Krwiak podtwardówkowy
Patofizjologia i mechanizm
Krwiak podtwardówkowy (SDH) to patologiczne nagromadzenie krwi pomiędzy oponą twardą a pajęczynówką, najczęściej spowodowane rozerwaniem żył mostkowych w wyniku urazu przyspieszeniowo-hamującego głowy. W ostrym SDH (ASDH) dochodzi do gwałtownego wzrostu ciśnienia wewnątrzczaszkowego, co może prowadzić do ucisku mózgu, niedokrwienia, przemieszczania struktur mózgowych i wklinowania, stanowiącego zagrożenie życia. Czynniki ryzyka obejmują atrofię mózgu, stosowanie leków przeciwzakrzepowych, nadużywanie alkoholu oraz obniżenie ciśnienia wewnątrzczaszkowego. W około 20% przypadków źródłem krwawienia są tętniczki korowe, co może wystąpić nawet przy niewielkim urazie. Patogeneza obejmuje mechanizmy uszkodzenia naczyń, narastanie krwiaka przez dodatnie sprzężenie zwrotne oraz zaburzenia hemodynamiczne i krzepnięcia.
- Patogeneza krwiaka podtwardówkowego
- Anatomia i mechanizm powstawania
- Czynniki predysponujące
- Mechanizm ostrego krwiaka podtwardówkowego
- Mechanizm przewlekłego krwiaka podtwardówkowego
- Ewolucja krwiaka podtwardówkowego
- Mechanizm powiększania krwiaka
- Podtypy etiologiczne krwiaka podtwardówkowego
- Konsekwencje patofizjologiczne
- Podsumowanie mechanizmów patogenetycznych
Patogeneza krwiaka podtwardówkowego
Krwiak podtwardówkowy (ang. subdural hematoma, SDH) to nieprawidłowe nagromadzenie krwi pomiędzy oponą twardą (dura mater) a pajęczynówką (arachnoid mater), które może prowadzić do ucisku mózgu i poważnych konsekwencji neurologicznych. Zrozumienie mechanizmów patogenetycznych powstawania tego schorzenia wymaga znajomości anatomii przestrzeni podtwardówkowej oraz procesów patofizjologicznych towarzyszących nagromadzeniu krwi w tej lokalizacji.123
Anatomia i mechanizm powstawania
Mózg jest chroniony przez czaszkę oraz opony mózgowe składające się z trzech warstw. Przestrzeń podtwardówkowa nie jest przestrzenią fizjologiczną, lecz potencjalną, która powstaje w wyniku patologicznego rozdzielenia warstwy komórek granicznych opony twardej (dural border cells). W stanie fizjologicznym ta przestrzeń nie istnieje, jednak w przypadku urazu może dojść do jej utworzenia.14
Głównym mechanizmem powstawania ostrego krwiaka podtwardówkowego (ASDH) jest uszkodzenie tzw. żył mostkowych (bridging veins), które przebiegają od powierzchni kory mózgowej do zatok żylnych opony twardej, przechodząc przez przestrzeń podpajęczynówkową. Te delikatne struktury naczyniowe są szczególnie podatne na uszkodzenie podczas nagłych zmian prędkości głowy (przyspieszenie-hamowanie), które powodują rozciąganie i rozrywanie ich cienkich ścian. W wyniku przerwania ciągłości tych naczyń, krew wydostaje się do przestrzeni podtwardówkowej.526
Gennarelli i Thibault wykazali w badaniach na modelu zwierzęcym, że głównym czynnikiem determinującym uszkodzenie żył mostkowych jest tempo przyspieszenia-hamowania głowy. Ich wyniki były spójne z klinicznymi przyczynami krwiaków podtwardówkowych, gdzie około 72% przypadków związanych jest z upadkami i napaściami, a tylko 24% z urazami komunikacyjnymi.7
Czynniki predysponujące
Istnieje kilka czynników zwiększających ryzyko powstania krwiaka podtwardówkowego:
- Zanik mózgu (atrofia) występujący u osób starszych – powoduje zwiększenie przestrzeni pomiędzy mózgiem a czaszką, co prowadzi do większego napięcia żył mostkowych i ich podatności na uszkodzenie28
- Przyjmowanie leków przeciwzakrzepowych (warfaryna, aspiryna) – utrudnia procesów krzepnięcia i zwiększa ryzyko krwawienia9
- Nadużywanie alkoholu – prowadzi do małopłytkowości, wydłużenia czasu krwawienia oraz zwiększonego ryzyka urazów głowy9
- Nadmierne obniżenie ciśnienia wewnątrzczaszkowego – np. po punkcji lędźwiowej lub nadmiernym drenażu płynu mózgowo-rdzeniowego1011
Mechanizm ostrego krwiaka podtwardówkowego
W ostrym krwiaku podtwardówkowym (ASDH) dochodzi do nagłego krwawienia do przestrzeni podtwardówkowej. Mechanizm obejmuje:212
- Przyspieszenie-hamowanie tkanki mózgowej względem unieruchomionych struktur opony twardej
- Rozerwanie żył mostkowych lub małych naczyń korowych (tętnic lub żył)
- Uwalnianie krwi do przestrzeni podtwardówkowej i gwałtowne narastanie ciśnienia wewnątrzczaszkowego
Typowo krwawienie żylne o niskim ciśnieniu odkleja pajęczynówkę od opony twardej, a krew rozprzestrzenia się wzdłuż wypukłości mózgu. W miarę narastania objętości krwiaka zwiększa się ciśnienie wewnątrzczaszkowe, co powoduje dalsze wyciskanie krwi do zatok żylnych opony twardej, zwiększając ciśnienie żylne i powodując dalsze krwawienie z uszkodzonych żył mostkowych. Ten mechanizm dodatniego sprzężenia zwrotnego powoduje narastanie krwiaka, aż do momentu gdy ciśnienie w krwiaku zrówna się z ciśnieniem wewnątrzczaszkowym lub nastąpi wykrzepienie krwi w przestrzeni krwiaka.131415
Należy podkreślić, że w około 20% przypadków krwiaków podtwardówkowych, źródłem krwawienia są uszkodzone tętniczki korowe, a nie żyły mostkowe. Taki ostry krwiak podtwardówkowy spowodowany pęknięciem tętnicy korowej może być związany z niewielkim urazem głowy, czasem nawet bez towarzyszącego stłuczenia mózgu.211
Mechanizm przewlekłego krwiaka podtwardówkowego
Przewlekły krwiak podtwardówkowy (CSDH) rozwija się w bardziej złożony sposób i ma wieloczynnikową patogenezę. Proces ten obejmuje kilka kluczowych mechanizmów:1617
Mechanizm zapalny
Proces zapalny odgrywa kluczową rolę w patogenezie przewlekłego krwiaka podtwardówkowego. Początkowo krwawienie do przestrzeni podtwardówkowej wywołuje reakcję zapalną, która prowadzi do:1819
- Aktywacji komórek zapalnych, które próbują naprawić uszkodzenie komórek granicznych opony twardej
- Proliferacji tych komórek, co prowadzi do tworzenia nowej błony (neomembrany)
- Rekrutacji mediatorów zapalnych, takich jak interleukiny (IL-1, IL-6, IL-8), które są znacząco podwyższone w płynie krwiaka w porównaniu z krwią obwodową
