LAUSR

Chronic subdural haematoma (CSDH) is invariably classified as 'neurotrauma'. However, whilst a history of trauma/fall is frequent, it is usually distant, mild or even absent. Serum S-100β > 1.38 μg/L is associated with a 100% specificity for mortality/poor outcome acutely after moderate-severe neurotrauma. Serum S-100β > 0.10 μg/L is used to screen mild neurotrauma cases for emergent neuro-imaging. Serum S-100 in controls is 0.057 μg/L. S-100β in serum or CSDH fluid (CSDHf) has not been studied. No normal 'subdural fluid' exists to compare CSDHf. We measured serum and CSDHf S-100β at surgical drainage in a novel prospective single-centre cohort. Of n = 86/86 (100%, M65, age 73 ± 13yrs), n = 66 (76%) reported mild trauma/fall 31 ± 23 days previously. N = 54 (63%) presented with good clinical Markwalder Grade (MG: 0-1). Paired serum and CSDHf S-100β samples were obtained in n = 45. CSDHf S-100β (n = 80) was elevated (0.9 ± 0.6 μg/L), was significantly higher than serum S-100β (n = 51) (0.33 ± 0.05 μg/L, P = 0.002), and was significantly correlated with midline-shift (r = 0.43, P = 0.005) and CSDH volume (r = 0.225, P = 0.046). CSDHf S-100β was not significantly associated with any demographic factor, co-morbidity or outcome measure. CONCLUSIONS: Despite expectations, S-100β was elevated in serum CSDH, but was significantly higher in CSDHf. Indeed, CSDHf S-100β approached serum levels associated with a poor prognosis after acute-neurotrauma. However, CSDHf S-100β did not represent a biomarker for trauma nor functional outcome. Whilst the non-traumatic source for on-going S-100β release could not be determined, prolonged compression of an atrophic brain, subsequent CSF leakage, or 'subdural-space' meningeal disruption/proliferation, represent theoretical possibilities. Elevated S-100β may therefore not be specific for mild-moderate-severe acute neurotrauma. Alternative non-traumatic intra-cranial mechanisms evidently also exist.