Journal articles: 'Drug-resistance epilepsy'

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Gorter, Jan, and Heidrun Potschka. "Drug resistance in epilepsy." Epilepsia 51 (December 2010): 91. http://dx.doi.org/10.1111/j.1528-1167.2010.02877.x.

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Sisodiya, S. M., W. ‐R Lin, B. N. Harding, M. V. Squier, and M. Thom. "Drug resistance in epilepsy: expression of drug resistance proteins in common causes of refractory epilepsy." Brain 125, no. 1 (January 1, 2002): 22–31. http://dx.doi.org/10.1093/brain/awf002.

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Millichap, J. Gordon. "Drug Resistance Proteins and Refractory Epilepsy." Pediatric Neurology Briefs 16, no. 2 (February 1, 2002): 16. http://dx.doi.org/10.15844/pedneurbriefs-16-2-11.

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Koepp, Matthias J. "Neuroimaging of drug resistance in epilepsy." Current Opinion in Neurology 27, no. 2 (April 2014): 192–98. http://dx.doi.org/10.1097/wco.0000000000000072.

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Sisodiya, Sanjay M. "Genetics of drug resistance in epilepsy." Current Neurology and Neuroscience Reports 5, no. 4 (August 2005): 307–11. http://dx.doi.org/10.1007/s11910-005-0076-2.

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French, Jacqueline A. "The Role of Drug-Resistance Proteins in Medically Refractory Epilepsy." Epilepsy Currents 2, no. 5 (September 2002): 166. http://dx.doi.org/10.1111/j.1535-7597.2002.00062.x.

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Drug Resistance in Epilepsy: Expression of Drug-resistance Proteins in Common Causes of Refractory Epilepsy Sisodiya SM, Lin WR, Harding BN, Squier MV, Thom M. Brain 2002;125(Pt 1):22–31 Epilepsy is resistant to drug treatment in about one third of cases, but the mechanisms underlying this drug resistance are not understood. In cancer, drug resistance has been studied extensively. Among the various resistance mechanisms, overexpression of drug-resistance proteins, such as multidrug resistance gene-1 P-glycoprotein (MDR1) and multidrug resistance–associated protein 1 (MRP1), has been shown to correlate with cellular resistance to anticancer drugs. Previous studies in human epilepsy have shown that MDR1 and MRP1 also may be overexpressed in brain tissue from patients with refractory epilepsy; expression has been shown in glia and neurons, which do not normally express these proteins. We examined expression of MDR1 and MRP1 in refractory epilepsy from three common causes, dysembryoplastic neuroepithelial tumors (DNTs; eight cases), focal cortical dysplasia (FCD; 14 cases), and hippocampal sclerosis (HS; eight cases). Expression was studied immunohistochemically in lesional tissue from therapeutic resections and compared with expression in histologically normal adjacent tissue. With the most sensitive antibodies, in all eight DNT cases, reactive astrocytes within tumor nodules expressed MDR1 and MRP1. In five of eight HS cases, reactive astrocytes within the gliotic hippocampus expressed MDR1 and MRP1. Of 14 cases of FCD, MDR1 and MRP1 expression was noted in reactive astrocytes in all cases. In five FCD cases, MRP1 expression also was noted in dysplastic neurons. In FCD and DNTs, accentuation of reactivity was noted around lesional vessels. Immunoreactivity was always more frequent and intense in lesional reactive astrocytes than in glial fibrillary acidic protein–positive reactive astrocytes in adjacent histologically normal tissue. MDR1 is able to transport some antiepileptic drugs (AEDs), and MRP1 also may do so. The overexpression of these drug-resistance proteins in tissue from patients with refractory epilepsy suggests one possible mechanism for drug resistance in patients with these pathologies. We propose that overexpressed resistance proteins reduce the interstitial concentration of AEDs in the vicinity of the epileptogenic pathology and thereby render the epilepsy caused by these pathologies resistant to treatment with AEDs. P-Glycoprotein and Multidrug Resistance–associated Protein Are Involved in the Regulation of Extracellular Levels of the Major Antiepileptic Drug Carbamazepine in the Brain Potschka H, Fedrowitz M, Loscher W. Neuroreport 2001;12:3557–3560 Despite considerable advances in the pharmacotherapy of epilepsy, about 30% of epilepsy patients are refractory to antiepileptic drugs (AEDs). In most cases, a patient who is resistant to one major AED also is refractory to other AEDs, although these drugs act by different mechanisms. The mechanisms that lead to drug resistance in epilepsy are not known. Recently, overexpression of multidrug transporters, such as P-glycoprotein (PGP) and multidrug resistance–associated protein (MRP), has been reported in surgically resected epileptogenic human brain tissue and suggested to contribute to the drug resistance of epilepsy. However, it is not known to what extent multidrug transporters such as PGP or MRP are involved in transport of AEDs. In the present study, we used in vivo microdialysis in rats to study whether the concentration of carbamazepine in the extracellular fluid of the cerebral cortex can be enhanced by inhibition of PGP or MRP, using the PGP inhibitor verapamil and the MRP inhibitor probenecid. Local perfusion with verapamil or probenecid via the microdialysis probe increased the extracellular concentration of carbamazepine. The data indicate that both PGP and MRP participate in the regulation of extracellular brain concentrations of the major AED carbamazepine.

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Rohracher, Alexandra, Judith Dobesberger, Claudia A. Granbichler, Julia Höfler, Giorgi Kuchukhidze, Martin Ortler, Iris Unterberger, Gerald Walser, Aljoscha Thomschewski, and Eugen Trinka. "The ILAE definition of drug resistant epilepsy and its clinical applicability compared with “older” established definitions." Journal of Epileptology 23, no. 1 (June 1, 2015): 39–44. http://dx.doi.org/10.1515/joepi-2015-0025.

