Objective: The intrathecal posttraumatic inflammation contributes to secondary brain damage as well as to the induction of neuroreparative mechanisms. In this context release of interleukin-10 (IL-10) has been reported to play a major role. However, initial IL-10 concentration in CSF remains incompletely characterized. Therefore, the aim was to analyze Il-10 in CSF and serum of patients early after TBI. Methods: For control, 10 volunteers receiving spinal puncture were enrolled. In patients with severe TBI (GCS< 8pts.), CSF and serum was drawn within 90±45min after intraventricular catheter insertion (0h), as well as 12h, 24h and 48h after TBI. Albumin for assessing Blood-Brain-Barrier (BBB) function and IL-10 (IMMULITE, DPC Biermann, Bad Nauheim, Germany) were analyzed.

Results: 23 patients were enrolled. 15 survived and 8 deceased within 24h. In controls, CSF IL-10 was below detection limit (< 5pg/ml). In contrast, IL-10 was elevated significantly in non-survivors at 0h vs. survivors and controls (30±6 vs. 9±1 vs.< 5pg/mL). This was accompanied by a significant increase of serum IL-10 in both groups at 0h vs. controls (survivors: 30±6pg/mL, non-survivors: 48±8pg/mL, controls: 10±7pg/mL, p< 0.001). Survivors revealed signs of a mild BBB dysfunction during the entire observation period. In contrast, non-survivors presented a severe BBB breakage.

Conclusions: We demonstrated an analysis of IL-10 CSF and serum concentration after TBI. These data support an intrathecal IL-10 synthesis. Although the significant increase of IL-10 might indicate a bad outcome of TBI, responsible mechanisms still have to be elucidated.