THE PHYSIOPATHOLOGY OF EPILEPTIC SEIZURES 



339 



activity extends proSiressi\elv from the telencephalon 

 to the diencephalon, and then to the mesencephalon 

 and the metencephalon, durintj which time the most 

 caudal structures, notably the reticular formation 

 (in the pons, medulla and the spinal cord) de\elop 

 or continue to show considerable electrical activit\'. 



1') Anoxic convulsions are no longer seen after the 

 bulbar part of the reticular formation has been de- 

 stroyed by diathermy (194). One must therefore con- 

 clude that anoxic seizures depend on the activity of 

 the caudal reticular formation when no longer under 

 the control of the higher nervous structures (fig. i). 



ft) Convulsions without loss of consciousness, char- 

 acterized by intense contractions in opisthotonus, 

 preceded and followed by clonic jerks, are provoked in 

 man and animals by the administration of strychnine 

 or other poisons (e.g. nitrogen mustards, di- 

 chlorodiphenyltrichloroethane). These convulsions 

 have been studied from the electrophysiological point 

 of view in animals by Bremer (21), Markham et a/. 



(136), Ruf (169), Marossero & Garrone (137), 

 Bremer & Bonnet (22), Johnson (112) and Gastaut 

 el al. (71). These studies give the following remarkably 

 similar results. 



/) .Strychnine convulsions are accompanied by a 

 hypersynchronous discharge in the whole of the retic- 

 ular formation of the spinal cord and the brain stem 

 but excluding the intralaminar and mid-line nuclei 

 of the thalamus, stimulation of which provokes the 

 recruiting response. 



-^) This reticular di.scharge secondarih extends to 

 the cerebellum. Bremer has shown that the discharges 

 recorded in the cerefiellar cortex are evoked by those 

 coming from the reticular formation which he con- 

 siders the site of the autorhythmic tetanic activity. 

 This reticular discharge also extends to the motor 

 neurons of the spinal cord, the hypersynchronous 

 activity of which is directly responsible for the con- 

 vul.sions. On the contrary, it does not extend to the 

 cerebral cortex which reacts by desynchronization. 



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FIG. I. Schematic representation of tlie mechanism of anoxic 

 convulsions. The density of the horizontal lines is proportional 

 to the damage to the neurons due to the anoxia. This damage 

 is maximum at the corticothalamic level where the bioelectric 

 rhythms are abolished also. It is diminished at the level of the 

 hypothalamus and especially of the mesencephalon, where 

 there are still slow rhythms. It is not present in the reticular 

 formation of the bulb where the electrical activity is normal. 

 It must thus be concluded that the anoxic convulsions (repre- 

 sented by the arrows) depend upon the normal activity of 

 the caudal reticular formation when it is no longer subject to 

 the control of the higher nervous centers. 



FIG. 2. Schematic representation of the mechanism of 

 strychnine convulsions. The cross-ruled areas of the brainstem 

 are those where the hypersynchronous discharge of the strych- 

 nine type occurs. The thalamocortical structures are completely 

 spared by this discharge and show only a desychronization 

 which is normal when there is an intense excitation of the 

 reticular formation. It must thus be concluded that strychnine 

 convulsions result from a caudal reticular discharge without 

 any participation of telencephalic structures or even of the 

 thalamus. 



