Formation Of Epilepsy Research Articles

The effect of the HMGB1/RAGE/TLR4/NF-κB signalling pathway in patients with idiopathic epilepsy and its relationship with toxoplasmosis.

This study aims to investigate the relationship between toxoplasmosis and this pathway, which may be effective in the formation of epilepsy by acting through the HMGB1/RAGE/TLR4/NF-κB signalling pathway in patients with idiopathic epilepsy. In the study, four different experimental groups were formed by selecting Toxoplasma gondii IgG positive and negative patients with idiopathic epilepsy and healthy controls. Experimental groups were as follows: Group 1: Epilepsy+/Toxo- (E+, T-) (n = 10), Group 2: Epilepsy-/Toxo- (E-, T-) (n = 10), Group 3: Epilepsy-/Toxo+ (E-, T+) (n = 10), Group 4: Epilepsy+/Toxo+ (E+, T+) (n = 10). HMGB1, RAGE, TLR4, TLR1, TLR2, TLR3, IRAK1, IRAK2, IKBKB, IKBKG, BCL3, IL1β, IL10, 1 L8 and TNFα mRNA expression levels in the HMGB/RAGE/TLR4/NF-κB signalling pathway were determined by quantitative simultaneous PCR (qRT-PCR) after collecting blood samples from all patients in the groups. Statistical analysis was performed by one-way ANOVA followed by LSD post-hoc tests, and p < 0.05 was considered to denote statistical significance. The gene expression levels of HMGB1, TLR4, IL10, IL1B, IL8, and TLR2 were significantly higher in the G1 group than in the other groups (p < 0.05). In the G3 group, RAGE and BCL3 gene expression levels were significantly higher than in the other groups (p < 0.05). In the G4 group, however, IRAK2, IKBKB, and IKBKG gene expression levels were significantly higher than in the other groups (p < 0.05). HMGB1, TLR4, IRAK2, IKBKB, IL10, IL1B, IL1B, and IL8 in this signalling pathway are highly expressed in epilepsy patients in G1 and seizures occur with the stimulation of excitatory mechanisms by acting through this pathway. The signalling pathway in epilepsy may be activated by HMGB1, TLR4, and TLR2, which are considered to increase the level of proinflammatory cytokines. In T. gondii, this pathway is activated by RAGE and BCL3.

Effects of epilepsy control following decompressive craniectomy on mortality and morbidity in epileptic patients with malignant MCA infarction

Aim: The present study aims to investigate the effects of seizure or epilepsy formation on mortality and morbidity in epileptic patients after craniectomy.Material and Methods: The patients were divided into the following groups: Group 1, those who had no seizures, but were routinely treated with 3x100 mg of epanutin daily (n=6), Group 2, those who had at least one or multiple seizures and were initiated a second antiepileptic drug in addition to 3x100 mg of epanutin daily (n=13), and Group 3, those who had multiple seizures and who were sedated or narcotized in addition to being treated with 3x100 mg of epanutin daily (n=7). All patients underwent decompressive craniectomy within a maximum period of 48 hours and their characteristics such as age, gender, localization of infarct, hemiplegia, monoplegia, operation time, Glasgow coma and outcome scales were recorded. Results: According to the Glasgow Outcome Scale, 1 patient in Group 1, 8 patients in Group 2 and 6 patients in Group 3 died and there was a significant increase in patient losses in Group 2 and Group 3 compared to Group 1 (p0.05). 10 patients continued to live their lives with the support of home-care services and 2 patients with other forms of help. Conclusion: It was seen that there is a high incidence of seizure and epilepsy in MMCA infarcts after decompressive craniectomy and this significantly increased mortality or dysfunctional recovery if epilepsy could not be brought under control.

Basic cellular and molecular mechanisms of refractory epilepsy: a review of current hypotheses

Clarification of refractory epilepsy mechanisms is of great significance for its precise diagnosis and adequate therapeutic approach. This review presents current hypotheses of refractory epilepsy formation: 1. Hypothesis of genetic factors; 2. Hypothesis of multi-drug transporters; 3. Target hypothesis; 4. Hypothesis of mechanisms related to antiepileptic drugs – development of tolerance and ineffective mechanisms of action 5. Hypothesis of epilepsy related factors – seizure etiology, epilepsy progression, structural brain changes or neural net alterations. The latter hypothesis is closely related to the hypothesis of intrinsic severity as a determinant of antiepileptic drug resistance. A combination of mechanisms is also a possible explanation of refractoriness. Each of these hypotheses characterizes refractory epilepsy to a different extent without attaining an explicit and complex explanation of epileptogenesis.

The Role of bcl‐2 Family of Genes During Kindling

Several experimental models of human temporal lobe epilepsy have shown that apoptotic death of neurons is an important part of this degenerative disease. However, the role of apoptotic regulators is not clear during the epileptogenesis. Therefore we investigated the expression pattern of bcl-2 family of genes during the formation of kindling model of epilepsy in rats. We examined the expression pattern of bax, bcl-2, bcl-xL, mtd, and bcl-w both at messenger RNA (mRNA) and protein level in the brain tissues during the formation of epilepsy with kindling model in adult rats, which has been the most acceptable form of experimental model of human epilepsy. We also assessed the onset of DNA fragmentation by using the terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) assay. Animals have started to have epileptic discharges after day 10 of kindling model. Recurrent subthreshold electrical stimuli induced not only epileptic foci but also the expression of bax, an inducer of apoptosis, in this time period. Conversely, bcl-xL, which is an inhibitor of apoptosis, had an opposite pattern of expression both at mRNA and protein level during the formation of epilepsy. We did not observe DNA fragmentation by TUNEL staining. Our study shows differential expression of Bax and Bcl-xL at the CA1 region during the formation of hippocampal kindling model. The absence of DNA fragmentation during this period suggests that epileptic changes in neurons have the potential to induce DNA fragmentation by altering the expression levels of Bax and Bcl-xL.

Depressive effect of nicardipine on penicillin-induced epileptiform activity in rats

It is believed that calcium ions have very important role in the formation of epilepsy. Calcium ion flux into the cell leads to secretion of excitatory neurotransmitters. During epileptic seizures, routine balance of excitation and inhibition is altered towards the excitation. In present study, the effect of nicardipine on penicillin-induced epilepsy was investigated. The left cerebral cortex was exposed by craniotomy in anaesthetized rats. The epileptic focus was produced by injection of penicillin G potassium (500 units) into the somatomotor cortex. Microinjection of nicardipine into the same area caused an inhibition for 4-5 minutes in electrocorticograms (ECoG). The results of this study suggest that nicardipine may be an effective anticonvulsant agent in treatment of epilepsy by preventing calcium flux into the cell.

Depressive effect of nicardipine on penicillin‐induced epileptiform activity in rats

It is believed that calcium ions have very important role in the formation of epilepsy. Calcium ion flux into the cell leads to secretion of excitatory neurotransmitters. During epileptic seizures, routine balance of excitation and inhibition is altered towards the excitation. In present study, the effect of nicardipine on penicillin-induced epilepsy was investigated. The left cerebral cortex was exposed by craniotomy in anaesthetized rats. The epileptic focus was produced by injection of penicillin G potassium (500 units) into the somatomotor cortex. Microinjection of nicardipine into the same area caused an inhibition for 4-5 minutes in electrocorticograms (ECoG). The results of this study suggest that nicardipine may be an effective anticonvulsant agent in treatment of epilepsy by preventing calcium flux into the cell.