To increase understanding into the specific networks involved in the pathophysiology of different types of epilepsy, we proposed extensive neurophysiological studies. First, we studied patients with photosensitive epilepsy since they represent a “model” of system epilepsy. Then, we focused on patients with focal (FE) and generalized epilepsies (GE) to unravel the neurophysiological basis of seizure generalization. Finally, we explored the motor cortex plasticity in juvenile myoclonic epilepsy (JME), the most common subtype of GE in adults. We used the paired transcranial magnetic stimulation (paired-TMS) to investigate the time related changes in functional connectivity between visual and primary motor cortex in healthy subjects and in patients with photosensitivity to study the visuomotor integration. We also studied the interhemispheric connection involved in seizure generalization in FE and GE; to explore the motor cortex synaptic plasticity in patients with JME we used the paired associative stimulation.The findings support a physiologically relevant visuomotor functional connectivity, which likely contributes to visuomotor integration. Substantial physiologic changes in this network underlie the photosensitivity, which may justify the origin of epileptic motor phenomena (i.e. myoclonus). We found significant differences in the interhemispheric connection of drug-treated patients with FE and those with IGE. Whilst interhemispheric inhibition changes would not be crucial for the IGE pathophysiology, they may represent one key factor for the contralateral spread of focal discharges, and seizure generalization. As to the patients with JME, we provided evidence of a defective long term potentiation-like plasticity, which may be primarily involved in the pathogenesis of myoclonus. In conclusion, we documented substantial changes in the epileptogenic networks involved in different types of epilepsy.

Neurophysiological study of epileptogenic networks in epilepsy / Strigaro, Gionata. - ELETTRONICO. - (2017). [10.20373/uniupo/openthesis/86981]

Neurophysiological study of epileptogenic networks in epilepsy

STRIGARO, Gionata
2017-01-01

Abstract

To increase understanding into the specific networks involved in the pathophysiology of different types of epilepsy, we proposed extensive neurophysiological studies. First, we studied patients with photosensitive epilepsy since they represent a “model” of system epilepsy. Then, we focused on patients with focal (FE) and generalized epilepsies (GE) to unravel the neurophysiological basis of seizure generalization. Finally, we explored the motor cortex plasticity in juvenile myoclonic epilepsy (JME), the most common subtype of GE in adults. We used the paired transcranial magnetic stimulation (paired-TMS) to investigate the time related changes in functional connectivity between visual and primary motor cortex in healthy subjects and in patients with photosensitivity to study the visuomotor integration. We also studied the interhemispheric connection involved in seizure generalization in FE and GE; to explore the motor cortex synaptic plasticity in patients with JME we used the paired associative stimulation.The findings support a physiologically relevant visuomotor functional connectivity, which likely contributes to visuomotor integration. Substantial physiologic changes in this network underlie the photosensitivity, which may justify the origin of epileptic motor phenomena (i.e. myoclonus). We found significant differences in the interhemispheric connection of drug-treated patients with FE and those with IGE. Whilst interhemispheric inhibition changes would not be crucial for the IGE pathophysiology, they may represent one key factor for the contralateral spread of focal discharges, and seizure generalization. As to the patients with JME, we provided evidence of a defective long term potentiation-like plasticity, which may be primarily involved in the pathogenesis of myoclonus. In conclusion, we documented substantial changes in the epileptogenic networks involved in different types of epilepsy.
2017
29
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11579/86981
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