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7 results

  • Clobazam as Add-on Therapy for Temporal Lobe Epilepsy and Hippocampal Sclerosis

  • Maria Augusta Montenegro, Claudio Meilman Ferreira, Fernando Cendes, Li M. Li, Carlos A.M. Guerreiro
  • Journal: Canadian Journal of Neurological Sciences / Volume 32 / Issue 1 / February 2005
  • Published online by Cambridge University Press: 02 December 2014, pp. 93-96
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  • Background:

    Clobazam is a benzodiazepine with known antiepileptic action; however, it is not considered first line therapy in the treatment of epilepsy. The objective of this study was to evaluate the efficacy of clobazam as add-on therapy in adults with temporal lobe epilepsy associated with MRI evidence of hippocampal sclerosis (HS).

    Method:

    This is a retrospective study, conducted at our epilepsy clinic which evaluated clobazam as add-on therapy in patients with temporal lobe epilepsy and MRI signs of HS. Clobazam was prescribed based on the minimum effective dose up to the maximum tolerated dose.

    Results:

    Seventy-eight patients met the inclusion criteria (51 women), ages ranging from 16 to 76 years old (mean=42.2). Dosage of clobazam ranged from 5 to 60 mg/day (mean=22.6 mg/day). Clobazam was used from one month to eight years (mean=29 months). Sixteen (20.5%) patients were seizure-free, 20 (25.5%) had more than 75% improvement in seizure control, eight (10%) had more than 50% and 20 (26%) were non responders to clobazam. In 14 (18%) we could not determine seizure frequency during follow-up. The improvement in seizure control lasted for more than one year in 30 (68%) patients.

    Conclusion:

    Our data suggest that clobazam should be considered as add-on therapy in the treatment of patients with temporal lobe epilepsy associated with MRI signs of HS.

  • Structural Abnormalities are Similar in Familial and Nonfamilial Mesial Temporal Lobe Epilepsy

  • Fabio Thadeu Ferreira, Eliane Kobayashi, Iscia Lopes-Cendes, Fernando Cendes
  • Journal: Canadian Journal of Neurological Sciences / Volume 31 / Issue 3 / August 2004
  • Published online by Cambridge University Press: 02 December 2014, pp. 368-372
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  • Background/Objective:

    Diffuse temporal lobe abnormalities can be observed on MRI of patients with mesial temporal lobe epilepsy (MTLE). Our objective was to perform qualitative and quantitative analyses of temporal lobe structures in patients with familial MTLE (FMTLE) and nonfamilial MTLE.

    Methods:

    Two groups of patients were ascertained: 67 FMTLE patients (14 with refractory seizures) and 30 patients with nonfamilial refractory MTLE. We performed qualitative analyses of MRI (with multiplanar reconstruction) and volumes of hippocampi and anterior temporal lobes in all patients, and in a normal control group of 23 individuals. We used the Chi-square test and ANOVA for statistical analyses.

    Results:

    We identified anterior temporal lobe abnormalities by visual analysis in only 4% of FMTLE patients and atrophy of the anterior temporal lobe by volumetric analysis in 19%. In the group of nonfamilial MTLE patients we found anterior temporal lobe abnormalities by visual analysis in 17% of patients and anterior temporal lobe atrophy in 13%. Hippocampal atrophy was present in 90% of FMTLE and in 83% of nonfamilial MTLE. No signs of cortical dysplasia were observed.

    Conclusion:

    Anterior temporal lobe atrophy and other abnormalities outside the mesial portion of temporal lobes were infrequent in both familial and nonfamilial MTLE patients. Despite the genetic basis, hippocampal atrophy in FMTLE is not associated with other abnormalities outside the mesial temporal regions.

  • Chapter 53 - Hippocampal sclerosis

  • from Section 3 - Symptomatic epilepsy
  • Edited by Simon D. Shorvon, Frederick Andermann, Renzo Guerrini
  • Book: The Causes of Epilepsy
  • Published online: 05 March 2012
  • Print publication: 14 April 2011, pp 363-372

  • Summary

    Genetically determined and acquired disorders leading to relative cobalamin deficiency result in hematologic changes characterized by megaloblastic anemia. Acquired disorders of cobalamin deficiency occur far more frequently than genetically determined disorders and often result in a variety of neurologic syndromes. Seizures are recognized as an uncommon manifestation of cobalamin deficiency, especially in adults. Early-onset cblC or cblD disorder, which results in both homocystinuria and methylmalonic aciduria, has been described in several reports to feature prominent seizures. Use of valproic acid, carbamazepine, and phenytoin has been shown in epileptic patients to lower serum cobalamin levels. Mutations affecting the proton-coupled folate transporter (PCFT) result in deficient uptake of folate at both the intestinal and choroid plexus levels and causes hereditary folate malabsorption. Neuroimaging studies detect non-specific cerebral atrophy and the intracranial, particularly occipital, calcifications noted especially in folate deficiency.