On the Provocation of Epileptiform Convulsions by Cardiazol [Experimental and Histopathological Investigations on Animals) [Über Provokation epilepti-former Anfälle durch Cardiazol—Experimentelle und histopathologische Untersuchungen an Tieren]. (Münch, med. Wochenschr., p. 1893, 1937.) Stender, A.

1938 ◽  
Vol 84 (352) ◽  
pp. 880-880
Author(s):  
S. L. Last
Keyword(s):  
Epileptiform Convulsions

scholarly journals A STUDY OF EPILEPTIFORM CONVULSIONS.

The Lancet ◽  
1919 ◽  
Vol 194 (5021) ◽  
pp. 914-917
Author(s):  
R.G. Gordon
Keyword(s):  
Epileptiform Convulsions

Experiments on the Prolongation of Induced Epileptiform Convulsions in the Cat

1952 ◽  
Vol 98 (412) ◽  
pp. 454-456 ◽  
Author(s):  
Hugo Ruf
Keyword(s):  
Electrical Activity ◽  
Intravenous Injection ◽  
Experimental Research ◽  
Electric Stimulation ◽  
List Type ◽  
Type Number ◽  
Convulsive Activity ◽  
Cortical Electrical Activity ◽  
Epileptiform Convulsions

THE present paper offers a brief summary of work which has been published in German journals dealing with the prolongation of induced convulsions. In the course of my experimental research the following phenomena were demonstrated:(1)Continuousconvulsionslastingup to oneand a half hours were produced by the administration of oxygen and adrenaline, preceded by the injection of phenyl-methyl-aminopropane.(2)Prolonged convulsions of 33 minutes were produced by the intravenous injection of 2 ml. of a io per cent. metrazol solution and continuous oxygen in suffiation.(3)Isolated continuous convulsive activity of the cerebellum was produced lasting 30 minutes after cessation of respiration and of all cortical electrical activity. This was achieved by continuous insuffiation of oxygen together with the injection of adrenaline and strychnine.(4)Activation of a prolonged convulsion up to 11 minutes, without further electric stimulation, was effected via the thalamus by the injection of adrenaline after administration of phenyl-methyl-aminopropane and continuous oxygen in sufflation.

American Retrospect

1898 ◽  
Vol 44 (184) ◽  
pp. 169-173
Author(s):  
C. Hubert Bond
Keyword(s):  
Cerebral Lesion ◽  
Special Relation ◽  
Anatomical Changes ◽  
Stratum Pyramidale ◽  
Cornu Ammonis ◽  
History Of ◽  
History Of Epilepsy ◽  
The One ◽  
Epileptiform Convulsions ◽  
Associated Abnormalities

Sclerosis of the Cornu Ammonis in Epilepsy.—Dr. W. L. Worcester (Journ. Nerv. and Ment. Disease, April and May, 1897) details his experience as to the frequency with which this lesion is found when systematically searched for, and discusses its relation to the pathology of epilepsy. He prefaces his own observations by a summary of previous ones, dating from those of Meynert in 1868. From these it would appear that the preponderance of authority is in favour of the view that the lesion in question is a result rather than a cause of the convulsions observed during life. Worcester's experience is based upon the appearances presented by the brains of forty-three epileptics, which he examined at the Arkansas and Danvers Asylums. In only nineteen of these was there an absence of any gross cerebral lesion. The one under consideration, namely, sclerosis of the cornu ammonis, was present on one or both sides in twenty cases, in eleven of which no other abnormality was found; while in nine it was accompanied by other and more extensive lesions which he believed had a common origin with it; and this association appeared to him to throw light on the nature of the connection between it and convulsions. Of these associated abnormalities the most frequent he found to be microgyria of an entire hemisphere. The histological characters of the diseased cornu ammonis seemed to have been remarkably uniform, and consisted of a general sclerosis, involving destruction of the neurons having their origin in the stratum pyramidale and nucleus fasciæ dentatæ. Such a condition the writer failed to note in a series of over a hundred and fifty brains of insane patients, save in those of epileptics. Exception, however, must be made to this generalisation, for the case of a patient dying subsequently to the printing of this monograph. It was that of a general paralytic in whom there was no history of epilepsy, nor had he suffered at all from convulsions; yet after death changes were noted identical with those above described. Still, the frequency of this condition in epileptics and its great rarity in those not subject to this disease, would seem to place it beyond the pale of mere coincidence. The question is whether the epilepsy causes the anatomical changes or they the epilepsy. The chief reason why the former view is held by the majority appears to be due, rather to the improbability of this convolution, from anything that is known, having any special relation to epilepsy, than to any definite theory as to the way in which epilepsy could bring about such changes in a single convolution. The writer himself would rather lean to the supposition that the condition of the cornu ammonis is the cause of the convulsions. In support of this view, he cites the fact that it is known that a cicatrix of the cortex may act as a focus of irritation, and gives references of evidence proving that irritation of the temporal lobe may excite convulsions. He does not wish it to be understood that he believes in this convolution having any special prerogative in this respect, but rather that a scar in any part of the cortex may have such an effect. Neither, also, would he assert that all epilepsies originate in any part of the cerebral cortex, for the certainty that epileptiform convulsions may be due to peripheral irritations and to toxæmic conditions is too clear.

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