Central Sensitization Severity in Chronic Low Back Pain: Associations with Sleep, Distress, Cortisol, and Visuospatial Working Memory.

Background: Central sensitization (CS) is increasingly recognized as a key mechanism underlying chronic low back pain (CLBP), and has been linked to disturbed sleep, psychological distress, altered hypothalamic-pituitary-adrenal (HPA) axis function, low-grade inflammation, and cognitive dysfunction. However, few studies have simultaneously examined these domains in patients with different levels of CS compared with pain-free individuals. Methods: In this cross-sectional study, adults with CLBP were classified into severe and mild CS groups using the Central Sensitization Inventory and were compared with healthy controls. Sleep quality, psychological distress, and pain-related cognition were assessed using the Pittsburgh Sleep Quality Index, Depression Anxiety Stress Scales-21, and pain measures. Morning salivary cortisol, interleukin-6 (IL-6), and fasting blood glucose were obtained as biological markers, and cognitive performance was evaluated using the Corsi Block-Tapping and Tower of London tasks. Group differences were analyzed using one-way ANOVA with Tukey post-hoc tests. Results: Forty-two participants (patients with CLBP and pain-free controls) completed the study. Compared with both mild CS patients and controls, the severe CS group showed markedly poorer sleep quality and higher levels of psychological distress. Morning cortisol concentrations were significantly elevated only in the severe CS group, whereas no statistically significant differences were detected for fasting glucose or IL-6 between groups. On the Corsi Block-Tapping task, healthy controls outperformed both CS groups, indicating reduced visuospatial working memory in patients, whereas no significant group differences were observed on the Tower of London planning task. Conclusion: Severe central sensitization in CLBP is associated with poor sleep, increased emotional distress, elevated morning cortisol, and deficits in visuospatial working memory, even in the absence of clear differences in IL-6 or fasting glucose. These findings support a biopsychosocial profile characterized by both neuroendocrine and cognitive alterations in patients with high levels of CS and highlight potential targets for multimodal assessment and intervention.