This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Iizuka, H. Articles by Young, W. Search for Related Content PubMed PubMed Citation Articles by Iizuka, H. Articles by Young, W.

Stroke, Vol 21, 790-794, Copyright © 1990 by American Heart Association

ARTICLES

Neural damage in the rat thalamus after cortical infarcts

H Iizuka, K Sakatani and W Young
Department of Neurosurgery, New York University Medical Center, New York 10016.

Histopathologic changes in the thalamus of 23 rats after somatosensory cortical infarction produced by middle cerebral artery occlusion were examined using the Fink-Heimer silver staining method, immunohistochemistry with antibodies against glial fibrillary acidic protein and laminin, and conventional stains. Middle cerebral artery occlusion produced cortical infarcts in the lateral parietal region, with variable involvement of the frontoparietal parasagittal sensorimotor cortex. Within 3 days after occlusion, massive terminal degeneration but no neuronal changes were apparent in the ipsilateral thalamus. By 1 week after occlusion, abnormal neurons with darkly stained, shrunken nuclei and atrophic perikarya were present in the ipsilateral thalamic nuclei. These neurons were densely argyrophilic in Fink-Heimer sections. Rats with small lateral parietal cortical lesions had degenerating neurons limited to the medial ventroposteromedial nucleus. Large lesions involving the parasagittal sensorimotor cortex resulted in widespread neuronal damage in the ventroposteromedial, ventroposterolateral, intralaminar, and posterior nuclear regions but nowhere else. Immunoreactivity to laminin antibody decreased, and astrocytic proliferation was abundant in affected thalamic areas. These findings are consistent with retrograde neuronal degeneration due to thalamocortical fiber damage in ischemic cortical regions. Such lesions remote from the infarct may influence functional recovery in patients with stroke.

This article has been cited by other articles:

				Y. Nonaka, A. Koumura, K. Hyakkoku, M. Shimazawa, S. Yoshimura, T. Iwama, and H. Hara Combination Treatment with Normobaric Hyperoxia and Cilostazol Protects Mice against Focal Cerebral Ischemia-Induced Neuronal Damage Better Than Each Treatment Alone J. Pharmacol. Exp. Ther., July 1, 2009; 330(1): 13 - 22. [Abstract] [Full Text] [PDF]

				C. Justicia, P. Ramos-Cabrer, and M. Hoehn MRI Detection of Secondary Damage After Stroke: Chronic Iron Accumulation in the Thalamus of the Rat Brain Stroke, May 1, 2008; 39(5): 1541 - 1547. [Abstract] [Full Text] [PDF]

				K.-J. Langen, D. Salber, K. Hamacher, G. Stoffels, G. Reifenberger, D. Pauleit, H. H. Coenen, and K. Zilles Detection of Secondary Thalamic Degeneration After Cortical Infarction Using cis-4-18F-Fluoro- D-Proline J. Nucl. Med., September 1, 2007; 48(9): 1482 - 1491. [Abstract] [Full Text] [PDF]

				M. Schroeter, P. Zickler, D. T. Denhardt, H.-P. Hartung, and S. Jander Increased thalamic neurodegeneration following ischaemic cortical stroke in osteopontin-deficient mice Brain, June 1, 2006; 129(6): 1426 - 1437. [Abstract] [Full Text] [PDF]

				W.-J. Moon, D. G. Na, S. S. Kim, J. W. Ryoo, and E. C. Chung Diffusion Abnormality of Deep Gray Matter in External Capsular Hemorrhage AJNR Am. J. Neuroradiol., February 1, 2005; 26(2): 229 - 235. [Abstract] [Full Text] [PDF]

				D Herve, N Molko, S Pappata, F Buffon, D LeBihan, M-G Bousser, and H Chabriat Longitudinal thalamic diffusion changes after middle cerebral artery infarcts J. Neurol. Neurosurg. Psychiatry, February 1, 2005; 76(2): 200 - 205. [Abstract] [Full Text] [PDF]

				M. Dihne, C. Grommes, M. Lutzenburg, O. W. Witte, and F. Block Different Mechanisms of Secondary Neuronal Damage in Thalamic Nuclei After Focal Cerebral Ischemia in Rats Stroke, December 1, 2002; 33(12): 3006 - 3011. [Abstract] [Full Text] [PDF]

				S. Miettinen, R. Roivainen, R. Keinanen, T. Hokfelt, and J. Koistinaho Specific Induction of Protein Kinase Cdelta Subspecies after Transient Middle Cerebral Artery Occlusion in the Rat Brain: Inhibition by MK-801 J. Neurosci., October 1, 1996; 16(19): 6236 - 6245. [Abstract] [Full Text] [PDF]