Glycosaminoglycans in subdural fluid and CSF after meningeal injury

Inflammatory mechanisms have an acknowledged role in the progression of chronic subdural hematoma (CSDH) and in tissue response after subarachnoid hemorrhage (SAH). The participation of extracellular matrix, especially glycosaminoglycans, in the cellular events during tissue repair is known to be important. We studied the production of glycosaminoglycans after two types of meningeal injury-one caused by rupture of the dural border cell layer after head injury, and the other caused by SAH.

Patients with CSDH (n = 28), subdural effusion (n = 8), and SAH (n = 33) were included in the study. Samples from subdural fluid or cerebrospinal fluid (CSF) were assayed for hyaluronic acid (HA) with an enzyme-linked assay and for sulfated glycosaminoglycans (sGAGs) with a dye-binding assay.

The median HA concentration was 3021 (range, 408-14,012) ng/ml in the CSDH fluid, 668 (392-3607) ng/ml in the effusion fluid, and 21.7 (5.8-195) ng/ml in the serum. In lumbar CSF after SAH, the median HA concentration was 246 (47-3686) ng/ml being 1.5-fold higher than that in control CSF. The median sGAG concentration was 52.8 (0-144) μg/ml in CSDH fluid, but only 5.32 (0-20.5) μg/ml in the effusion fluid, where the concentration was similar to that in the serum.

We found high, but variable, concentrations of sGAGs and HA in the CSDH and effusion fluid after head injury and HA in the CSF after SAH. Our results show that HA and sGAGs are induced after meningeal injury and that these proteins may participate in a reactive process.