="D L" last="Sherman">D L Sherman</name></author><author><name sortKey="Thakor, N V" sort="Thakor, N V" uniqKey="Thakor N" first="N V" last="Thakor">N V Thakor</name></author><author><name sortKey="Hanley, D F" sort="Hanley, D F" uniqKey="Hanley D" first="D F" last="Hanley">D F Hanley</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2000">2000</date><idno type="RBID">pubmed:10755267</idno><idno type="pmid">10755267</idno><idno type="wicri:Area/PubMed/Corpus">003F95</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Early electrophysiological and histologic changes after global cerebral ischemia in rats.</title><author><name sortKey="Geocadin, R G" sort="Geocadin, R G" uniqKey="Geocadin R" first="R G" last="Geocadin">R G Geocadin</name><affiliation><nlm:affiliation>Department of Neurology, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Muthuswamy, J" sort="Muthuswamy, J" uniqKey="Muthuswamy J" first="J" last="Muthuswamy">J. Muthuswamy</name></author><author><name sortKey="Sherman, D L" sort="Sherman, D L" uniqKey="Sherman D" first="D L" last="Sherman">D L Sherman</name></author><author><name sortKey="Thakor, N V" sort="Thakor, N V" uniqKey="Thakor N" first="N V" last="Thakor">N V Thakor</name></author><author><name sortKey="Hanley, D F" sort="Hanley, D F" uniqKey="Hanley D" first="D F" last="Hanley">D F Hanley</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="ISSN">0885-3185</idno><imprint><date when="2000" type="published">2000</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Brain Ischemia (pathology)</term><term>Brain Ischemia (physiopathology)</term><term>Brain Mapping</term><term>Cerebral Cortex (pathology)</term><term>Cerebral Cortex (physiopathology)</term><term>Electroencephalography</term><term>Epilepsies, Myoclonic (pathology)</term><term>Epilepsies, Myoclonic (physiopathology)</term><term>Evoked Potentials, Somatosensory (physiology)</term><term>Hypoxia, Brain (pathology)</term><term>Hypoxia, Brain (physiopathology)</term><term>Male</term><term>Myoclonus (pathology)</term><term>Myoclonus (physiopathology)</term><term>Neurons (pathology)</term><term>Neurons (physiology)</term><term>Rats</term><term>Rats, Wistar</term><term>Ventral Thalamic Nuclei (pathology)</term><term>Ventral Thalamic Nuclei (physiopathology)</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Brain Ischemia</term><term>Cerebral Cortex</term><term>Epilepsies, Myoclonic</term><term>Hypoxia, Brain</term><term>Myoclonus</term><term>Neurons</term><term>Ventral Thalamic Nuclei</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Evoked Potentials, Somatosensory</term><term>Neurons</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Brain Ischemia</term><term>Cerebral Cortex</term><term>Epilepsies, Myoclonic</term><term>Hypoxia, Brain</term><term>Myoclonus</term><term>Ventral Thalamic Nuclei</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Brain Mapping</term><term>Electroencephalography</term><term>Male</term><term>Rats</term><term>Rats, Wistar</term></keywords></textClass></profileDesc></teiHeader><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></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">10755267</PMID><DateCreated><Year>2000</Year><Month>05</Month><Day>25</Day></DateCreated><DateCompleted><Year>2000</Year><Month>05</Month><Day>25</Day></DateCompleted><DateRevised><Year>2007</Year><Month>11</Month><Day>14</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0885-3185</ISSN><JournalIssue CitedMedium="Print"><Volume>15 Suppl 1</Volume><PubDate><Year>2000</Year></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Early electrophysiological and histologic changes after global cerebral ischemia in rats.</ArticleTitle><Pagination><MedlinePgn>14-21</MedlinePgn></Pagination><Abstract><AbstractText Label="INTRODUCTION" NlmCategory="BACKGROUND">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.</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">Two cohorts of rats were subjected to sham and graded asphyxic-cardiac arrest. EEG was collected during baseline, at injury, and 90 minutes into recovery in the first rat cohort. EEG bursting during the first 90 minutes of recovery was visually analyzed and correlated with the neurologic recovery at 24 hours after injury. The neurologic recovery was assessed using a neurodeficit score (NDS) with 80 as normal and 0 as brain dead. The next rat cohort subjected to asphyxic-cardiac arrest was studied using SEP and multiunit recording in the VPL; brain histologic studies were performed at 4 hours after the asphyxia.