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The role of synaptic weight changes in the epileptic destabilization of neuronal nets
S164 P26.10 T H E R O L E O F SYNAPTIC W E I G H T C H A N G E S IN T H E EPILEPTIC D E S T A B I L I Z A T I O N O F N E U R O N A L NETS.
P26.12 S U B D U R A L E L E C T R O E N C E P H A L O G R A P H Y IN C A N D I D A T E S F O R SURGERY F O R U N C O N T R O L L E D P A R T I A L E P I L E P T I C SEIZURES: T E C H N I Q U E AND RESULTS.
W. Trabka, J. Trabka and Z. Mikrut D.C. Jones, W.T. Blume, J.P. Girvin and R.S. McLachlan
(Krakow. Poland) (London, Canada) Stable function of a neuronal net depends mainly upon the synaptic weights. We would like to explain this problem according to the theory of regulation, mathematical modelling and computer simulation, briefly reported in the previous poster. The chosen weight differences between excitatory and inhibitory synapses ranged from +0.8 to - 2 . 0 . Changing only the synaptic weight differences we could observe the following states: Stability: Keeping constant synaptic weights, the selfsustained discharge was not observed, in spite of other parametric shifts. Conditional or potential stability: if even 0.2 weight difference changes were applied (i.e., about 10% of general amplification level) destabilization appeared. Destabilization: when the weight difference crossed the stabilization threshold, resulting from the ratio of synaptic configuration to general amplification, the neuronal net fell into continuous destablized discharge. The most interesting feature was the great sensitivity of neuronal nets in the conditional stability state.
P26.11 AXONAL C O N D U C T I V I T Y DELAYS AS C A U S E O F C O M P U T E R S I M U L A T E D EPILEPTIC DESTABILIZATION. J. Trabka and W. Trabka
(Krakow, Poland) This work tries to explain the conditions for the occurrence of seizure discharges in neuronal nets. Having constructed a mathematical model and computer program we could, in simulation experiments, verify hypotheses concerning the mechanisms of paroxysmal destabilization. The net consisted of 25 cells, each connected with 8 neighbours in a synaptic linkage. For each experiment we had to define thresholds, interneuronal connections and axonal delays. In the experiment there were 300 simulation steps, each one lasting 0.5 msec. In order to estimate the influence of the axonal delays, the only problem to be discussed here, we used 6 values: from 0.3 to 9.0 msec. For 0.3 and 0.8 msec dllays the impulses expired; for delays: 1.0, 1.5, 4.0, 9.0 msec the net fell into synchronous, self-sustained high frequency discharges. The results show that the shifting delays from 0.8 to 1.0 msec caused totally different reactions. During the destabilization we observed a spontaneous discharge frequency fluctuation of waxing and waning type.
Although depth EEG is widely used to delineate the origin of partial seizures, its limitations are becoming recognised. Arrays of subdural electrodes require large craniotomies prohibiting bilateral implantation. As an alternative, we have used strings of subdural electrodes. Four to eight such strings of seven contacts each are inserted bilaterally through burr holes and fed along regions to be recorded. Recording contacts consist of platinum rings encircling 1 mm. diameter polyethylene tubing at 20 mm. intervals, seven rings per tubing. Teflon coated stainless steel wires, soldered to the inside of each ring, enter the tubing and feed through it to a seven-pin amphenol connector which is secured to the tubing with an epoxy adhesive. Silastic medical adhesive coats the entire structure except for the platinum rings and the connector. Temporal lobes were studied in five patients, frontal lobes in two, and temporal-occipital in three. Seizure origin was delineated in eight of ten patients; excision of the epileptogenic area has improved seven of seven. One patient had no seizures during implantation; origin remained undetermined in one.
P26.13 T H E C O R R E L A T I O N B E T W E E N D I S C H A R G E P A I q ' E R N S DURING S L E E P STAGES AND O U T C O M E O F S U R G I C A L T R E A T M E N T IN P A T I E N T S W I T H TEMP O R A L LOBE EPILEPSY. 72 Bacia and C. Fryze
(Warsaw', Poland) Since Gibbs and Gibbs (1947) it has been common experience that sleep is an effective method of activating epileptic discharges. From 1972 in the Neurosurgical Department in Warsaw, all-night sleep records have been used as a diagnostic tool in epileptic patients. From this material we have chosen 50 consecutive patients treated by temporal lobectomy from 1975-1980. Right temporal lobectomy was performed in 29 patients, left temporal lobectomy in 21 patients. Follow-up after surgical intervention was from 5 to 9 years. Surgical outcome was rated on a scale from 1 to 2, with a score of 1 indicating that the patient became seizure-free following lobectomy and a score of 2 indicating that the patient was not seizure free, regardless of the degree of improvement. Spiking property rates in sleep stages were related to the surgical outcome. The present study reveals a strong relation-
P26.12 S U B D U R A L E L E C T R O E N C E P H A L O G R A P H Y IN C A N D I D A T E S F O R SURGERY F O R U N C O N T R O L L E D P A R T I A L E P I L E P T I C SEIZURES: T E C H N I Q U E AND RESULTS.
