The pathophysiology of chronic subdural hematoma revisited: emphasis on aging processes as key factor

Chronic subdural hematoma (CSH) affects mostly elderly subjects. Previously, pathophysiological concepts suggested that CSH is secondary to degradation of subdural collections of blood and its products exerting merely a mass effect on the underlying brain. During the last decades, however, new insights into the pathogenetic mechanisms urge us to reconsider such a simplistic view. Here, we critically review novel pathophysiological, imaging, interventional, and medical treatment aspects and establish an integrative concept of the pathogenesis of CSH stressing the role of age as key factor. Trauma is considered a trigger event that unleashes a cascade of immunological and angiogenic age-dependent responses. These are associated with hypervascularization of the outer hematoma membrane, rebleeding, and exsudation which are crucial determinants for further development and propagation of CSH. Neurosurgical evacuation of the hematoma has long been thought the only viable treatment option, and it is still the method of choice in the majority of cases. Only more recently, embolization of the middle meningeal artery has been introduced as an alternative to surgery, and pharmacological treatment options are being investigated. Persons with advanced age trauma and other trigger events encounter a repair system with characteristics of senescence. This repair system implies a dysfunctional secretory phenotype of senescent cells and results in an insufficient repair process including chronic inflammation and fibrosis. Increased knowledge about the pathomechanisms of CSH will inform future studies and open new perspectives for its treatment and possibly also for its prevention.