Proces zapalny, który pierwotnie ma na celu naprawę tkanek, staje się przewlekły i patologiczny, prowadząc do ciągłego wzrostu błony i gromadzenia się płynu.2021
Angiogeneza
Charakterystyczną cechą przewlekłego krwiaka podtwardówkowego jest tworzenie się dwóch błon otaczających zbiornik krwi: zewnętrznej (przylegającej do opony twardej) i wewnętrznej (przylegającej do pajęczynówki). Szczególnie ważna jest błona zewnętrzna, która zawiera liczne, wysoce przepuszczalne naczynia krwionośne o cienkich ścianach, z cienką lub nieobecną błoną podstawną, pozbawione komórek mięśni gładkich i perycytów.2223
W procesie angiogenezy kluczową rolę odgrywają czynniki wzrostu, takie jak:2425
- Czynnik wzrostu śródbłonka naczyniowego (VEGF)
- Angiopoetyna
- Transformujący czynnik wzrostu (TGF-1)
Te nowo utworzone naczynia są kruche i przepuszczalne, co prowadzi do mikrokrwawień i przesięku płynu do przestrzeni podtwardówkowej, przyczyniając się do powiększania się krwiaka.19
Procesy fibrynolityczne
W przewlekłym krwiaku podtwardówkowym dochodzi do zaburzenia równowagi pomiędzy procesami krzepnięcia a fibrynolizy. Zwiększona aktywność fibrynolityczna w przestrzeni krwiaka zapobiega tworzeniu się skrzepów, co prowadzi do:1626
- Ciągłego krwawienia z kruchych naczyń w błonie zewnętrznej
- Rozpuszczania istniejących skrzepów
- Utrzymywania płynnej konsystencji krwiaka
Ten mechanizm, w połączeniu z procesami zapalnymi i angiogennymi, tworzy błędne koło prowadzące do powiększania się krwiaka.27
Ewolucja krwiaka podtwardówkowego
Krwiak podtwardówkowy przechodzi charakterystyczną ewolucję w czasie:715
- Faza ostra (0-3 dni) – świeża krew gromadzi się w przestrzeni podtwardówkowej
- Faza podostra (3-21 dni) – skrzep ulega upłynnieniu, można zaobserwować efekt hematokrytu na obrazach CT
- Faza przewlekła (>21 dni) – elementy komórkowe ulegają dezintegracji, pozostaje kolekcja płynu surowiczego w przestrzeni podtwardówkowej; w rzadkich przypadkach może wystąpić zwapnienie
Proces przejścia z ostrego do przewlekłego krwiaka podtwardówkowego obejmuje:2829
- Tworzenie błon otaczających krwiak
- Rozwój patologicznych naczyń krwionośnych w błonie zewnętrznej
- Nawracające mikrokrwawienia z tych naczyń
- Przenikanie płynu mózgowo-rdzeniowego do przestrzeni podtwardówkowej w wyniku przerwania ciągłości pajęczynówki
Mechanizm powiększania krwiaka
Powiększanie się krwiaka podtwardówkowego jest uwarunkowane wieloma czynnikami. Zasadniczo wyróżnia się kilka głównych teorii:2627
- Teoria mikrokrwawień – nawracające krwawienia z patologicznych naczyń w błonie zewnętrznej krwiaka
- Teoria osmotyczna/onkotyczna – gradient ciśnienia osmotycznego/onkotycznego pomiędzy krwiakiem a otaczającymi tkankami powoduje przenikanie płynu do przestrzeni krwiaka
- Teoria równowagi produkcji i resorpcji – zaburzenie równowagi między wytwarzaniem a wchłanianiem płynu w przestrzeni podtwardówkowej
- Teoria naczyniowo-limfatyczna – upośledzenie funkcji naczyń limfatycznych oponowych (meningeal lymphatic vessels), które w warunkach fizjologicznych uczestniczą w usuwaniu płynu z przestrzeni podtwardówkowej25
Większość aktualnych danych wskazuje, że najbardziej prawdopodobny jest wieloczynnikowy mechanizm powiększania się krwiaka, obejmujący kombinację teorii mikrokrwawień, zaburzeń fibrynolitycznych oraz procesów zapalnych i angiogennych.3026
Podtypy etiologiczne krwiaka podtwardówkowego
Poza klasycznym mechanizmem pourazowym, krwiak podtwardówkowy może powstawać również w innych okolicznościach:1531
- Krwiak podtwardówkowy spowodowany pęknięciem tętniaka – rzadki, ale poważny stan, gdy tętniak penetruje do przestrzeni podtwardówkowej lub pęka z taką siłą, że przerywa ciągłość błony pajęczej
- Krwiak podtwardówkowy w zespole dziecka potrząsanego – powstaje w wyniku gwałtownych ruchów przyspieszająco-hamujących głowy niemowlęcia podczas potrząsania, co prowadzi do rozerwania żył mostkowych
- Krwiak podtwardówkowy spontaniczny – występujący u pacjentów z koagulopatiami, stosujących leki przeciwzakrzepowe lub z wrodzonymi zaburzeniami naczyniowymi
- Krwiak podtwardówkowy rdzenia kręgowego – rzadka jednostka chorobowa, której dokładna patogeneza pozostaje niewyjaśniona, ale może być związana z uszkodzeniem żył mostkowych w przestrzeni kręgowej lub nagłym wzrostem ciśnienia wewnątrznaczyniowego3233
Konsekwencje patofizjologiczne
Krwiak podtwardówkowy powoduje szereg patologicznych zmian w obrębie mózgowia:1434
Wzrost ciśnienia wewnątrzczaszkowego
Akumulacja krwi w przestrzeni podtwardówkowej prowadzi do zwiększenia ciśnienia wewnątrzczaszkowego, co może skutkować:635
- Uciskiem na korowe naczynia krwionośne, co powoduje niedokrwienie mózgu
- Skurczem naczyniowym wywołanym przez substancje uwalniane z krwiaka
- Zmniejszeniem objętości układu komorowego
- Przemieszczeniem linii środkowej mózgu w kierunku przeciwnym do krwiaka
Wklinowanie mózgu
W miarę narastania ciśnienia wewnątrzczaszkowego i przemieszczania struktur mózgowia może dojść do wklinowania mózgu, które stanowi zagrożenie życia:3634
- Wklinowanie części hakowej płata skroniowego
- Ucisk na pień mózgu
- Przemieszczenie struktur mózgowych w kierunku otworu wielkiego
Nieleczony duży krwiak podtwardówkowy może prowadzić do śpiączki i śmierci wskutek wklinowania mózgu.37
Zaburzenia neurologiczne
Krwiak podtwardówkowy może również powodować inne konsekwencje neurologiczne:38
- Wtórny parkinsonizm – w wyniku ucisku na jądra podstawy lub przerwania dróg dopaminergicznych
- Deficyty ogniskowe – w zależności od lokalizacji krwiaka
- Encefalopatia – w wyniku globalnego niedokrwienia mózgu
Podsumowanie mechanizmów patogenetycznych
Patogeneza krwiaka podtwardówkowego jest złożonym procesem obejmującym wiele mechanizmów działających równocześnie lub sekwencyjnie:3039
- Mechanizm inicjujący – uraz powodujący rozerwanie żył mostkowych lub naczyń korowych
- Procesy zapalne – reakcja zapalna w przestrzeni podtwardówkowej prowadząca do tworzenia neomembran
