THE PHVSIOPATHOLOGY OF EPILEPTIC SEIZURES 



349 



under the form of a self-sustained electrographic ac- 

 tivity known as a postdischarge. 



This postdischarge has most of the features char- 

 acteristic of the evoked electrical or strychnine po- 

 tential : /) diffusion to the whole of the area contain- 

 ing the stimulated spot; 2) propagation to the contra- 

 lateral homologous area, j) subcortical propagation 

 to allied structures; and ^) development on a strip of 

 vascularized but neuronally isolated cortex. On the 

 other hand, it differs in that it has the peculiar at- 

 tribute of being self-sustained and of continuing 

 rhythmically for a shorter or longer time after the end 

 of the stimulation. It is no longer a single bioelectrical 

 oscillation of great amplitude repeated at variable 

 intervals, but a series of oscillations slowing pro- 

 gressively and soon interrupted by intervals of elec- 

 trical silence of which the last represents a long phase 

 of postictal extinction. 



French et al. (50) have observed that all cortical 

 regions can be made to show a postdischarge follow- 

 ing supramaximal electrical stimulation, but that 

 only some regions show a postdischarge from stimu- 

 lation which is only just above threshold. On this 

 basis they describe zones as ' epileptogenic' in the fol- 

 lowing descending scale: the motor and premotor cor- 

 tex (motor area for the face and the hand), and the 

 teletemporal and uncinate cortex being most sus- 

 ceptible; next the posterior insular and superior 

 temporal cortex; and after that the parietal cortex. 

 On the other hand the frontal and especially the 

 occipital cortex are resistant to experimental epilepsy. 



The clinical effects of electrical stimulation have 

 been studied only in respect of the somatomotor region 

 for the same reason as in the case of strychnine con- 

 vulsions. The potential evoked by a single electric 

 shock is accompanied by an isolated contralateral 

 ' clonus' identical with the ' cortical strychnine clonus' 

 of Baglioni & Magnini (15). The electrical after dis- 

 charge is accompanied by a convulsive attack (which 

 might be termed a motor after discharge) involving 

 the appropriate contralateral part, each cortical 

 oscillation corresponding to a clonic jerk and to a 

 burst of high frequency activity in the corticospinal 

 pathways. 



As in the case of strychnine, one can facilitate or 

 prolong the clinical and EEG effects of electrical 

 stimulation of the cortex by stimulating the appro- 

 priate cutaneous reflexogenic areas or the parts of 

 the brain that project to that particular cortical zone. 

 In this way subthreshold stimulation of the sensori- 

 motor region facilitates the provocation of a seizure 

 from the homologous contralateral area. With supra- 



maximal stimulation applied to the subcortical white 

 matter after removal of the corresponding somato- 

 motor area, it is even possible to provoke a seizure in 

 the homologous opposite region (27). 



f) Epileptogenic cortical lesions. These are caused by 

 local application of aluminum hydroxide, according 

 to the technique of Kopeloff et al. (127), and appear 

 as fibroglial scars developing slowly around a foreign 

 body. Attacks of partial epilepsy are seen 4 to 1 2 wk. 

 after application and persist for several years. 



The clinical effects of such lesions ha\e been 

 studied most frequently when they were located in 

 the somatomotor area of the monkey. These take 

 the form of Jacksonian seizures beginning in one limb 

 or the face on the contralateral side and spreading 

 progressively (with Jacksonian march) to include the 

 rest of that half of the body. Between seizures, there 

 may be isolated twitches of the muscles involved in 

 the beginning of the paroxysm (epilepsia partialis 

 continua). Peripheral stimulation of all kinds, chiefly 

 of the special sense organs (e.g. a loud and continuous 

 noise), may precipitate or reinforce isolated clonic 

 jerks and may even fire off a Jack.sonian fit. 



\'ery few authors have had the curiosity to apply 

 aluminum cream to cortical areas other than the 

 somatomotor. Cure & Rasmussen (34), however, ap- 

 plied it to the insula of monkeys and they mention 

 spontaneous seizures but unfortunately describe 

 only one, characterized by a bilateral tonic -clonic 

 spasm without any localized feature. Kopeloff et al. 

 (127) applied aluminum cream to the occipital, 

 frontal, middle and anteriortemporal cortex of the 

 monkey without producing seizures in which there 

 was any detectable motor phenomenon. Nor did 

 Gastaut et al. (83) observe any paroxysmal motor 

 effects after subpial injection of aluminum hydroxide 

 in the cat in regions corresponding to the occipital 

 lobe and to the tip of the temporal loije and the 

 temporal lobe proper. These negative findings are 

 very important, chiefly in so far as they show that 

 temporal and teletemporal scars, at least in the 

 monkey and the cat, do not provoke 'psychomotor' 

 seizures, sometimes attributed in man to similarly 

 placed lesions. 



The EEG manifestations resulting from experi- 

 mental .scars appear in the form of slow variations of 

 local potential in a sporadic or in a rhythmical man- 

 ner. The sporadic variations are analogous to those 

 provoked i^y a single electric shock or the application 

 of strychnine, since they appear as predominantly 

 negati\e polyphasic variations in the form of a spike 

 followed b\' a single slow wave or a spike-and-wave 



