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(Stroke. 2002;33:3006.)
© 2002 American Heart Association, Inc.

Original Contributions

Different Mechanisms of Secondary Neuronal Damage in Thalamic Nuclei After Focal Cerebral Ischemia in Rats

Marcel Dihné, MD; Christian Grommes, MD; Michael Lutzenburg, PhD; Otto W. Witte, MD Frank Block, MD

From the Department of Neurology, Rheinisch Westfälische Technische Hochschule–Aachen, Aachen (M.D., F.B.); Department of Neurology, Rheinische Friedrich-Wilhelm Universität, Bonn (C.G.); Department of Neurology, Heinrich-Heine Universität, Düsseldorf (M.L.); and Department of Neurology, Friedrich-Schiller Universität, Jena (O.W.W.), Germany.

Correspondence to F. Block, MD, Department of Neurology, RWTH-Aachen, Pauwelsstrasse 30, D-52057 Aachen, Germany. E-mail fblock{at}post.klinikum.rwth-aachen.de

Background and Purpose— After focal cerebral ischemia, depending on its localization and extent, secondary neuronal damage may occur that is remote from the initial lesion. In this study differences in secondary damage of the ventroposterior thalamic nucleus (VPN) and the reticular thalamic nucleus (RTN) were investigated with the use of different ischemia models.

Methods— Transient middle cerebral artery occlusion (MCAO) leads to cortical infarction, including parts of the basal ganglia such as the globus pallidus, and to widespread edema. Photothrombotic ischemia generates pure cortical infarcts sparing the basal ganglia and with only minor edema. Neuronal degeneration was quantified within the ipsilateral RTN and VPN 14 days after ischemia. Glial reactions were studied with the use of immunohistochemistry.

Results— MCAO resulted in delayed neuronal cell loss of the ipsilateral VPN and RTN. Glial activation occurred in both nuclei beginning after 24 hours. Photothrombotic ischemia resulted in delayed neuronal cell loss only within the VPN. Even 2 weeks after photothrombotic ischemia, glial activation could only be seen within the VPN.

Conclusions— Pure cortical infarcts after photothrombotic ischemia, without major edema and without effects on the globus pallidus of the basal ganglia, only lead to secondary VPN damage that is possibly due to retrograde degeneration. MCAO, which results in infarction of cortex and globus pallidus and which causes widespread edema, leads to secondary damage in the VPN and RTN. Thus, additional RTN damage may be due to loss of protective GABAergic input from the globus pallidus to the RTN or due to the extensive edema. Retrograde degeneration is not possible because the RTN, in contrast to the VPN, has no efferents to the cortex.

Key Words: brain ischemia • neuronal damage • thalamus • rats

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