Roberta Monterazzo Cysneiros

Evaluation of physical exercise habits in Brazilian patients with epilepsy

In this study we present data from a survey that aimed to assess the physical activity of a sample of adult outpatients with epilepsy. One hundred adult outpatients of both sexes with epilepsy answered a survey addressing exercise habits. Fifty-eight males and forty-two females participated in this study. The mean age of onset of seizures was 18.6 years and the mean duration of epilepsy was 16.1 years. Sixty patients had controlled or rare seizures, 8 infrequent seizures, 17 frequent seizures, and 11 very frequent seizures. Eighty-six had partial epilepsy and only 3 had abnormal neurological examinations. Of the total, 51 engaged in physical activity, 85 did not believe that sports precipitate seizures, and 15 were forbidden by their physicians to engage in physical activities. Moreover, 14 were cautioned against participation in sports by their relatives and friends. Eight-four patients had never experienced seizures during physical exercise, 36 believed that physical activity has a positive influence on treatment, and only 1 related injuries associated with seizures. Forty-five are afraid of having seizures during exercise because the seizures might attract the attention of others and they would make fools of themselves. Our data show that although most of our patients do not regularly engage in physical activity, they believe that it might improve medical treatment.

Neuroprotective activity of omega-3 fatty acids against epilepsy-induced hippocampal damage: Quantification with immunohistochemical for calcium–binding proteins

To investigate whether n-3 polyunsaturated fatty acids (n-3 PUFAs) would promote different morphological changes in the hippocampal formation of rats with epilepsy, we performed an immunocytochemical study using parvalbumin (PV) and calretinin (CR) distribution as a marker. Animals subjected to the experimental model of epilepsy with a single dose of pilocarpine were randomly divided into the following groups: animals with epilepsy treated daily with vehicle (EV) and animals with epilepsy treated daily with 85 mg/kg n-3 PUFAs (EW). Control animals administered saline were also randomly divided into two other groups: animals treated daily with vehicle (CV) and animals treated daily with 85 mg/kg n-3 PUFAs (CW). A larger number of PV-positive neurons were observed in EW when compared with EV, CV, and CW. Similarly, there were significantly more CR-positive neurons in EW than in EV. These findings demonstrate that omega-3 fatty acids prevent status epilepticus-associated neuropathological changes in the hippocampal formation of rats with epilepsy.

Avaliação de parâmetros cardíacos em animais com epilepsia: possível causa de morte súbita?

Among the causes for sudden death in epilepsy, cardiac dysfunction has been an area of interest. Based on this, the aim of our study was to evaluate the heart rate (in vivo and in vitro) and ventricular pressure in vitro of rats with epilepsy induced by pilocarpine. Adult male Wistar rats (n=6) were given pilocarpine hydrochloride to induce status epilepticus. Control rats (n=6) received saline solution instead pilocarpine. Our results showed significant differences in the mean of heart rate in vivo between the groups. In contrast, we did not find differences during in vitro experiments. Our results suggest a central nervous system modulation on the heart, which could explain the sudden unexpected death in epilepsy.

Exercise paradigms to study brain injury recovery in rodents.

Exercise has been found to influence molecular systems important for maintaining neural function and plasticity as well as treatment of neurologic disorders. The stimuli required to elicit plasticity are thought to be activity dependent. Several protocols of physical exercise have been used to explore its effects on brain function. However, it is becoming increasingly recognized that no single physical exercise model is likely to fulfill all therapeutic needs. Varied interpretations of data derived from animal models have given rise to the lack of uniformity in the description and control of various features of the physical exercise stimulus, ranging from low to high intensity, intermittent to sustained, short to long durations, and different modes of activity. This article first describes the characteristics of the most frequently used animal models and goes on to review brain plasticity in intact animals and the usefulness of these models for the study of brain disorders. In this regard, animal models that investigate the beneficial effects of exercise on the brain before and after brain injury are discussed. A challenge for future studies is to better evaluate the usefulness of physical exercise protocols for preventing or treating brain disorders.