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SUMMARY Background. Early identification of potential epilepsy surgery candidates is essential to the treatment process. Aim. To evaluate the clinical applicability of the ILAE definition of drug resistant epilepsy and its potential in identifying surgical candidates earlier compared to three established “older” definitions of drug resistant epilepsy. Material and Methods. Retrospective analysis of 174 patients who underwent epilepsy surgery between 1998 and 2009. Clinical factors and course of disease were extracted from patients' charts. Drug resistant epilepsy was classified according to four definitions and the time until fulfillment of criteria compared. Results. Mean time to fulfillment of criteria of drug resistant epilepsy ranged from 11.8 (standard deviation (SD) 9.8) to 15.6 years (SD 11.3). Time to drug resistance was significantly longer applying the only definition, requiring failure of three antiepileptic drugs (AEDs) (Canada definition), whereas time to fulfillment of all other definitions did not differ. Fifty percent of all patients experienced a seizure free period of ≥1 year prior to being classified as drug resistant, 13% entered another 1-year remission after fulfilling any criteria for drug resistance. Conclusion. We conclude that the ILAE definition identifies drug resistant epilepsy, with similar latency like two of three formerly used definitions. It is an easy applicable tool to minimize the delay of referral to a specialized center. Intermittent remissions delay assessment of drug resistance for all definitions and 13% of patients enter a remission despite established drug resistance.

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Malyshev, S. M., T. M. Alekseeva, W. A. Khachatryan, and M. M. Galagudza. "Pathogenesis of drug resistant epilepsy." Epilepsia and paroxysmal conditions 11, no. 1 (April 27, 2019): 79–87. http://dx.doi.org/10.17749/2077-8333.2019.11.1.79-87.

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Pharmacotherapy is the first-line treatment modality for epilepsy. However, in 20-40% of patients, epilepsy is resistant to pharmacotherapy. These numbers have not changed for decades despite the development and use of antiepileptic drugs with novel mechanisms of action. Drug-resistant epilepsy is now considered a separate pathophysiologic and clinical entity. The existing hypotheses on its pathogenesis could be divided in two groups. Firstly, drug-resistance might be caused by an abnormal pharmacokinetics or pharmacodynamics of antiepileptic drugs as a result of congenital or acquired dysfunction of the transporter or receptor proteins. Secondly, it might be a consequence of inherent features of epilepsy per se, such as the so-called “intrinsic severity” or some disorder of the connectome. Taking into account the complexity of this phenomenon, the issue of drug resistance continues to remain in the focus of the current research efforts.

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Xiong, Jie, Ding-an Mao, and Li-qun Liu. "Research Progress on the Role of ABC Transporters in the Drug Resistance Mechanism of Intractable Epilepsy." BioMed Research International 2015 (2015): 1–10. http://dx.doi.org/10.1155/2015/194541.

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The pathogenesis of intractable epilepsy is not fully clear. In recent years, both animal and clinical trials have shown that the expression of ATP-binding cassette (ABC) transporters is increased in patients with intractable epilepsy; additionally, epileptic seizures can lead to an increase in the number of sites that express ABC transporters. These findings suggest that ABC transporters play an important role in the drug resistance mechanism of epilepsy. ABC transporters can perform the funcions of a drug efflux pump, which can reduce the effective drug concentration at epilepsy lesions by reducing the permeability of the blood brain barrier to antiepileptic drugs, thus causing resistance to antiepileptic drugs. Given the important role of ABC transporters in refractory epilepsy drug resistance, antiepileptic drugs that are not substrates of ABC transporters were used to obtain ABC transporter inhibitors with strong specificity, high safety, and few side effects, making them suitable for long-term use; therefore, these drugs can be used for future clinical treatment of intractable epilepsy.

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Yegorova, N. V., and N. N. Maslova. "Therapy of epilepsy: analysis of pseudo-drug resistance." Bulletin of Siberian Medicine 7, no. 5-1 (December 30, 2008): 132–34. http://dx.doi.org/10.20538/1682-0363-2008-5-1-132-134.

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Sisodiya, Sanjay. "Drug resistance in epilepsy: not futile, but complex?" Lancet Neurology 2, no. 6 (June 2003): 331. http://dx.doi.org/10.1016/s1474-4422(03)00402-2.

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Odintsova, G., W. Khachatryan, and V. Guzeva. "Catamenial epilepsy as a predictor of drug resistance." Journal of the Neurological Sciences 357 (October 2015): e153-e154. http://dx.doi.org/10.1016/j.jns.2015.08.519.

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Sivakova, N., and E. Korsakova. "P.165 Neurophysiological correlates of drug-resistance epilepsy." European Neuropsychopharmacology 40 (November 2020): S96. http://dx.doi.org/10.1016/j.euroneuro.2020.09.128.

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Bazhanova, Elena D., Alexander A. Kozlov, and Anastasia V. Litovchenko. "Mechanisms of Drug Resistance in the Pathogenesis of Epilepsy: Role of Neuroinflammation. A Literature Review." Brain Sciences 11, no. 5 (May 19, 2021): 663. http://dx.doi.org/10.3390/brainsci11050663.

