Editing Subdural hematoma (section)

==Pathophysiology==

=== Acute ===
Acute subdural hematoma 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.{{citation needed|date=February 2021}}

[[Intracerebral hemorrhage]] and ruptured cortical vessels (blood vessels on the surface of the brain) can also cause subdural hematoma. 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,<ref name="JNS Acute">{{Cite journal |vauthors=Miller JD, Nader R |date=June 2014 |title=Acute subdural hematoma from bridging vein rupture: a potential mechanism for growth |journal=Journal of Neurosurgery |volume=120 |issue=6 |pages=1378–1384 |doi=10.3171/2013.10.JNS13272 |pmid=24313607 |s2cid=25404949}}</ref> and two, [[vasoconstriction]] due to the substances released from the hematoma, which causes further [[ischemia]] by restricting blood flow to the brain.<ref name="graham">{{Cite book |title=Head Injury |vauthors=Graham DI, Gennareli TA |date=2000 |publisher=Morgan Hill |veditors=Cooper P, Golfinos G |edition=4th |location=New York |chapter=Chapter 5: Pathology of brain damage after head injury}}</ref> 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]].<ref>{{Cite journal |vauthors=Tandon PN |date=March 2001 |title=Acute subdural haematoma : a reappraisal |url=http://www.neurologyindia.com/article.asp?issn=0028-3886;year=2001;volume=49;issue=1;spage=3;epage=10;aulast=Tandon |journal=Neurology India |volume=49 |issue=1 |pages=3–10 |pmid=11303234 |access-date=26 November 2017 |quote=. The possibility of direct effect of some vasoactive substances released by the blood clot, being responsible for the ischaemia, seems attractive.}}</ref>

Subdural hematomas 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 hematoma equalizes with the intracranial pressure, as the space for expansion shrinks.<ref name="JNS Acute" />

=== Chronic ===

[[Image:Subdural hematoma - very low mag.jpg|thumb|right|[[Micrograph]] of a chronic subdural hematoma, as demonstrated by thin strands of collagen and neovascularization. [[HPS stain]]]]

In chronic subdural hematomas, blood accumulates in the dural space as a result of damage to the dural border cells.<ref name="Pathophysiology of CSDH" /> 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 cell]]s, [[white blood cell]]s, and [[Blood plasma|plasma]] into the hematoma cavity. Traumatic tearing of the [[arachnoid mater]] also causes leakage of cerebrospinal fluid into the hematoma cavity, increasing the size of the hematoma over time. Excessive [[fibrinolysis]] also causes continuous bleeding.{{citation needed|date=July 2021}}

Pro-inflammatory mediators active in the hematoma 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 metalloproteinase]]s remove surrounding collagen, providing space for new blood vessels to grow.<ref name="Pathophysiology of CSDH">{{Cite journal |vauthors=Edlmann E, Giorgi-Coll S, Whitfield PC, Carpenter KL, Hutchinson PJ |date=May 2017 |title=Pathophysiology of chronic subdural haematoma: inflammation, angiogenesis and implications for pharmacotherapy |journal=Journal of Neuroinflammation |volume=14 |issue=1 |pages=108 |doi=10.1186/s12974-017-0881-y |pmc=5450087 |pmid=28558815 |doi-access=free}}</ref>

[[Craniotomy]] for unruptured [[intracranial aneurysm]] is another risk factor for the development of chronic subdural hematoma. 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.<ref>{{Cite journal |vauthors=Tanaka Y, Ohno K |date=June 2013 |title=Chronic subdural hematoma – an up-to-date concept |url=http://lib.tmd.ac.jp/jmd/6002/01_Tanaka.pdf |url-status=dead |journal=Journal of Medical and Dental Sciences |volume=60 |issue=2 |pages=55–61 |pmid=23918031 |archive-url=https://web.archive.org/web/20170813054647/http://lib.tmd.ac.jp/jmd/6002/01_Tanaka.pdf |archive-date=13 August 2017 |access-date=26 November 2017}}</ref>