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HANDBOOK OF PHYSIOLOGY 



NEUROPHYSIOLOGY I 



allied structures or even to the whole brain. Numerous 

 authors have studied propagation of epileptic activity 

 and we may summarize their work as follows, a) Local 

 propagation of the discharge proceeds very slowly 

 like a ' drop of oil' through the filjrillary network of 

 grev matter. This explains the Jacksonian ' march' 

 so characteristic of seizures provoked by the discharge 

 of structures somatotopically arranged (for example 

 the jerks which extend from the face to the hand 

 while the cortical discharge travels from one repre- 

 sentative part of the cortex to the next adjacent 

 part). 6) Remote propagation takes place very 

 rapidly along fibers of large diameter. This explains 

 the almost immediate bringing into play of the whole 

 group of structures of a corticosubcortical ' sector' and 

 the stereotyped symptomatology during one or subse- 

 quent seizures when the discharge remains localized 

 to such a sector. On the contrary, when propagation 

 takes place to various '.sectors' successively, a variety 

 of disturbances appear during the course of one or 

 subsequent seizures. 



The discharge in partial epilepsy is propagated by 

 means of normally functioning nerve fibers and 

 synapses from an epileptogenic center which is 

 anatomically altered to allied centers which are 

 anatomically healthy. This implies that the discharge 

 originates as a lesional (or more likely perilesional) 

 phenomenon but that its propagation is an exclusively 

 functional phenomenon. Moruzzi says: " It is ordinary 

 nervous activity which determines that allied neurones 

 pass from a state of normal activity to one of epileptic 

 functioning." 



Although involving only normal functions, this 

 mode of propagation is nonetheless pathological since 

 it does not exist in the normal subject. Indeed, the 

 following two conditions are necessary for its produc- 

 tion, a) Hyperexcitaijility of the neuronal population 

 allied to the epileptic center, explaining the sensi- 

 tivitv \\ hich it acquires under epileptogenic iiombard- 

 ment. VVe have already shown that this is always the 

 case in generalized epilepsy; and according to John- 

 son & Walker (114): "Not only the primary focus is 

 hypersensitive, but this hypersensitivity is found in 

 the other cortical and subcortical structures with 

 which it is intimately connected. This hypersensitivity 

 manifests itself by a lowered threshold for electrical 

 and chemical stimulation and seems to result from 

 functional disturbance at the level of the normal 

 neurons, as a result of the influence of the epilepto- 

 genic focus." 



fe) The epileptic discharge cannot be propagated 

 unless the bombardment from the epileptogenic cen- 



ter is efficacious. For this, it requires the following 

 properties: the bonii)ardment discharges must be of 

 high frequency (1,000 cps); these discharges must 

 activate a sufficient number of terminals on the same 

 cells in order to pro\oke spatial summation; these dis- 

 charges must be rhythmically spaced so as to use the 

 facilitation of supranormality provoked in each neuron 

 by the previous discharge and thus to produce tem- 

 poral summation; and the bombardment must con- 

 tinue long enough to produce a progressive effect. 



Although hypcrexcitability of allied centers is al- 

 ways required, all the conditions necessary to make 

 bombardment effective are not necessarily present at 

 one time. Certain ones, indeed, depend on the func- 

 tional or anatomical characteristics of the bombarded 

 or bombarding centers and of the pathways which 

 unite them. The phenomena of spatial summation, 

 for example, depend exclusively on the number of 

 fibers transmitting the bombardment and on their 

 mode of terminating on allied neurons. All of these 

 conditions vary from one system to another and make 

 certain epileptic propagations easier than others. 



A center allied to an epileptogenic focus reacts 

 differently, according to its degree of excitability and 

 according to the efficacy of bombardment, a) It 

 may remain indifferent, b) Its spontaneous activity 

 may simply i)e increased, r) It may respond stroke for 

 stroke to the fjombarding discharges as they arrive; 

 thus true evoked potentials are produced in answer to 

 the convulsive waves of the primary focus, with a 

 latency corresponding to the propagation along axons 

 and across synapses. Under these conditions the allied 

 center can be said to have become epileptic because 

 of the primary focus, d) The allied center may become 

 epileptic on its own account, that is, it may dissociate 

 itself from the epileptogenic focus and show secondary 

 autonomous convulsive activity. This may persist 

 after the end of the primary discharge and be propa- 

 gated to allied structures as a tertiary discharge (so- 

 called ' erratic' discharge). 



A ' center' secondarily made epileptic by bombard- 

 ment from a primary epileptogenic focus thus modifies 

 the seizure according to its own anatomical and func- 

 tional characteristics. One of two things usually fol- 

 lows; either the seizure remains partial but is en- 

 riched by electroclinical symptoms consequent upon 

 the new discharge and this discharge may lead to 

 another, or the fit becomes generalized. 



In the first case a seizure may begin with focal 

 clinical and electroencephalographic signs and pass 

 through a series of equally focal episodes. Many psy- 

 chomotor attacks have this pattern, notably those in 