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Epilepsy is a chronic neurological disorder characterized by recurring spontaneous seizures. Drug resistance appears in 30% of patients and it can lead to premature death, brain damage or a reduced quality of life. The purpose of the study was to analyze the drug resistance mechanisms, especially neuroinflammation, in the epileptogenesis. The information bases of biomedical literature Scopus, PubMed, Google Scholar and SciVerse were used. To obtain full-text documents, electronic resources of PubMed Central and Research Gate were used. The article examines the recent research of the mechanisms of drug resistance in epilepsy and discusses the hypotheses of drug resistance development (genetic, epigenetic, target hypothesis, etc.). Drug-resistant epilepsy is associated with neuroinflammatory, autoimmune and neurodegenerative processes. Neuroinflammation causes immune, pathophysiological, biochemical and psychological consequences. Focal or systemic unregulated inflammatory processes lead to the formation of aberrant neural connections and hyperexcitable neural networks. Inflammatory mediators affect the endothelium of cerebral vessels, destroy contacts between endothelial cells and induce abnormal angiogenesis (the formation of “leaky” vessels), thereby affecting the blood–brain barrier permeability. Thus, the analysis of pro-inflammatory and other components of epileptogenesis can contribute to the further development of the therapeutic treatment of drug-resistant epilepsy.

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Margineanu, Doru Georg, and Henrik Klitgaard. "Mechanisms of drug resistance in epilepsy: relevance for antiepileptic drug discovery." Expert Opinion on Drug Discovery 4, no. 1 (December 15, 2008): 23–32. http://dx.doi.org/10.1517/17460440802611729.

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Mangunatmadja, Irawan, Raden Muhammad Indra, Dwi Putro Widodo, and Achmad Rafli. "Risk Factors for Drug Resistance in Epileptic Children with Age of Onset above Five Years: A Case-Control Study." Behavioural Neurology 2021 (November 10, 2021): 1–7. http://dx.doi.org/10.1155/2021/9092824.

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Background. Children with epilepsy with onset above five years encompass distinct epidemiological and clinical characteristics that may have specific risk factors for resistance to antiseizure medications (ASMs). Studies on this age group are limited. Purpose. To identify risk factors for drug resistance in children with epilepsy with the age of onset above five years. Methods. A case-control study was conducted on children with epilepsy with the age of onset above five years visiting the Pediatric Neurology Clinic of Cipto Mangunkusumo and Mohammad Hoesin Hospital between September 2015 and August 2016. Cases consisted of drug-resistant children while control consisted of drug-responsive children according to 2010 ILAE classification. Risk factors studied include onset, number of seizures, illness duration before treatment, cause, seizure type, status epilepticus, initial and evolution of EEG, brain imaging, and initial treatment response. Results. Thirty-two pairs of children were included in the study. After logistic regression analysis, symptomatic etiology and failure to achieve early response to treatment were found to be associated with drug resistance with adjusted OR of 84.71 (95% CI: 5.18-1359.15) and 72.55 (95% CI: 7.08-743.85), respectively. Conclusion. Poor initial response to ASM and symptomatic etiology are independent risk factors for drug resistance in children with epilepsy with the age of onset above five years.

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Zaer, Nael Husain. "Drug Resistant Epilepsy Among Patients Attended The Neurosciences Hospital." AL-Kindy College Medical Journal 13, no. 1 (November 21, 2019): 108–15. http://dx.doi.org/10.47723/kcmj.v13i1.138.

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Background: Drug resistant epilepsy is defined as failure of adequate trials of two tolerated, appropriately chosen and used antiepileptic drug schedules to achieve sustained seizure freedom. Up to 30% of patients referred to clinics with a diagnosis of pharmaco-resistant epilepsy may have been misdiagnosed, and many can be helped by optimizing their treatment.Pseudoresistance, in which seizures persist because the underlying disorder has not been adequately or appropriately treated, must be ruled out or corrected before drug treatment can be considered to have failed. Objectives: The objectives of this study were to determine the causes of drug failure in patients with epilepsy and to differentiate between drug resistant epilepsy and pseudoresistant epilepsy. Type of the study: This is a retrospective study. Method: It is conducted in Baghdad governorate at the epilepsy clinic in the neurosciences hospital during the period from the 1st of February through July 2013. Two hundred patients with refractory epilepsy were involved. These patients attended the epilepsy clinic during 2011 and 2012. The data was collected from the files of the patients including age, gender, weight, history of presenting illness, type of seizure, drugs used, duration of disease, EEG and imaging findings, compliance and follow up. Results: Drug resistance epilepsy constituted a prevalence of 24% (128) as the total number of patients with epilepsy attending the hospital during the same period was 527.The mean age of patients with refractory epilepsy was 25 years. Male were 56.5% (113/200) and urban residents were 70.5% (141/200). The study revealed that 64% (128/200) of refractory epilepsy was attributed to drug resistance; while the remaining proportion was pseudoresistance 36% (72/200). The main cause of pseudoresistance was poor compliance 36.1% (26/72).The most common type of seizure in the sampled patients was generalized tonic clonic seizures in 51.5% (103/200).Compliance was found to be statistically associated with abnormal EEG finding, past medical history (hypertension, cardiac diseases, encephalitis, diabetes mellitus and any significant history) and quality of follow up. The follow-up was found to be statistically associated with the family history, past medical history( encephalitis and hypertension) and compliance of patient. Conclusion:A considerable number of patientsdiagnosed as cases of drug resistant epilepsy had another explanation causing drug failure.The study recommends the application of consensus definition for drug resistant epilepsy and periodic evaluation of patients with drug resistant epilepsy to exclude pseudoresistance.

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Lattanzi, Simona, Claudia Rinaldi, Claudia Cagnetti, Nicoletta Foschi, and Mauro Silvestrini. "Can we predict drug resistance in post-stroke epilepsy." Journal of the Neurological Sciences 429 (October 2021): 117844. http://dx.doi.org/10.1016/j.jns.2021.117844.

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Feldmann, Maria, and Matthias Koepp. "ABC Transporters and Drug Resistance in Patients with Epilepsy." Current Pharmaceutical Design 22, no. 38 (November 30, 2016): 5793–807. http://dx.doi.org/10.2174/1381612822666160810150416.

