The results of a long-term study of prophylactic treatment of posttraumatic epilepsy performed in Czechoslovakia during the years 1963 through 1980 are reported. The prophylactically treated group of 144 patients with severe brain injuries was compared with a control group of 24 equally damaged cases without prophylactic treatment. The preventive treatment lasting 2 years in the great majority of cases was performed with relatively low doses of phenytoin (160--240 mg/day) and phenobarbital (30--60 mg/day) administered orally. The incidence of late posttraumatic epilepsy was 25% in the control and 2.1% in the prophylactically treated group. Only one patient (0.7%), however, developed seizures during the course of the prophylactic treatment. The efficiency of prophylactic pharmacotherapy has been proved in long-term observations lasting 8 to 13 years.
In experiments on animals, airflow through the nasal cavity elicits rhythmic synchronized activity that can trigger and/or elicit epileptic electrographic activities in the limbic structures of the brain. This could be demonstrated in studies of lower vertebrates (frogs and turtles). In the turtle the elicited paroxysmal activity often had the shape of regular high-voltage activity in the theta-frequency range (average frequency, 4.1 Hz). It was further proven in clinical experiments that nasal deep breathing with a closed mouth effectively activates epileptic electrographic phenomena of a temporal (limbic) origin. The activating effect was more pronounced on the side ipsilateral to the ventilated nasal meatus. It could also be evoked by air insufflation into the nasal cavity. This effect was suppressed by anesthesia of the mucous membrane in the upper nasal meatus. Possible mechanisms of this, probably reflex, phenomenon are discussed.
SUMMARY
The role of reflex mechanisms in the genesis of epilepsy is classified into the following groups:
Reflex provocation of an epileptic attack by a constant, more or less defined stimulus.
Reflex elevation of paroxysmal susceptibility.
Reflex arrest of the development of the crisis.
Reflex diminution of the paroxysmal susceptibility and limitation of activity of the focus.
Reflex modification of the symptomatology, duration and sequelae of epileptic seizures.
Most of these questions are recommended to the attention of the symposium.
RÉSUMÉ
Le rô1e des mécanismes réflexes dans la génèse de l'carépilepsie a été classe de la manière suivante:
Provocation réflexe d'une crise épileptique par un stimulus constant plus ou moins défini.
Elévation réflexe de la susceptibilité paroxystique.
Inhibition réflexe du développement de la crise.
Diminution réflexe de la susceptibilité paroxystique et limitation de l'caractivité du foyer épileptogène.
Modification réflexe de la symptomatologie, de la durée et des séquelles de crises épileptiques.
La plupart de ces questions sont recommandées a l'caràttention du symposium.
SUMMARY
By means of statistical processing of anamnestic data of a group of 895 patients it was stated that in approximately 40% one or more activating or inhibitory stimuli were identified which seriously influenced the number of attacks. The activating and inhibitory influences assert themselves in almost the same measure. To the most outstanding aptivating influences belong the neurotizing situation and inactivity, and/or mental and physical relaxation, whereas to the inhibitory factors belongs concentration upon some motor or psychical activity.
RÉSUMÉ
L'Car etude statistique de dates anamnésiques d'un groupe de 895 malades a révélé qu'a peu pres en 40% de ces cas, on a pu identifier un ou plusieurs stimuli activateurs ou inhibiteurs susceptibles d'influencer serieusement le nombre des attaques. Les influences d'activation et d'inhibition se manifestent a peu pres dans la meme mesnre. On compte parmi les influences activatrices les plus importantes la situation neurotisante et l'inactivite, et/ou la relaxation mentale et physique, tandis que la concentration sur une activite psychique ou motriee appartient aux facteurs inhibiteurs.
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