gms | German Medical Science

59th Annual Meeting of the German Society of Neurosurgery (DGNC)
3rd Joint Meeting with the Italian Neurosurgical Society (SINch)

German Society of Neurosurgery (DGNC)

1 - 4 June 2008, Würzburg

Cortical necrosis occurs independently of vasospasm in a primate model of subarachnoid hemorrhage – the first animal model of delayed ischemic deficits?

Zerebrale kortikale Nekrosen treten unabhängig von Vasospasmen auf – Ist das Primatenmodell der Subarachnoidalblutung das erste experimentelle Modell verzögerter ischämischer Defizite?

Meeting Abstract

  • corresponding author B. Schatlo - Surgical Neurology Branch, National Institutes of Health, Bethesda, USA
  • A. O. Vortmeyer - Surgical Neurology Branch, National Institutes of Health, Bethesda, USA
  • S. Gläsker - Surgical Neurology Branch, National Institutes of Health, Bethesda, USA
  • E. H. Oldfield - Surgical Neurology Branch, National Institutes of Health, Bethesda, USA
  • R. M. Pluta - Surgical Neurology Branch, National Institutes of Health, Bethesda, USA
  • J. P. Dreier - Department of Experimental Neurology, Charité - Universitätsmedizin Berlin

Deutsche Gesellschaft für Neurochirurgie. Società Italiana di Neurochirurgia. 59. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie e.V. (DGNC), 3. Joint Meeting mit der Italienischen Gesellschaft für Neurochirurgie (SINch). Würzburg, 01.-04.06.2008. Düsseldorf: German Medical Science GMS Publishing House; 2008. DocMI.09.05

The electronic version of this article is the complete one and can be found online at:

Published: May 30, 2008

© 2008 Schatlo et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.



Objective: Delayed ischemic neurological deficits (DIND) are a devastating consequence of aneurysmal subarachnoid hemorrhage (SAH). A majority of patients with DIND show patches of selective cortical necrosis upon pathologic examination. These lesions have been discussed as a possible pathological correlate of DIND. However, there is currently no animal model mimicking this entity. The present study was conducted to assess whether a widely used primate model of vasospasm can reproduce the changes occurring in the brains of patients with DIND.

Methods: 16 cynomolgus monkeys were subjected to clot placement around the middle cerebral artery (MCA); 3 more animals underwent sham-surgery without clot placement. Animals were sacrificed on postoperative days 1–28 and the brains were examined.

Results: Two animals were excluded because of death secondary to complications during angiography or surgery. Of the remaining 14 study animals, all showed fronto-temporal siderosis; 8 animals displayed marked pathology, out of which 6 had cortical laminar necrosis and 3 had a wedge-shaped infarct. In 3 cases, a pillar-like cortical infarct, corresponding to the supply area of a single leptomeningeal artery branch was observed. Sham-operated animals had no pathologic changes. Infarct occurrence was not correlated with the degree of MCA vasospasm or the time-point of sacrifice.

Conclusions: Similarly to patients with DIND, primates with SAH demonstrated pathomorphological cortical infarcts limited to the cerebral cortex adjacent to the subarachnoid blood clot. This finding confirmed the direct pathological effect of blood on the cortex in primates which was independent of the development and degree of delayed cerebral vasospasm and may be related to alternative mechanisms including cortical spreading ischemia. Thus, this well established primate model of vasospasm following SAH can be used to enhance our understanding of the pathophysiology and relationship of vasospasm and DIND.