Pharmacological inhibition of ictal and interictal epileptiform discharges

Background: epilepsy is a brain disorder characterized by an enduring predisposition to generate epileptic seizures. Seizures are a transient occurrence of signs and/or symptoms due to abnormal excessive and synchronous neuronal activity in the brain. Electroencephalogram (EEG), a non-invasive instrumental test, has an important role in the diagnosis of epilepsy, as well as in monitoring the results and long-term treatment because it can detect interictal and ictal discharges that are crucial for confirmation and classification of seizures. Antiepileptic drugs are the first treatment option in patients with epilepsy, although the effectiveness of such drugs is limited only to symptom control and requires a regular intaking by the patient. These drugs exploit the cell membrane channels, modifying their permeability, allowing either an increase in the inhibitory neurotransmission or the reduction in the excitatory one, by hyperpolarizing neurons and avoiding the recurrence of the epileptic seizures without reversing or stopping the underlying mechanism of epileptogenesis. Materials and Methods: the internship took place in the Neurophysiopathology department of the Antonio, Biagio and Cesare Arrigo’s hospital in Alessandria, from October 2022 to March 2023. During this period, it was possible to attend the emergency treatment of prolonged and recurrent epileptic seizures during EEGrafic recording and the consequential amendments of the ictal discharges induced by the administration of antiepileptic drugs. Follow up EEG was also performed to investigate the modifications of interictal activity after a period of treatment with antiepileptic drugs. The patient who has been analyzed in this paper, underwent EEG recordings obtained by using bridge electrodes placed on the scalp according to the international 10-20 system. Objectives: the aim of this study is to analyze the mechanisms of action of the main antiepileptic drugs, in relation to the physiological cellular mechanisms regulating the neuronal excitability and their effect on the ictal and interictal epileptiform discharges in the EEG recordings.