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Bedside Diagnosis of Mitochondrial Dysfunction After Malignant Middle Cerebral Artery Infarction

Nielsen, T. H.; Schalén, Wilhelm LU ; Ståhl, Nils LU ; Toft, P.; Reinstrup, Peter LU and Nordstrom, C. H. (2014) In Neurocritical Care 21(1). p.35-42
Abstract
The study explores whether the cerebral biochemical pattern in patients treated with hemicraniectomy after large middle cerebral artery infarcts reflects ongoing ischemia or non-ischemic mitochondrial dysfunction. The study includes 44 patients treated with decompressive hemicraniectomy (DCH) due to malignant middle cerebral artery infarctions. Chemical variables related to energy metabolism obtained by microdialysis were analyzed in the infarcted tissue and in the contralateral hemisphere from the time of DCH until 96 h after DCH. Reperfusion of the infarcted tissue was documented in a previous report. Cerebral lactate/pyruvate ratio (L/P) and lactate were significantly elevated in the infarcted tissue compared to the non-infarcted... (More)
The study explores whether the cerebral biochemical pattern in patients treated with hemicraniectomy after large middle cerebral artery infarcts reflects ongoing ischemia or non-ischemic mitochondrial dysfunction. The study includes 44 patients treated with decompressive hemicraniectomy (DCH) due to malignant middle cerebral artery infarctions. Chemical variables related to energy metabolism obtained by microdialysis were analyzed in the infarcted tissue and in the contralateral hemisphere from the time of DCH until 96 h after DCH. Reperfusion of the infarcted tissue was documented in a previous report. Cerebral lactate/pyruvate ratio (L/P) and lactate were significantly elevated in the infarcted tissue compared to the non-infarcted hemisphere (p < 0.05). From 12 to 96 h after DCH the pyruvate level was significantly higher in the infarcted tissue than in the non-infarcted hemisphere (p < 0.05). After a prolonged period of ischemia and subsequent reperfusion, cerebral tissue shows signs of protracted mitochondrial dysfunction, characterized by a marked increase in cerebral lactate level with a normal or increased cerebral pyruvate level resulting in an increased LP-ratio. This biochemical pattern contrasts to cerebral ischemia, which is characterized by a marked decrease in cerebral pyruvate. The study supports the hypothesis that it is possible to diagnose cerebral mitochondrial dysfunction and to separate it from cerebral ischemia by microdialysis and bed-side biochemical analysis. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
Mitochondrial dysfunction, Cerebral metabolism, Microdialysis, Malignant, middle cerebral artery infarction
in
Neurocritical Care
volume
21
issue
1
pages
35 - 42
publisher
Humana Press
external identifiers
  • wos:000339350500006
  • scopus:84904133589
ISSN
1541-6933
DOI
10.1007/s12028-013-9875-5
language
English
LU publication?
yes
id
898288b5-7971-4e35-854f-ef3b4de12607 (old id 4591849)
date added to LUP
2014-09-05 08:05:31
date last changed
2017-08-27 03:13:41
@article{898288b5-7971-4e35-854f-ef3b4de12607,
  abstract     = {The study explores whether the cerebral biochemical pattern in patients treated with hemicraniectomy after large middle cerebral artery infarcts reflects ongoing ischemia or non-ischemic mitochondrial dysfunction. The study includes 44 patients treated with decompressive hemicraniectomy (DCH) due to malignant middle cerebral artery infarctions. Chemical variables related to energy metabolism obtained by microdialysis were analyzed in the infarcted tissue and in the contralateral hemisphere from the time of DCH until 96 h after DCH. Reperfusion of the infarcted tissue was documented in a previous report. Cerebral lactate/pyruvate ratio (L/P) and lactate were significantly elevated in the infarcted tissue compared to the non-infarcted hemisphere (p &lt; 0.05). From 12 to 96 h after DCH the pyruvate level was significantly higher in the infarcted tissue than in the non-infarcted hemisphere (p &lt; 0.05). After a prolonged period of ischemia and subsequent reperfusion, cerebral tissue shows signs of protracted mitochondrial dysfunction, characterized by a marked increase in cerebral lactate level with a normal or increased cerebral pyruvate level resulting in an increased LP-ratio. This biochemical pattern contrasts to cerebral ischemia, which is characterized by a marked decrease in cerebral pyruvate. The study supports the hypothesis that it is possible to diagnose cerebral mitochondrial dysfunction and to separate it from cerebral ischemia by microdialysis and bed-side biochemical analysis.},
  author       = {Nielsen, T. H. and Schalén, Wilhelm and Ståhl, Nils and Toft, P. and Reinstrup, Peter and Nordstrom, C. H.},
  issn         = {1541-6933},
  keyword      = {Mitochondrial dysfunction,Cerebral metabolism,Microdialysis,Malignant,middle cerebral artery infarction},
  language     = {eng},
  number       = {1},
  pages        = {35--42},
  publisher    = {Humana Press},
  series       = {Neurocritical Care},
  title        = {Bedside Diagnosis of Mitochondrial Dysfunction After Malignant Middle Cerebral Artery Infarction},
  url          = {http://dx.doi.org/10.1007/s12028-013-9875-5},
  volume       = {21},
  year         = {2014},
}