gms | German Medical Science

58. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie e. V. (DGNC)

Deutsche Gesellschaft für Neurochirurgie (DGNC) e. V.

26. bis 29.04.2007, Leipzig

Degeneration of cholinergic basal forebrain neurons after experimental subarachnoid hemorrhage

Degeneration cholinerger Neurone im basalen Vorderhirn nach experimenteller Subarachnoidalblutung

Meeting Abstract

  • corresponding author M. Löhr - Klinik für Allgemeine Neurochirurgie der Universität zu Köln
  • G. Tzouras - Klinik für Allgemeine Neurochirurgie der Universität zu Köln
  • R. I. Ernestus - Klinik für Allgemeine Neurochirurgie der Universität zu Köln
  • T. Arendt - Paul-Flechsig-Institut für Hirnforschung, Universität Leipzig
  • J. A. Hampl - Klinik für Allgemeine Neurochirurgie der Universität zu Köln
  • W. Härtig - Paul-Flechsig-Institut für Hirnforschung, Universität Leipzig

Deutsche Gesellschaft für Neurochirurgie. 58. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie e.V. (DGNC). Leipzig, 26.-29.04.2007. Düsseldorf: German Medical Science GMS Publishing House; 2007. DocDO.01.07

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

Published: April 11, 2007

© 2007 Löhr 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: The reasons for neuropsychological deficits after subarachnoid hemorrhage (SAH) are still unknown. Cholinergic neurons of the basal forebrain (BFB) are essential for attention, memory and emotion, provided by its hippocampal and neocortical terminals. We investigated possible changes in the cholinergic BFB and its projections after experimental SAH.

Methods: In 15 male Wistar rats, SAH was induced by stereotactical injection of 200µl autologous blood into the prechiasmatic cistern, keeping the intracranial pressure (ICP) at the mean arterial blood pressure level. Three control animals were treated with 200µl saline. Continuous monitoring of brain tissue oxygen tension (ptiO2) was performed. Arterial blood gases were kept in physiological ranges by assisted ventilation. Animals were perfused on day four (n=5) and fourteen (n=6) after the experiment. For cell counts serial sections of the BFB were stained for choline acetyltransferase (ChAT), low-affinity neurotrophin receptor p75 and parvalbumin (Parv). The number of cholinergic terminals in the hippocampus and neocortex was calculated by optical densitometry.

Results: Immediately after SAH, ICP increased but soon returned to normal levels. PtiO2 declined considerably and continued to stay below baseline in SAH, but returned to normal values after saline injection. Animals killed four days after SAH showed a marked decrease (>30%) of cholinergic BFB-neurons in the medial septum and the horizontal limb of the diagonal band. There was a similar drop in the density of the hippocampal and neocortical cholinergic terminals. In animals sacrificed on day fourteen, cell counts of cholinergic neurons and density of its projection fibers were reduced by about 20%. In animals that received saline, cell counts showed a 10% loss of cholinergic BFB neurons. In contrast to the cholinergic loss, Parv-positive neurons seemed to be unaffected.

Conclusions: Experimental SAH resulted in a distinct decrease of cholinergic BFB neurons, that might underly the cognitive decline. This might be in part due to the marked ICP elevation after SAH induction, as cholinergic loss occurred to a lower extent even after saline administration. However, the direct effect of blood in the basal cisterns seemed to result in an enduring tissue hypoxia as another probable mechanism for cholinergic degeneration. Our findings indicate the clinical relevance of early ICP and ptiO2 management to minimize persisting neuropsychological sequelae after SAH.