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Ralf Weigel. 1 Division of Neurosurgical Research, Medical Faculty Mannheim, Ruprecht-Karls-University Heidelberg, Heidelberg, Germany. 2 Current address: Department of Neurosurgery, St. Katharinen Hospital, Frankfurt/Main, Germany.
Axel Hohenstein. 1 Division of Neurosurgical Research, Medical Faculty Mannheim, Ruprecht-Karls-University Heidelberg, Heidelberg, Germany. 3 Current address: Bioassay, Biological Analytics GmbH, Heidelberg, Germany.
Lothar Schilling. 1 Division of Neurosurgical Research, Medical Faculty Mannheim, Ruprecht-Karls-University Heidelberg, Heidelberg, Germany.
Address correspondence to: Lothar Schilling, MD, PhD, Division of Neurosurgical Research, Medical Faculty Mannheim, Ruprecht-Karls-University Heidelberg, Theodor Kutzer-Ufer 1-3, 68165 Mannheim, Germany, E-mail: [email protected]
Introduction
Chronic subdural hematoma (CSH) is considered a rather benign disease of the elderly, although mortality rates up to 13% are reported in the contemporary literature.1 Minor head trauma preceding development of CSH is documented in two thirds of patients; however, a CSH may also occur without such an obvious insult.2 Clinically, patients present with neurological impairment of varying intensity, which is classified using the scoring system suggested by Markwalder some 30 years ago.3 Diagnosis is usually corroborated by computed tomography (CT) scanning showing different levels of density within the hematoma,2 commonly based on the classification suggested by Nomura and coworkers.4 According to this classification, CSH images may appear as hypodense, isodense, hyperdense, or display mixed density.
The pathophysiology of CSH is not yet clear. Minor head trauma may lead to shear stress on the loose junction between the inner and outer layer of the dura and may initiate a cascade of bleeding, rebleeding, and exudation, which finally results in the formation of an increasing cavity within the dura mater. In this sequence of pathophysiological events, the parietal membrane adjacent to the subdural space appears to play an important role. Morphologically, the microvasculature of the parietal layer is grossly altered with an increase of vessel density, capillary diameter, and the occurrence of large intercellular gaps between the endothelial cells (ECs).5,6 These alterations have been related to increased local inflammatory activity,7 intermittent episodes of (re)bleeding,8 and exudation of proteins and plasma water.9 Recently, our group has reported extremely high concentrations of vascular endothelial growth factor (VEGF) in hematoma fluid.10,11 In addition, we found an inverse angiopoietin-1/angiopoietin-2 (Ang-1/Ang-2) messenger RNA ratio in tissue samples obtained from the parietal membrane.11