[Incidence of brain tumors in cases of chronic epilepsy treated surgically]. / Wystepowanie guzów mózgu w przypadkach chronicznych padaczek leczonych operacyjnie.

An incidence of tumors of the brain as a cause of drug-resistant epilepsy have been analysed. The analysis included patients operated for epilepsy at the Department of Neurosurgery, Medical Academy in Warsaw between 1987 and 1991. Malignant tumors were found in 21 out 85 patients (24.7%) treated surgically, 22.4% were benign tumors, and 52.9%--lesions of cicatricial character. The most frequent malignant tumor was fibrillary astrocytoma, noted in 57.1% of cases. Neurological examination has revealed discrete symptoms only in 2 out of 21 patients. CT scans have showed non-characteristic focus of decreased density in 12 patients (57.1%). Differentiation of tumor-produced epilepsy and those due to other focal lesions could not be made with the clinical course of seizures and EEG records. Actually, an incidence of tumors of the brain causing seizures refractory to pharmacologic treatment is increasing. Not characteristic clinical course and EEG records as well as CT scans are the main causes of delays in the surgery.

[A focus and pathologically tuned circuit in pathogenesis of epilepsy]. / Ognisko a patologicznie przestrojony obwód w patogenezie padaczki.

A model of the functional relationship between epileptic focus and neuronal circuit is presented. Such a relationship decides on spreading epileptic discharges in CNS and formation of pathologically tunned circuits during epileptogenesis. Basing on the analysis of kindling and plastic changes in networks and neuronal circuits, a role of these factors in the interpretation of the secondary epilepsy and mirror foci is discussed.

[Regulatory model of pathologic mechanisms in activation of epileptic foci]. / Regulacyjny model mechanizmów patologicznej aktywnosci w ognisku padaczkowym.

A concept of regulatory mechanism of abnormal activity in epileptic foci is discussed, basing on the results of current experimental studies. Such a model is illustrated with an example of basket and pyramidal cell in the hippocampus, results of simulation studies of the role of stimulating and inhibiting junctions in synchronous discharges of high frequency which are an equivalent of epileptic activity in the foci.

[Numeric description of circadian rhythm of TSH in patients with cold tumors of the thyroid gland before and after surgery]. / Numeryczny opis rytmu dobowego TSH u pacjentów z guzkami zimnymi tarczycy przed i po zabiegu operacyjnym.

Circadian rhythm of TSH was analyzed in patients with cold tumors of the thyroid before and after surgical removal of the tumors and in control subjects. By using special computer program BIOR based on harmonic and regression analysis, designed for verifying and comparing various biorhythms, significant differences were found between TSH biorhythms in patients with cold thyroid tumors before and after the operation.

Spreading of epileptic afterdischarges between entorhinal cortex and hippocampus in acute experiments and the kindling model of epilepsy in the rat--comparing different methods of analysis.

Spreading of epileptiform activity in the central nervous system is one of the fundamental problems in epileptology. The patterns of spreading of after-discharges in the hippocampus and entorphinal cortex were studied in acute experiments and using the kindling model of epileptogenesis. Three methods were used to determine the time relations between EEG signals from different brain areas; visual inspections, average amount of mutual information (AAMI) and phase spectrum method. The analysis methods used are adequate for quantification of the degree of coupling between different EEG signals during an afterdischarge, but should be used jointly since different signal features are taken into consideration by different methods. During an afterdischarge only at the beginning the focal area is clearly leading the other brain areas; thereafter the pattern becomes more complex.

[Studies of the mechanisms of spreading of epileptic discharges in the central nervous system]. / Badania nad mechanizmami szerzenia sie padaczkowych wyladowan w osrodkowym ukladzie nerwowym.

The process of spreading of epileptic discharges in central nervous system has to be discussed in two points of view; as a propagation of signals in neuronal networks and as a process of dynamics changes in neuronal circuits and nets. On the base of the spreading of afterdischarges between entorhinal cortex and both hippocampi we discussed time and space relations in spreading of epileptic discharges, and automatic analytical methods in localization of epileptic focus. Spreading epileptic discharge is not only the symptom of pathologic function of system but it simultaneously changes the dynamics of system in which it spreads and causes epileptic destabilization of neuronal circuits and nets. The above mechanisms after theoretical investigations play also important role in evaluation of secondary epileptic foci and posttraumatic epilepsy.

[Changes in synaptic potentials and axonal delays as factors causing epileptic instability of neuronal networks]. / Zmiany wag synaptycznych oraz opóznien aksonowych jako czynniki padaczkowo destabilizujace siec nerwowa.

Synaptic weights, axonal delays and excitability thresholds are three basic parameters influencing the function of neuronal network as a dynamic system. Changes of the general level of the signal flow, without changes in relation between excitatory and inhibitory connections can cause pathologic oscillations in the network. The conductivity in neuronal nets depends on electrochemical processes and may be influenced by the pH-status, ion concentrations, among other parameters. Also different pathological processes can change it. Even slight changes of axonal delays, as shown above, can cause in certain situations unstable, epileptic oscillations of the net.

[Study of the mechanisms of the development of epileptic activity in neuronal networks using a simulation model]. / Badanie mechanizmów wystepowania padaczkowej aktywnosci sieci nerwowej na modelu symulacyjnym.

The occurrence of synchronous, self-sustaining seizure activity is one of the basic mechanisms underlying epileptic attacks. Using a mathematical model of neuronal network in various simulation experiments carried out in digital computer the conditions were studied of the development of pathological epileptic activity and the conditions of the parameters of this network affecting its stable function. After exceeding of a threshold value in the relation between the weights of the stimulating and inhibiting synapses an unstable epileptic response appears. In the state of the so called conditional stability the network is highly sensitive to even small changes of the parameters. These observations make possible a new look at a number of phenomena found in clinical cases and in experiments.

Kindled seizures: anticonvulsant drugs and agents.

Repeated administration of an initially subconvulsive electrical stimulation results in a progressive intensification of the seizure activity, which is known as a kindling phenomenon. The stability of the kindling model of seizures is particularly useful for evaluation of the action of anticonvulsant drugs. In the present study the action of different substances on kindled seizures is reviewed. In general, there are two groups of substances; 1--classical antiepileptic drugs, which are widely used in treatment of human epilepsy and 2--a group of different kinds of biochemical and pharmacological agents, which have been shown to have an anticonvulsant action. In relation to the first group we present here only a brief review. As to the other group, physiological and pharmacological data are reported in order to explain the mechanisms of the anticonvulsant action.

A trial of cybernetic explanation of the development and regression of benign child epilepsy.

Using as an example the verification of a hypothetic mechanism of the course of benign child epilepsy the authors demonstrate a method of simulation investigations of neuron-like networks. The structure and possibilities of a digital system for network modelling are discussed, including the properties of the neuron-like element used presently for the experiments. The results of the simulation investigations described in the second part of the paper confirm the hypothesis that an attack of benign child epilepsy is a result of transgressing of the stability border by a fragment of the neuronal network with development in it of a self-exciting activity of a neuronal group.