Chronic subdural hematoma (CSDH) is one of the most common neurosurgical diseases, characterized by a pathological hematoma between the dura mater and the arachnoid mater, with an insidious onset and slow progression. In recent years, its incidence has been increasing year by year. The formation and development of chronic subdural hematomas remains unclear. As the hematoma expands, intracranial pressure increases, forcing the nearby brain parenchyma and may cause different clinical manifestations, including headache, nausea or vomiting, altered mental status, seizures, weakness, sensory disturbances, gait abnormalities, and coma.
There are five risk factors for chronic subdural hematoma formation.
Trauma. The incidence of chronic subdural hematoma among U.S. veterans is as high as 79 per year due to trauma4 100,000. In the general population, trauma is also the most important risk factor for chronic subdural hematoma, accounting for 50% to 70% of patients with chronic subdural hematoma**, and the vast majority of patients have minor trauma with a history of motor vehicle accidents and falls. In addition, indirect head jolts have also been found in patients with cerebral atrophy to induce chronic subdural hematomas.
Eld. The incidence of chronic subdural hematomas also increases with age, and most chronic subdural hematomas occur in people aged 65 years due to the aging of the population. From 1990 to 2015, the incidence of chronic subdural hematoma remained stable in adults under 70 years of age, while in 80-year-olds, the incidence increased significantly, from 46 per year9 100,000 increased to 1295 100,000. Chronic subdural hematoma is expected to become the most common cranial neurosurgical condition in the elderly by 2030.
Use of anticoagulant and antiplatelet drugs.
The increased frequency of anticoagulant and antiplatelet drug use is associated with a high incidence of chronic subdural hematoma, and with the increase in the incidence of cardiovascular disease, the risk of anticoagulant and antiplatelet drugs for chronic subdural hematoma is also increasing year by year.
List of high-quality authors Low intracranial pressure.
Hypocrillary pressure refers to a decrease in cerebrospinal fluid pressure that may be caused by a spontaneous or iatrogenic CSF leak, such as after a lumbar puncture. When cerebrospinal fluid pressure drops, its buoyancy to brain tissue decreases, causing traction on the bridging veins, causing these vessels to tear and rupture. In addition, low intracranial pressure may cause cerebral venous congestion, which can lead to fluid leakage into the subdural space.
Other factors. Tumors or vascular lesions may lead to acute subdural hematomas through mass effect or vascular injury due to neovascular rupture and progression to chronic subdural hematomas. The prevalence of chronic subdural hematoma in men is 23 times higher than in women. In younger patients, arachnoid cysts and ventriculoperitoneal shunts are risk factors for chronic subdural hematomas.
So what is the pathogenesis of chronic subdural hematoma?
At present, it is believed that factors such as local hyperfibrinolysis, extravascularization and rebleeding of the hematoma, and local inflammation play an important role in the pathogenesis of chronic subdural hematoma, and related cytokines are involved and play an important role. After a risk event, the loosely connected boundary cells of the dural lining are lysed, activating fibroblast growth signals, triggering a cascade of age-dependent responses associated with immunity, angiogenesis, and inflammation, forming a "new membrane" with abundant neovascularization and abnormal permeability, resulting in the subdural space being filled with blood, blood degradation products, and extravasate. Subsequently, immune cells undergo chemotaxis, and the levels of IL-6, HIF, TNF-, and COX-2 increase, inducing the secretion of vascular endothelial growth factor. Overexpression of vascular endothelial growth factor activates the MEK ERK signaling pathway, resulting in extravasation of neovascularization. In addition, persistently high levels of IL-6 increase vascular permeability through the JAK STAT pathway, resulting in sustained extravasation of plasma proteins, resulting in expanded hematoma volume. The absence of anti-inflammatory cytokines (eg, IL-10 and IL-13) in the hematoma leads to the occurrence of chronic subdural hematoma.