مروری بر صرع کوچک با رویکرد به علوم پایه

Abstract Background: Epilepsy is one of the most common neurological disorders. Seizures could be presented as general or focal attacks. Absence epilepsy is one of the main forms of the general epilepsy and associated with sudden impairment of consciousness and non/convulsive generalized attacks. The prevalence of absence epilepsy was estimated about 10% of all types of seizures and seizures onset usually started between 3-8 years old. The genetic factors play a crucial role in the absence epilepsy. Dysfunction in the thalamocortical network seems to be a main factor in the pathogenesis of the absence epilepsy. Due to abnormal interaction between the reticular neurons, thalamocortical neurons and pyramidal neurons absence epilepsy can be occurred. Extra release of GABA from the reticular neurons leads to suppress the relay neurons in the thalamus. Hyperpolarization of these neurons can open T-type-Ca+2 channels. The burst activity of relay neurons causes extra release of glutamate. These hyperactivities of relay neurons trigger spike-wave discharges in the neocortex. Methods: In this manuscript the epidemiology, etiology, epidemiology, animal models, pathophysiology and the treatment of absence epilepsy were collected by studying the original and review articles. Conclusions: It seems that we should notice this disorder because of its prevalence and side effects. The results of many studies indicated that there are several types of reasons for the onset of this disease. Thus for treatment of these patients we should consider all of the involved elements. Keywords: Absence epilepsy, EEG, Pathophysiology.