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      Neuropsychiatric Disease and Treatment (submit here)

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      Treating Lennox–Gastaut syndrome in epileptic pediatric patients with third-generation rufinamide

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          Abstract

          Lennox–Gastaut syndrome (LGS) is a rare but debilitating pediatric epileptic encephalopathy characterized by multiple intractable seizure types. Treatment of LGS is challenging because of the small number of antiepileptic drugs (AEDs) which are effective for this syndrome, as well as the need for polytherapy in the majority of patients. This review focuses on the treatment of LGS with rufinamide, a recently approved third-generation AED with reported efficacy as adjunctive therapy for LGS. All relevant papers identified through a PubMed search on the treatment of LGS with rufinamide were reviewed. To date, the literature suggests improvements in seizure frequency for pediatric patients with LGS on rufinamide. Rufinamide appears to be especially effective for atonic or drop attack seizures. Rufinamide also displays a favorable adverse event profile compared with the older anticonvulsants, as well as a minimal number of drug interactions, making it a promising option for the adjunctive treatment of seizures associated with LGS.

          Most cited references24

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          Epilepsy in children.

          10.5 million children worldwide are estimated to have active epilepsy. Over the past 15 years, syndrome-oriented clinical and EEG diagnosis, and better aetiological diagnosis, especially supported by neuroimaging, has helped to clarify the diversity of epilepsy in children, and has improved management. Perinatal and postinfective encephalopathy, cortical dysplasia, and hippocampal sclerosis account for the most severe symptomatic epilepsies. Ion channel defects can underlie both benign age-related disorders and severe epileptic encephalopathies with a progressive disturbance in cerebral function. However, the reasons for age-related expression in children are not understood. Neither are the mechanisms whereby an epileptic encephalopathy originates. Several new drugs have been recently introduced but have provided limited therapeutic benefits. However, treatment and quality of life have improved because the syndrome-specific efficacy profile of drugs is better known, and there is heightened awareness that compounds with severe cognitive side-effects and heavy polytherapies should be avoided. Epilepsy surgery is an important option for a few well-selected individuals, but should be considered with great caution when there is no apparent underlying brain lesion.
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            Lennox-Gastaut syndrome: a consensus approach on diagnosis, assessment, management, and trial methodology.

            Lennox-Gastaut syndrome is one of the most severe epileptic encephalopathies of childhood onset. The cause of this syndrome can be symptomatic (ie, secondary to an underlying brain disorder) or cryptogenic (ie, has no known cause). Although Lennox-Gastaut syndrome is commonly characterised by a triad of signs, which include multiple seizure types, slow spike-wave complexes on electroencephalographic (EEG) recordings, and impairment of cognitive function, there is debate with regard to the precise limits, cause, and diagnosis of the syndrome. Tonic seizures, which are thought to be a characteristic sign of Lennox-Gastaut syndrome, are not present at onset and the EEG features are not pathognomonic of the disorder. There are few effective treatment options for the multiple seizures and comorbidities, and the long-term outlook is poor for most patients. Probably as a result of the complexity of the disorder, only a few randomised trials have studied Lennox-Gastaut syndrome, and thus many of the drugs that are more commonly used have little or no supporting evidence base from controlled trials. In this Review, we discuss the main issues with regard to the diagnosis and treatment options available. We also suggest key considerations for future trials and highlight the importance of a comprehensive approach to the assessment and management of this syndrome.
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              The cost of epilepsy in the United States: an estimate from population-based clinical and survey data.

              To provide 1995 estimates of the lifetime and annual cost of epilepsy in the United States using data from patients with epilepsy, and adjusting for the effects of comorbidities and socioeconomic conditions. Direct treatment-related costs of epilepsy from onset through 6 years were derived from billing and medical chart data for 608 population-based incident cases at two sites in different regions of the country. Indirect productivity-related costs were derived from a survey of 1,168 adult patients visiting regional treatment centers. Direct costs separate the effects of epilepsy and comorbidity conditions. Indirect costs account for the effects of other disabilities and socioeconomic conditions on foregone earnings and household activity. The estimates were applied to 1995 population figures to derive national projections of the lifetime and annual costs of the disorder. The lifetime cost of epilepsy for an estimated 181,000 people with onset in 1995 is projected at $11.1 billion, and the annual cost for the estimated 2.3 million prevalent cases is estimated at $12.5 billion. Indirect costs account for 85% of the total and, with direct costs, are concentrated in people with intractable epilepsy. Direct costs attributable to epilepsy are below previous estimates. Indirect costs adjusted for the socioeconomic conditions of patients are above previous estimates. Findings indicate that epilepsy is unique in the large proportion of costs that are productivity-related, justifying further investment in the development of effective interventions.
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                Author and article information

                Journal
                Neuropsychiatr Dis Treat
                Neuropsychiatric Disease and Treatment
                Neuropsychiatric Disease and Treatment
                Dove Medical Press
                1176-6328
                1178-2021
                5 October 2010
                2010
                2010
                : 6
                : 639-645
                Affiliations
                [1 ] Auburn University, Harrison School of Pharmacy (AUHSOP)
                [2 ] Department of Pharmacy Practice, AUHSOP
                [3 ] University of Alabama, School of Medicine, Huntsville Regional Medical Campus
                [4 ] University of South Alabama School of Medicine, Department of Pediatrics, Mobile, Alabama, USA
                Author notes
                Correspondence: Allison M Chung, Auburn University, Harrison School of Pharmacy, Technology and Research Park, Bldg 3, Suite 2100, 307 University, Blvd N, Mobile, AL 36688, USA, Tel +1 251 445 9300, Fax +1 251 445 9341, Email chungam@ 123456auburn.edu
                Article
                ndt-6-639
                10.2147/NDT.S6465
                2951747
                20957124
                e0170cf9-9e6c-4ba6-a36a-c780ea070326
                © 2010 Gresham et al, publisher and licensee Dove Medical Press Ltd.

                This is an Open Access article which permits unrestricted noncommercial use, provided the original work is properly cited.

                History
                Categories
                Review

                Neurology
                pediatrics,lennox-gastaut syndrome,seizure,epilepsy,rufinamide
                Neurology
                pediatrics, lennox-gastaut syndrome, seizure, epilepsy, rufinamide

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