Chronic Subdural Hematoma: A Historical and Clinical Perspective

Abstract

Background: This review aims to highlight the clinical complexity of chronic subdural hematoma (cSDH) while presenting a brief historical discussion of cSDH.

Methods: A thorough literature search of published English-language papers was performed in PubMed, Ovid, and Cochrane databases.

Results: cSDH affects 1-5.3 per 100,000 individuals annually, with the incidence expected to rise as the U.S. population ages. The symptoms of cSDH are often nonspecific, with headaches being the most common complaint. Other symptoms include weakness, balance and gait problems, and memory problems.

Conclusions: A variety of clinical factors must be taken into account in the treatment of cSDH, and the multifaceted treatment paradigms continue to evolve.

Keywords: Chronic; Hematoma; Membrane; Neurosurgery; Subdural; Trauma.

Figure 1.

(A) Diagram illustrating a chronic subdural hematoma (cSDH) between the dura-arachnoid interface (coronal view). (B) Axial view of a computed tomography (CT) scan depicting a cSDH. The arrowhead depicts the fluid level with higher density blood products in the posterior region of the subdural compartment. (C) Sagittal view of a CT scan depicting cSDH, with the asterisk depicting an intradural membrane that is tenting the neuroparenchyma.

Figure 2.

Timeline depiction of the major historical events in chronic subdural hematoma history. cSDH, chronic subdural hematoma; CSF, cerebrospinal fluid.

Figure 3.

Depiction of the various molecules implicated in chronic subdural hematoma formation. Of note, inflammatory cell recruitment (green), angiogenesis of leaky and permeable capillaries (red), factors supporting membrane formation (brown), and fibrinolysis (blue). The dura would be located adjacent to the external/outer membrane. Ang, angiopoietin; CSDH, chronic subdural hematoma; FDPs, fibrin/fibrinogen degradation products; HIF, hypoxia-inducible factor; IL, interleukin; JAK-STAT, Janus kinase-signal transducer and activator of transcription; MAPK, mitogen-activated protein kinase; MMP, matrix metalloproteinase; NO, nitric oxide; PGE, prostaglandin E; PI3 kinase Akt, phosphatidylinositol 3-kinase-serine/threonine kinase; PICP, procollagen type 1; PIIINP, procollagen type 3; tPA, tissue plasminogen activator; VEGF, vascular endothelial growth factor. (Adapted from Edlmann E, Giorgi-Coll S, Whitfield PC, Carpenter KL, Hutchinson PJ. Pathophysiology of chronic subdural haematoma: inflammation, angiogenesis and implications for pharmacotherapy. J Neuroinflammation. 2017;14:108, distributed under the terms of the Creative Commons Attribution 4.0 International License [https://creativecommons.org/licenses/by/4.0/]).