1. ¹In-vivo-NMR-Laboratory, Max-Planck-Institute for Neurological Research, Cologne, Germany
2. ²Department of Neurology, Charité Universitaetsmedizin Berlin, Berlin, Germany

Correspondence: Dr S Wegener, Center for Functional Magnetic Resonance Imaging and Department of Radiology, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0677, USA. E-mail: swegener@ucsd.edu

Received 10 February 2005; Revised 30 March 2005; Accepted 27 April 2005; Published online 29 June 2005.

Abstract

Transient middle cerebral artery occlusion (MCAO) by an intraluminal thread leads to primarily subcortical infarctions with little sensorimotor impairment in the Wistar rat strain. We investigated the course of infarct development in this lesion type for 10 weeks using magnetic resonance imaging (MRI) along with histological characterization. MCAO was induced in male Wistar rats (260 to 300 g) for 60 mins. Animals received follow-up T₁- and T₂-weighted MRI from day 1 until week 10. Separate groups of animals were analyzed histologically after 2, 6, and 10 weeks. Histology included immunohistochemistry for neuronal and astrocytic markers as well as hematoxylin eosin and luxol fast blue-cresyl violet staining. In contrast to lesions involving the cortex, exclusively subcortical infarctions were characterized by a complete resolution of initially increased T₁ and T₂ relaxation times by 10 weeks. Between 2 and 10 weeks, neuronal death and gliosis as well as a dense inflammatory infiltrate were evident in these lesions, without damage to fiber tracts or development of cystic cavities. Exclusively subcortical lesions in Wistar rats are characterized by normalization of T₁ and T₂ relaxation times, which might, however, not be mistaken for tissue recovery. Despite this MRI normalization, selective neuronal death and gliosis develop. Although MRI at individual time points might therefore be ambiguous, the temporal profile of relaxation time changes over the chronic time period allows discrimination of the lesion development into selective neuronal death or pannecrosis.