- Angiogeneza – powstawanie patologicznych naczyń krwionośnych w błonach krwiaka
- Fibrynoliza – zaburzenie równowagi między krzepnięciem a fibrinolizą
- Mikrokrwawienia – nawracające krwawienia z kruchych naczyń w błonie zewnętrznej
- Zaburzenia resorpcji – upośledzenie mechanizmów wchłaniania płynu z przestrzeni podtwardówkowej
Zrozumienie złożonych mechanizmów patogenetycznych krwiaka podtwardówkowego ma kluczowe znaczenie dla opracowania skutecznych strategii terapeutycznych, zwłaszcza w kontekście leczenia farmakologicznego przewlekłych krwiaków podtwardówkowych oraz zapobiegania ich nawrotom.4025
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Materiały źródłowe
- #1 Subdural Hematoma – StatPearls – NCBI Bookshelfhttps://www.ncbi.nlm.nih.gov/books/NBK532970/
A subdural hematoma, as its name implies, forms because of an abnormal collection of blood under the dura mater. […] A subdural hematoma forms because of an accumulation of blood under the dura mater, one of the protective layers to the brain tissue under the calvarium. […] The understanding of subdural hematoma relies on the knowledge of neuroanatomical sheets covering the brain. […] The brain finds its protection under the skull by the meninges that comprise three layers. […] These so-called bridging veins may rupture when direct opposing forces rupture their thin walls, releasing blood under the dura mater forming a subdural hematoma. […] When there is a larger space between the dura mater and the brain, as seen in the young, growing brain or an aging brain (because of contraction), the cerebrospinal fluid (CSF) flows between bridging veins occupying a larger space.
- #2 Subdural Hematoma: Background, Pathophysiology, Etiologyhttps://emedicine.medscape.com/article/1137207-overview
A subdural hematoma (SDH) is a collection of blood below the inner layer of the dura but external to the brain and arachnoid membrane. Subdural hematoma is the most common type of traumatic intracranial mass lesion. […] The usual mechanism that produces an acute subdural hematoma (SDH) is a high-speed impact to the skull. This causes brain tissue to accelerate or decelerate relative to the fixed dural structures, tearing blood vessels. […] Often, the torn blood vessel is a vein that connects the cortical surface of the brain to a dural sinus (termed a bridging vein). In elderly persons, the bridging veins may already be stretched because of brain atrophy (shrinkage that occurs with age). […] Alternatively, a cortical vessel, either a vein or small artery, can be damaged by direct injury or laceration. An acute SDH due to a ruptured cortical artery may be associated with only minor head injury, possibly without an associated cerebral contusion.
- #3 Subdural hematoma in adults: Etiology, clinical features, and diagnosis – UpToDatehttps://www.uptodate.com/contents/subdural-hematoma-in-adults-etiology-clinical-features-and-diagnosis
Subdural hematoma (SDH) is a form of intracranial hemorrhage characterized by bleeding into the space between the dural and arachnoid membranes surrounding the brain. […] The pathophysiology, etiology, clinical features, and diagnostic evaluation of SDH will be discussed here.
- #4 Understanding Subdural Collections in Pediatric Abusive Head Trauma | American Journal of Neuroradiologyhttp://www.ajnr.org/content/40/3/388
Typically, injuries of the BVs cause extra-axial hemorrhage, predominantly within the subarachnoid and subdural spaces. […] The resulting hemorrhage from the injured BVs fosters opening of the subdural space. This pathologic space does not exist under physiologic conditions and has been recognized as an intradural lesion caused by cleavage of the innermost part of the dura mater, the dura border cell layer. […] Nevertheless, the traditional term subdural is still widely in use; thus, BV hemorrhage leads to what is generally referred to as SDH. […] Due to shearing forces, the arachnoid membrane may also tear (eg, in the vicinity of strained BVs or at Pacchionian granulations). […] If this is the case, transfer of CSF from the subarachnoid space to the subdural space is possible. Thus, an SDHy or SDHHy may develop additionally or subsequently. […] The laceration of the arachnoid membrane may function as a valve preventing backflow of CSF. […] A pathologically expanding SDHy or SDHHy is considered the precursor of the cSDH.
- #5 Subdural hematoma | Mechanism, Symptoms, & Management | Britannicahttps://www.britannica.com/science/subdural-hematoma
subdural hematoma, bleeding into the space between the brain and its outermost protective covering, the dura. It typically results when a traumatic force applied to the head creates significant fast-changing velocities of the contents inside the skull. The expanding hemorrhage can increase the pressure inside the skull and compress the underlying brain tissue. […] A network of veins traverses the space between the surface of the brain and the dura. These veins, the bridging veins, can tear if the contents of the skull experience sudden changes in velocity. Blood leaking from the bridging veins then collects in the subdural space, creating a hematoma. The size of the hematoma and the speed with which it expands depend primarily on the number and size of the tears in the bridging veins. […] The expanding subdural hematoma increases the intracranial pressure and can lead to damage of the underlying brain.
- #6 Subdural Haematoma – Clinical Features – Management – TeachMeSurgeryhttps://teachmesurgery.com/neurosurgery/traumatic-injuries/subdural-haematoma/
Bleeding in a SDH occurs from tearing of the bridging veins that cross from the cortex to the dural venous sinuses, which are vulnerable to deceleration injury. […] This subsequently leads to accumulation of blood between the dura and arachnoid and results in a gradual rise in intracranial pressure (ICP). This can lead to herniation and brainstem death if left untreated.
