title: Report of selective cortical infarcts in the primate clot model of vasospasm after subarachnoid hemorrhage.
abstract: BACKGROUND
  In human autopsy studies, 70% to 80% of patients with aneurysmal subarachnoid hemorrhage (SAH) showed infarcts in cerebral cortex covered by subarachnoid blood. Thus far, no animal model of SAH is known to produce this peculiar infarct pattern, and its pathogenesis remains enigmatic.
  
  
  OBJECTIVE
  To investigate whether such infarcts occur in the clot model of SAH in primates.
  
  
  METHODS
  We performed a retrospective pathological review of 16 primate brains. In 13 cynomolgus monkeys, a blood clot was placed around the middle cerebral artery after additional removal of the arachnoid membrane from the basal surface of the frontal and temporal cortexes. Three animals underwent sham surgery without placement of a blood clot (controls). The brains were harvested between days 1 and 28 after SAH and examined by a neuropathologist blinded to study group.
  
  
  RESULTS
  We identified 2 types of cortical infarcts. A band of selective cortical laminar necrosis parallel to the cortical surface ("horizontal") was found in 5 animals. The second category of cortical lesions had a "vertical" extension. It included wedge-shaped (n = 2) or pillarlike (n = 2) necrosis. Both horizontal and vertical infarcts were located exclusively in areas adjacent to subarachnoid blood. The presence of a cortical infarct did not correlate with the degree of middle cerebral artery vasospasm (r2 = .24, P = .13).
  
  
  CONCLUSIONS
  The presence of cortical infarcts suggests that a modified nonhuman primate model of SAH is suitable to examine the pathogenesis of proximal vasospasm and permits investigation of cortical lesions similar to those reported in patients after SAH. Furthermore, it indicates that direct effects of the blood clot on the brain and microcirculation contribute to the development of cortical infarcts after SAH.
authors.affiliation: Surgical Neurology Branch, National Institutes of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892-1414, USA.
authors.forename: Bawarjan
authors.initials: B
authors.lastname: Schatlo
authors.forename: Jens P
authors.initials: JP
authors.lastname: Dreier
authors.forename: Sven
authors.initials: S
authors.lastname: Gläsker
authors.forename: Ali-Reza
authors.initials: AR
authors.lastname: Fathi
authors.forename: Travis
authors.initials: T
authors.lastname: Moncrief
authors.forename: Edward H
authors.initials: EH
authors.lastname: Oldfield
authors.forename: Alexander O
authors.initials: AO
authors.lastname: Vortmeyer
authors.forename: Ryszard M
authors.initials: RM
authors.lastname: Pluta
mesh_terms: D000818:Animals; D001798:Blood Proteins / Q000378:metabolism / Q000633:toxicity; D002536:Cerebral Arteries / Q000473:pathology / Q000503:physiopathology; D002540:Cerebral Cortex / Q000098:blood supply / Q000473:pathology* / Q000503:physiopathology*; D002544:Cerebral Infarction / Q000209:etiology / Q000473:pathology* / Q000503:physiopathology*; D002560:Cerebrovascular Circulation / Q000502:physiology; D004195:Disease Models, Animal; D008252:Macaca fascicularis; D008833:Microcirculation / Q000502:physiology; D012189:Retrospective Studies; D013345:Subarachnoid Hemorrhage / Q000150:complications / Q000503:physiopathology*; D013927:Thrombosis / Q000503:physiopathology; D020301:Vasospasm, Intracranial / Q000209:etiology / Q000503:physiopathology*
chemical_list: D001798:Blood Proteins