Centro-median stimulation yields additional seizure frequency and attention improvement in patients previously submitted to callosotomy

AbstractRationaleDeep brain stimulation (DBS) has been increasingly used in the treatment of refractory epilepsy over the last decade. We report on the outcome after thalamic centro-median (CM) DBS in patients with generalized epilepsy who had been previously treated with extended callosal section.MethodsFour consecutive patients with generalized epilepsy who were previously submitted to callosal section and had at least 1 year of follow-up after deep brain implantation were studied. Age ranged from 19 to 44 years. All patients were submitted to bilateral CM thalamic DBS. Post-operative CT scans documented the electrode position in all patients. All patients had pre- and post-stimulation prolonged interictal scalp EEG recordings, including spike counts. Attention level was evaluated by means of the SNAP-IV questionnaire. The pre-implantation anti-epileptic drug regimen was maintained post-operatively in all patients.ResultsPost-operative CT documented that all electrodes were correctly located. There was no morbidity or mortality. Seizure frequency reduction ranging from 65 to 95% and increased attention level was seen in all patients. Interictal spiking frequency was reduced from 25 to 95%, but their morphology remained the same. There was re-synchronization of interictal discharges during slow-wave sleep in 2 patients.ConclusionAll patients benefit from the procedure. The CM seems to play a role in modulating the epileptic discharges and attention in these patients. On the other hand, it is not the generator of the epileptic abnormality and appeared not to be involved in non-REM sleep-related interictal spiking modulation

Cardiac troponin I levels in patients with refractory temporal lobe epilepsy after cortico-amygdalo-hippocampectomy

PURPOSE: Sudden unexpected death in epilepsy (SUDEP) is the main cause of death in patients with epilepsy. Morphologic and functional changes in the heart are related to SUDEP. The aim of our study was to verify the concentration of troponin I, an important marker of myocardium damage, in patients with temporal lobe epilepsy who were submitted to surgical resection and were not seizure-free after the procedure. METHODS: Eleven non-consecutive patients participated in the study and all of them presented poor seizure control after surgical procedure. Troponin I levels higher then 1 ng/ml indicate myocardium damage. The detection level of the kit used in our study was 0,15 ng/ml. RESULTS: Only three patients showed detectable troponin I levels. The troponin I levels found in our study is not related with sex, age or side of the lesion. CONCLUSIONS: In spite of we did not find positive results in our study, an active role of the heart in SUDEP cannot be discarded, since some injuries, even so not being capable to modify troponin I levels, can be enough to generate arrhythmogenic foci.OBJETIVOS: A morte súbita em epilepsia (SUDEP) é a principal causa de morte entre os pacientes com epilepsia. Alterações morfológicas e funcionais do coração estão relacionadas com a SUDEP. Nesse sentido, o objetivo deste estudo foi avaliar a concentração de troponina I, um importante marcador de lesão do miocárdio, em pacientes com epilepsia do lobo temporal de difícil controle e que foram submetidos à ressecção cirúrgica e que não obtiveram sucesso com esta abordagem terapêutica. METODOLOGIA: Onze pacientes participaram do estudo e todos continuaram a apresentar crises após o tratamento cirúrgico. Os valores de troponina I indicativos de lesão seriam aqueles maiores de 1 ng/ml e o valor mínimo detectável pelo kit utilizado em nosso estudo foi de 0,15 ng/ml. RESULTADOS: Apenas três pacientes apresentaram níveis de troponina I detectáveis. Em relação aos níveis detectáveis de troponina I, não encontramos nenhuma relação com sexo, idade e lateralidade da lesão. CONCLUSÕES: APESAr de não termos encontrado resultados positivos em nosso estudo, o papel do coração na SUDEP não pode ser descartado, já que algumas lesões, embora não sendo capazes de alterar os níveis séricos de troponina I, podem ser suficientes na gênese de focos arritmogênicos.Universidade Federal de São Paulo (UNIFESP) Escola Paulista de MedicinaUniversidade de Mogi das Cruzes Núcleo de Pesquisas TecnológicasHospital Brigadeiro Departamento de Neurologia e NeurocirurgiaCentro Universitário São CamiloHospital Israelita Albert EinsteinUniversidade Federal de São João del-Rei Departamento de Engenharia BiomédicaUniversidade Federal de São Paulo (UNIFESP) Escola Paulista de Medicina Departamento de FisiologiaUNIFESP, EPM, Depto. de FisiologiaSciEL