Epilepsy Unit, IRCCS Foundation Carlo Besta Neurological Institute, Milan, Italy.
Epilepsia. 2021 Mar;62(3):583-595. doi: 10.1111/epi.16824. Epub 2021 Jan 25.
Loss of myelin and altered oligodendrocyte distribution in the cerebral cortex are commonly observed both in postsurgical tissue derived from different focal epilepsies (such as focal cortical dysplasias and tuberous sclerosis) and in animal models of focal epilepsy. Moreover, seizures are a frequent symptom in demyelinating diseases, such as multiple sclerosis, and in animal models of demyelination and oligodendrocyte dysfunction. Finally, the excessive activity reported in demyelinated axons may promote hyperexcitability. We hypothesize that the extracellular potassium rise generated during epileptiform activity may be amplified by the presence of axons without appropriate myelin coating and by alterations in oligodendrocyte function. This process could facilitate the triggering of recurrent spontaneous seizures in areas of altered myelination and could result in further demyelination, thus promoting epileptogenesis.
大脑皮质中髓鞘的丢失和少突胶质细胞分布的改变，在不同局灶性癫痫（如局灶性皮质发育不良和结节性硬化症）的术后组织以及局灶性癫痫的动物模型中均很常见。此外，脱髓鞘疾病（如多发性硬化症）和脱髓鞘及少突胶质细胞功能障碍的动物模型中，癫痫发作是一种常见症状。最后，报道称脱髓鞘轴突的过度活动可能会促进过度兴奋。我们假设，癫痫样活动期间产生的细胞外钾升高可能会因缺乏适当髓鞘包被的轴突的存在以及少突胶质细胞功能的改变而被放大。这个过程可能会促进在髓鞘改变区域中反复发作的自发性癫痫发作，并可能导致进一步的脱髓鞘，从而促进癫痫发生。
