title: Aggravation of infarct formation by brain swelling in a large territorial stroke: a target for neuroprotection?
abstract: OBJECTIVE
  In territorial stroke vasogenic edema formation leads to elevated intracranial pressure (ICP) and can cause herniation and death. Brain swelling further impairs collateral blood flow to the ischemic penumbra and causes mechanical damage to adjacent brain structures. In the present study the authors sought to quantify the impact of this space-occupying effect on ischemic lesion formation.
  
  
  METHODS
  Wistar rats were assigned to undergo bilateral craniectomy or a sham operation and then were subjected to temporary middle cerebral artery occlusion (MCAO) for 90 minutes. A clinical evaluation and 7-T MR imaging studies were performed 5 and 24 hours after MCAO. The absolute brain water content was determined at 24 hours by using the wet/dry method.
  
  
  RESULTS
  Bilateral craniectomy before MCAO led to a drastic reduction in lesion volume at both imaging time points (p < 0.0001). Ischemic lesion volume was 2.7- and 2.3-fold larger in sham-operated animals after 5 and 24 hours, respectively. Clinical scores were likewise better in rats that had undergone craniectomy (p < 0.05). After 24 hours the midline shift differed significantly between the 2 groups (p < 0.001), but not after 5 hours. The relation between brain water content and ischemic lesion volume as well as the T2 relaxation time within the infarcted area was not different between the groups (p > 0.05).
  
  
  CONCLUSIONS
  The data indicated that collateral damage caused by the space-occupying effect of a large MCA territory stroke contributes seriously to ischemic lesion formation. The elimination of increased ICP thus must be regarded as a highly neuroprotective measure, rather than only a life-saving procedure to prevent cerebral herniation. Further clinical trials should reveal the neuroprotective potential of surgical and pharmacological ICP-lowering therapeutic approaches.
authors.affiliation: Experimental Neurology Research Group, Justus-Liebig-University Giessen, Germany.
authors.forename: Maureen
authors.initials: M
authors.lastname: Walberer
authors.forename: Nouha
authors.initials: N
authors.lastname: Ritschel
authors.forename: Max
authors.initials: M
authors.lastname: Nedelmann
authors.forename: Kai
authors.initials: K
authors.lastname: Volk
authors.forename: Clemens
authors.initials: C
authors.lastname: Mueller
authors.forename: Marlene
authors.initials: M
authors.lastname: Tschernatsch
authors.forename: Erwin
authors.initials: E
authors.lastname: Stolz
authors.forename: Franz
authors.initials: F
authors.lastname: Blaes
authors.forename: Georg
authors.initials: G
authors.lastname: Bachmann
authors.forename: Tibo
authors.initials: T
authors.lastname: Gerriets
mesh_terms: D000818:Animals; D001929:Brain Edema / Q000209:etiology / Q000473:pathology* / Q000601:surgery*; D003399:Craniotomy; D019299:Decompression, Surgical; D038524:Diffusion Magnetic Resonance Imaging; D004195:Disease Models, Animal; D020244:Infarction, Middle Cerebral Artery / Q000150:complications / Q000473:pathology* / Q000601:surgery*; D019586:Intracranial Hypertension / Q000209:etiology / Q000473:pathology / Q000601:surgery; D008297:Male; D051381:Rats; D017208:Rats, Wistar