Introduction. Dravet syndrome (DS) is an epileptic and developmental infantile onset encephalopathy, characterized by a polymorphic evolution of seizures and resistant to antiepileptic drugs. Purpose of the research. Analysis of data from the literature and our patients to highlight evolving electroencephalographic (EEG) features in DS patients. Material and methods. Prospective review of Pubmed data studies including: ≥ 1 patient with clinical diagnosis of SD and SCN1A pathogenic variant, and for each such patient, a description of ≥ 1 EEG and age at time of EEG. We also reviewed our research database for Dravet patients with available EEG reports that included 5 patients. We extracted data from reported EEG abnormalities (generalized/focal epileptiform abnormalities, focal/diffuse slowing). We determined the earliest ages at which various abnormalities were observed, as well as the percentage of abnormalities reported for different age ranges. The SPSS program was used for the statistical analysis. Results. An analysis was performed on EEG data (no. 108 recordings) from 56 patients with Dravet syndrome (from 19 studies and our research base). The following EEG changes were reported at the onset of the disease in 43.6% – normal appearance or non-specific changes (age 4-6 months), later over 12 months: 43.2% – with generalized and focal epileptiform discharges, diffuse background slowing and focal slowings, and 30.8% showed atypical epileptic activity in the form of absences. Thus, the EEG was normal in most patients in the first year of life, followed later by the appearance of generalized, focal and multifocal discharges. Conclusions. Normal EEG findings in patients with genetic DS at disease onset often confuse and delay early diagnosis, and the low rate of specific developmental epileptiform abnormalities confounds treatment. Molecular-genetic examinations are recommended in infants with epileptic seizures without electrographic changes. According to these electroclinical criteria, it is possible to divide the population into two groups, both sharing common genetic mechanisms but with a different clinical outcome.