W. Trabka, J. Trabka and Z. Mikrut D.C. Jones, W.T. Blume, J.P. Girvin and R.S. McLachlan
(Krakow. Poland) (London, Canada) Stable function of a neuronal net depends mainly upon the synaptic weights. We would like to explain this problem according to the theory of regulation, mathematical modelling and computer simulation, briefly reported in the previous poster. The chosen weight differences between excitatory and inhibitory synapses ranged from +0.8 to - 2 . 0 . Changing only the synaptic weight differences we could observe the following states: Stability: Keeping constant synaptic weights, the selfsustained discharge was not observed, in spite of other parametric shifts. Conditional or potential stability: if even 0.2 weight difference changes were applied (i.e., about 10% of general amplification level) destabilization appeared. Destabilization: when the weight difference crossed the stabilization threshold, resulting from the ratio of synaptic configuration to general amplification, the neuronal net fell into continuous destablized discharge. The most interesting feature was the great sensitivity of neuronal nets in the conditional stability state.
P26.11 AXONAL C O N D U C T I V I T Y DELAYS AS C A U S E O F C O M P U T E R S I M U L A T E D EPILEPTIC DESTABILIZATION. J. Trabka and W. Trabka
(Krakow, Poland) This work tries to explain the conditions for the occurrence of seizure discharges in neuronal nets. Having constructed a mathematical model and computer program we could, in simulation experiments, verify hypotheses concerning the mechanisms of paroxysmal destabilization. The net consisted of 25 cells, each connected with 8 neighbours in a synaptic linkage. For each experiment we had to define thresholds, interneuronal connections and axonal delays. In the experiment there were 300 simulation steps, each one lasting 0.5 msec. In order to estimate the influence of the axonal delays, the only problem to be discussed here, we used 6 values: from 0.3 to 9.0 msec. For 0.3 and 0.8 msec dllays the impulses expired; for delays: 1.0, 1.5, 4.0, 9.0 msec the net fell into synchronous, self-sustained high frequency discharges. The results show that the shifting delays from 0.8 to 1.0 msec caused totally different reactions. During the destabilization we observed a spontaneous discharge frequency fluctuation of waxing and waning type.
Although depth EEG is widely used to delineate the origin of partial seizures, its limitations are becoming recognised. Arrays of subdural electrodes require large craniotomies prohibiting bilateral implantation. As an alternative, we have used strings of subdural electrodes. Four to eight such strings of seven contacts each are inserted bilaterally through burr holes and fed along regions to be recorded. Recording contacts consist of platinum rings encircling 1 mm. diameter polyethylene tubing at 20 mm. intervals, seven rings per tubing. Teflon coated stainless steel wires, soldered to the inside of each ring, enter the tubing and feed through it to a seven-pin amphenol connector which is secured to the tubing with an epoxy adhesive. Silastic medical adhesive coats the entire structure except for the platinum rings and the connector. Temporal lobes were studied in five patients, frontal lobes in two, and temporal-occipital in three. Seizure origin was delineated in eight of ten patients; excision of the epileptogenic area has improved seven of seven. One patient had no seizures during implantation; origin remained undetermined in one.
P26.13 T H E C O R R E L A T I O N B E T W E E N D I S C H A R G E P A I q ' E R N S DURING S L E E P STAGES AND O U T C O M E O F S U R G I C A L T R E A T M E N T IN P A T I E N T S W I T H TEMP O R A L LOBE EPILEPSY. 72 Bacia and C. Fryze
(Warsaw', Poland) Since Gibbs and Gibbs (1947) it has been common experience that sleep is an effective method of activating epileptic discharges. From 1972 in the Neurosurgical Department in Warsaw, all-night sleep records have been used as a diagnostic tool in epileptic patients. From this material we have chosen 50 consecutive patients treated by temporal lobectomy from 1975-1980. Right temporal lobectomy was performed in 29 patients, left temporal lobectomy in 21 patients. Follow-up after surgical intervention was from 5 to 9 years. Surgical outcome was rated on a scale from 1 to 2, with a score of 1 indicating that the patient became seizure-free following lobectomy and a score of 2 indicating that the patient was not seizure free, regardless of the degree of improvement. Spiking property rates in sleep stages were related to the surgical outcome. The present study reveals a strong relation-