THE I'HVSIOPATHOLOGY OF EPILEPTIC SEIZURES 



347 



dominance in petit mal ol the thalamocaudate system 

 from which are generated the slow waves and a process 

 of active inhibition. 



a) The loss of consciousness can be related to the 

 hypersynchronous discharge which is propagated 

 from the thalamus to the whole of the brain and pre- 

 vents normal cerebral functioning. The lack of con- 

 vulsions may depend on the fact that the reticular 

 activation is rhythmically inhibited and can e.xpress 

 itself only by a slight muscular contraction with each 

 spike of the spike-and-wave. 



/)) This hypothesis of the predominance of the in- 

 hibitory system from which are generated the slow 

 waves may explain why petit mal is seen especially in 

 patients with a well-marked tendency to ictal and 

 interictal slow hypersynchronization. Certain ' alj- 

 sences' are characterized solely by a discharge of slow 

 waves. There is also a prevalence of slow rhythms in 

 iaetween petit mal .seizures (theta rhythms, delta 

 rhvthms in the frontal and occipital regions, and 

 hypersynchronous bursts during overbreathing). 



f) This same hypothesis may explain \vhy the ' ab- 

 sences' are frequently precipitated by conditions 

 which favor this slow hypersynchronization (hy- 

 perpnea, sleep, closure of the eyes, and administra- 

 tion of pentylenetetrazol, pentothal, chlorpromazine, 

 etc.). These synchronizing; measures depress the 

 mesorhombencephalic reticular formation and thus 

 ■ release' the thalamocortical system of spindles, the 

 hypersynchronous discharges which depend on this 

 same thalainocortical system and the accompanying 

 ' braking' slow waves. 



(T) The relative antagonism between the rostral 

 and caudal parts of the reticular formation may throw 

 light on the fact that certain physiological conditions 

 (such as puberty) or therapeutic agents (such as the 

 diones) can transforin petit mal ' absences' into grand 

 mal seizures. Petit mal is distinguished from grand 

 mal by this functional predominance of thalamo- 

 caudate inhibition, so that the hypersynchronous 

 thalamic discharge is prematurely inhibited and 

 liberation of the caudal reticular formation is pre- 

 vented. One has but to suppose that endocrine modi- 

 fications or certain medications selectively depress 

 the inhibitory system; this lessened inhibition mav 

 explain the prolongation of the hypersynchronous 

 thalamic discharge, the bulbar 'release' and the 

 transformation of petit mal into grand mal. 



One common theoretical basis thus may explain 

 the three varieties of generalized epilepsy which have 

 been shown by empirical observation to he closely 



linked. Grand mal and petit mal in their pure forms 

 are indeed exceptional, whereas the association, 

 either temporary or permanent, of two or three forms 

 is the general rule. This theory of common causalitv 

 may help in understanding the characteristics of the 

 EEG discharge and the .somatic manifestations of the 

 three types of generalized epilepsy; it may explain 

 the loss of consciousness which is a feature of grand 

 mal and the 'absence' of petit mal. Myoclonic petit 

 mal is too brief to interrupt the chain of psychological 

 events whose temporal dimensions are greater than 

 the duration of the seizure. Indeed one cannot en- 

 visage the receipt and transmission of messages, their 

 analysis and transformation into sensations, ideas or 

 actions, and their storage in the form of memory, at 

 a time when most of the cerebral neurons are col- 

 lecti\-ely occupied in discharging simultaneouslv and 

 when the source of this discharge is exactly the struc- 

 ture whose function is to regulate the whole of cerebral 

 activitv. 



PHYSIOP.'kTHOLOGV OF P.ARTI.AL EPILEPSIES 



ExperimeiUal Results 



Seizures of partial epilepsy have been reproduced 

 in animals only by provoking a localized cerebral dis- 

 turbance. Since this necessitates opening the skull, 

 the method cannot be applied to man. All experi- 

 mental results have therefore been obtained in ani- 

 mals, but relevant information may be gathered from 

 patients with a \'erified epileptogenic lesion. 



A localized experimental cereljral disturbance can 

 be epileptogenic either directly by acting on the 

 neurons or indirectly by causing a lesion which is 

 later epileptogenic. In the first case, no actual lesion 

 is produced in the brain; the epileptogenic stimula- 

 tion is either an electric current applied locally, a 

 source of heat or cold, or a chemical irritant (strych- 

 nine, penicillin, carbachol, creatine, physostigmine, 

 acetylcholine, nicotine, picrotoxin, etc.). On the con- 

 trary, in the second case, the cerebral as.sault does not 

 directly precipitate a seizure but leads to localized 

 cicatrization which is responsible for the irritation 

 that later provokes seizures. Aluminum hydroxide, 

 acting as a foreign body without immediate chem- 

 ical action, is the substance commonly used to pro- 

 voke this type of irritation. In both cases, the cere- 

 bral disorder may be produced in the cortex or in 

 the depths of the brain in various subcortical struc- 

 tures; in both cases, it gives rise to seizures which may 



