Browsing by Author "Eskazan, Esat"

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    Are Absence and Limbic Seizures Mutually Exclusive?: An Experimental Approach to Enigmatic Clinical Concept
    (GEORG THIEME VERLAG KG, 2021-01-01) Onat, Filiz Yilmaz; Eskazan, Esat
    The impressive advances in the several disciplines including neurophysiology, molecular biology, neuroimmunology, neurogenetics, neuroimaging, and neuropharmacology of epilepsies have been stimulating a mutual interaction among basic scientists, clinicians, and professionals from other disciplines, leading to the identification of clinical questions and then the design of basic science paradigms to test enigmatic clinical issues. Based on a clinical observation that the coexistence of genetic (idiopathic) generalized typical absence and mesial temporal lobe epilepsy in the same patient is extremely rare and debatable, we addressed the rare coexistence in the same individual, designed an experimental approach to test the validity of this clinical concept and to study the underlying mechanisms involved. Here we presented evidence of a mutual cross-interaction in the circuits involved in typical absence and temporal lobe epilepsy. This article delineates a phenomenological picture and comprehends a theoretical understanding of a mutual cross-interaction in typical absence as a representative of genetic generalized epilepsies and limbic epilepsy in which seizures often start from the mesial temporal lobe.
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    Pharmacologically induced absence seizures versus kindling in Wistar rats
    (KARE PUBL, 2020-01-01) Carcak, Nihan; Sahiner, Melike; Akman, Ozlem; Idrizoglu, Medine Gulcebi; Cortez, Miguel A.; Snead, O. Carter; Eskazan, Esat; Onat, Filiz
    OBJECTIVE: This study aimed to investigate the effects of gamma-butyrolactone (GBL), a prodrug of gamma-Hydroxybutyric acid-induced absence seizures on the development of kindling in Wistar rats. METHODS: Three groups of adult male Wistar rats under anesthesia were implanted with bilateral cortical recording elec- trodes for the GBL group (GBL) and/or bipolar stimulation electrodes into the right basolateral amygdala for the Kindling group (KI) alone and Kindling plus GBL group (GBL+KI). Rats in the KI and GBL+KI groups were stimulated twice daily at the afterdischarge threshold until they reached Racine's stage 5 seizure state. The animals in the GBL + group had an i.p injection of GBL 20 minutes before each electrical stimulation, and the effects of GBL-induced seizures on the development of kindling were investigated. The animals in the GBL group were injected GBL twice daily i.p. for 15 days without receiving any electrical stimulation. RESULTS: The KI animals reached stage 5 seizure stage at 12th stimulations, whereas the GBL+KI rats reached at 27th stimulations. The mean numbers of stimulations needed for the development of the first stage 3, 4, or 5 generalized seizures were significantly higher in the GBL+KI group than the KI group. CONCLUSION: The resistance to amygdala kindling in the GBL model can be modulated by the absence seizure mechanism alone, without the intervention of an abnormal genetic background.