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Gelisse, P. "Clinical factors of drug resistance in juvenile myoclonic epilepsy." Journal of Neurology, Neurosurgery & Psychiatry 70, no. 2 (February 1, 2001): 240–43. http://dx.doi.org/10.1136/jnnp.70.2.240.

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Zhang, Lin, Xi Zhu, Anjiao Peng, Wanlin Lai, Shixu He, Xiangmiao Qiu, Xiaoyi Zou, and Lei Chen. "Predictors of drug-resistance in epilepsy with auditory features." Epilepsy Research 164 (August 2020): 106353. http://dx.doi.org/10.1016/j.eplepsyres.2020.106353.

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Binder, Devin K. "Mechanisms of Drug Resistance in Epilepsy: Lessons from Oncology." Drug Discovery Today 7, no. 24 (December 2002): 1205. http://dx.doi.org/10.1016/s1359-6446(02)02441-8.

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Schmidt, Dieter, and Wolfgang Loscher. "Drug Resistance in Epilepsy: Putative Neurobiologic and Clinical Mechanisms." Epilepsia 46, no. 6 (June 2005): 858–77. http://dx.doi.org/10.1111/j.1528-1167.2005.54904.x.

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Sisodiya, Sanjay M., and David B. Goldstein. "Drug resistance in epilepsy: More twists in the tale." Epilepsia 48, no. 12 (December 10, 2007): 2369–70. http://dx.doi.org/10.1111/j.1528-1167.2007.01260_1.x.

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Remy, Stefan, Siegrun Gabriel, Bernd W. Urban, Dirk Dietrich, Thomas N. Lehmann, Christian E. Elger, Uwe Heinemann, and Heinz Beck. "A novel mechanism underlying drug resistance in chronic epilepsy." Annals of Neurology 53, no. 4 (March 24, 2003): 469–79. http://dx.doi.org/10.1002/ana.10473.

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Emich-Widera, Ewa, Wirginia Likus, Beata Kazek, Paweł Niemiec, Anna Balcerzyk, Aleksander L. Sieroń, and Iwona Żak. "CYP3A5*3 and C3435T MDR1 Polymorphisms in Prognostication of Drug-Resistant Epilepsy in Children and Adolescents." BioMed Research International 2013 (2013): 1–7. http://dx.doi.org/10.1155/2013/526837.

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Drug-resistant epilepsies still remain one of the most profound problems of contemporary epileptology. Several mechanisms of drug resistance are possible; among them, genetic factors have a prominent place. Much importance is attached to genes, which encode enzymes that metabolize antiepileptic drugs CYP 3A, which belong to the family of cytochromes P450 and the genome of multidrug resistance, such as multidrug resistance 1 (MDR1) that expresses P-glycoprotein (P-gp), a drug transporter protein. The aim of the study was to assess the relation between polymorphism of gene CYP3A5 and polymorphism C3435T of MDR1 gene with the occurrence of focal, drug-resistant epilepsy in children and youths up to 18 years of age. The study comprised 85 patients, and their age range was from 33 months to 18 years of age, suffering from epilepsy, partly responding well to treatment, partly drug resistant. The polymorphism of both genes has been analysed using the PCR-RFLP method. The study failed to corroborate association between polymorphism CYP3A5*3 and C3435T polymorphism in MDR1 gene and pharmacoresistant epilepsy. The results of our research do not confirm the prognostic value of the polymorphisms examined in the prognostication of drug resistance in epilepsies.

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Dubenko, A. Ye, and M. V. Naboka. "Management of symptomatic epilepsy after surgery due to drug resistance." INTERNATIONAL NEUROLOGICAL JOURNAL 17, no. 3 (June 11, 2021): 18–24. http://dx.doi.org/10.22141/2224-0713.17.3.2021.231571.

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The issue of managing patients who were operated due to drug resistance has not been accomplished not only in Ukraine, but throughout the world. But these patients exist, their number is growing, and the neurologists who observe them need a direct understanding of this process. Nowadays, there is no enough evidence base to substantiate rational recommendations regarding the post-surgical drug treatment. Despite the fact that the International League Against Epilepsy (ILAE) classification and the classification previously proposed by J. Engel Jr have many headings that indicate the improvement of patients and possible improvement in their quality of life, the treatment that has achieved seizure control can be considered successful only in patients who meet qualification point 1 according to the ILAE classification or IA according to the Engel classification, and only those who meet these criteria for at least one year. This understanding is very important when choosing further therapeutic management. Taking into account the fact that after surgical treatment the drug resistance should be overcome, further drug treatment should be carried out in the same way as in patients without drug resistant epilepsy. The issue of managing people with epilepsy who received surgical treatment due to drug resistance requires further studies, especially in the context of an increase in the number of such patients. The authors indicate that all the questions and aspects that were presented in the work are controversial and can be adjusted depending on the clinical situation.

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Biketov, Oleg. "DRUG-RESISTANT EPILEPSY IN CASE OF CRANIOCEREBRAL DISPROPORTION. A PILOT STUDY." Manual Therapy 83, no. 3 (October 31, 2021): 19–23. http://dx.doi.org/10.54504/1684-6753-2021-83-3-19-23.

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The problem of ineff ective drug therapy of epilepsy continues to be relevant during many decades and determines many key research trends in clinical and fundamental epileptology. Despite the emergence of a large number of various antiepileptic drugs the eff ectiveness of drug therapy for epilepsy has remained almost unchanged over the past decades. In this article drug-resistance in epilepsy is considered as a consequence of a concomitant pathological process in the form of craniocerebral disproportion.

