مکانیسم کنترل تشنج ابسنس با محرک مغزی عمیق اعمال شده در هسته زیر تالاموسی Controlling mechanism of absence seizures by deep brain stimulus applied on subthalamic nucleus

Introduction Absence epilepsy is one kind of generalized non-convulsive brain seizure disease, mainly occurred in childhood (Loiseau et al. 1995). The typical features of absence seizures are transient loss of consciousness, and then suddenly stop, at the same time, along with the specific electrophysiological characteristics, i.e., bilateral synchronous spike wave discharges (SWDs) with slow oscillation frequency (2–4 Hz) (Loiseau et al. 1995; Crunelli and Leresche 2002), which usually shown on the electroencephalogram (EEG) [which also used to check other brain nerve diseases, such as the Parkinson’s disease (Yi et al. 2017)] of patients. The brain anatomical structure and medical experiments have shown that the SWDs of absence seizures mainly induced by abnormal interactions between the cortex and thalamus neurons, they form the cortical–thalamic (CT) loop system. The CT network is an important anatomical structure of the brain, the firing activity of which is closely related to the neurophysiological state of the brain, such as sleep, epilepsy seizure, etc. The physiological activity record of the cerebral cortex and thalamus on rodent models and clinical patients is the direct evidence of epileptic seizure arising from the CT system (Marescaux and Vergnes 1995; Coenen and Luijtelaar 2003). Subsequently, there have developed many concepts on the pathophysiology of epilepsy, such as the cortical focus theory (Meeren et al. 2005). At present, there are also many mathematical models, especially the mean field model, used to study the pathogenesis of epilepsy and have obtained a series of results are in good agreement with experiments (Robinson et al. 2002; Rodrigues et al. 2006, 2009; Takeshita et al. 2007; Marten et al. 2009a, b; Wilson et al. 2006; Case and Soltesz 2011; Dadok et al. 2012; Chen et al. 2014, 2015; Hu et al. 2015; Hu and Wang 2015; Hu et al. 2017; Paz et al. 2011; Paz and Huguenard 2015). Breakspear et al. employed the bifurcation analysis to give an unifying mechanism of primary generalized seizures (Breakspear et al. 2006). The detailed cellular and network mechanisms of genetically-determined absence seizures referred to (Pinault and O’Brien 2005). The gap junctions also play an important role in the process of epileptic seizure (Volman et al. 2011). Volman and Perc found that the rewiring and forming of new links between neurons may greatly affect the generation of seizures (Volman and Perc 2010). Recently, Fan and Wang et al. discussed the disinhibition-induced transition mechanism between absence and tonic–clonic seizures in detail (Fan et al. 2015).