Fuchs endothelial corneal dystrophy (FECD) is the most common corneal endothelial dystrophy. It is characterized by the progressive loss of corneal endothelial cells (CECs), guttae formation on the Descemet membrane, and corneal edema, leading to visual impairment. Corneal transplantation remains the standard treatment, but it has limitations such as donor shortages, infection risk, and graft rejection. Rho-kinase (ROCK) inhibitors have emerged as a promising pharmacological alternative. These agents promote CEC proliferation, migration, and adhesion while inhibiting apoptosis and enhancing corneal endothelial wound healing. Several studies have demonstrated the efficacy of ROCK inhibitors in improving corneal clarity and endothelial function, particularly when used as an adjunct to Descemet Stripping Only (DSO) surgery. Additionally, they show potential in preventing corneal edema in FECD patients undergoing cataract surgery. The methodology involved a literature search through the PubMed and Medline databases using relevant keywords. Only peer-reviewed articles in English were included, with additional references from selected articles reviewed to ensure comprehensive coverage. ROCK inhibitors offer a novel pharmacological approach to managing FECD. They have shown potential in promoting endothelial cell regeneration and improving corneal functIion. Despite promising results, further research is required to determine ROCK inhibitors’ long-term safety, optimal dosing, and efficacy in surgical and non-surgical FECD patients. Their potential to delay or prevent corneal transplantation represents a significant advancement in FECD management.

Objective: Psychogenic non‐epileptic seizures (PNES) are functional neurological disorders that are often misdiagnosed and treated as epileptic seizures (ES). Video‐electroencephalography (v‐EEG) is the gold standard for differentiating ES from PNES. However, blood biomarkers provide a faster and more accessible methodology, particularly for unwitnessed events. Ubiquitin C‐terminal hydrolase L1 (UCH‐L1) and protein S100B are key biomarkers released following neuronal and glial damage. Previous experimental and clinical studies have shown increased postictal serum and cerebrospinal fluid (CSF) levels of UCH‐L1 and S100B in patients with ES.Methods: This prospective cohort pilot study compared postictal serum levels of UCH‐L1 and S100B proteins in subjects with ES to those with PNES, aiming to identify specific biomarkers for distinguishing these conditions. To exclude confounding factors, the inclusion criteria required normal magnetic resonance (MR) findings of the brain. Strict timing of blood sampling and v‐EEG monitoring were used for diagnosing PNES. The study included 32 subjects with epilepsy, 36 with PNES, and 30 healthy controls.Results: A significant difference in postictal UCH‐L1 levels was observed among the groups. Subjects with ES had significantly higher postictal UCH‐L1 levels (pg/mL) compared to those with PNES (p = 0.049) and healthy controls (p = 0.029). No significant differences were found between PNES subjects and healthy controls (p = 0.756). Postictal protein S100B levels did not differ significantly between the groups (p = 0.515).Significance: This study confirms the potential of postictal UCH‐L1 levels as a biomarker for distinguishing ES from PNES. However, it also raises questions about the utility of protein S100B as a biomarker in epilepsy. Given the pilot nature of this study, UCH‐L1 cannot yet be adopted for clinical use due to the small sample size, as statistical significance may have been driven by a subset of eight patients.Plain Language Summary: This study evaluated two potential biomarkers, UCH‐L1 and S100B, to differentiate ES from PNES in clinical practice. Our findings showed elevated postictal UCH‐L1 levels in subjects with epilepsy compared to those with PNES, while no significant differences in S100B levels were observed among the groups.