- #7 Subdural Hematoma: Background, Pathophysiology, Etiologyhttps://emedicine.medscape.com/article/1137207-overview
The head trauma may also cause associated brain hematomas or contusions, subarachnoid hemorrhage, and diffuse axonal injury. […] Typically, low-pressure venous bleeding from bridging veins dissects the arachnoid away from the dura, and the blood layers out along the cerebral convexity. […] In the subacute phase, the clotted blood liquefies. […] In the chronic phase, cellular elements have disintegrated, and a collection of serous fluid remains in the subdural space. […] It has been asserted that the primary brain injury associated with SDH plays a major role in mortality. However, most SDHs are thought to result from torn bridging veins, as judged by surgery or autopsy. […] Using a primate model, Gennarelli and Thibault demonstrated that the rate of acceleration-deceleration of the head was the major determinant of bridging vein failure. […] Gennarelli and Thibault reported that their results were consistent with the clinical causes of subdural hematoma, in that 72% are associated with falls and assaults and only 24% are associated with vehicular trauma.
- #8 Subdural Haematoma: Symptoms and Treatment | Doctorhttps://patient.info/doctor/subdural-haematoma-pro
A subdural haematoma (SDH) is a collection of clotting blood that forms in the subdural space. This may be: […] An acute SDH is usually caused by either: Tearing of bridging veins from the cortex to one of the draining venous sinuses – typically occurring when bridging veins are sheared during rapid acceleration-deceleration of the head. […] Blunt head trauma is the usual mechanism of injury but spontaneous SDH can arise as a consequence of clotting disorder, arteriovenous malformations/aneurysms or other conditions. […] In the subacute phase the collection of clotted blood liquifies. In the chronic phase it becomes a collection of serous fluid in the subdural space. […] Cerebral atrophy can occur in people over the age of 60, causing tension on the veins, which may also be weaker and more susceptible to injury as a consequence of age.
- #9 Subdural Haematoma: Symptoms and Treatment | Doctorhttps://patient.info/doctor/subdural-haematoma-pro
Chronic SDH is more common in the older age group. […] Alcohol misuse leads to a risk of thrombocytopenia, prolonged bleeding times and blunt head trauma and is a risk factor for SDH. […] Anticoagulation treatment (including with aspirin or warfarin) is another risk factor. […] SDH can occur in about one third of people with a severe head injury. […] The incidence is gradually increasing, but the reason for this is unknown. […] A UK-based epidemiological study found that the annual incidence of SDH/effusion in infants is approximately 12.5 cases per 100,000 population in 0- to 2-year-olds and approximately 24 cases per 100,000 in 0- to 1-year-olds. […] Surgery is needed if there are focal signs, deterioration, a large haematoma, raised intracranial pressure or midline shift. […] SDH is treated by emergency craniotomy, or decompressive craniectomy and clot evacuation. […] There is a growing body of evidence for using middle meningeal artery embolisation to treat chronic subdural haematoma as recurrence may occur in 5-30% of those treated with burr hole or craniectomy.
- #10 Pulsenotes | CSDHhttps://app.pulsenotes.com/surgery/neurosurgery/notes/chronic-subdural-haematoma
Subdural haematoma is a collection of blood in the subdural space. […] The most common cause of CSDH is trauma in nearly 50% of patients. […] A CSDH may develop if the patient has a shunt inserted for cerebrospinal fluid (CSF) drainage. Over-drainage can cause a bleed. […] Tearing of a bridging or surface vein causes blood to escape into the subdural space. […] A CSDH invariably starts out as an acute subdural haematoma. […] The mechanism behind CSDH formation is likely multifactorial and goes beyond a tear of a bridging vein. […] The subdural blood provokes an inflammatory response with likely neoangiogenesis (growth of new blood vessels) and coagulopathy (abnormal clotting). […] CSDH tends to affect elderly patients more than younger patients and the mechanism of injury is usually innocuous.
- #11 Subdural hematoma pathophysiology – wikidochttps://www.wikidoc.org/index.php/Subdural_hematoma_pathophysiology
Rupture of small cortical atreries and hemorrhage into the space between dura matter and arachnoid, leading to subdural hematoma. […] Intracranial hypotension (mostly due to lumbar punctue) and traction of bridging veins which leads to subdural hematoma. […] Subdural hematomas as a result of arterial rupture accounts for 20% of SDH cases and are mostly in temporoparietal region. […] Since most of the SDH cases are due to vein rupture, the bleeding will stop on its own as a result of a clot formation or increased intracranial pressure.
- #12 Subdural hematoma – Wikipediahttps://en.wikipedia.org/wiki/Subdural_hematoma
A subdural hematoma (SDH) is a type of bleeding in which a collection of blood usually but not always associated with a traumatic brain injury gathers between the inner layer of the dura mater and the arachnoid mater of the meninges surrounding the brain. It usually results from rips in bridging veins that cross the subdural space. […] Subdural hematomas may cause an increase in the pressure inside the skull, which in turn can cause compression of and damage to delicate brain tissue. Acute subdural hematomas are often life-threatening. Chronic subdural hematomas have a better prognosis if properly managed. […] 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.
- #13 Acute subdural hematoma from bridging vein rupture: a potential mechanism for growth in: Journal of Neurosurgery Volume 120 Issue 6 (2014) Journalshttps://thejns.org/view/journals/j-neurosurg/120/6/article-p1378.xml
Most acute subdural hematomas (ASDHs) develop after rupture of a bridging vein or veins. The anatomy of the bridging vein predisposes to its tearing within the border cell layer of the dura mater. Thus, the subdural hematoma actually forms within the dura. The hematoma grows by continued bleeding into the border cell layer. However, the venous pressure would not be expected to cause a large hematoma. Therefore, some type of mechanism must account for the hematoma’s expansion. […] A hypothesis is derived to explain the mechanism of ASDH enlargement. Tearing of one or more bridging veins causes these vessels to bleed into the dural border cell layer. Subsequent ICP elevation from the ASDH, cerebral swelling, or other cause results in elevation of the CVP by increased outflow resistance in the intact bridging veins. The increased ICP causes further bleeding into the hematoma cavity via the torn bridging veins. Thus, the ASDH enlarges via a positive feedback mechanism. […] Enlargement of an ASDH would cease as blood within the hematoma cavity coagulates. This would stop the dissection of the dural border cell layer, and pressure within the hematoma cavity would equalize with that in the torn bridging vein or veins.
- #14 Subdural hematoma – Wikipediahttps://en.wikipedia.org/wiki/Subdural_hematoma
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, and two, vasoconstriction due to the substances released from the hematoma, which causes further ischemia by restricting blood flow to the brain. […] 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.
