Recent epidemiological studies indicate that neurological disorders are currently the leading cause of disability and the second leading cause of mortality worldwide. In recent decades, considerable progress has been made in understanding the aetiology and treatment of neurological disorders. To achieve an adequate therapeutic effect and reduce the possibility of unwanted reactions, it is necessary to gain a thorough understanding of the factors that influence pharmacokinetics and pharmacodynamics. For many years, females have not been sufficiently included in clinical studies of drugs. The reasons are primarily related to the fear of adverse effects of the tested drugs during pregnancy and breastfeeding. However, at the beginning of the current millennium, females began to be increasingly included in clinical trials in response to recommendations from the United States Food and Drug Administration (FDA). Therefore, knowledge of sex differences in the pharmacokinetics and pharmacodynamics of drugs is increasing. Nevertheless, there are currently no specific recommendations regarding the dosage differentiation of most drugs between females and males. This article aims to summarize current knowledge on current knowledge on sex differences in the pharmacokinetics, efficacy, and safety of drugs commonly used to treat neurological patients to achieve a personalized approach. In the future, attention should be devoted to evaluating differences in the pharmacokinetics of drugs under development to optimize their therapeutic effects and reduce the number of adverse reactions in both sexes.

Background: Status epilepticus (SE) is a neurological emergency associated with neuronal injury and activation of apoptotic pathways. While these mechanisms are well described in experimental models, evidence in humans is limited. This study evaluated Bcl-2 and FAS—key apoptosis-related proteins—in the serum and cerebrospinal fluid (CSF) of patients with convulsive SE. Methods: Between February 2024 and January 2025, CSF and serum samples were collected from 18 adults with convulsive SE within 48 h of onset, and from 15 control subjects. Patients with acute brain injury, stroke, tumors, or central nervous system infections were excluded. Bcl-2 and FAS concentrations were quantified using ELISA. Serum samples were obtained at diagnosis (S1), 24 h (S2), and 7 days (S3). Results: CSF Bcl-2 levels were significantly higher in SE patients compared with controls (z = 4.1, p < 0.001). CSF FAS levels did not differ significantly (z = 0.07, p = 0.94). No differences in serum Bcl-2 were observed. In contrast, serum FAS concentrations were significantly elevated at all three time points in SE patients compared with controls (S1–S3; all p < 0.001). Conclusions: Convulsive SE is associated with distinct apoptotic responses in the central nervous system and periphery. Elevated CSF Bcl-2 may reflect acute neuroprotective or stress-related responses, whereas persistently increased serum FAS suggests systemic apoptotic activation. These findings highlight the potential prognostic and therapeutic relevance of apoptosis-related biomarkers in SE.