Note to users. If you're seeing this message, it means that your browser cannot find this page's style/presentation instructions -- or possibly that you are using a browser that does not support current Web standards. Find out more about why this message is appearing, and what you can do to make your experience of our site the best it can be.

Science 8 October 1982:
Vol. 218. no. 4568, pp. 177 - 179
DOI: 10.1126/science.7123229
Prev | Table of Contents | Next

Articles

Science, Vol 218, Issue 4568, 177-179
Copyright © 1982 by American Association for the Advancement of Science

articles

Focal cortical seizures cause distant thalamic lesions

RC Collins and JW Olney

Topical application of convulsants to the rat sensorimotor cortex in concentrations sufficient to cause repetitive focal motor seizures resulted in acute neuropathology (dark cell neuronal degeneration and spongiform neurophil changes) involving both the cortical seizure focus and certain thalamic nuclei within seizure pathways. Changes in the cortex were localized primarily in layer IV and those in the thalamus in nuclei having reciprocal connections with the cortical focus. The spongiform neuropil changes consisted of massively dilated presynaptic axon terminals in the cortex and postsynaptic dendrites in the thalamus. The dendritic and dark cell changes resemble the excitotoxic damage caused by glutamate and aspartate. Since these putative transmitters may be released locally from recurrent collaterals and remotely from corticothalamic axons, excessive release of glutamate or aspartate may account for the changes in both sites. The abnormal axons in sensory cortex appear to be terminals of thalamocortical neurons. Swelling of these axons may be caused by excessive anti- and orthodromic firing in the course of focal motor seizures.


THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES:
Possible Mechanisms in Infants for Selective Basal Ganglia Damage From Asphyxia, Kernicterus, or Mitochondrial Encephalopathies.
M. V. Johnston and A. H. Hoon JR (2000)
J Child Neurol 15, 588-591
   Abstract »    PDF »
Local Release of GABAergic Inhibition in the Motor Cortex Induces Immediate-Early Gene Expression in Indirect Pathway Neurons of the Striatum.
S. Berretta, H. B. Parthasarathy, and A. M. Graybiel (1997)
J. Neurosci. 17, 4752-4763
   Abstract »    Full Text »    PDF »
Glutamate Currents in Morphologically Identified Human Dentate Granule Cells in Temporal Lobe Epilepsy.
M. Isokawa, M. Levesque, I. Fried, and J. Engel Jr. (1997)
J Neurophysiol 77, 3355-3369
   Abstract »    Full Text »    PDF »
Cerebellar Atrophy in Patients With Long-term Phenytoin Exposure and Epilepsy.
G. C. Ney, G. Lantos, W. B. Barr, and N. Schaul (1994)
Arch Neurol 51, 767-771
   Abstract »    PDF »
Selective Vulnerability of the Brain: New Insights into the Pathophysiology of Stroke.
R. C. Collins, B. H. Dobkin, and D. W. Choi (1989)
Ann Intern Med 110, 992-1000
   Abstract »    PDF »
Analytic Reviews : Potential New Therapies for Acute Ischemic Stroke.
L. R. Wechsler (1988)
J Intensive Care Med 3, 258-264
   Abstract »    PDF »
Synaptic activity mediates death of hypoxic neurons.
S. Rothman (1983)
Science 220, 536-537
   Abstract »    PDF »
Systemic cholinergic agents induce seizures and brain damage in lithium-treated rats.
M. Honchar, J. Olney, and W. Sherman (1983)
Science 220, 323-325
   Abstract »    PDF »


To Advertise     Find Products

Science. ISSN 0036-8075 (print), 1095-9203 (online)