gms | German Medical Science

57th Annual Meeting of the German Society of Neurosurgery
Joint Meeting with the Japanese Neurosurgical Society

German Society of Neurosurgery (DGNC)

11 - 14 May, Essen

Prevention of global brain atrophy after unilateral parietal cryolesion by early neuroprotective treatment with erythropoietin

Prävention globaler Hirnatrophie nach parietaler Kryoläsion durch einen frühen neuroprotektiven Therapieansatz mit Erythropoietin

Meeting Abstract

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  • corresponding author A.L. Sirén - Neurochirurgische Klinik und Poliklinik, Universität Würzburg
  • H. Ehrenreich - Max-Planck-Institut für experimentelle Medizin, Göttingen

Deutsche Gesellschaft für Neurochirurgie. Japanische Gesellschaft für Neurochirurgie. 57. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie e.V. (DGNC), Joint Meeting mit der Japanischen Gesellschaft für Neurochirurgie. Essen, 11.-14.05.2006. Düsseldorf, Köln: German Medical Science; 2006. DocSO.04.02

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

Published: May 8, 2006

© 2006 Sirén 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: In humans, neurotrauma is suspected to cause brain atrophy and accelerate slowly progressive neurodegenerative disorders (Alzheimer's, Parkinson disease, schizophrenia). However, a direct link between brain injury and subsequent delayed global neurodegeneration has remained elusive. The issue we have addressed here is (i) whether or not a small localized lesion in the developing parietal cortex is sufficient to trigger global morphological changes in the mature brain, (ii) what the behavioral consequences of such a cascade might be, and (iii) whether a novel neuroprotective strategy involving recombinant erythropoietin (EPO) might prevent these changes.

Methods: Juvenile (4 week-old) mice were given a unilateral cryolesion of the right parietal cortex. High-resolution three-dimensional magnetic resonance imaging (MRI) and behavioral testing (hole board, elevated plus-maze, Rotarod, open-field, prepulse inhibition of startle, Morris water maze) were performed 3 and 9 months after lesioning. EPO (5 U/g, i.p.) or placebo (0.01 ml/g, i.p.) was administered immediately after setting of the lesion, and every other day for 14 days thereof.

Results: Significant reduction in brain volume and ventricular enlargement by in vivo 3D MRI were evident at 3 and 9 months after unilateral parietal cortical lesion. This brain atrophy was accompanied with distinct behavioral alterations and spatial learning deficits. EPO therapy prevented behavioral abnormalities, cognitive dysfunction and brain atrophy at 9 months after parietal cortical injury.

Conclusions: A discrete lesion to the parietal cortex of juvenile mice, i.e. during brain maturation, is by itself the primary cause of a global neurodegeneration, with significant changes in brain morphology and function upon long-term follow-up. The delayed global neurodegeneration can be efficiently counteracted by neuroprotective therapy.