Lovastatin reduces neuronal cell death in hippocampal CA1 subfield after pilocarpine-induced status epilepticus: preliminary results

OBJECTIVE To further characterize the capacity of lovastatin to prevent hippocampal neuronal loss after pilocarpine-induced status epilepticus (SE) METHOD: Adult male Wistar rats were divided into four groups: (A) control rats, received neither pilocarpine nor lovastatin (n=5); (B) control rats, received just lovastatin (n=5); (C) rats that received just pilocarpine (n=5); (D) rats that received pilocarpine and lovastatin (n=5). After pilocarpine injection (350 mg/kg, i.p.), only rats that displayed continuous, convulsive seizure activity were included in our study. Seizure activity was monitored behaviorally and terminated with an injection of diazepam (10 mg/kg, i.p.) after 4 h of convulsive SE. The rats treated with lovastatin received two doses of 20 mg/kg via an oesophagic probe immediately and 24 hours after SE induction. Seven days after pilocarpine-induced SE, all the animals were perfused and their brains were processed for histological analysis through Nissl method. RESULTS The cell counts in the Nissl-stained sections performed within the hippocampal formation showed a significant cell loss in rats that received pilocarpine and presented SE (CA1=26.8 +/- 13.67; CA3=38.1 +/- 7.2; hilus=43.8 +/- 3.95) when compared with control group animals (Group A: CA1=53.2 +/- 9.63; CA3=63.5 +/- 13.35; hilus=59.08 +/- 10.24; Group B: CA1=74.3 +/- 8.16; CA3=70.1 +/- 3.83; hilus=70.6 +/- 5.10). The average neuronal cell number of CA1 subfield of rats that present SE and received lovastatin (44.4 +/- 17.88) was statically significant increased when compared with animals that just presented SE. CONCLUSION Lovastatin exert a neuroprotective role in the attenuation of brain damage after SE.

Estudo qualitativo da formação hipocampal de animais hipertensos com epilepsia

RESUMO - O objetivo deste estudo foi avaliar qualitativamente o hipocampo e o giro dentado de ratos es-pontaneamente hipertensos (SHR) com epilepsia. Metodo: Os animais foram divididos em 4 grupos: Wistarcontrole, Wistar com epilepsia, SHR controle e SHR com epilepsia. Para inducao da epilepsia, utilizamos omodelo da pilocarpina. Apos os animais apresentarem crises espontâneas e recorrentes, o tecido cerebraldos animais foi encaminhado para analise histologica atraves dos metodos de Nissl e neo-Timm. Resultados:Nos animais Wistar e SHR controle submetidos a coloracao de Nissl observamos a manutencao das camadascelulares da formacao hipocampal. Nos animais Wistar com epilepsia verificamos intensa morte neuronalna regiao CA1 e CA3 do hipocampo e no hilo do giro dentado. Nos animais SHR com epilepsia verificou-se a presenca de atrofia hipocampal com dilatacao do sistema ventricular. A coloracao de neo-Timm reve-lou a presenca de brotamento supragranular em todos os animais com epilepsia. Conclusao: Foram encon-tradas alteracoes neuropatologicas na citoarquitetura hipocampal nos animais Wistar com epilepsia e SHRcom epilepsia, demonstrando que a epilepsia isoladamente ou associadamente a hipertensao sao capazesde causar destruicao neuronal. PALAVRAS-CHAVE: epilepsia, hipertensao arterial, crise epileptica, pilocarpina.Qualitative study of hippocampal formation in hypertensive rats with epilepsy.ABSTRACT - The aim of our study was to investigate the hippocampus and dentate gyrus neuropathologicalfeatures of spontaneous hypertensive rats (SHR) with epilepsy. Method: Animals were randomly dividedinto 4 groups: control Wistar, Wistar with epilepsy, control SHR and SHR with epilepsy. The pilocarpine modelof epilepsy was used in this experiement. After spontaneous recurrent seizures, all animals were perfusedand their brains processed for histological analysis through Nissl and neo-Timm methods. Results: In theWistar rats with epilepsy we observed cell loss in hippocampal subfields CA1, CA3 and hilus of the dentategyrus when compared with control animals. In the SHR with epilepsy we observed hippocampal formationatrophy with ventricular dilatation. No morphological alterations were observed in SHR and Wistar controlrats. The neo-Timm staining of hippocampal formation has shown supragranular sprouting in Wistar andSHR with epilepsy. Conclusion: We found neuropathological alterations in hippocampal formation in Wis-tar with epilepsy and SHR with epilepsy, suggesting that epilepsy per se or associated to hypertention areable to cause neuronal damage.KEY WORDS: epilepsy, arterial hypertension, seizure, pilocarpine.

