Summary
We analyzed neuronal alterations in a distant nonischemic area, particularly focusing on the delayed changes in the ipsilateral thalamus and substantia nigra, after focal cerebral ischemia. In the rat middle cerebral artery occlusion model, the ipsilateral thalamus progressively shrank in the course of several months. The thalamic atrophy is most likely due to disconnection of neuronal fibers between the cerebral cortex and the thalamus. In the ipsilateral substantia nigra, neuronal loss, gliosis, and marked atrophy were observed in and after the 2nd week. The nigral degeneration may have resulted from excessive excitation due to loss of an inhibitory GABAergic input as a result of striatal infarct. To clarify whether or not similar changes in the thalamus or substantia nigra exist in patients with cerebral infarction in the territory of the middle cerebral artery, these areas were observed using computed tomography or magnetic resonance imaging. Consequently, the neuropathological changes in the ipsilateral thalamus and substantia nigra initially found in the rat model similarly occurred in clinical cases of cerebral infarction.
This work was supported in part by a Grant-in-Aid for Scientific Research from the Ministry of Education, Science, and Culture of Japan and by a Research Grant for Cardiovascular Diseases from the Ministry of Health and Welfare of Japan.
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Tamura, A. et al. (1992). Neuropathological Changes in Remote Areas After Focal Cerebral Ischemia. In: Ito, U., Kirino, T., Kuroiwa, T., Klatzo, I. (eds) Maturation Phenomenon in Cerebral Ischemia. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-77134-7_7
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DOI: https://doi.org/10.1007/978-3-642-77134-7_7
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