- #15 Subdural Hematoma | Top Neuro Docshttps://www.topneurodocs.com/subdural-hematoma/
Typically, low-pressure venous bleeding from bridging veins dissects the arachnoid away from the dura, and the blood layers out along the cerebral convexity. Cerebral injury results from direct pressure, increased intracranial pressure (ICP), or associated intraparenchymal insults. […] In the subacute phase, the clotted blood liquefies. Occasionally, the cellular elements layer can appear on CT imaging as a hematocrit-like effect. In the chronic phase, cellular elements have disintegrated, and a collection of serous fluid remains in the subdural space. In rare cases, calcification develops. […] Less common causes of subdural hematoma involve coagulopathies and ruptured intracranial aneurysms. Subdural hematomas have even been reported to be caused by intracranial tumors. […] It has been asserted that the primary brain injury associated with subdural hematoma plays a major role in mortality. However, most subdural hematomas are thought to result from torn bridging veins, as judged by surgery or autopsy. Furthermore, not all subdural hematomas are associated with diffuse parenchymal injury. As mentioned earlier, many patients who sustain these lesions are lucid before their condition deteriorates an unlikely scenario in patients who sustain diffuse damage.
- #16 Pathophysiology of chronic subdural haematoma: inflammation, angiogenesis and implications for pharmacotherapyhttps://pmc.ncbi.nlm.nih.gov/articles/PMC5450087/
Chronic subdural haematoma (CSDH) is an encapsulated collection of blood and fluid on the surface of the brain. […] This review focuses on several key processes involved in CSDH development: angiogenesis, fibrinolysis and inflammation. […] The characteristic membrane surrounding the CSDH has been identified as a source of fluid exudation and haemorrhage. Angiogenic stimuli lead to the creation of fragile blood vessels within membrane walls, whilst fibrinolytic processes prevent clot formation resulting in continued haemorrhage. […] An abundance of inflammatory cells and markers have been identified within the membranes and subdural fluid and are likely to contribute to propagating an inflammatory response which stimulates ongoing membrane growth and fluid accumulation. […] It has been hypothesised that inflammation is a key factor in the development of a CSDH.
- #17 Pathophysiology of chronic subdural haematoma: inflammation, angiogenesis and implications for pharmacotherapy | Journal of Neuroinflammation | Full Texthttps://jneuroinflammation.biomedcentral.com/articles/10.1186/s12974-017-0881-y
Chronic subdural haematoma (CSDH) is an encapsulated collection of blood and fluid on the surface of the brain. Historically considered a result of head trauma, recent evidence suggests there are more complex processes involved. Trauma may be absent or very minor and does not explain the progressive, chronic course of the condition. This review focuses on several key processes involved in CSDH development: angiogenesis, fibrinolysis and inflammation. The characteristic membrane surrounding the CSDH has been identified as a source of fluid exudation and haemorrhage. Angiogenic stimuli lead to the creation of fragile blood vessels within membrane walls, whilst fibrinolytic processes prevent clot formation resulting in continued haemorrhage. An abundance of inflammatory cells and markers have been identified within the membranes and subdural fluid and are likely to contribute to propagating an inflammatory response which stimulates ongoing membrane growth and fluid accumulation.
- #18 Pathophysiology of chronic subdural haematoma: inflammation, angiogenesis and implications for pharmacotherapy | Journal of Neuroinflammation | Full Texthttps://jneuroinflammation.biomedcentral.com/articles/10.1186/s12974-017-0881-y
It has been hypothesised that inflammation is a key factor in the development of a CSDH. This is not a new concept and indeed one of the earliest reports by Virchow in 1857, referred to the condition as pachymeningitis haemorrhagica interna. This was based on the assumption that bacterial infection (meningitis) was driving a chronic inflammatory response in the dura, resulting in fibrin exudation and growth of new capillaries. However, it has long become accepted that inflammation can occur in response to any injury, including trauma or cellular injury, and not just infection. The primary purpose of inflammation is for the body’s immune system to activate repair, but despite this intention to heal, persistent or chronic activation of inflammation can occur and lead to pathology. […] While inflammation can aid tissue repair, it is the sustained inflammatory response in CSDH which results in new membrane growth and fluid accumulation over time. Damage to the dural border cells, rather than acute haemorrhage itself, may be what initiates this inflammatory response and may not occur in all patients. Inflammatory cells recruited to the subdural space will attempt to repair the border cell damage, but instead proliferate and result in the new membrane formation. Many of the inflammatory cells have pro-angiogenic roles which support the development of new blood vessels in this subdural region. These vessels are leaky, allowing micro-haemorrhages and fluid exudation into the new membrane-bound subdural space. This process is summarised in the so-called CSDH cycle.
- #19 Pathophysiology of chronic subdural haematoma: inflammation, angiogenesis and implications for pharmacotherapy | springermedizin.dehttps://www.springermedizin.de/pathophysiology-of-chronic-subdural-haematoma-inflammation-angio/12326566
Chronic subdural haematoma (CSDH) is an encapsulated collection of blood and fluid on the surface of the brain. […] This review focuses on several key processes involved in CSDH development: angiogenesis, fibrinolysis and inflammation. […] It has been hypothesised that inflammation is a key factor in the development of a CSDH. […] The primary purpose of inflammation is for the body’s immune system to activate repair, but despite this intention to heal, persistent or chronic activation of inflammation can occur and lead to pathology. […] Inflammatory cells recruited to the subdural space will attempt to repair the border cell damage, but instead proliferate and result in the new membrane formation. […] Many of the inflammatory cells have pro-angiogenic roles which support the development of new blood vessels in this subdural region.
- #19 Pathophysiology of chronic subdural haematoma: inflammation, angiogenesis and implications for pharmacotherapy | springermedizin.dehttps://www.springermedizin.de/pathophysiology-of-chronic-subdural-haematoma-inflammation-angio/12326566
The external membrane, however, is considered more crucial in driving CSDH growth. […] Importantly, CSDH membranes also contain numerous highly permeable capillaries with thin walls containing thin or absent basement membrane and lacking smooth muscle cells and pericytes. […] The inflammatory process involved in CSDH membrane and fluid formation is localised to the subdural space, exemplified by the fact that the mediators are consistently significantly higher in and around the CSDH compared with peripheral blood. […] Following the pathological delamination of the dural border cells, two membranes are formed, enclosing the new subdural cavity which fills with the fluid and blood. […] The SMAD signalling pathway is an important mediator of the persistent fibrosis which contributes to membrane development, and is activated by transforming growth factor (TGF-1), expressed by eosinophils.
