Topiramate for the treatment of juvenile myoclonic epilepsy

Sousa, Patrícia da Silva; Filho, Gerardo Maria de Araújo; Garzón, Eliana; Sakamoto, Américo Ceiki; Yacubian, Elza Márcia Targas

doi:10.1590/s0004-282x2005000500001

Cited by 30 publications

(17 citation statements)

References 9 publications

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“…Response rate for myoclonias was 58.3% versus 23.3% for placebo, and 80% of cases were reported to be free of epileptic seizures 32 . Topiramate therapy during one year was able to control GTCS in 62.5% of patients and myoclonic jerks in 68.8%, although 13.6% had an increase in frequency of absence seizures 34 . Clonazepam may also be utilized 4 , as it helps to control myoclonic jerks in association with VPA, although it has a lesser effect on GTCS 1,32 .…”

Section: Differential Diagnosismentioning

confidence: 91%

Juvenile myoclonic epilepsy

Alfradique¹,

Vasconcelos

2007

Arq. Neuro-Psiquiatr.

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-Juvenile myoclonus epilepsy (JME) is a common epileptic syndrome, the etiology of which is genetically determined. Its onset occurs from 6 through 22 years of age, and affected patients present with myoclonic jerks, often associated with generalized tonic-clonic seizures -the most common association -and absence seizures. JME is non-progressive, and there are no abnormalities on clinical examination or intellectual deficits. Psychiatric disorders may coexist. Generalized polyspike-and-waves are the most characteristic electroencephalographic pattern. Usual neuroimaging studies show no abnormalities. Atypical presentations should be entertained, as they are likely to induce misdiagnosis. Prevention of precipitating factors and therapy with valproic acid (VPA) are able to control seizures in the great majority of patients. Whenever VPA is judged to be inappropriate, other antiepileptic drugs such as lamotrigine may be considered. Treatment should not be withdrawn, otherwise recurrences are frequent.KEY WORDS: juvenile myoclonic epilepsy, diagnosis, etiology, treatment. Epilepsia mioclônica juvenilRESUMO -A epilepsia mioclônica juvenil é uma síndrome epiléptica comum, cuja etiologia é fundamentada na genética. Inicia-se entre 6 e 22 anos e os indivíduos apresentam mioclonias, que podem ser acompanhadas por crises tônico-clônicas generalizadas -associação mais comum -e crises de ausência. A doença não é progressiva, e não há alterações detectáveis no exame físico ou déficits intelectuais. Distúrbios psiquiátri-cos podem coexistir. Polipontas-ondas lentas generalizadas constituem o padrão eletrencefalográfico ictal típico. Não há anormalidades em exames de imagem convencionais. Apresentações atípicas devem ser consideradas, pois predispõem a erros de diagnóstico. A prevenção de fatores desencadeantes e o uso de áci-do valpróico (VPA) controlam as crises epilépticas na grande maioria dos casos. Quando o VPA é inapropriado, outras drogas como a lamotrigina podem ser utilizadas. O tratamento não deve ser interrompido, visto que as recidivas são freqüentes.

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Section: Differential Diagnosismentioning

confidence: 91%

Juvenile myoclonic epilepsy

Alfradique¹,

Vasconcelos

2007

Arq. Neuro-Psiquiatr.

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“…GTCS were completely controlled in 62.5% of patients, and a reduction of 50% in 25.0%, and 50% in 12.5% were observed. Myoclonias were controlled in 68.8% and persisted in 31.2% of patients [91].…”

Section: Juvenile Myoclonic Epilepsymentioning

confidence: 90%

Topiramate: Its Pharmacological Properties and Therapeutic Efficacy in Epilepsy

Latini¹,

Verrotti²,

Manco³

et al. 2008

MRMC

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Since 1990 eight new antiepileptic drugs (AEDs) have been developed. Among these new drugs, Topiramate (TPM) is one of the latest AEDs available for treating drug resistant partial epilepsy both in adults and in children. The mechanisms underlying TPM antiepileptic activity are still incompletely understood. However, TPM, a sulfamate-substituted derivative of the naturally occurring monosaccharide D-fructose, has a different structure from other known AEDs. The antiepileptic activity of TPM in animal models of partial and generalized tonic-clonic seizures has been shown to be more effective as compared to other AEDs. Proposed mechanisms of action include reduction of epileptiform discharges through a voltage-dependent block of Na(+) channels, enhancement of the activity of gamma-aminobutyrate at some subtypes of gamma-aminobutyrate receptors, and antagonism of non- N-methyl-D-aspartate (NMDA) glutamate receptors. The pharmacokinetic profile of TPM, which is characterized by its rapid and almost complete absorption after oral administration, linear pharmacokinetics, minimal protein binding and predominantly renal excretion, makes the drug a good option for the treatment. TPM was found to be effective and well tolerated in many studies conducted in adults and pediatric patients suffering from epilepsy. This review, summarising the main studies in this field, provides an overview of the current knowledge about the relevant pharmacological and clinical information on the efficacy and tolerability of TPM.

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“…Lamotrigin (LTG), iako efikasan kod većine, može dovesti do pogoršanja miokloničnih napada, posebno pri primeni visokih doza [41,42]. Topiramat je efikasan u kontroli GTKN i mioklonih napada kod oko 60% pacijenata [43]. Sve je više dokaza da bi levetiracetam (LEV) mogao biti prva alternativa za VPA jer se dobro podnosi, ima mali interaktivni potencijal i efikasan je u kontroli i mioklonič-nih napada (58,3% vs 23,3% placebo).…”

Section: Lečenje I Prognozaunclassified