Over the past decade, there has been a large amount of evidence indicating neuroendocrine, biochemical, and immune disorders in many acute and chronic central nervous system (CNS) diseases, including epilepsy, which made the authors consider the inflammatory theory of epileptogenesis. The chronic inflammatory process in epilepsy is believed to be facilitated by the activation of microglia and astrogliosis, which are accompanied by neuronal damage. The main postulate of this type of investigation is the assumption that the basis for CNS inflammation is blood-brain barrier (BBB) damage. Cytokines are presumed to play the greatest role in this process, mainly because they are natural pro- and anticonvulsants. Patients and methods. Examinations were made in 160 patients with epilepsy (drug-resistant epilepsy (n = 80) and controlled epilepsy (n = 80)) and 30 apparently healthy donors. The blood and cerebrospinal fluid (CSF) levels of the cytokines interleukin (IL)-1β, IL-2, IL-6, IL-8, IL-10, tumor necrosis factor-α (TNF-α), IL-1 receptor antagonist (IL-1RA), soluble IL-2 receptor (sIL-2R), brain-derived neurotrophic factor (BDNF), S100b protein, C-reactive protein (CRP), and albumins were analyzed using a solid-phase enzyme-linked immunoabsorbent assay. Statistical analysis was performed using Student's t-test and Mann-Whitney U-test. Differences at p < 0.05 were regarded as statistically significant. Results and discussion. The investigation showed that the patients with epilepsy had a substantially impaired plasma cytokine profile: higher levels of proinflammatory cytokines, such as Il-1β, IL-8, and TNF, and a lower concentration of IL-1 RA. The elevated CSF levels of the cytokines Il-1β and IL8 in patients with epilepsy suggest that BBB is impaired and a systemic inflammatory process exists while the absence of IL-1RA indicates that protective inflammation factors in blood and CSF are reduced.