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HANDBOOK OF PHYSIOLOGY 



NEUROPHYSIOLOGY I 



must mention Binswanger (i8) and Wortis & Klenke 

 (198} who obtained only tonic seizures by mechanical 

 or electric stimulation of the pons and the hypothal- 

 amus, and Ziehen (201) who was unable to obtain 

 clonic con\ulsions after cortical ablation. These re- 

 sults have been confirmed by Samaja (171), Prevost 

 (161) and Bouche (19). This difference between the 

 sites of origin of clonic and tonic convulsions was 

 elevated into a law by Bechterew (16). Horsley offered 

 an even more eclectic opinion when he wrote in 1886 

 (100), "tonic and clonic spasms may be produced by 

 any motor center, but the combination and sequence 

 of tonic-clonic could originate only from the cerebral 

 motor cortex." Such an interpretation however is not 

 uni\ersally accepted. Bubnoff & Heidenhain (23), 

 Pollock & Davis (159), Pike et al. (157), Spiegel (180), 

 and Marinesco et al. (135) insist upon the fact that 

 clonic as well as tonic convulsions may originate e.x- 

 clusiveh' in subcortical structures. 



MEGH.^NISM OF THE BIOELECTRIC DISCH.^RGES IN GEN- 



ER.-^LiZED EPILEPSY. Certainly the most striking aspect 

 of generalized seizures recorded from the cortex is 

 the excessive synchrony of the elements responsible 

 for each wave of activity. For this reason the epileptic 

 seizure has .sometimes been called a 'paroxysmal 

 hypersynchrony'. Actually, the synchrony of the 

 components is always imperfect and what mainly 

 characterizes them is isorhythmicity (48). This iso- 

 rhythmicity, as well as the approximate synchrony, is 

 partly explained by the fact that different cortical 

 regions, primarily passive, are connected with one or 

 several subcortical foci of acti\it\' which act as their 

 common pace maker or pace makers. We know that 

 when several pace makers compete, only one is dom- 

 inant, although changeover from one to another may 

 take place. 



This community and this unity of control rep- 

 resent what one might call the external factors of 

 isorhythmicity; there is a synchrony or at least a 

 grouping of elements when the controls are mediated 

 by fast conducting pathways. 



On the other hand, the mechanism of internal 

 synchronization, which engenders and organizes the 

 convulsive subcortical pace makers of the passive 

 cortical areas, is much more complicated, depending 

 on many intricate factors. Here interactions between 

 neighboring neurons of the same type may arise 

 either from synaptic connections or from reciprocal 

 field effects at a short distance. The seizure occurs 

 when these interactions become unusually important 

 and especially when they thus create the conditions 



for explosive autorecruitment. This may come from 

 different causes, according to Fessard (48) : lowering 

 of the excitability threshold of neurons, failure of 

 inhibitory mechanisms, structural arrangements favor- 

 able to synaptic or ephaptic interactions, alterations 

 of the recovery cycles so that those of a whole popula- 

 tion of neurons come to have more similar perio- 

 dicities, etc. Even chance can be invoked, for if the 

 other conditions are favorable, a fortuitous and ini- 

 tially restricted synchrony may hiring on synchroniza- 

 tion of excitable elements of a larger population of 

 neurons as a result of intense interactions which will 

 be powerful in proportion to the number of units al- 

 ready recruited. The fact that the synchrony, whatever 

 its cause, results in wider synchronization is the basic 

 principle of the paroxysmal character of seizures. 



The generalized nature of the seizure discharge 

 which accompanies tonic-clonic conxulsions was 

 demonstrated by workers who studied its distribution 

 in the brain of animals. Thus Jung (116) by using 

 electroshock, and Gastaut & Hunter (66) and Starzl 

 ('/ al. (184) by injecting pent\lenetetrazol recorded 

 such a discharge from the whole of the cerebellar and 

 cerebral cortex (i.so- and allocortex) and all the sub- 

 cortical structures from the caudate nucleus to the 

 mesencephalon. Jung observed that electrical stimu- 

 lation, which was insufficient to provoke a generalized 

 fit, caused the discharge to appear in subcortical 

 (thalamic and subthalamic) structures and the allo- 

 cortex (Amnion's horn) and spared only the isocortex. 

 These results agree well with those of Gastaut & 

 Hunter (66) who observed that following an injection 

 of pentylenetetrazol, bisynchronous discharges appear 

 first in the diencephalon.' 



Thus one may suppose that generalized discharges 

 originate in diencephalic structures, whence they 

 irradiate to the whole of the brain, a hypothesis which 

 is confirmed by direct stimulation of the median 

 diencephalon. 



Electrical stimulation of the nonspecific thalamic 

 structures at low frequency provokes a 'recruiting' 

 response (38-40, 106, 109, 183). Such responses, when 



' These results do not however agree with those of Starzl 

 et al. (184) who found that a convulsant dose of pentylenetet- 

 razol pro\oked first a cortical discharge which was secondarily 

 'driven' to the subcortical structures by projection fibers. 

 Starzl et at. even concluded that, in the animal with an en- 

 tirely' isolated corte.x, the convulsant dose of pentylenetetrazol 

 caused a generalized cortical discharge without any response 

 in the diencephalon. These are obviously disturbing differences 

 which are difficult to reconcile, but may be due to differences 

 in technique. 