Seizure occurrence in patients with chronic renal insufficiency in regular hemodialysis program

Hemodialysis-associated seizure is a complication of hemodialysis. This report describes the occurrence of seizures in patients with end stage renal disease on dialysis therapy at the Nephrology Institute of Mogi das Cruzes, São Paulo State, Brazil. A retrospective medical history of 189 patients was reviewed to investigate the occurrence of convulsive seizures during dialytic program. Seven patients with history of seizures were selected but five of them were included in our study. Three patients presented generalized tonic-clonic seizures, one had partial seizure with secondary generalization, and one presented unclassified seizure. Three patients presented seizure just during the dialysis (unique seizure) and one of them presented convulsive status epilepticus. The two other patients had already presented seizures prior the beginning of dialysis. We conclude that seizures in renal failure could be considered as occasional events that do not usually become chronic.

The effects of alcohol intake and withdrawal on the seizures frequency and hippocampal morphology in rats with epilepsy

The aim of our study, using the pilocarpine model of epilepsy, was to investigate the effects of alcohol administration and withdrawal on the spontaneous recurrent seizures (SRSs). Four groups of adult, male Wistar rats were studied: (A). control rats (n=10), received neither pilocarpine nor alcohol, (B). alcohol-treated rats (n=10), received a daily dose of 3.0 g x kg(-1) of a 30% alcohol solution via an oesophagic probe for 30 days, (C). rats with epilepsy (n=10), (D). rats with epilepsy with alcohol intake (n=10). SRSs were induced by a single dose of pilocarpine (i.p.) and the basal frequency of SRSs was video monitored (24h per day) for 30 days. Following this period, the animals of group D received a daily dose of alcohol solution as described above and at the end of this period, alcohol administration was stopped and the seizure frequency was assessed for more 30 days. The basal seizure frequency observed in groups C and D during the first 30 days was 2.2+/-1.8 seizures per week per animal. In group D, it was observed an increase to 12.2+/-5.8 during the first 2 weeks of alcohol administration. During the last 2 weeks of alcohol administration, the number of SRSs returned to the previous basal level. During alcohol withdrawal the seizure frequency increased to 14.3+/-7.4 seizures per week per animal for the first 2 weeks, and returned to the basal level in the remaining period of observation. The Neo-Timm and Nissl staining of hippocampal formation and of the dentate gyrus in rats with epilepsy showed a cell loss in the hippocampal subfield CA1 and in the hillus of dentate gyrus. In rats with epilepsy with alcohol intake, we observed a cell loss in hippocampal subfields CA3 and hillus of the dentate gyrus, with significant neuronal death in subfield CA1, when compared with control animals. The alcohol withdrawal syndrome is a crucial event for the development of functional and neuropathological alterations associated with epilepsy.

Níveis cardíacos de troponina I em pacientes com epilepsia do lobo temporal refratária após cortico-amígdalo-hipocampectomia

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.

Serum magnesium and sudden unexpected death in epilepsy: A curious clinical sign or a necessity of life

Universidade Federal de Sao Paulo, Escola Paulista Med UNIFESP EPM, Disciplina Neurol Expt, Sao Paulo, Brazil