Étude électrographique du cycle d'excitabilité cortical

Abstract

Les auteurs décrivent une technique pour mesurer le cycle d'excitabilité chez l'animal et chez l'homme. Ils indiquent la forme et la valeur des points caractéristiques de la courbe qui représente ce cycle. Ils étudient la signification théorique des variations de cette courbe suivant le paramètre du temps et celui des amplitudes et individualisent un certain nombre de critères: a) un temps de récupération, caractétrisant l'aptitude d'un système neuronique à répondre ⪡plus ou moins vite⪢ à une stimulation itérative; b) une amplitude moyenne de la ⪡courbe conditionnante ⪢ trasuisant l'aptitude du dit système à répondre ⪡ plus ou moins fort ⪢ à stimulus unique (degré de synchronisation neuronique); c) une amplitude moyenne de la ⪡ courbe exploratice ⪢ exprimant l'extennce d'un état de subnormalité (ou de supernormalité) post-excitatoire; d) une élongation des oscillations de la ⪡ courbe exploratrice ⪢ exprimant l'existence et l'importance du recrutement dans la frange subliminaire et traduisant l'aptitude du système exploréà répondre plus ou moins fort à des stimuli répétitifs. Ils envisagent les variations de ces différents critères sous l'effet de produits pharmacologiques agissant électivement sur un ou plusieurs des paramètres du cycle d'excitabilité. Ils étudient les corrélations entre le cycle d'excitabilité et, d'une part l'activité corticale spontanée, d'autre part l'activité corticale provoquée par des afférences corticipètes. Ils envisagent enfin les corrélations qui peuvent exister entre le cycle d'excitabilité, l'activitéélectrique corticale spontanée et provoquée et les principales activités psycho-somatiques physiologiques et pathologiques. L'attention est surtout attirée sur les corrélations du cyle avec: 1° l'état de conscience, 2° l'aptitude à présenter des crises épileptiques généralisée. Un dernier aperçu e st jeté sur l'application possible de la mesure du cycle d'excitabilité à l'étude pharmacodynamique des produits anti-épileptiques. The “Cycle of Excitability” consists in the whole of the modifications of excitability of a neuronal population following a preliminary excitation. The authors have studied the excitability cycle in men and in animals by means of photic conditioning and test stimuli. They describe the form and value of the characteristic points of the curve which represents this cycle and they discuss the theoretical significance of this curve according to the parameters of time and amplitude, thus deriving certain criteria of excitability: figure 3 shows that by increasing progressively the interval between the conditioning and test stimuli, one finds first an absolute refractory period (20 msec.) of the cortex, then a relative refractory period (40 msec.) followed by alternative periods of increased and decreased excitability (120 and 220 msec.) The time taken by the two refractory periods represents the time of recuperation of transitory normal excitability. The time taken by all the periods of the whole cycle represents the time of recuperation of definitely normal excitability. The refractory periods (recuperation time) could serve as a measure of a “time constant” of a neuronal system, i.e. it characterizes the ability of a neuronal system to respond “more or less quickly” to repetitive stimulation. The average amplitude of the “conditioning curve” depends on the ability of a given system to respond “more or less strongly” to a single stimulus (degree of neuronal synchronization). The average amplitude of the “test curve” expresses a post-excitatory state of subnormality (or supernormality). The lengthening of the oscillations of the test curve, following the relative refractory period depends on the ability of a system to respond in a more or less stable manner to repetitive stimulation. This phenomenon could probably be explained on the basis of the subliminal fringe following the first stimulus. They study the variations of these criteria under the influence of drugs acting electively on one or many parameters of the cycle of excitability. Barbiturates lengthen the time of recuperation of transitory normal excitability. They also decrease the amplitude of the response to the first and following photic stimuli; it is an excellent sedative. Ether acts similarly though less markedly. Trimethadione acts mostly by decreasing the amplitude of the response to the first and particularly to repetitive photic stimuli; it is a strong anti-convulsant. Chloralose both lengthens the time of recuperation and decreases the amplitude to isolated or repetitive responses; it is both convulsive and an anesthetic drug. Cardiazol increases the response to a single or repetitive stimuli; it is a powerful convulsant. Amphetamines considerably decrease the time of recuperation. They are known for their “wakening” properties. Correlations between the cycle of excitability with spontaneous cortical activity and with evoked cortical potentials were studied. As regards spontaneous cortical activity they have noticed that on the whole the cycle of excitability is lengthened or shortened somewhat proportionally to the decrease or increase in the frequency of the most highly synchronized neuronal system (alpha rhythm, barbiturate bursts). However, there does not seem to be an obvious relation between the duration of the absolute refractory period of the cycle and the frequency of the rhythms. With regards to the relations between the amplitude of evoked cortical responses and the phase of spontaneous waves, no constant findings were observed. The probable conclusion reached is that “fast” cycles of excitability represented by short periods of oscillation and short refractory periods are usually seen with fast rhythms; “slow” cycles of excitability represented by lengthened periods of oscillation and long refractory periods are usually found with slow rhythms. There is undoubtedly a relation between the cycle of excitability and an evoked potential (primary specific response) since it is the variations of the later which permit measurement of the former. The presence of such a cycle of excitability at the various levels of the central nervous system will cause a profound reorganization of peripheral signals. On their way towards the highest levels of cerebral function some will be attenuated, others amplified. The experimental or therapeutic modifications of the rhythm and amplitude of transmitted signals should in some way modify the psychosomatic function of an individual. This proves to be the case. For instance amphetamines, which considerably decrease the time of recuperation of neurones, cause a person to be agitated and hyper-excitable; barbiturates acting in the reverse direction would induce sleep. Calm individuals have a slow, high voltage alpha rhythm (8–10 c/sec.) with hardly no “driving” of occipital rhythms by photic stimulation, their neuronal time of recuperation is long, synchrony is obvious and recruitment is poor; nervous individuals have a high frequency, low voltage alpha rhythm (10–13 c/sec.), at times not perceptible and they show considerable driving by photic stimulation. They have a short neuronal recuperation time, little synchrony and good recruitment. The electrographic picture and the clinical “absence” of petit mal epilepsy can be explained on the basis of the cycle of excitability. In these cases recruitment would be such in the fronto-central regions that the total amount of neurones would discharge synchronously after two or more signals (as seen in photically evoked wave and spike, fig. 15). After one discharge they could fire again only some 300 msec. later, i.e. after having recovered normal excitability. During such a discharge large areas of the cortex, being unable to receive other impulses, could not function normally. Hence the “absence” starting abruptly with the first discharge and ending no less abruptly after the refractory period of the last hypersynchronous discharge. “Grand mal” could be explained by a lesser degree of recruitment. The polyspikes and wave would represent the intermediate form of recruitment between petit mal and grand mal. The durable state of facilitation produced by a sustained discharge may explain the “grand mal” seizure following a rhythmical discharge of spikes and prolonged photic stimulation. Antiepileptic drugs are considered from the oint of view of their action on various parts of the cycle of excitability. Trimethadione decreases hypersynchrony and recruitment; barbiturates decrease the amount of afferent impulses by lengthening the neuronal recovery time.