Abstract
Recent clinical practice has found that the spike-wave discharge (SWD) scopes of absence seizures change from small cortical region to large thalamocortical networks, which has also been proved by theoretical simulation. The best biophysics explanation is that there are interactions between coupled cortico-thalamic and thalamocortical circuits. To agree with experiment results and describe the phenomena better, we constructed a coupled thalamocortical model with bidirectional channel (CTMBC) to account for the causes of absence seizures which are connected by the principle of two-way communication of neural pathways. By adjusting the coupling strength of bidirectional pathways, the spike-wave discharges are reproduced. Regulatory mechanism for absence seizures is further applied to CTMBC via four different targeted therapy schemes, such as deep brain stimulation (DBS), charge-balanced biphasic pulse (CBBP), coordinated reset stimulation (CRS) 1 : 0, and (CRS) 3 : 2. The new CTMBC model shows that neurodiversity in bidirectional interactive channel could supply theory reference for the bidirectional communication mode of thalamocortical networks and the hypothesis validation of pathogenesis.
Highlights
Absence seizures characterized by spike-wave activity were first discovered in 1941 by the electroencephalograms (EEGs) of patients [1], whose frequency is shown at a range of approximately 2–4 Hz [2]
There are four types of neuronal populations shown in the original Taylor model [19], which are comprised of thalamic reticular nucleus (TRN) and specific relay nucleus (SRN) in the subcortical pathway and inhibitory interneuronal population (IN) and pyramidal neuronal population (PY) in the cortex, where pathological spike-wave discharge (SWD) activity is reproduced and a single pulse stimulation is given to control epileptic seizures
It is necessary to analyze the relationship between TRN activation and caused absence seizures in our coupled thalamocortical model with bidirectional channel
Summary
Absence seizures characterized by spike-wave activity were first discovered in 1941 by the electroencephalograms (EEGs) of patients [1], whose frequency is shown at a range of approximately 2–4 Hz [2]. The model embodies the dynamics of cerebral cortex incorporating stereotactic space and distance [16,17,18] Due to their coupling interactions with each other, dynamical behaviors of firing neurons can be reproduced, which can be regarded as a reference model of macroscopic absence seizures in epilepsy. It is necessary to construct a theoretical model to explore a wide range of pathogenic possibilities It remains uncertain whether or not absence seizures exist in coupled thalamocortical model with interactional channel. A coupled thalamocortical network evolved from a neural field model is composed mainly of four neuronal populations with unidirectional information transfer Inspired by these excellent results, a large amount of unknown space is found in coupled thalamocortical model with interactional channel [39, 40].
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