Epileptic Studies Research Articles

Sida cordifolia Linn- An widely used herbs in the village of Falta, west Bengal, India: Pharmacological evaluation of antiepileptic activity of root extract of Sida cordifolia Linn.

As per the observation of the social work activitist it was found that the raw extract of the root of Sida cordifolia Linn. Are been used by some old people in the village of Falta Block of South 24 PGS district of West Bengal, India to treat epileptic attack on some villagers. The identified plant were collected and handed over the research scientists for the further study. The dried coarse powder of the root of Sida cordifolia Linn. Were soxheleted successively with petroleum ether (PESC), methanol (MESE), with boiled water (AESC) and the epileptic study was performed on the Albino mice using 100 and 300 mg/kg body weight of PESC, MESE and using clonazepam as standard using Maximum Electroshock induced seizure model and result depicted that PESC exhibited a significant antiepileptic effect at both low and high doses where as MESC exhibited the significant antiepileptic effect only at high dose. Hence, the petroleum ether extract may be chosen to be more effective than that of the methanol extract.

A New Signal Processing Approach for Discrimination of EEG Recordings

Classifying brain activities based on electroencephalogram (EEG) signals is one of the important applications of time series discriminant analysis for diagnosing brain disorders. In this paper, we introduce a new method based on the Singular Spectrum Analysis (SSA) technique for classifying brain activity based on EEG signals via an application into a benchmark dataset for epileptic study with five categories, consisting of 100 EEG recordings per category. The results from the SSA based approach are compared with those from discrete wavelet transform before proposing a hybrid SSA and principal component analysis based approach for improving accuracy levels further.

Sensitivity analyses for partially observed recurrent event data.

Recurrent events involve the occurrences of the same type of event repeatedly over time and are commonly encountered in longitudinal studies. Examples include seizures in epileptic studies or occurrence of cancer tumors. In such studies, interest lies in the number of events that occur over a fixed period of time. One considerable challenge in analyzing such data arises when a large proportion of patients discontinues before the end of the study, for example, because of adverse events, leading to partially observed data. In this situation, data are often modeled using a negative binomial distribution with time-in-study as offset. Such an analysis assumes that data are missing at random (MAR). As we cannot test the adequacy of MAR, sensitivity analyses that assess the robustness of conclusions across a range of different assumptions need to be performed. Sophisticated sensitivity analyses for continuous data are being frequently performed. However, this is less the case for recurrent event or count data. We will present a flexible approach to perform clinically interpretable sensitivity analyses for recurrent event data. Our approach fits into the framework of reference-based imputations, where information from reference arms can be borrowed to impute post-discontinuation data. Different assumptions about the future behavior of dropouts dependent on reasons for dropout and received treatment can be made. The imputation model is based on a flexible model that allows for time-varying baseline intensities. We assess the performance in a simulation study and provide an illustration with a clinical trial in patients who suffer from bladder cancer.

The rearrangement of synaptic actin networks after pilocarpine-induced status epilepticus and pentylenetetrazol-induced kindling

Post status epilepticus (SE) and chemical kindling are two widely used animal models for epileptic studies The pilocarpine-treated C57BL/6 mice exhibited stereotypical alterations of F-actin networks, including a severe reduction of F-actin in area CA1-CA3 and in the hilum. By contrast, F-actin networks seemed less affected by pentylenetetrazol kindling, and almost no remarkable alterations were noted in area CA1 or in the hilum. The overall labeling of F-actin in the hippocampus was generally consistent with the pathological observations on dendritic spines reported in both the epileptic models. Because the reorganized F-actin network can lead to long-term stabilization of synaptic changes and to consolidation of the enhanced neuronal activity, the alterations of F-actin networks may be related to the aberrant hyperexcitability in the epileptic animals.

Convulsant agent pentylenetetrazol does not alter the structural and dynamical properties of dipalmitoylphosphatidylcholine model membranes

Pentylenetetrazol (PTZ) is an epileptogenic agent, which is widely used in the determination of epilepsy-induced alterations and in the assessment of anticonvulsant agents in epileptic studies. Even though PTZ is suggested to induce repetitive firing of nerve fibers and shorten the refractory, its mechanism of action is only partially understood. In the literature there are discrepancies for its action mechanism. While some studies stated that primary sites of PTZ are membrane proteins, some reports indicated that PTZ acts on membrane lipids. In order to gain new insight for this we tested the possibility of interaction of PTZ with a simplified model system called dipalmitoylphosphatidylcholine (DPPC) multilamellar vesicles (MLVs) at agent concentrations (0–24 mol%) using differential scanning calorimetry (DSC), Fourier transform infrared (FTIR), electron spin resonance (ESR) and steady-state fluorescence spectroscopy. The results showed that PTZ at concentrations used (1–24 mol%), does not cause any significant change in lipid phase behavior, lipid dynamics (fluidity), lipid acyl chain flexibility (order), hydration state of the head group and/or the region near the head group of DPPC MLVs. These results clearly revealed that PTZ does not change the structural and dynamical parameters of neutral DPPC lipid vesicles and does not locate within the bilayer.