A new hypothesis of drug refractory epilepsy: Neural network hypothesis

Drug-Resistant Epilepsy: Multiple Hypotheses, Few Answers

“…Recently, Fang et al (51) proposed the neural network hypothesis, which states that seizure-induced degeneration and remodeling of the neural network suppress the endogenous antiseizure system and inhibit ASDs from accessing neuronal targets. Specifically, molecular evidence shows that the growth cone at the tip of an exon receives abnormally expressed guidance and signaling molecules in the epileptic brain (51).…”

“…Specifically, molecular evidence shows that the growth cone at the tip of an exon receives abnormally expressed guidance and signaling molecules in the epileptic brain (51). In addition, the formation of new excitatory circuits as a result of progressive sprouting has been widely investigated in TLE (51). The authors postulate that neurogenesis and astrogliosis in TLE could contribute to the development of abnormal neural networks and eventually ASD resistance.…”

“…The authors postulate that neurogenesis and astrogliosis in TLE could contribute to the development of abnormal neural networks and eventually ASD resistance. However, the major weakness of this hypothesis is that alterations in the neural network do not lead to refractoriness in all epilepsy patients, and therefore, further biological evidence on potential differences in the changes of brain plasticity between drug-responsive and drug-resistant epilepsy is needed to support this hypothesis (51). …”

Activation of LILRB2 signal pathway in temporal lobe epilepsy patients and in a pilocarpine induced epilepsy model

“…The main pathological changes of TLE, including neuron degeneration, neurogenesis, gliosis, mossy fiber sprouting and synaptic reorganization, have been observed in the epileptic zone (Bae et al, 2010;O'Dell et al, 2012). Obviously, aberrant excitatory neural networks provide the anatomic basis for epilepsy (Fang et al, 2011). For instance, it has been confirmed that increased excitatory synaptic input to granule cells from CA3 and hilar areas composing the positive-feedback circuits might contribute to epileptogenesis in a rat model of TLE .…”

Kangxian capsules: Effects on convulsive injuries, N -methyl- d -aspartate (NMDA) receptor subunit expression, and free Ca 2+ concentration in a rat hippocampal neuron epileptic discharge model

“…This disease is characterized by excessive discharge of neurons that result in sudden, repeated, and transient central nervous system dysfunction. Numerous studies have shown that abnormal neuronal discharge is related to a number of factors, such as neurotransmitter abnormalities [2][3][4], ion channel mutations [5], glial cell dysfunction [6,7], synaptic connection dysfunction [8], heredity, and immunity [9,10]. Because A c c e p t e d M a n u s c r i p t children and rat models, thus reducing seizure frequency, and the underlying mechanisms are not clear [11].…”