- #20 Pathophysiology of chronic subdural haematoma: inflammation, angiogenesis and implications for pharmacotherapyhttps://pmc.ncbi.nlm.nih.gov/articles/PMC5450087/
The primary purpose of inflammation is for the body’s immune system to activate repair, but despite this intention to heal, persistent or chronic activation of inflammation can occur and lead to pathology. […] However, some authors did recognise that inflammation and trauma may be co-existing factors in CSDH development and that the trauma need only be very trivial. […] Following histological analysis of several cases, he identified that the dura is lined with a layer of specialised, modified connective tissue cells. […] These cells have two essential roles: they can phagocytose, and they can develop into fibro-cellular connective tissue, allowing formation of new membranes as seen in CSDH. […] While inflammation can aid tissue repair, it is the sustained inflammatory response in CSDH which results in new membrane growth and fluid accumulation over time.
- #21 Pathophysiology of chronic subdural haematoma: inflammation, angiogenesis and implications for pharmacotherapy | springermedizin.dehttps://www.springermedizin.de/pathophysiology-of-chronic-subdural-haematoma-inflammation-angio/12326566
The large number of reports linking CSDH to trauma clouded this early insight regarding inflammation and led to the popular view that CSDH was an entirely traumatic condition. […] However, some authors did recognise that inflammation and trauma may be co-existing factors in CSDH development and that the trauma need only be very trivial. […] It is clear there is more to this condition than trauma causing bleeding into the subdural space. […] The subsequent array of molecules found within the CSDH fluid provide evidence for a role of localised hyperfibrinolysis and continuous inflammation contributing to the haematoma expansion.
- #22 Pathophysiology of chronic subdural haematoma: inflammation, angiogenesis and implications for pharmacotherapy | Journal of Neuroinflammation | Full Texthttps://jneuroinflammation.biomedcentral.com/articles/10.1186/s12974-017-0881-y
Importantly, CSDH membranes also contain numerous highly permeable capillaries with thin walls containing thin or absent basement membrane and lacking smooth muscle cells and pericytes. Gap junctions are also numerous, allowing continued migration of erythrocytes, leucocytes and plasma from these vessels into the subdural haematoma cavity. The external membrane also shows evolutionary changes over time with progressive inflammation followed by scarring, and persistence of areas capable of recurrent bleeding. […] The inflammatory process involved in CSDH membrane and fluid formation is localised to the subdural space, exemplified by the fact that the mediators are consistently significantly higher in and around the CSDH compared with peripheral blood. Each of these mediators may have a unique and important role in CSDH formation and propagation.
- #23 Pathophysiology of chronic subdural haematoma: inflammation, angiogenesis and implications for pharmacotherapyhttps://pmc.ncbi.nlm.nih.gov/articles/PMC5450087/
Inflammatory cells recruited to the subdural space will attempt to repair the border cell damage, but instead proliferate and result in the new membrane formation. […] Many of the inflammatory cells have pro-angiogenic roles which support the development of new blood vessels in this subdural region. […] The internal membranes are generally reported as containing collagen and fibroblasts only and therefore relatively non-functional with respect to driving CSDH growth. […] The external membrane, however, is considered more crucial in driving CSDH growth. […] Importantly, CSDH membranes also contain numerous highly permeable capillaries with thin walls containing thin or absent basement membrane and lacking smooth muscle cells and pericytes. […] The inflammatory process involved in CSDH membrane and fluid formation is localised to the subdural space, exemplified by the fact that the mediators are consistently significantly higher in and around the CSDH compared with peripheral blood.
- #24 Subdural hematoma – Wikipediahttps://en.wikipedia.org/wiki/Subdural_hematoma
In chronic subdural hematomas, 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 hematoma cavity. […] Pro-inflammatory mediators active in the hematoma expansion process include Interleukin 1 (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).
- #25 Expert consensus on drug treatment of chronic subdural hematoma | Chinese Neurosurgical Journal | Full Texthttps://cnjournal.biomedcentral.com/articles/10.1186/s41016-021-00263-z
The secretion of inflammatory cytokines and vascular endothelial growth factor (VEGF) leads to the proliferation of immature blood vessels on the hematoma wall, damage to vascular endothelial cells, opening of gap junctions, and increase of permeability. The continuous leakage of circulating substances results in the gradual increase in hematoma growth. […] At the same time, the lack of anti-inflammatory and pro-repair factors, such as regulatory T (Treg) cells and endothelial progenitor cells (EPCs), leads to the recurrence of immature angiogenesisendothelial cell damagevascular leakage on the hematoma wall, which may be the key factor for CSDH formation. […] A recent study showed that meningeal lymphatic vessels (mLVs) were also an important pathway for subdural hematoma (SDH) clearance. The presence of SDH hampers the formation and normal functioning of mLVs, which may form a vicious circle and accelerate the accumulation of SDH. […] These observations indicate that CSDH may be formed because of the malfunction of mLVs and be cleared through mLVs. Other studies have confirmed that immune regulation abnormity and decrease in vascular repair and maturation ability play important roles in the formation and development of CSDH.
- #25 Expert consensus on drug treatment of chronic subdural hematoma | Chinese Neurosurgical Journal | Full Texthttps://cnjournal.biomedcentral.com/articles/10.1186/s41016-021-00263-z
Chronic subdural hematoma (CSDH) is a chronic space-occupying lesion formed by blood accumulation between arachnoid and dura mater, which is usually formed in the third week after traumatic brain injury. […] The mechanism of CSDH development and absorption is not very clear. A series of studies were carried out on the pathogenesis of CSDH, such as bleeding from the avulsion of the pontine vein, increased osmotic pressure, hematoma capsule hemorrhage, and local hyperfibrinolysis. All studies were considered to be related to the formation and development of CSDH, but the pathogenesis of CSDH is still unclear up to now. […] Recent evidence shows that trauma and other causes can lead to the accumulation of blood and/or cerebrospinal fluid in the local subdural cavity. Hematoma-derived exosomes promote abnormal angiogenesis with high permeability by delivering miR-144-5p into endothelial cells, which results in re-bleeding and inhibits hematoma absorption.
- #26 Evidence-Based Treatment of Chronic Subdural Hematoma | IntechOpenhttps://www.intechopen.com/chapters/46053
The factors responsible for the maintenance or enlargement of cSDH over time are still ambiguous. It is most likely influenced by multiple factors, which vary from case to case. Over the years, several theories have been debated: Osmotic theory, Oncotic theory, Microbleeds theory, Anticoagulant and profibrinolytic theory, Inflammatory and growth factors theory. […] Current evidence suggests that the maintenance or enlargement of cSDH is caused by multiple factors. The stimulus is probably a mixture of the microbleed theory, the anticoagulant and profibrinolytic theory, and the inflammatory and growth factors theory.
