(Stroke. 2004;35:758.)
© 2004 American Heart Association, Inc.
Original Contributions |
From the Departments of Neurology (S.T.C., D.K.), Pediatrics, and Pharmacology and the University of California at Los Angeles Department of Energy Center for Molecular Medicine (K.T., N.T., H.I.K.), David Geffen School of Medicine at University of California at Los Angeles.
Correspondence to S. Thomas Carmichael, MD, PhD, Department of Neurology, David Geffen School of Medicine at University of California at Los Angeles, 710 Westwood Plaza, Los Angeles, CA 90095. E-mail scarmichael{at}mednet.ucla.edu
Background and Purpose Stroke produces diaschisis in adjacent and connected regions. The sequential changes in diaschisis over time and the relationship of regions of diaschisis to functional cortical areas and regions of poststroke neuroplasticity have not been determined.
Methods Small cortical strokes were produced in the barrel cortex of rats. Relative glucose metabolism was determined in vivo over time with [18F]fluorodeoxyglucose small-animal positron emission tomography. Cerebral blood flow was measured with [14C]iodoantipyrine. Regions of hypometabolism and hypoperfusion were compared with histological damage in the same animals.
Results Small cortical strokes produce an initial network of hypometabolism in a broad region of cortex adjacent to the stroke and in the striatum and thalamus on day 1. Cerebral blood flow is diminished only immediately around the cortical infarct on day 1. A substantial area of cortex adjacent to the stroke remains hypometabolic on day 8. This persistent cortical hypometabolism occupies the somatosensory cortex, forelimb motor cortex, and second somatosensory area.
Conclusions Focal stroke produces ipsilateral diaschisis in connected cortical regions that is clearly distant from subtotal damage and may play a role in poststroke neuroplasticity.
Key Words: cerebral cortex neuronal plasticity somatosensory cortex tomography, emission computed
This article has been cited by other articles:
![]() |
F. C. Hummel, B. Steven, J. Hoppe, K. Heise, G. Thomalla, L. G. Cohen, and C. Gerloff Deficient intracortical inhibition (SICI) during movement preparation after chronic stroke Neurology, May 19, 2009; 72(20): 1766 - 1772. [Abstract] [Full Text] [PDF] |
||||
![]() |
Y. Dong, G. Zhang, B. Zhang, R. D. Moir, W. Xia, E. R. Marcantonio, D. J. Culley, G. Crosby, R. E. Tanzi, and Z. Xie The Common Inhalational Anesthetic Sevoflurane Induces Apoptosis and Increases {beta}-Amyloid Protein Levels Arch Neurol, May 1, 2009; 66(5): 620 - 631. [Abstract] [Full Text] [PDF] |
||||
![]() |
S. B Rafnsson, I. J Deary, and F. Fowkes Peripheral arterial disease and cognitive function Vascular Medicine, February 1, 2009; 14(1): 51 - 61. [Abstract] [PDF] |
||||
![]() |
P. T. Tsai, J. J. Ohab, N. Kertesz, M. Groszer, C. Matter, J. Gao, X. Liu, H. Wu, and S. T. Carmichael A Critical Role of Erythropoietin Receptor in Neurogenesis and Post-Stroke Recovery J. Neurosci., January 25, 2006; 26(4): 1269 - 1274. [Abstract] [Full Text] [PDF] |
||||
![]() |
T. van Groen, K. Puurunen, H.-M. Maki, J. Sivenius, and J. Jolkkonen Transformation of Diffuse {beta}-Amyloid Precursor Protein and {beta}-Amyloid Deposits to Plaques in the Thalamus After Transient Occlusion of the Middle Cerebral Artery in Rats Stroke, July 1, 2005; 36(7): 1551 - 1556. [Abstract] [Full Text] [PDF] |
||||
![]() |
B. H. Dobkin Rehabilitation after Stroke N. Engl. J. Med., April 21, 2005; 352(16): 1677 - 1684. [Full Text] [PDF] |
||||
|
Stroke Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 2004 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |