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HANDBOOK OF PHYSIOLOGY' 



NEUROPHYSIOLOGY I 



on the contralateral side, but they are never bilateral 

 and synchronous. Independent contralateral dis- 

 charges may indicate a secondary vascular extension 

 of the lesion to the other side (69) but may also indi- 

 cate a functional ' unleashing' of these homologous 

 contralateral structures which have acquired an 

 epileptogenic potential through being bombarded. 

 For these reasons, ablation of the epileptogenic focus 

 on the side of the lesion does not necessarily lead to 

 the disappearance of the contralateral discharges 

 which mav persist for several months after operation 

 (84). 



During seizures, the discharges show a great variety 

 of forms: /) rhythmical discharges of spikes or slow 

 waves observed around the lesion, propagated to the 

 same cortical areas as the interictal discharges, chiefly 

 to the orbitoinsuloteletemporal cortex; 2) propaga- 

 tion of the discharge to subcortical structures, chiefly 

 the septum, the hypothalamus and the tegmentum 

 mesencephali, generally accompanied by diffuse cor- 

 tical manifestations like desynchronization or slow 

 hypersynchronization occupying all or part of one or 

 both hemispheres (78, 84, 167). Sloan, Ransohoff & 

 Pool emphasize the bisynchronous 4 to 6 cps ictal 

 discharges which they recorded in monkeys with 

 amygdaloid scars. 



EXPERIMENTAL PARTIAL EPILEPSY OF SUBCORTICAL 



ORIGIN. If one excludes the amygdala and septum 

 which have been linked to the rhinencephalon, few 

 subcortical structures have been studied from the 

 point of view of experimental epilepsy. Different parts 

 of the thalamus, subthalamus and tegmentum mesen- 

 cephali have, however, received indwelling electrodes 

 or been injected with aluminum cream (72, 73). 



The clinical manifestations produced by limited 

 electrical stimulation include autonomic and devia- 

 tional phenomena which bear only a distant and frag- 

 mentary resemblance to the seizures provoked by 

 stimulation of the basal rhinencephalon. The scars 

 from aluminum implantation have never given rise 

 to spontaneous seizures, probably because the di- 

 encephalic structures have a high convulsant thresh- 

 old. However, injection of subliminal doses of pentyl- 

 enetetrazol in cats with diencephalic scars have always 

 precipitated seizures very similar to those provoked 

 from the basal rhinencephalon. This led Gastaut & 

 Roger (78) to believe that at least some of the aspects 

 of rhinencephalic seizures depend on the fact that 

 allied diencephalic formations are brought into play. 



The electroencephalographic manifestations are of 



several types. With hypothalamic, subthalamic and 

 tegmental epileptogenic lesions there are sporadic 

 and local interictal discharges, transmitted to the 

 orbitoinsulouncotemporal region which, as we have 

 already seen, is involved when the rhinencephalon 

 discharges. This curious observation is explained by 

 the findings of physiological neuronography and of 

 histology which demonstrate a large number of con- 

 nections between the orbitoinsuloteletemporal region 

 on the one hand and the hypothalamus, subthalamus 

 and tegmentum mesencephali on the other (67). 



Irritative lesions of other subcortical structures 

 cause discharges in other parts of the cerebral cortex. 

 Thus lesions of the lateral (dorsal and posterior) and 

 of the posterior nuclei of the thalamus produce their 

 effects in the posterior temporal and the parietal cor- 

 tex, whereas lesions of the pulvinar, the lateral genicu- 

 late and the corresponding region of the nucleus 

 reticularis affect the occipital cortex. Lesions of the 

 medial geniculate, the suprageniculate nucleus and 

 the corresponding region of the nucleus reticularis act 

 on the superior temporal cortex. 



EXPERIMENTAL PARTIAL EPILEPSY, SECONDARILY GEN- 

 ERALIZED. All partial epilepsies may become gener- 

 alized whether they are of cortical or subcortical 

 origin, and whether caused by direct chemical or elec- 

 trical stimulation or resulting indirectly from an epi- 

 leptogenic scar. The partial epilepsy which has been 

 best studied from the point of view of generalization 

 is that caused by localized cortical electrical stimu- 

 lation. Generalized convulsions develop when the 

 strength of local stimulation passes a threshold value 

 wherever this cortical stimulation may be, even after 

 sagittal section of the telencephalon, diencephalon 

 and mesencephalon (181); it is thus certain that the 

 subcortical structures extending as far as the rhomben- 

 cephalon are responsible for the generalization of the 

 convulsions. 



A study of epilepsy of the Openshowski-Speranski 

 variety leads to the same conclusions. Here generalized 

 seizures, so frequent that they constitute status epilep- 

 ticus, are provoked by refrigeration of a small part of 

 cerebral cortex on one side. This is a generalized 

 epilepsy which is at first partial, for immediate abla- 

 tion of the refrigerated zone abolishes it, but the 

 generalization is of subcortical origin since convul- 

 sions (which are bilateral) still appear after ablation 

 of the somatomotor region of both hemispheres (45) 

 and after section of the corpus callosum (179). 



Subcortical structures influence the generalization 



