SUMMARY A method is described for creating lesions in subcortical nuclear structures of cats. With small amounts of granular aluminum oxide, a primary focus “discharging” into the hippocampus can be localized. Discrete epileptogenic lesions in deep structures can be associated with development of secondary discharges at sites in the opposite hemisphere. Continuous epileptiform bombardment in networks produces synaptic or cellular changes which are evidenced by the secondary epileptic focus in the contralateral hippocampus. These changes can be recorded in other structures connected to the hippocampus, such as the amygdaloid nucleus, septal region and tegmentum mesencephali. We postulate that the secondary discharges are accompanied by a neurohumoral mechanism at the synaptic level. This mechanism is altered by the continuous epileptiform bombardment emanating from the epileptogenic primary focus. We attribute the changes from normal to abnormal epileptiform activity in the cell to metabolic alteration of the cell. Sectioning of the anterior commissure, fornix and corpus callosum before injection of alumina into the hippocampus prevented development of the secondary discharges. Sectioning after development of secondary discharges did not modify the epileptogenic discharges in the opposite hemisphere. Total isolation of the side with the lesion after development of discharges in the secondary focus did not produce significant change in the mirror focus. Intraperitoneal or intramuscular injection of phenobarbital prevented or decreased the spread of epileptiform hippocampal discharges. Intracerebral administration of this drug into the primary epileptiform focus had no notable effect, but administration into the site of the secondary focus exerted a slightly inhibitory action on the secondary focus and a suppressive effect on the further spread of epileptiform discharges. In contrast, intracerebral administration of dilantin produced a blockade of primary as well as secondary epileptiform discharges. On the other hand, intraperitoneal or intramuscular dilantin had inhibitory or facilitatory effects, depending on dosages of the drug. RÉSUMÉ Description d'une méthode pour l'obtention de lésions dans les structures nucléaires sous‐corticales des chats; on peut, avec de petites quantités d'oxyde d'aluminium granulaire, provoquer des décharges primaires dans l'hippocampe d'un côté et des décharges secondaires dans l'hippocampe contralatéral et dans d'autres structures reliées à l'hippocampe, telles que le noyau amygdaloïde, la région septale et la calotte du mésencéphale. Nous supposons que les décharges secondaires sont accompagnées d'un mécanisme neurohumoral au niveau synaptique; mécanisme qui serait altéré par le bombardement épileptiforme continu émanant du foyer épileptogène primaire. Nous attribuons les changements de l'activité normale en activité anormale à une altération métabolique de la cellule. Une section de la commissure antérieure, du fornix et du corps calleux faite avant l'injection d'aluminium dans l'h...
in 1942. The technique does not readily lend itself, however, to the creation of focal deep lesions, since the fluid irritative agent backs up through the needle tract and often spreads through the ventricles or subarachnoid spaces. In our laboratories a method was introduced to produce epileptogenic foci in deep structures of the brain.2 Crystalline aluminum oxide was stereotaxically introduced into specific subcortical structures of the brain. A primary epileptogenic focus developed at the site of the alumina, and, subsequently, secondary discharge developed in the homotopic structure of the contralateral hemisphere. This report is concerned with the induction of petit mal-like patterns after the introduction of crystalline aluminum oxide into deep structures of the brains of kittens. Reports in the literature point to the importance of specific subcortical structures in the development of three per second spike and wave patterns.3"" This, however, is not a universal opinion. For example, Shimizu, Ref sum, and Gibbs 7 in 1952 contended that petit mal spike and wave discharges have a localized cortical origin and transmit over the entire cortex by means of corticocortical association pathways.In the study described here, introduction of aluminum oxide into the intralaminar nuclei of the thalamus and the mesencephalic reticular formation led to the development of spike and wave patterns in the electro¬ encephalographic recordings. The spike and wave patterns, typical of petit mal, did not develop, however, when aluminum oxide was introduced into several other deep structures or on the cortex. MethodThe experiments were carried out on 38 kittens between 21 and 30 days of age (200 to 300 gm body weight). Electrodes were introduced under pentobarbital (Nembutal) anesthesia by the tech¬ nique of Heath et al8 into deep structures, includ¬ ing the ventral mesencephalic reticular formation, the intralaminar nuclei of the thalamus, amygdala, hippocampus, septal region, and the following corti¬ cal areas : coronal gyrus, medial ectosylvian gyrus, posterior suprasylvian gyrus, and sigmoid gyrus. The epileptogenic foci were induced by a previously described technique employing aluminum oxide ( Fig 1 ). Recordings were obtained with a cathode ray oscilloscope and by an ink-writing electroen¬ cephalographic machine with eight or 16 channels. Hyperventilation of the animals was accomplished by manual manipulation of the thorax. Photostimu¬ lation of the animals was performed with a Grass Model PS-2 photostimulator at frequencies of 3, 6, 9, 12 and 18 cps. At the conclusion of the study the animals were sacrificed, and the brains were perfused and stained for location of the electrode tracts and site of the implanted aluminum oxide (Fig 2).Sites of alumina implantation were the reticular formation, intralaminar thalamic nuclei, hippo¬ campus, and over selected cortical areas. Alumina was introduced into only one site in each animal. Results Recordings in Animals WithFoci in the Thalamus and Reticular Formation.-The electroenc...
SUMMARY Kittens with epileptogenic lesions and electroencephalographic 3/sec spike wave discharges like petit mal pattern as well as adult cats with epileptogenic lesions and paroxysmal spike wave discharges were subjected to specific study. Attentive factors (visual, acoustic, olfactory and skin stimulation) had a high inhibitory effect on 3/sec spike wave discharges and on some types of paroxysmal spike wave discharges. Also the stimulation of the mesencephalic reticular formation showed evidence of inhibitory effect on the epileptiform activity previously described. The topical application of acetyl‐choline into the epileptogenic focus produces activation of epileptiform discharges. Also some sensory stimulation (photic, acoustic and tooth stimulation) provokes activation of 3/sec spike and wave discharges which are associated with accelerated liberations of free acetyl‐choline. The inhibitory effect of y‐aminobutyric acid on 3/sec spike wave and paroxysmal discharges had been considered as dependent on the activation of the non‐specific system. RÉSUMÉ Des chatons ayant des lésions épileptogènes et des décharges électroencéphalogra‐phiques de pointes‐ondes de 3/sec du type petit mal et, tout aussi bien, des chats adultes avec lésions épileptogènes et décharges de pointes‐ondes paroxysmales ont fait l'objet d'une étude spécifique. Des facteurs d'attention (visuelle, acoustique, olfactive et une stimulation de la peau) ont un effet inhibiteur élevé sur les décharges de pointes‐ondes de 3/sec et sur quelques types de décharges de pointes‐ondes paroxysmales. La stimulation de la formation réticulaire mésencéphalique a présenté, de même, l'évidence d'un effet inhibiteur sur l'activitéépileptiforme décrite auparavant. L'application topique de l'acétylcholine dans le focus épileptogène produit une activation de décharges épileptiformes. Une certaine stimulation sensorielle (lumineu‐se, acoustique ou stimulation des dents) provoque de même une activation des décharges de pointes‐ondes de 3/sec qui sont associeAes à une libération accélérée d'acétylcholine libre. L'effet inhibiteur de l'acide gamma‐amino‐butyrique sur les décharges paroxysmales de pointes‐ondes de 3/sec a été considéré comme dépendant de l'activation du système non‐spécifique.
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