RESUMO
OBJECTIVE: To explore the efficacy and tolerability of levetiracetam in medical treatment of trigeminal neuralgia. BACKGROUND: Antiepileptic drugs (AEDs) are considered as first-line treatment for trigeminal neuralgia, although their use is often limited due to incomplete efficacy and tolerability. Newer AEDs with improved safety profile may be useful in this disorder. METHODS: Patients suffering from trigeminal neuralgia (either primary or secondary) refractory to previous treatments were recruited to be treated with levetiracetam (3-4 g/day) for 16 weeks as add-on therapy, after a 2-week baseline period. Rescue medication was allowed in both the baseline and treatment phases. The primary efficacy measure was the number of attacks per day. The patients' efficacy evaluation, the patients' global evaluation for both safety and efficacy, changes in the Hamilton Depression Scale, the Hamilton Anxiety Scale, and the Quality of Life Measure Short Form-36 were secondary parameters. RESULTS: Twenty-three patients were included in the analysis. After treatment and compared to the baseline phase, the number of daily attacks decreased by 62.4%. All secondary parameters changed significantly with the exception of the Quality of Life Measure Short Form-36 score. Seven patients withdrew from the study. Five patients (21.7%) reported side effects and 2 withdrew. CONCLUSIONS: Levetiracetam may be effective and safe in trigeminal neuralgia treatment. Confirmation in a randomized controlled study is needed.
Assuntos
Anticonvulsivantes/administração & dosagem , Piracetam/análogos & derivados , Neuralgia do Trigêmeo/tratamento farmacológico , Adolescente , Adulto , Idoso , Anticonvulsivantes/efeitos adversos , Feminino , Humanos , Levetiracetam , Masculino , Pessoa de Meia-Idade , Projetos Piloto , Piracetam/administração & dosagem , Piracetam/efeitos adversos , Estudos Prospectivos , Resultado do Tratamento , Adulto JovemRESUMO
Twenty-one unrelated patients with a history of suspected familial Alzheimer disease (FAD) were screened for mutations in PSEN1, PSEN2, and APP, the known FAD genes encoding the presenilins (PS1 and PS2) and the amyloid precursor protein (APP). The mutation detection rate was 57%. Of the nine pathogenic mutations found in 12 cases, three were in APP, one in PSEN2, and five in PSEN1, including two novel Greek mutations (L113Q and N135S). Whereas our findings suggest the possibility of single founders for the majority of mutations, we found evidence of recurrence of the APP mutations V717L and V717I.