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French, Jacqueline A. "Response to Early AED Therapy and Its Prognostic Implications." Epilepsy Currents 2, no. 3 (May 2002): 69–71. http://dx.doi.org/10.1111/j.1535-7597.2002.00025.x.

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Determining the prognosis of patients when they first present with epilepsy is a difficult task. Several clinical studies have shed light on this very important topic. Potential predictors of the refractory state, including seizure etiology, duration of epilepsy before treatment, and epilepsy type, have not been successful indicators of long-term outcome. One predictor of the refractory state appears to be early response to AED therapy. Inadequate seizure control after initial treatment is a poor prognostic sign. Recent research into genetic causes of the refractory state has included investigation of the multiple drug resistance gene, and polymorphisms at drug targets. More work is needed to determine the causes and predictors of drug resistance.

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Hao, Xiao-Ting, and Patrick Kwan. "Update and Overview of the International League Against Epilepsy Consensus Definition of Drug-resistant Epilepsy." US Neurology 06, no. 02 (2010): 122. http://dx.doi.org/10.17925/usn.2010.06.02.122.

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Drug-resistant epilepsy remains a major clinical challenge. Diverse criteria have been used to define drug resistance by different researchers, making it difficult or even impossible to compare the results across different studies. To improve patient care and facilitate clinical research, the International League Against Epilepsy (ILAE) recently proposed a consensus definition to define drug-resistant epilepsy. This is the failure of adequate trials of two tolerated, appropriately chosen and used antiepileptic drug schedules (whether as monotherapies or in combination) to achieve sustained seizure freedom. This article outlines the framework of the consensus definition, explains how to apply it in practice, and discusses the future development of its use.

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Hao, Xiao-Ting, and Patrick Kwan. "Update and Overview of the International League Against Epilepsy Consensus Definition of Drug-resistant Epilepsy." European Neurological Review 6, no. 1 (2011): 57. http://dx.doi.org/10.17925/enr.2011.06.01.57.

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Drug-resistant epilepsy remains a major clinical challenge. Diverse criteria have been used to define drug resistance by different researchers, making it difficult or even impossible to compare the results across different studies. To improve patient care and facilitate clinical research, the International League Against Epilepsy (ILAE) recently proposed a consensus definition to define drug-resistant epilepsy. This is the failure of adequate trials of two tolerated, appropriately chosen and used antiepileptic drug schedules (whether as monotherapies or in combination) to achieve sustained seizure freedom. This article outlines the framework of the consensus definition, explains how to apply it in practice and discusses the future development of its use.

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Algahtani, Rami, Qamar ALhothaly, Raghd Alabdullah, Omniyh Fatani, Asmaa Alsaeigh, Amal Alamri, Abdullah Tawakul, and Jihad Muglan. "Knowledge and awareness toward surgical treatment of epilepsy among medical students at Umm Al-Qura University." SAGE Open Medicine 10 (January 2022): 205031212211460. http://dx.doi.org/10.1177/20503121221146065.

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Objective: This study aims to evaluate knowledge and awareness toward surgical treatment of epilepsy among medical students at Umm Al-Qura University. Methods: A survey composed of 10 questions was distributed to medical students concerning surgical neurological disorders. It was used to collect data from 401 samples. Questions addressed general knowledge of epilepsy surgery and drug-resistant epilepsy, students’ attitude toward epilepsy surgery, and techniques. The chi-square test was utilized. Results: The familiar surgical techniques were lobectomy (11.2%), followed by hemispherotomy (8.2%). The term “drug-resistant epilepsy” was known to 24.4%. More than half of the students 259 (64.6%) would refer patients with drug-resistant epilepsy to a neurosurgeon and neurologist, knowledge and awareness of epilepsy surgery were high for 30.7% of students. Statistically, significant relationship was observed between the level of awareness and academic years ( p = 0.000131). Conclusions: Medical students have a positive attitude toward epilepsy surgery. Students are less aware of drug resistance in epilepsy. Knowledge and awareness were better among students at higher levels. We conclude that highlighting the importance of epilepsy surgery should be continued. Moreover, additional educational effort should be invested in expressing the term drug-resistant epilepsy.

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Panina, Yulia S., Elena E. Timechko, Anna A. Usoltseva, Kristina D. Yakovleva, Elena A. Kantimirova, and Diana V. Dmitrenko. "Biomarkers of Drug Resistance in Temporal Lobe Epilepsy in Adults." Metabolites 13, no. 1 (January 4, 2023): 83. http://dx.doi.org/10.3390/metabo13010083.

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Temporal lobe epilepsy (TLE) is the most common type of focal epilepsy in adults. Experimental and clinical data indicate that neuroinflammation and neurodegeneration accompanying epileptogenesis make a significant contribution to the chronicity of epilepsy and the development of drug resistance in TLE cases. Changes in plasma and serum concentrations of proteins associated with neuroinflammation and neurodegeneration can be predictive biomarkers of the course of the disease. This study used an enzyme-linked immunosorbent assay of the following plasma proteins: brain-derived neurotrophic factor (BDNF), tumor necrosis factor alpha (TNFa), and high-mobility group protein B1 (HMGB1) in patients with mesial TLE to search for biomarkers of the disease. The objective of the study was to examine biomarkers of the neuroinflammation and neurodegeneration of plasma: BDNF, TNFa, and HMGB1. The aim of the study was to identify changes in the concentration of circulating pro-inflammatory and neurotrophic factors that are prognostically significant for the development of drug resistance and the course of TLE. A decrease in the concentration of BDNF, TNFa, and HMGB1 was registered in the group of patients with TLE compared with the control group. A significant decrease in the concentration of HMGB1 in patients with drug-resistant TLE was observed. Aberrations in plasma concentrations of BDNF, TNFa, and HMGB1 in patients with TLE compared with the controls have been confirmed by earlier studies. A decrease in the expression of the three biomarkers may be the result of neurodegenerative processes caused by the long course of the disease. The results of the study may indicate the acceptability of using HMGB1 and TNFa as prognostic biological markers to indicate the severity of the disease course and the risk of developing drug resistance.

