Chronic Subdural Hematoma-Evolution of Etiology and Surgical Treatment

Abstract

In this paper, I review the historical changes in the etiological concepts and surgical treatments for chronic subdural hematoma (CSDH) across the world and in Japan. I also examine future problems associated with its surgical procedures and medical costs. CSDH was first reported by Wepfer in 1657 as "delayed apoplexy." In 1857, Virchow described the famous concept of so-called "pachymeningitis hemorrhagica interna." He considered that the etiology of CSDH involved inflammation. In 1914, Trotter described the origin of CSDH as traumatic. Currently, CSDH is considered to arise with a first leak of blood from dural border cells after mild trauma. Inflammatory cells are then drawn to the border cell layer. At this point, new membranes form from activated inflammation; then, the hematoma enlarges, promoted by angiogenic factors and new capillaries. In 1883, Hulke reported successful trepanning of a patient with CSDH. Burr holes and craniotomy for removal of the hematoma were subsequently reported, and new methods were developed over the course of several decades around the world. In Japan, after the first report by Nakada in 1938, many Japanese pioneering figures of neurological surgery have studied CSDH. After Mandai reported the middle meningeal artery embolization in 2000, this method is now considered useful as an initial or second treatment for CSDH. However, the age of patients is increasing, so more minimally invasive surgeries and useful pharmacotherapies are needed. We must also consider the costs for treating CSDH, because of the increasing numbers of surgical cases.

Keywords: chronic subdural hematoma; etiology; history; outcome; surgical treatment.

Fig. 1

Contemporary etiological concept of chronic subdural hematoma. A: Anatomical schema of dural border cells. These cells exist between the arachnoid and dura mater. B: After minor trauma, bleeding occurs from dural border cells. C: After inflammatory reaction and additional minor trauma, the subdural space is noted to enlarge. D: Blood leaks and inflammatory reactions are repeated; then, an outer membrane forms. Next, an inner membrane forms. Granulation and angiogenesis of the membrane gradually induce thickening of the dural border cell layer. E: The outer membrane participates in the enlargement of the hematoma associated with various actions, and the inner membrane participates in liquefaction of the hematoma. These reactions lead to the enlargement of the hematoma and, ultimately, formation of the chronic subdural hematoma.

Fig. 2

Historical review of reports from around the world regarding middle meningeal artery embolization (MMAE) for chronic subdural hematoma (CSDH).