Changes in interictal pretreatment and posttreatment EEG in childhood absence epilepsy

Abstract

Spike and wave discharges (SWDs) are the characteristic manifestation of childhood absence epilepsy (CAE). It has long been believed that they unpredictably emerge from otherwise almost normal interictal EEG. Herein, we demonstrate that pretreatment closedeyes theta and beta EEG wavelet powers of CAE patients (20 girls and 10 boys, mean age 7.4 ± 1.9 years) are much higher than those of age-matched controls at multiple sites of 10-20 system. For example, at C4 site, we observed a 91% and 62% increase in power of theta and beta rhythms, respectively. We were able to compare the baseline and posttreatment wavelet power in 16 patients. The pharmacotherapy brought about a statistically significant decrease in delta and theta wavelet power in all the channels, e.g. for C4 the reduction was equal to 45% (delta) and 65% (theta). We also observed a less pronounced attenuation of posttreatment beta rhythm in several channels. We hypothesize that the increased theta and beta powers result from cortical hyperexcitability and propensity for epileptic spikes generation, respectively. We argue that the distinct features of CAE wavelet power spectrum may be used to define an EEG biomarker which could be used for diagnosis and monitoring of patients.

Role of Biomarkers in Epileptogenesis: A Concise Review

“…All things considered, an exceptionally prescient attractive reverberation imaging (MRI) or electroencephalogram (EEG) biomarker would be more adequate. As depicted over, a basic thought is the 'window' when the biomarker is communicated corresponding to the sickness [24]. For instance, on account of epileptogenesis, it is basic to know when after a head injury or stroke, the biomarker first shows up and how long it endures.…”

Nghiên Cứu Đặc Điểm Điện Não Đồ Ngoài Cơn Ở Bệnh Nhân Động Kinh Tâm Thần Vận Động

“…Theo nghiên cứu của Glaba P. (2020) thì thấy rằng biên độ sóng theta tăng lên ở nhiều vị trí trên hệ thống điện não đồ 10-20. Đặc biệt ở vị trí các điện cực C4, P3 và O1 thì biên độ đã biến đổi từ 46% -63% so với người bình thường [7].…”

Parallel changes in the promoter methylation of voltage-gated T-type calcium channel alpha 1 subunit G and histone deacetylase activity in the WAG/Rij model of absence epilepsy

“…In patients with the absence of epilepsy, genetic analyses indicated the CACNA1G gene, which is located on chromosome 19 and encodes the poreforming α1A subunit of Cav2.1 channels, linked to the epileptic phenotype (8). Functional expression studies on CACNA1G demonstrated that the E147K mutation impairs calcium channel function and is related to abnormal neuronal firing (9). Further studies revealed that Cav2.1 channels are expressed in the cerebellar Purkinje and granule cells at high levels, directly related to the initiation point of absence seizures (10).…”