THE PHYSIOPATHOLOGV OF EPILEPTIC SEIZURES 



355 



milted to the other side. This was reproduced experi- 

 mentally by Gastaut et al. (84). The\ provoked bi- 

 lateral and symmetrical spike foci with a one-sided 

 lesion resulting from aluminum scarring and then ob- 

 served that the contralateral focus persisted after 

 ablation of the single lesion. 



This instability and variability of the epileptic dis- 

 charge is seen even in patients who only show peri- 

 lesional discharges. These discharges originate at 

 some point on the periphery of the lesion; when the 

 lesion is extensive and surrounded Ijy a large ' halo' 

 of neuronal hyperexcitaljility, the discharges may 

 arise in different seizures at places far removed from 

 each other. This was recorded experimentally by 

 Roger (167) in whose experience the seizure dis- 

 charges around a single ijut extensive lesion involv- 

 ing most of the amygdaloid nucleus sometimes began 

 in the hippocampus and sometimes in the ento- 

 peduncular nucleus or the anterior amygdaloid zone 

 or the lateral amygdaloid nucleus. Pathological hyper- 

 excitability maintained around and at a distance from 

 epileptogenic lesions thus plays an essential part in the 

 development of the seizures of partial epilepsy. 



Of equivalent or greater importance is the part 

 played by the innate hyperexcitability of certain 

 regions which show a low convulsant threshold and 

 a striking epileptogenic predisposition. The various 

 authors who have studied these local difTerences in 

 the convulsant thresholds have come to the following 

 conclusions. The hippocampus has the lowest thresh- 

 old of excitability of all the cerebral structures so far 

 explored (11, 25, 31, 86, 94, 119-121, 142). The 

 motor cortex has the next lowest threshold (168), es- 

 pecially in the region corresponding to motor repre- 

 sentation of the face and hand (50). In order of de- 

 creasing e.xcitability there follows the cingular region, 

 the tip of the temporal lobe and the uncinate region 

 with the underlying amygdala, the first temporal con- 

 volution and, finally, the parietal region. The frontal 

 region and particularly the occipital region have the 

 highest epileptogenic threshold. It is hardly neces- 

 sary to stress the importance of these findings which 

 explain why the majority of partial epilepsies have a 

 somatomotor or tempororhinencephalic symptoma- 

 tology and why focal frontal or occipital epilepsies are 

 so rare. 



Spontaneous regional hyperexcitability and hyper- 

 excitability developing around and remote from a 

 cerebral lesion thus play a fundamental part in the 

 development of seizures of partial epilepsy. It is 

 similar to the part played by general neuronal hyper- 



excitaljility in the development of generalized seizures, 

 and which we have already termed a 'predisposing 

 role'." 



The precipitating factor is also the same in the 

 partial as in generalized epilepsies. This factor is a 

 volley of afferent stimuli which, although without 

 pathological effect under normal conditions, can pro- 

 voke paroxysmal hypersynchrony when local hyper- 

 excitability is present. The precipitating role of 

 afferent stimuli was physiologically demonstrated 

 once (and perhaps for all) by the remarkable experi- 

 ments of Clementi (28), in which strychninization of 

 the visual cortex is in no way detectable until \isual 

 stimulation is applied, whereupon it provokes myo- 

 clonic movements of the eyelids and sometimes even 

 a generalized convulsive seizure. The experiments of 

 Amantea (8) exemplify the same principle, showing 

 that strychninization of the somatomotor area, is in- 

 sufficient to produce strychnine clonus yet precipi- 

 tates Jacksonian or even generalized seizures when 

 the appropriate reflexogenic cutaneous territory is 

 stimulated. It is indeed hardly necessary to remind 

 clinicians of the numerous cases of parietal, temporal, 

 amygdaloid or hippocampal partial epilepsy precipi- 

 tated by an unexpected movement (7), a noise (13, 

 74), music (33, 97), rapid ingestion of a large quantity 

 of water (20) or an emotion (62, i 78).'- 



In most cases, however, the fact that afferent 

 stimuli precipitate a seizure is not clinically apparent 

 because local hyperexcitability increases at the ap- 

 proach of an attack and is finally so marked that any 

 volley of nervous impulses resulting from an insignifi- 

 cant stimulus is sufficient to fire off a paro.xysm. 



PROPAGATION AND TERMINATION OF NEURONAL DIS- 

 CHARGE IN PARTIAL EPILEPSY. We have already seen 

 that a localized discharge may extend locally or be 

 propagated concomitantly or successively to various 



" An epileptogenic lesion may obviously develop in a patient 

 with a predisposition for epilepsy expressed as generalized 

 neuronal hypere.\citability, either constitutional or acquired. 

 The two factors are then added together. For this reason a ce- 

 rebral lesion will frequently provoke seizures of partial epilepsy 

 in one subject and not in another. For the same reason, Lennox 

 found a degree of familial predisposition in the parents of 

 symptomatic epileptics, because partial epilepsy dc\"elops 

 particularly in those who are already so predisposed. 



'- Conversely the continuous physiological bombardment of 

 the discharging region may entail its desynchronization and 

 abort a seizure; that is the reason why certain epileptics abort 

 their somatomotor or psychomotor fits by forcible extension of 

 the limb in which the jerks first appear or by concentrating 

 their attention fixedly on an idea or a perception. 