- #27 Chronic Subdural Hematoma: Concepts of Physiopathogenesis A Review | Canadian Journal of Neurological Sciences | Cambridge Corehttps://www.cambridge.org/core/journals/canadian-journal-of-neurological-sciences/article/chronic-subdural-hematoma-concepts-of-physiopathogenesis-a-review/B6EA3285217ED67594CA97E9794D4BBA
A larger body of clinical evidence exists supporting the concept that plasma and/or erythrocytes continuously penetrate into the subdural cavity, where enhanced fibrinolytic activity is present. […] However, this chronic rebleeding cannot fully explain the observed growth, because the composition of the hematoma fluid is somewhat different from serum or plasma, and the protein content is also progressively diluted by fluid arising from an unknown source. […] There is some clinical and experimental evidence to suggest that a production – reabsorption balance may be a significant growth variable. […] No work has been done to define the role, if any, of local inflammatory mechanisms in the chronic subdural hematoma. […] Sound clinical evidence has shown that after the initial formation of the subdural clot, growth follows, then a slow, complete reabsorption usually occurs. Aside from the plausible production – reabsorption balance concept, it is not known why the evolution proceeds in this manner.
- #27 Chronic Subdural Hematoma: Concepts of Physiopathogenesis A Review | Canadian Journal of Neurological Sciences | Cambridge Corehttps://www.cambridge.org/core/journals/canadian-journal-of-neurological-sciences/article/chronic-subdural-hematoma-concepts-of-physiopathogenesis-a-review/B6EA3285217ED67594CA97E9794D4BBA
From the present review it seems clear that the physiopathogenesis of the chronic subdural hematoma is far from being completely understood. […] The development of subdural hematomas most likely occurs following minimal trauma in those patients with predisposing factors. […] Experimental data substantiates the fact that an accumulation of clotted blood in the subdural or subcutaneous space induces the formation of the fibroplastic neomembrane. […] The hypothesis that blood must come in contact with cerebrospinal fluid in order for the growth to occur, is still controversial. […] It has been virtually disproven that osmosis, referring to the electrolyte gradient as measured by freezing point depression, has any significance as a growth inducing factor. […] The protein oncotic gradient theory, having been the most widely accepted explanation as to the progressive enlargement of the subdural hematoma sac, has little experimental data supporting it.
- #28 Journal of the Korean Medical Associationhttps://jkma.org/m/journal/view.php?number=3536
Chronic SDH mainly originates from an SDG and acute SDH. […] SDG is usually triggered by trauma but only occurs in patients in whom sufficient potential space is available and may occur spontaneously in such cases. […] Separation of the dural border cell layer causes inflammation, indicated by fibroblast proliferation and neovascularization. […] Conversion of an SDG into a chronic SDH or enlargement of a chronic SDH is attributable to formation of neomembranes, neovascularization, and repeated microhemorrhages from fragile capillaries. […] Outcomes of chronic SDH depend on the absorptive-expansion capacity dynamics.
- #29 Management of Chronic Subdural Haematoma | ACNRhttps://acnr.co.uk/articles/management-of-chronic-subdural-haematoma/
Chronic subdural haematoma (CSDH) is one of the most common clinical entities encountered in daily neurosurgical practice. It generally occurs in the elderly population in whom age related reductions in brain volume with a corresponding increase in the size of the subdural space increase the vulnerability to this disease. […] Two mechanisms, either alone or in combination, appear to play an aetiological role in the development of a CSDH. […] An acute subdural haematoma that has not been evacuated may evolve into a CSDH. As the acute haematoma matures an inflammatory membrane forms and envelopes the clot. Repeated minor haemorrhages from neovascular structures in the membrane may contribute to haematoma expansion. […] In addition the acute haematoma liquefies within days of the initial bleed. Fluid ingress, driven by an osmotic gradient generated by fibrinolytic products within the haematoma has been postulated to cause expansion during the conversion of an acute to a chronic subdural haematoma.
- #30 Pathophysiology of chronic subdural haematoma: inflammation, angiogenesis and implications for pharmacotherapy | Journal of Neuroinflammation | Full Texthttps://jneuroinflammation.biomedcentral.com/articles/10.1186/s12974-017-0881-y
- #31https://journals.lww.com/neur/fulltext/2023/71040/detailed_demonstration_of_the_mechanism_of_acute.31.aspx
In cases of acute subdural hematomas (ASDHs) caused by ruptured intracranial aneurysms, it is challenging to confirm the diagnosis when the hemorrhage is limited to the subdural space and the subarachnoid hemorrhage (SAH) is not evident. […] the precise mechanism of nontraumatic ASDH is unknown. […] The arachnoid at the tip of the aneurysm was thickened with clots, and arachnoid perforation was observed at the tip of the aneurysm, which was identified as the rupture point of the ASDH. […] Clarke and Walton reported four mechanisms of subdural hemorrhage due to ruptured aneurysms. First, previous minor hemorrhage causes adhesion between the arachnoid and the aneurysm. Second, the high bleeding pressure of the ruptured aneurysm causes a rupture of the arachnoid membrane, which was also present in our case. Third, intracerebral hemorrhage bleeding spreads from the brain’s surface into the subdural space. Fourth, aneurysms directly exposed to the subdural space cause bleeding. […] If the tip of the aneurysm protrudes into the epi-arachnoid space and ruptures at the tip, it breaks through the arachnoid membrane and causes ASDH. […] In summary, ASDH due to a ruptured aneurysm is rare, but a precise preoperative diagnosis is crucial to avoid fatal re-rupture.
- #32 Pathogenesis of Spinal Subdural Hematoma Based on Histopathological Findings: A Case Reporthttps://www.jstage.jst.go.jp/article/nmccrj/12/0/12_2024-0214/_html/-char/ja
Spinal subdural hematoma is a rare condition whereas intracranial chronic subdural hematoma is well-recognized and documented in clinical settings. […] Despite various theories that have been proposed, the exact pathogenesis of spinal subdural hematoma remains to be elucidated. […] The exact pathogenesis of sSDH remains unknown, with various theories proposed. One theory suggests that disruption of bridging veins in the spine, caused by direct trauma or lumbar puncture, leads to hematoma formation, similar to intracranial hematomas. […] However, bridging veins exist not only in intracranial structures but also in the spine, suggesting that disruption of these veins can also cause a sSDH. […] A third theory suggests a different mechanism for the formation of sSDH from that of iCSDH.