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Almanbekova, Aiperi. "A Review of Clinical Management of Drug Resistant Epilepsy." International Journal of Health Sciences and Research 12, no. 6 (June 20, 2022): 89–92. http://dx.doi.org/10.52403/ijhsr.20220611.

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Epilepsy is one of the most prevalent chronic neurological illnesses, with an estimated frequency of 0.5% to 1%. Currently, the majority of epilepsy treatment methods include the provision of symptomatic medicine. When treating individuals with drug-resistant epilepsy (DRE), it is essential to provide anti-seizure medicines (ASDs) at an appropriate daily dose to prevent seizures with DRE. Because of drug resistance, about one-third of epileptic patients are still unable to take their drugs, despite the fact that the number of ASDs accessible continues to expand. Several risk factors, including epilepsy that started in infancy, symptoms of epilepsy, and abnormal neurological examination, increase the likelihood that a newly diagnosed epileptic patient would proceed to DRE. ASD poly-therapy is a kind of pharmacological treatment that is widely used. When assessing the influence of DRE on mental health and social integration, it is vital to make complete therapy modifications in order to improve the overall quality of life of patients. Key words: Seizure, Epilepsy, Drug Resistant Epilepsy.

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Manganaro, Sheryl, Tobias Loddenkemper, and Alexander Rotenberg. "The Need for Antiepileptic Drug Chronotherapy to Treat Selected Childhood Epilepsy Syndromes and Avert the Harmful Consequences of Drug Resistance." Journal of Central Nervous System Disease 9 (January 1, 2017): 117957351668588. http://dx.doi.org/10.1177/1179573516685883.

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Antiepileptic drug (AED) chronotherapy involves the delivery of a greater AED dose at the time of greatest seizure susceptibility usually associated with predictable seizure peaks. Although research has proven AED chronotherapy, commonly known as differential dosing, to be safe, well tolerated, and highly effective in managing cyclic seizure patterns in selected childhood epilepsies, conventional, equally divided AED dosing remains the standard of care. Differential dosing is more often applied in the emergency management of acute seizure clustering resulting from drug resistance—a harmful epilepsy-related consequence that affects 30% of children. Moreover, drug resistance is a major risk factor in status epilepticus and sudden, unexpected death in epilepsy. Although these facts should promote the wider use of differential dosing in selected cases, a credible hypothesis is needed that defines the differential dosing strategy and application in cyclic epilepsy and for the greater purpose of preventing harmful outcomes.

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Lalitha, Sree, Ranjana W. Minz, and Bikash Medhi. "Understanding the controversial drug targets in epilepsy and pharmacoresistant epilepsy." Reviews in the Neurosciences 29, no. 3 (March 28, 2018): 333–45. http://dx.doi.org/10.1515/revneuro-2017-0043.

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AbstractAccumulating experimental data suggests a number of successful drug targets against epilepsy which eventually failed in the clinical setup. Mammalian target of rapamycin inhibitors, multi-drug resistance transporter inhibitors, cyclo-oxygenase-2 inhibitors, statins, etc. are the most promising and well studied among them. Drugs aiming at these targets produced beneficial response in most of thein vitroandin vivoseizure models. However, in certain situations, they have produced differential rather controversial results. Their effects varied with the seizure model, species, time and route of administration, different drugs from the same class, etc. This review emphasises on such drugs which presented with variability in their beneficial effects against seizures and epilepsy. This review critically summarises the preclinical evidence of these targets in the context of seizures and the probable reasons for their variability and clinical failures.

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Smolarz, Beata, Marianna Makowska, and Hanna Romanowicz. "Pharmacogenetics of Drug-Resistant Epilepsy (Review of Literature)." International Journal of Molecular Sciences 22, no. 21 (October 28, 2021): 11696. http://dx.doi.org/10.3390/ijms222111696.

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Pharmacogenomic studies in epilepsy are justified by the high prevalence rate of this disease and the high cost of its treatment, frequent drug resistance, different response to the drug, the possibility of using reliable methods to assess the control of seizures and side effects of antiepileptic drugs. Candidate genes encode proteins involved in pharmacokinetic processes (drug transporters, metabolizing enzymes), pharmacodynamic processes (receptors, ion channels, enzymes, regulatory proteins, secondary messengers) and drug hypersensitivity (immune factors). This article provides an overview of the literature on the influence of genetic factors on treatment in epilepsy.

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Mancini, Kerri L., Vince Fazio, Sanjay Awasthi, Sharad Singhal, Luca Cucullo, Gabriele Dini, and Damir Janigro. "RLIP-76: A novel mechanism of drug resistance in epilepsy." Journal of Cerebral Blood Flow & Metabolism 25, no. 1_suppl (August 2005): S276. http://dx.doi.org/10.1038/sj.jcbfm.9591524.0276.

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Hernández-Ronquillo, Lizbeth, Scott Adams, Stephanie Ballendine, and Jose F. Téllez-Zenteno. "Epilepsy in an elderly population: Classification, etiology and drug resistance." Epilepsy Research 140 (February 2018): 90–94. http://dx.doi.org/10.1016/j.eplepsyres.2017.12.016.

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French, Jacqueline A. "The Role of Drug-resistance Proteins in Medically Refractory Epilepsy." Epilepsy Currents 2, no. 5 (September 2002): 166–67. http://dx.doi.org/10.1046/j.1535-7597.2002.00062.x.

