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Glycosaminoglycans in subdural fluid and CSF after meningeal injury

  • Clinical Article - Brain Injury
  • Published:
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Abstract

Background

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.

Methods

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.

Results

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.

Conclusions

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.

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Acknowledgments

This research was supported in part by The National Graduate School of Clinical Investigation (ALH)

Conflict of interest

All authors certify that they have no affiliations with or involvement in any organization or entity with any financial interest (such as honoraria; educational grants; participation in speakers’ bureaus; membership, employment, consultancies, stock ownership, or other equity interest; and expert testimony or patent-licensing arrangements), or non-financial interest (such as personal or professional relationships, affiliations, knowledge or beliefs) in the subject matter or materials discussed in this manuscript.

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Correspondence to Anna-Leena Heula or Kari Majamaa.

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Comment

Glycosaminoglycans (GAGs) act like sponges, retain water, and reduce diffusion of molecules. It is interesting to see that production of GAGs is induced by trauma of the meninges. It is also interesting to see another mechanism used by nature to promote repair and keep the process local. Questions raised after reading the manuscript and stimulating further research are: When and how is it harmful? How do we influence the processes with medication and intervention? How could we take advantage of it and improve outcome? How could we modulate it?

Philippe Bijlenga

Geneva, Switzerland

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Figure 1

Concentrations of total protein, hyaluronic acid, and sulfated glycosaminoglycans in chronic subdural hematoma (CSDH) fluid (A), subdural effusion fluid (B) and lumbar CSF after SAH (C, excluding sulfated glycosaminoglycans). The samples were obtained at the time points indicated after head injury (A, B) or SAH (C). (PDF 294 kb)

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Heula, AL., Sajanti, J. & Majamaa, K. Glycosaminoglycans in subdural fluid and CSF after meningeal injury. Acta Neurochir 157, 2105–2110 (2015). https://doi.org/10.1007/s00701-015-2591-5

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  • DOI: https://doi.org/10.1007/s00701-015-2591-5

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