Serum Neuron-Specific Enolase as a Prognostic Biomarker in Pediatric Convulsive Status Epilepticus: A Single-Center...

Serum neuron-specific enolase (NSE) is a biomarker of neuronal injury, but its prognostic role in pediatric convulsive status epilepticus (CSE) remains uncertain. We evaluated the association between serum NSE levels and short-term neurological outcome, assessed model calibration with internal bootstrap validation, and examined whether NSE provides incremental discrimination beyond established clinical severity scores.

This was a single-center retrospective cohort study of children aged 1 month to 18 years admitted to a tertiary pediatric intensive care unit (PICU) with CSE as the primary admission diagnosis between January 2024 and November 2025. The primary outcome was poor neurological outcome at hospital discharge, defined as a worsening of ≥1 point in the Pediatric Cerebral Performance Category (PCPC) score from baseline (ΔPCPC ≥ 1) or in-hospital death. A multivariable logistic regression model adjusting for NSE, PRISM III, acute symptomatic etiology, and mechanical ventilation was developed, with bootstrap optimism-corrected internal validation (2000 resamples) and formal calibration assessment. Separate models for in-hospital mortality and for neurological deterioration among survivors were conducted as secondary analyses. Diagnostic operating characteristics were reported with 95% Wilson confidence intervals. The study followed the STROBE and TRIPOD reporting guidelines.

Of 132 children included (median age 26 months, 56.1% male), 60 (45.5%) had a poor neurological outcome including 18 deaths (13.6%). Serum NSE was significantly higher in the poor-outcome group (median 22.0 vs. 14.4 μg/L; p < 0.001). In the primary multivariable model, NSE (adjusted OR 1.11 per μg/L; 95% CI 1.06-1.19; p = 0.001) and PRISM III (adjusted OR 1.15; 95% CI 1.03-1.37; p = 0.013) were independently associated with poor outcome. The model showed acceptable calibration (Hosmer-Lemeshow p = 0.130) and a bootstrap optimism-corrected AUC of 0.759. NSE remained independently associated with both in-hospital mortality (aOR 1.13) and with ΔPCPC ≥ 1 in survivors (aOR 1.09). The AUC for NSE alone was 0.741 (95% CI 0.65-0.82) for poor outcome and 0.885 (0.79-0.96) for mortality. The combined PRISM III + NSE model showed a numerically higher but not statistically significant AUC compared with PRISM III alone (0.784 vs. 0.726; DeLong p = 0.103).

Higher serum NSE is independently associated with adverse short-term neurological outcome and mortality in pediatric CSE, including in survivor-only analysis. However, the present data do not demonstrate clinically meaningful incremental prognostic value beyond PRISM III, and the proposed cutoff was derived and tested in the same cohort and is therefore optimistic. These findings are hypothesis-generating and require external validation in prospective multicenter cohorts with serial sampling and long-term neurodevelopmental follow-up before routine clinical use can be advocated.