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Xu, Cenglin, Yi Wang, Shuo Zhang, Jiazhen Nao, Yao Liu, Ying Wang, Fang Ding, et al. "Subicular pyramidal neurons gate drug resistance in temporal lobe epilepsy." Annals of Neurology 86, no. 4 (August 12, 2019): 626–40. http://dx.doi.org/10.1002/ana.25554.

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Liu, Song Yan, Rui Tao Mao, Hua Cai, and Xue Mei Han. "Research on the Correlation between Neuronal Damage and Drug Resistance Gene Product P-Gp Following Status Epilepsy." Advanced Materials Research 550-553 (July 2012): 1010–13. http://dx.doi.org/10.4028/www.scientific.net/amr.550-553.1010.

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Objective: To study the association between neuronal injury following status epilepsy and expression of P-glycoprotein, discuss the association between intractable epilepsy and neuronal injury. Method: To establish a mice status epilepticus model by lithium-pilocarpine injected intraperitoneal, The mice were randomly divided into control group 6h, 12h, 1d, 3d, 5d and 7d after status epilepticus(SE) .To research the neuronal injury by image analysis method, expression of P-gp in blood was studied by flow cyometry .To analyze the association between neuronal injury and expression of P-gp by Pearson statistics. Result: The neuronal injury was observed after status epilepsy. Neuronal injury is most obvious 3-7 days after status epilepsy, expression of P-gp increased simultaneously. The severity of neuronal injury has a positive correlation to expression of P-gp. Conclusion: Association between intractable epilepsy and neuronal injury exists.

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Manguoğlu, E., S. Akdeniz, N. Dündar, Ö. Duman, B. Aktekin, Ş. Haspolat, U. Bilge, D. Özel, and G. Lüleci. "RLIP76 Gene Variants are not Associated with Drug Response in Turkish Epilepsy Patients." Balkan Journal of Medical Genetics 14, no. 1 (January 1, 2011): 25–30. http://dx.doi.org/10.2478/v10034-011-0014-3.

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RLIP76Gene Variants are not Associated with Drug Response in Turkish Epilepsy PatientsApproximately 30% of epileptic patients remain untreated, in spite of trials with maximum tolerable doses of more than one drug. The RalA binding protein 1 (RALBP1/RLIP76), a multifunctional, anti-apoptotic, multidrug transporter protein, has been proposed as being responsible for the drug resistance mechanism in epilepsy. We have investigated polymorphic differences in the coding regions and exon-intron boundaries of theRLIP76gene, between 146 refractory and 155 non refractory epileptic patients in Turkey, using denaturing high performance liquid chromatography (HPLC) and sequencing analysis techniques. We have detected the following sequence variants: c.160-4G>A, c.187C>G, c.1562-38G>A, c.1670+107G>A, c.1670+93G>A, c.1670+96G>A, c.1670+100C>T, c.1670+130C>T, c.1670+131G>C, c.1670+140 G>C, and found no statistically significant correlation between allele frequencies and drug response status. We conclude that sequence variants of this gene are not involved in drug resistance in epilepsy.

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Chiosa, Vitalie, Dumitru Ciolac, Viorica Chelban, Daniela Gasnas, Anatolie Vataman, Cristina Munteanu, and Stanislav Groppa. "Drug-resistant epilepsy: modern concepts, integrative mechanisms, and therapeutic advances." Moldovan Medical Journal 64, no. 4 (October 2021): 72–85. http://dx.doi.org/10.52418/moldovan-med-j.64-4.21.14.

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Background: Drug-resistant epilepsy is the cause of severe disability. Multiple questions remain unanswered both in terms of pathogenesis and therapeutic management. For this narrative review, PubMed database and Infomedica library were searched by using “drug-resistance in epilepsy” and “treatment of drug-resistant epilepsy” as key words. The following filters were applied: “Clinical Trial”, “Meta-analysis”, “Multicenter Study”, and “Randomized Controlled Trial”, covering the period of 01.01.2005–06.01.2021.Several hypotheses have been proposed, i.e., pharmacokinetic, intrinsic severity, gene, target, transporter, and neural network hypotheses. Many controlled trials showed different results in terms of seizure control after combined methods of therapies. Immunotherapy, palliative epilepsy surgery alone or associated with neurostimulation procedures including vagus nerve, trigeminal nerve, or deep brain stimulation may be efficient, however, seizure freedom is not always achieved. Genetic epilepsies might benefit from gene and exosome therapy; however, further studies are needed to verify their safety. Conclusions: Neuroscience of drug-resistant epilepsy faces many challenges. Inflammatory mediators, biomarkers, and genes might allow the identification of new treatment targets, contribute to an earlier diagnosis, and assess the clinical outcomes.

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Maqbool, Hafsa, Tayyaba Saleem, Nadeem Sheikh, and Aqsa Ashfaq. "Genetic Analysis of CYP2C9 with Reference to Drug Response in Epilepsy Patients of Pakistan." Genetics Research 2022 (January 29, 2022): 1–6. http://dx.doi.org/10.1155/2022/1451007.

