As stated above, an SDH is classified as subacute if the clinical symptoms take more than 48-72 h, but less than 3 weeks to appear (Fig. 7.16a). Coagulation of the blood has usually occurred, with signs of leukocyte emigration, ingestion of erythrocytes, and/or digestion as demonstrated by Fe-containing macrophages, plus the formation of granulation tissue comprised of fibroblasts, collagenous fibers, macrophages, and endothelial cells. A dense network of precipitated fibrin holds the hematoma together.
Chronic SDH requires a survival time of about 3 weeks or more to develop. It expands very gradually due to successive bleeding, so that clinical symptoms develop very slowly. The morphology, which is largely characterized by resorption and organization, varies according to the survival time. Chronic SDH is characterized by a clearly delineated collection of a clot between the dura mater and arachnoid. The SDH is typically encapsulated by a neomembrane (Figs. 7.16d, c, 7.17) formed by the dura mater as a non-specific reaction to blood or its degradation products (Apfelbaum et al. 1974). Whereas the outer membrane contains giant neovessels, the inner membrane is only poorly vascularized.
The neomembrane (Fig. 7.16d) that forms on the inner aspect creates a small space or a cavity into which recurrent bleeding may occur. The rebleeding phenomenon can make it difficult or nearly impossible to determine the age of an SDH. Bleeding that recurs after a single traumatic event must be distinguished from multiple episodes of bleeding caused by one or several, temporally distinct, traumatic or spontaneous events. Though most neuropathologists suggest that any neomembrane will result from sub-dural hemorrhages, we have to accept that neomem-
branes are seen in newborn infants as well as in the elderly without any morphological indication of former hemorrhage and without a traumatic event.
Under clinical conditions in the elderly, chronic SDH can present diagnostic problems. The brain atrophy often associated with advanced age is a well-recognized factor facilitating development of SDH (Fogelholm et al. 1975; Spallone et al. 1989). Chronic SDH, though present, is often not suspected in elderly patients for a number of reasons: the neurological symptomatology is frequently protean and slow
Fig. 7.17a-c. Chronic subdural hematoma associated with age-related external brain atrophy. a The external lamina of the right part of the dura is still removed and parts of the internal lamina are visible; b within this secondary (intradural) space the hema toma is located; c a transverse section of the hematoma gives evidence of the membrane structure, the color, and consistence of the hematoma
Fig. 7.17a-c. Chronic subdural hematoma associated with age-related external brain atrophy. a The external lamina of the right part of the dura is still removed and parts of the internal lamina are visible; b within this secondary (intradural) space the hema toma is located; c a transverse section of the hematoma gives evidence of the membrane structure, the color, and consistence of the hematoma to progress, and may closely mimic cerebrovascular disease; the causative traumatic event may have been so mild, such as walking on irregular ground or stepping into a gopher hole, as to elude the notice of even the victim.
A special problem may be the question of why chronic SDH continues to grow slowly and does not coagulate. Murakami and his colleagues (2002) evaluated thrombomodulin expression and stated that thrombomodulin is expressed on the sinusoidal vessels and, thus, the blood coagulation system is inhibited in the hematoma. As a result, bleeding from the sinusoidal vessels may persist and the hematoma may grow slowly and fail to coagulate.
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