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">The first rat cohort subjected to graded asphyxic-cardiac arrest emerged from EEG isoelectricity by burst-suppression pattern during the first 90 minutes after asphyxia. Six rats in the good outcome group (NDS >60) showed increased frequency of bursting, leading to return of EEG background activity. Six rats with a bad outcome (NDS <60) had low-intensity and persistent bursting without return of EEG background activity within 90 minutes of observation. Visual assessment showed increased EEG peak burst counts during the first 90 minutes of recovery for the rats with a good outcome compared with the rats with a bad outcome. In the second cohort, the rats were subjected to 3 minutes, 5 minutes, and 7 minutes of asphyxia. The N20 recovered to 60% of baseline in all three cases. The recovery profile of VPL is similar to that of cortical N2O for the animal with 3 minutes of asphyxia. However, VPL response is suppressed after 7 minutes of asphyxia leading to a divergence in the rate of recovery of the cortical N20 and VPL response. In both the animals (with mild and intermediate injury) in which the early response in VPL recovered to more than 50% of baseline, the recovery profile was similar to the N20 in cortical evoked potential (EP). The rats were killed 4 hours after asphyxia and the hematoxylin and eosin stain performed on the brains showed evidence of neuronal injury in the thalamic reticular nucleus (TRN) which seemed to correlate with the duration of asphyxia.</AbstractText><AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">We present a multimodality assessment of early neurologic recovery following resuscitation from cardiac arrest. The recovery of bursting and high-frequency oscillations may be regulated by interneurons in the TRN. The early selective vulnerability of these interneurons in the TRN may be crucial to the early neurologic recovery as assessed by EP, multiunit recording, EEG, and neurologic behavioral recovery.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Geocadin</LastName><ForeName>R G</ForeName><Initials>RG</Initials><AffiliationInfo><Affiliation>Department of Neurology, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Muthuswamy</LastName><ForeName>J</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Sherman</LastName><ForeName>D L</ForeName><Initials>DL</Initials></Author><Author ValidYN="Y"><LastName>Thakor</LastName><ForeName>N V</ForeName><Initials>NV</Initials></Author><Author ValidYN="Y"><LastName>Hanley</LastName><ForeName>D F</ForeName><Initials>DF</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>NS 24282</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013487">Research Support, U.S. Gov't, P.H.S.</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>UNITED STATES</Country><MedlineTA>Mov Disord</MedlineTA><NlmUniqueID>8610688</NlmUniqueID><ISSNLinking>0885-3185</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000818">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D002545">Brain Ischemia</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000473">pathology</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000503">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D001931">Brain Mapping</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D002540">Cerebral Cortex</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000473">pathology</QualifierName><QualifierName MajorTopicYN="N" UI="Q000503">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D004569">Electroencephalography</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D004831">Epilepsies, Myoclonic</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000473">pathology</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000503">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D005073">Evoked Potentials, Somatosensory</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000502">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D002534">Hypoxia, Brain</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000473">pathology</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000503">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008297">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D009207">Myoclonus</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000473">pathology</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000503">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D009474">Neurons</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000473">pathology</QualifierName><QualifierName MajorTopicYN="N" UI="Q000502">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D051381">Rats</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D017208">Rats, Wistar</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D020651">Ventral Thalamic Nuclei</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000473">pathology</QualifierName><QualifierName MajorTopicYN="N" UI="Q000503">physiopathology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2000</Year><Month>4</Month><Day>8</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2000</Year><Month>6</Month><Day>8</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2000</Year><Month>4</Month><Day>8</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">10755267</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Santé/explor/MovDisordV3/Data/PubMed/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 003F95 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/PubMed/Corpus/biblio.hfd -nk 003F95 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Wicri/Santé
|area= MovDisordV3
|flux= PubMed
|étape= Corpus
|type= RBID
|clé= pubmed:10755267
|texte= Early electrophysiological and histologic changes after global cerebral ischemia in rats.
}}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/PubMed/Corpus/RBID.i -Sk "pubmed:10755267" \
| HfdSelect -Kh $EXPLOR_AREA/Data/PubMed/Corpus/biblio.hfd \
| NlmPubMed2Wicri -a MovDisordV3
| This area was generated with Dilib version V0.6.23. |  |