354 



HANDBOOK OF PHYSIOLOGY 



NEUROPHYSIOLOGY I 



marked neuronal degeneration or necrosis, associated 

 with reactional gliosis. The cerebral atrophy may in- 

 volve the whole of one hemisphere and sometimes also 

 the contralateral cerebellar hemisphere, but it gen- 

 erally predominates in the temporal lobe and may in- 

 volve it alone. The lesion is maximal in most cases in 

 the internal aspect of the temporal lol)e and the in- 

 ferior surface of the frontal lobe in the region which 

 comprises the anterior part of the hippocampal gy- 

 rus — including the uncus and amygdala — Ammon's 

 horn, the temporal tip, the insula and its opercula, the 

 anterior perforated space and the posterior part of the 

 orbital convolutions. This is a region which is fur- 

 rowed from front to back by the rhinal fissure lined 

 by the endorhinal fissure, and which Gastaut pro- 

 posed to name the ' pararhinal region' for this has the 

 advantage of connoting the allopcriallocortical (rhin- 

 encephalic) nature of the parts inxoKed. 



Phruiipatliogenesis of Partial Epilepsies 



ORIGIN ."KND CAUSE OF NEURON.AL DISCHARGE IN PARTI.\L 



EPILEPSY. The discharge in the partial epilepsies gen- 

 erally starts in the immediate neighborhood of the 

 epileptogenic lesion where the neurons show hyper- 

 excitability, as demonstrated by Walker & Johnson 

 (192). These workers found that around an alumi- 

 num-produced scar weaker electric stimulation pro- 

 duced a postdischarge, or smaller doses of pen- 

 is lenetetrazol were recjuired to evoke local spikes. 



In certain cases, however, the discharge begins at a 

 distance from the epileptogenic lesions, either in al- 

 lied structures or even in structures which are entirely 

 independent. We have already seen that an experi- 

 mental epileptogenic lesion in the right amygdala in 

 a cat can cause ictal discharges in the left amygdala, 

 and in man a right-sided temporal epileptogenic 

 lesion. This is seen in the experiments of Walker & 

 or left temporal or in the occipital regions. These facts, 

 emphasized by the Marseilles school, may be ex- 

 plained by the conception that neuronal excitability 

 is heightened at a distance from the epileptogenic 

 lesion. This is seen in the experiments of Walker & 

 Johnson (192) and of KopelofTc^ al. (127) who demon- 

 strated a lowered convulsant threshold in cortical or 

 allied subcortical structures, and even in the whole 

 jjrain in animals with an epileptogenic scar. 



It is a very important conception that neuronal 

 excitability may be intensified remotely from the 

 epileptogenic lesion in structures anatomically allied 

 to the lesion but not themselves showing anv organic 



alteration. The degree of excitability may indeed be 

 so high that, under the influence of an afferent volley, 

 the allied structure may discharge as well as, if not 

 more intensely than, the epileptogenic focus itself 

 (61). One concludes therefore (53-55, 57) that, al- 

 though the existence of a sporadic spike or a rh\ thmic 

 discharge in an EEG or a corticogram constitutes 

 the most reliable proof of a local epileptic process, it 

 in no way guarantees that the epileptogenic lesion is 

 seated in the same place. Working on this general 

 principle, Gastaut & Roger (78) demonstrated the 

 following facts. 



o) The epileptogenic lesion may or may not coin- 

 cide with a given EEG focus; it may even be a long 

 way off. Gastaut (82) showed that a large number of 

 occipital seizure discharges appear in patients with 

 an anterior temporalpararhinal lesion, while Segundo 

 et al. (175) observed true electric occipital seizures in 

 the monkey following postdischarges induced in the 

 amygdala. 



h) The existence of an EEG spike focus is always 

 a valuable criterion for localization in partial epilepsy, 

 but only as a physiological argument in relation to the 

 clinical facts; it never permits one to incriminate a 

 lesion of the underlying cortex directly and with 

 certainty. 



c) A spike focus in the electrocorticogram is always 

 a useful finding for the neurosurgeon, allowing him to 

 judge where the primary epileptogenic focus probably 

 lies on the basis of anatomophysiological reasoning. It 

 ne\'er unfailingly indicates the territory to be resected 

 nor its lioundaries; the surgeon has to remove the 

 lesion or the structure insolved and not just the spike- 

 ijearing area. 



(/) The existence of several, concomitant or inde- 

 pendent spike foci does not necessarily signify a cor- 

 responding number of lesions. Also, the existence of a 

 focus of bilateral and symmetrical spikes, concomitant 

 or independent, does not necessarily signify a bi- 

 lateral lesion. 



<") The persistence of a spike focus after ablation of 

 an epileptogenic focus does not necessarily mean that 

 the whole or a part of the lesion persists nor that a new 

 lesion has been created by the operation; it may be 

 that the local perilesional hyperexcitability persists or 

 is enhanced for a shorter or longer time. In the same 

 wav, the persistence or appearance of a contralateral 

 spike focus after ablation of an apparently unilateral 

 lesion does not necessarily imply that a previously 

 unobserved contralateral lesion exists; it may be a 

 matter again of local hyperexcitability which is trans- 



