Ricardo Mario Arida

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.

Biophysical Aspects of the Nonsynaptic Epileptiform Activity

Since the demonstration that the hippocampus slice exposed to low calcium external solution is able to sustain nonsynaptic epileptiform activity, it has been accepted that nonsynaptic interactions may be sufficient, in some conditions, for generating seizure like activity in cortical network. Recently, evidences have suggested that the reductions in calcium are not essential for nonsynaptic mechanisms to contribute to epileptic activity. Therefore, evidences allow demonstrating that the conjoint actuation of nonsynaptic mechanisms and nonsynaptic connections are able to induce and sustain seizures. The nonsynaptic mechanisms considered in this context are all mechanisms which are not directly involved with synaptic transmission, but comprehending important action on the homeostasis equilibrium and, consequently, on the neuronal excitability. The non-synaptic connections are all types of neuronal coupling that are not mediated by synaptic transmission. The concomitant actuation of nonsynaptic mechanisms and connections seems to be a relevant process for the seizure intensity modulation. Therefore, it may be conjectured that the nonsynaptic mechanisms and connections could be considered a natural target for investigations aiming to control refractory seizures. Within this perspective, the scope of the present chapter will cover the following topics: • nonsynaptic events: experimental induction and electrophysiological characteristics; • nonsynaptic mechanisms; • nonsynaptic connections; • biophysical aspects of the nonsynaptic epileptiform activities; • possible targets for controlling refractory seizures.

Physical Exercise as a Strategy to Reduce Seizure Susceptibility

Effective strategies for preventing or treating epilepsy have been extensively used. Exercise has gained substantial attention to stimulate brain plasticity as well as noninvasive therapeutic strategy for achieving rehabilitation after brain damage. This chapter focuses on the beneficial effects of exercise programs observed in clinical studies and animal models of epilepsy, and their importance as complementary therapy for epilepsy. Information about the antiepileptogenic and neuroprotective effects of physical exercise is emphasized. Considering that exercise can promote beneficial actions such as reduction of seizure susceptibility, reduction of anxiety and depression, and improvement of quality of life of people with epilepsy, it can be suggested to be integrated with conventional therapy for epilepsy.