- #33 Pathogenesis of Spinal Subdural Hematoma Based on Histopathological Findings: A Case Reporthttps://www.jstage.jst.go.jp/article/nmccrj/12/0/12_2024-0214/_html/-char/ja
In this theory, sSDH occurs due to a rapid increase in intravascular pressure of the intraspinal segments of lateral spinal vessels, caused by increased abdominal and thoracic pressure. […] Finally, some researchers have stated that the subarachnoid hemorrhage is thought to extend into the subdural space. […] These potential pathogenesis may be more likely to be induced by the use of antithrombotics or because of bleeding diathesis. […] In conclusion, we demonstrated that sSDH may have various potential pathogeneses, which can be elucidated through histopathological examination as in our case.
- #34 Subdural Hematoma: What It Is, Causes, Symptoms & Treatmenthttps://my.clevelandclinic.org/health/diseases/21183-subdural-hematoma
A subdural hematoma develops from a tear in a blood vessel. Blood leaks out of the torn vessel into the space between your dura mater and your arachnoid mater. Active bleeding into this space is called a subdural hemorrhage. A buildup of blood is a subdural hematoma. […] More broadly, a subdural hematoma is a type of traumatic brain injury (TBI). […] Subdural hematomas can be life-threatening and need immediate medical care. […] About half of people with large acute hematomas survive, but they often have permanent brain damage. Younger people have a higher chance of survival than older adults. […] Without treatment, large hematomas can lead to coma and death. Other complications include: Brain herniation: Increased pressure from a pool of blood can squeeze and push brain tissue so it moves from its normal position. A brain herniation is often fatal.
- #35 Subdural hematoma – Symptoms, diagnosis and treatment | BMJ Best Practice UShttps://bestpractice.bmj.com/topics/en-us/416
Subdural hematoma (SDH) has a variable disease course, depending on size of hematoma, age of the patient, presenting neurologic signs/symptoms, presence of underlying coagulopathy or neoplasm, and associated injuries. […] SDH is a collection of blood between the dural and arachnoid coverings of the brain. As the volume of the hematoma increases, brain parenchyma is compressed and displaced, and the intracranial pressure may rise and cause herniation. […] While the presence of SDH can be inferred by neurologic decline and mechanism of traumatic injury, the diagnosis is typically made radiographically (computed tomography or magnetic resonance imaging).
- #36 Subdural Hematoma – StatPearls – NCBI Bookshelfhttps://www.ncbi.nlm.nih.gov/books/NBK532970/
In this context, the structure stretches bridging veins and renders them prone to rupture. […] A larger bleed may augment the distance between the bridging veins and trigger an extensive amount of blood layering around the brain, slowly augmenting subdural space, decreasing the space of the brain leading to herniation of the cerebral structures. […] In shaken baby syndrome or battered infant syndrome, the acceleration and decelerating forces of the brain during violent shaking of the head causes the brain to move in an opposite direction to the meninges causing the bridging veins to rupture and bleed in the subdural space. […] This potential space may accumulate a significant quantity of blood in various stages to exist in an acute or sub-acute form. […] When there is a sufficient accumulation of blood to occupy a large intracranial space, the brain midline shifts toward the opposite side, encroaching on the brain structures against the inner surface of the calvarium after decreasing the volume of the lateral third and fourth ventricles. […] As the intracranial space becomes limited, the volumetric forces push the uncal portion of the temporal lobe toward the foramen magnum causing herniation of the brain.
- #37 Subdural Hematomahttps://mobile.fpnotebook.com/Neuro/CV/SbdrlHmtm.htm
Cranial Trauma results in Subdural Hemorrhage. […] Tear of bridging veins between Dura Mater and the arachnoid membrane on the surface of the brain. […] Sudden acceleration-deceleration is typical cause. […] Subdural Hematoma accumulation exerts pressure on the brain. […] Results in neurologic tissue ischemia. […] May progress to Cerebral Herniation (esp. acute Subdural Hematoma).
- #38 Parkinsonsim due to a Chronic Subdural Hematomahttps://www.e-jmd.org/journal/view.php?number=91
Subdural hematoma is a rare cause of parkinsonism. […] The pathomechanism of secondary parkinsonism may involve interruption of presynaptic or postsynaptic dopaminergic transmission. […] The mechanism leading to parkinsonism in patients with a subdural hematoma is not well understood. It has been suggested that direct compression on the basal ganglia by space-occupying lesions can cause the decreased number of dopaminergic receptors in the striatum which explains parkinsonism secondary to brain tumor. […] Furthermore, the mass effect that compress the midbrain and thus interfere nigro-striatal dopaminergic transmission may also induce parkinsonism. […] In those mechanism, the levodopa-responsiveness may be depending on the region of compression and the involvement in the midbrain tend to be more responsive rather than basal ganglia compression. […] Although parkinsonism secondary to CSH is rare etiology, it is important to recognize because it is potentially treatable.
- #39 BIOCELL | The pathogenesis of chronic subdural hematoma in the perspective of neomembrane formation and related mechanismshttps://www.techscience.com/biocell/v48n6/57033
Chronic subdural hematoma (CSDH) is a disease characterized by capsuled blood products that progressively occupy the intracranial space, causing intracranial hypertension and compression in the brain. […] the pathogenesis of CSDH remains unclear. […] For the first time, we analyzed the cellular and molecular compositions of hematoma membranes with a focus on neomembrane formation, a complex early-stage interactive event in hematoma pathogenesis. […] We hypothesize that in patients with CSDH, dural border cells (DBCs) might be induced to synthesize collagen or serum proteins might accumulate at the dura and arachnoid layers at the site of injury, thereby encapsulating the hemorrhage. […] Membrane formation may trigger inflammatory responses after subdural hemorrhage, promoting fibroblast-involved extracellular matrix (ECM) deposition and aberrant angiogenesis within the outer membrane.
- #40 Chronic Subdural Hematoma: Epidemiology, Etiology, Pathogenesis, Treatment and Outcome | Frontiers Research Topichttps://www.frontiersin.org/research-topics/11547/chronic-subdural-hematoma-epidemiology-etiology-pathogenesis-treatment-and-outcome/articles
Chronic subdural hematoma (CSDH), a disorder that mainly affects the elderly, is predicted to be the most common cranial neurosurgical disease in America by 2030. […] Therefore, delineating the pathophysiologic mechanisms to further improve the outcome of non-surgical treatment is beneficial to CSDH patients, especially those elderly patients who are unable to tolerate surgery. […] This Research Topic aims to advance our understanding of the pathogenesis of CSDH and to improve the treatment and prognosis of CSDH patients. […] Whether Atorvastatin therapy can prevent the recurrence and the mechanisms of CSDH needs to be further addressed through clinical and animal studies. […] Specifically, we welcome original research articles and reviews that focus on the etiology, pathogenesis, epidemiology and treatment of CSDH including papers on: Studies on animal models to examine the pathogenesis of CSDH.