Literature ReviewChronic Subdural Hematoma: A Perspective on Subdural Membranes and Dementia
Introduction
Chronic subdural hematoma (cSDH) is a relatively common and debilitating pathologic entity that affects 1–5.3 per 100,000 individuals annually.1, 2 cSDH is particularly prevalent in elderly men, with >50% of cSDH cases occurring in patients >60 years old and the highest incidence (7.35 cases per 100,000) in adults 70–79 years old. It is projected to affect 60,000 Americans >65 years old annually by 2030.3, 4 Reasons for this lie in the increased risk factors, such as falls and use of anticoagulants, in elderly adults coupled with age-related cortical atrophy that distends small cerebral vessels and bridging veins.5, 6, 7, 8, 9
cSDH commonly develops over the course of ≥3 weeks following mild to moderate head trauma coupled with a chronic inflammatory reaction.10 After cSDH development, natural physiologic sequelae lead to a gradual enlargement of the cSDH, primarily through the formation of a subdural neomembrane.11 This subdural membrane is composed of inner and outer layers (Figure 1) that release antithrombotic and fibrinolytic molecules to liquefy the hematoma to prevent clot formation and facilitate cSDH reabsorption.12, 13 However, in cases where reabsorption is impaired or absent, the cSDH can expand and result in mass effects, blood flow impairment, and metabolic disturbances in the underlying cortex.14 The presence of blood alone in the subdural space is inadequate to induce cSDH; rather, chronic inflammation and other contributing factors, such as cerebral atrophy, may be the true etiologic factors underlying cSDH.15 We provide a brief overview of subdural membrane formation and discuss potential links between cSDH, dementia, and intracranial lymphatic systems.
Section snippets
Subdural Membrane Formation
The subdural membrane is an important contributor to the pathogenesis and clinical symptoms of cSDH. It consists of an inner and outer layer and forms within the dura-arachnoid meningeal interface.16 This interface creates a potential space, termed the subdural space, that consists of a tight group of cells known as the interface layer. This layer lines the inner dural border and forms the outermost arachnoid barrier. These 2 cellular components fuse within the interface layer and form a tight
Linking cSDH to Dementia and Dural Lymphatics
The clinical effects of treated and untreated cSDH have been broadly explored and overshadow the physiologic effects of cSDH on the underlying brain parenchyma. In addition to overt mass effect, the presence of a large cSDH can alter cerebral blood flow and result in ischemia and deleterious metabolic changes within the neuroparenchyma.37 cSDH evacuation has been shown to improve cerebral blood flow and cognitive function in patients.
Although the exact extent of the adverse physiologic effects
Conclusions
cSDH results from head injuries and is a type of TBI that affects approximately 1–5 in 100,000 individuals each year. cSDH is a leading cause of reversible dementia, in that surgical evacuation can lead to symptomatic improvement, yet multiple treatment options exist. Furthermore, an increasingly greater emphasis must be placed on the short-term and long-term effects of cSDH and the subdural membrane that accompanies it on the pathogenesis of dementia and the mechanistic role of newly
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Conflict of interest statement: R.S. is funded in part by a Medical Scientist Training Program grant from the National Institutes of Health (grant number T32-GM08620). All other authors have no conflicts to report.