Quantitative Electroencephalography in Cerebral Ischemia. Detection of Abnormalities in “Normal” EEGs

Author(s):  
A.C. Van Huffelen ◽  
D.C.J. Poortvliet ◽  
C.J.M. Van Der Wulp
1995 ◽  
Vol 81 (1) ◽  
pp. 80-83 ◽  
Author(s):  
David C. Adams ◽  
Eric J. Heyer ◽  
Ronald G. Emerson ◽  
James R. Moeller ◽  
Henry M. Spotnitz ◽  
...  

1996 ◽  
Vol 40 (1) ◽  
pp. 46
Author(s):  
D. C. ADAMS ◽  
E. J. HEYER ◽  
R. G. EMERSON ◽  
J. R. MOELLER ◽  
H. M. SPOTNITZ ◽  
...  

1996 ◽  
Vol 82 (6) ◽  
pp. 1300-1301
Author(s):  
David C. Adams ◽  
Eric J. Heyer ◽  
Ronald G. Emerson

1996 ◽  
Vol 82 (6) ◽  
pp. 1300-1301 ◽  
Author(s):  
David C. Adams ◽  
Eric J. Heyer ◽  
Ronald G. Emerson

1995 ◽  
Vol 81 (1) ◽  
pp. 80-83
Author(s):  
David C. Adams ◽  
Eric J. Heyer ◽  
Ronald G. Emerson ◽  
James R. Moeller ◽  
Henry M. Spotnitz ◽  
...  

Author(s):  
R.V.W. Dimlich ◽  
M.H. Biros

In severe cerebral ischemia, Purkinje cells of the cerebellum are one of the cell types most vulnerable to anoxic damage. In the partial (forebrain) global ischemic (PGI) model of the rat, Paljärvi noted at the light microscopic level that cerebellar damage is inconsistant and when present, milder than in the telencephalon, diencephalon and rostral brain stem. Cerebellar injury was observed in 3 of 4 PGI rats following 5 minutes of reperfusion but in none of the rats after 90 min of reperfusion. To evaluate a time between these two extremes (5 and 90 min), the present investigation used the PGI model to study the effects of ischemia on the ultrastructure of cerebellar Purkinje cells in rats that were sacrificed after 30 min of reperfusion. This time also was chosen because lactic acid that is thought to contribute to ischemic cell changes in PGI is at a maximum after 30 min of reperfusion.


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