Micrograph of a chronic<unk> , as demonstrated by thin strands of collagen and neovascularization. HPS stain Acute Acute<unk>  is usually caused by external trauma that creates tension in the wall of a bridging vein as it passes between the arachnoid and dural layers of the brain's lining—i.e., the subdural space. The circumferential arrangement of collagen surrounding the vein makes it susceptible to such tearing. Intracerebral hemorrhage and ruptured cortical vessels (blood vessels on the surface of the brain) can also cause<unk> . In these cases, blood usually accumulates between the two layers of the dura mater. This can cause ischemic brain damage by two mechanisms: one, pressure on the cortical blood vessels, and two, vasoconstriction due to the substances released from the<unk> , which causes further ischemia by restricting blood flow to the brain. When the brain is denied adequate blood flow, a biochemical cascade known as the ischemic cascade is unleashed, and may ultimately lead to brain cell death.<unk> s grow continually larger as a result of the pressure they place on the brain: As intracranial pressure rises, blood is squeezed into the dural venous sinuses, raising the dural venous pressure and resulting in more bleeding from the ruptured bridging veins. They stop growing only when the pressure of the<unk>  equalizes with the intracranial pressure, as the space for expansion shrinks. Chronic In chronic<unk> s, blood accumulates in the dural space as a result of damage to the dural border cells. The resulting inflammation leads to new membrane formation through fibrosis and produces fragile and leaky blood vessels through angiogenesis, permitting the leakage of red blood cells, white blood cells, and plasma into the<unk>  cavity. Traumatic tearing of the arachnoid mater also causes leakage of cerebrospinal fluid into the<unk>  cavity, increasing the size of the<unk>  over time. Excessive fibrinolysis also causes continuous bleeding. Pro-inflammatory mediators active in the<unk>  expansion process include Interleukin 1α (IL1A), Interleukin 6, and Interleukin 8, while the anti-inflammatory mediator is Interleukin 10. Mediators that promote angiogenesis are angiopoietin and vascular endothelial growth factor (VEGF). Prostaglandin E2 promotes the expression of VEGF. Matrix metalloproteinases remove surrounding collagen, providing space for new blood vessels to grow. Craniotomy for unruptured intracranial aneurysm is another risk factor for the development of chronic<unk> . The incision in the arachnoid membrane during the operation causes cerebrospinal fluid to leak into the subdural space, leading to inflammation. This complication usually resolves on its own.
Subdural hematoma
Hepatic encephalopathy
Subdural empyema
Epidural hematoma
Subarachnoid hemorrhage
ROSAH syndrome
Migraine
Migraine 