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Epilepsy is a major global issue. Epilepsy patients are treated with AED (antiepileptic drugs). Interindividual variability in drug response has been documented in several studies. The resistance to drug response may be attributed to genetic polymorphism. The current study was undertaken to investigate the CYP2C9 gene polymorphism associated with antiepileptic drug (AED) resistance in the Pakistani population. The current study included 337 individuals including 100 control subjects, 110 drug-resistant subjects, and 127 drug responders. Genomic DNA was isolated from blood, and amplification of rs1799853 (430C > T) and rs1057910 was carried out by polymerase chain reaction. Genotypes of CYP2C9 SNPs were determined by Sanger’s sequencing. Astounding results were observed in the current study that none of the well-known reported SNPs of CYP2C9 was found in our Pakistani cohorts. However, a novel missense variant (c.374G > A) was found only in drug-resistant patients of the current study. According to the in silico analysis performed by PolyPhen-2, it was observed that this nonsynonymous substitution is likely to be pathogenic. The results of our study demonstrated that rs1799853 and rs1057910 may be involved in drug resistance in the Pakistani population. However, some other variants on CYP2C9 may play a critical role in AED resistance that needs to be explored.

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Jésus, Pierre, Bertrand Godet, Lucile Darthou-Pouchard, Philippe Fayemendy, Françoise Abdallah-Lebeau, Olivier Villeneuve, Claire Marcon, et al. "Vitamin D status among patients with drug-resistant and non-drug-resistant epilepsy." International Journal for Vitamin and Nutrition Research 90, no. 3-4 (June 2020): 205–9. http://dx.doi.org/10.1024/0300-9831/a000459.

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Abstract. Background & Aims: Epilepsy affects nearly 70 million people worldwide. Vitamin D deficiency may influence the balance of certain epilepsies. The purpose of this study was to determine the vitamin D status and anthropometric measurements of people with epilepsy (PWE), according to their pharmacosensitivity. Methods: Forty-six PWE, with or without drug resistance, underwent nutritional assessment after giving consent. Weight, body mass index (BMI), triceps skinfold thickness (TSF), fat mass (FM) and free fat mass (FFM) by bioelectrical impedance analysis were measured. Serum vitamin D was determined without supplementation. Deficiency was defined as a level < 30 ng/mL. Statistical analysis involved Student t test, ANOVA and Chi2. Results: Patients were aged 44.5 ± 14.3 years, with 60.9% of drug-resistance. BMI was 28.7 ± 7.0, 2.2% were malnourished and 30.4% obese according to the BMI. The average vitamin D level was 15.3 ± 9.9 ng/mL, with 87.0% of deficiency, and 40.0% of severe deficiency (<10 ng/mL). The TSF was higher in drug-resistant cases (p = 0.03). There was no link between drug resistance and anthropometric measurements, FM, FFM or vitamin D concentration. Conclusions: Although limited in size, this study showed that PWE are more often obese. Vitamin D deficiency is more common than in the general population, with a much higher prevalence of severe deficiency.

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Chouchi, Malek, Hedia Klaa, Ilhem Ben-Youssef Turki, and Lamia Hila. "ABCB1 Polymorphisms and Drug-Resistant Epilepsy in a Tunisian Population." Disease Markers 2019 (December 2, 2019): 1–16. http://dx.doi.org/10.1155/2019/1343650.

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Background. Epilepsy is one of the most common neurological disorders with about 30% treatment failure rate. An interindividual variations in efficacy of antiepileptic drugs (AEDs) make the treatment of epilepsy challenging, which can be attributed to genetic factors such as ATP-Binding Cassette sub-family B, member1 (ABCB1) gene polymorphisms. Objective. The main objective of the present study is to evaluate the association of ABCB1 C1236T, G2677T, and C3435T polymorphisms with treatment response among Tunisian epileptic patients. Materials and Methods. One hundred epileptic patients, originated from north of Tunisia, were recruited and categorized into 50 drug-resistant and 50 drug-responsive patients treated with antiepileptic drugs (AEDs) as per the International League Against Epilepsy. DNA of patients was extracted and ABCB1 gene polymorphisms studied using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. Results. The C1236T, G2677T, and C3435T polymorphisms were involved into AED resistance. Significant genotypic (C1236T TT (p≤0.001); G2677T TT (p=0.001); C3435T TT (p≤0.001)) and allelic associations (C1236T T (3.650, p≤0.001); G2677TT (1.801, p=0.044); C3435T T (4.730, p≤0.001)) with drug resistance epilepsy (DRE) were observed. A significant level of linkage disequilibrium (LD) was also noted between ABCB1 polymorphisms. Patients with the haplotypes CT and TT (C1236T-G2677T); GT, TC, and TT (G2677T-C3435T); CT and TT (C1236T-C3435T); CTT, TTC, TGT, and TTT (C1236T-G2677T-C3435T) were also significantly associated to AED resistance. Conclusions. The response to antiepileptics seems to be modulated by TT genotypes, T alleles, and the predicted haplotypes for the tested SNPs in our population. Genetic analysis is a valuable tool for predicting treatment response and thus will contribute to personalized medicine for Tunisian epileptic patients.

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Radhakrishnan, Kurupath, Abhijit Das, Shabeesh Balan, and Moinak Banerjee. "Drug resistance in epilepsy and the ABCB1 gene: The clinical perspective." Indian Journal of Human Genetics 17, no. 4 (2011): 12. http://dx.doi.org/10.4103/0971-6866.80353.

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Alpman, Asude, Ferda Ozkinay, Hasan Tekgul, Sarenur Gokben, Sacide Pehlivan, Martin Schalling, and Cihangir Ozkinay. "Multidrug Resistance 1 (MDR1) Gene Polymorphisms in Childhood Drug-Resistant Epilepsy." Journal of Child Neurology 25, no. 12 (May 6, 2010): 1485–90. http://dx.doi.org/10.1177/0883073810368997.

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Sisodiya, Sanjay M., and Susan E. Bates. "Treatment of drug resistance in epilepsy: one step at a time." Lancet Neurology 5, no. 5 (May 2006): 380–81. http://dx.doi.org/10.1016/s1474-4422(06)70422-7.

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Journal articles on the topic 'Drug-resistance epilepsy'

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