Cerebral venous sinus thrombosis pathophysiology: Difference between revisions
Line 6: | Line 6: | ||
There are two mechanisms for [[cerebral venous thrombosis]]. The first is [[thrombosis]] of [[cerebral veins]] causing local effects due to [[venous]] [[obstruction]] and the second cause is [[thrombosis]] of the [[cerebral]] [[sinuses]] leading to [[intracranial hypertension]]. Both of these processes occur in the majority of [[patients]] with CVT. Increased [[venous]] [[pressure]] due to the [[occlusion]] of the [[cerebral]] [[vein]] causes cytotoxic [[edema]] and [[venous]] [[infarction]],[[blood brain barrier]] disruption associated vasogenic [[edema]] and [[parenchymal]] [[hemorrhage]] due to [[venous]] and [[capillary]] [[rupture]]. | There are two mechanisms for [[cerebral venous thrombosis]]. The first is [[thrombosis]] of [[cerebral veins]] causing local effects due to [[venous]] [[obstruction]] and the second cause is [[thrombosis]] of the [[cerebral]] [[sinuses]] leading to [[intracranial hypertension]]. Both of these processes occur in the majority of [[patients]] with CVT. Increased [[venous]] [[pressure]] due to the [[occlusion]] of the [[cerebral]] [[vein]] causes cytotoxic [[edema]] and [[venous]] [[infarction]],[[blood brain barrier]] disruption associated vasogenic [[edema]] and [[parenchymal]] [[hemorrhage]] due to [[venous]] and [[capillary]] [[rupture]]. | ||
<img src="https://www.ahajournals.org/cms/asset/01aa1024-5777-4e2b-8efb-f1b93ffed164/zhc0131205700002.jpg" alt="Figure 2."/> | |||
<img src="https://www.ahajournals.org/cms/asset/01aa1024-5777-4e2b-8efb-f1b93ffed164/zhc0131205700002.jpg" alt="Figure 2."/><ref name="Piazza2012">{{cite journal|last1=Piazza|first1=Gregory|title=Cerebral Venous Thrombosis|journal=Circulation|volume=125|issue=13|year=2012|pages=1704–1709|issn=0009-7322|doi=10.1161/CIRCULATIONAHA.111.067835}}</ref> | |||
Revision as of 04:35, 15 July 2021
Cerebral venous sinus thrombosis Microchapters |
Differentiating Cerebral venous sinus thrombosis from other Diseases |
---|
Diagnosis |
Treatment |
Case Studies |
Cerebral venous sinus thrombosis pathophysiology On the Web |
American Roentgen Ray Society Images of Cerebral venous sinus thrombosis pathophysiology |
Cerebral venous sinus thrombosis pathophysiology in the news |
Directions to Hospitals Treating Cerebral venous sinus thrombosis |
Risk calculators and risk factors for Cerebral venous sinus thrombosis pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Pathophysiology=
There are two mechanisms for cerebral venous thrombosis. The first is thrombosis of cerebral veins causing local effects due to venous obstruction and the second cause is thrombosis of the cerebral sinuses leading to intracranial hypertension. Both of these processes occur in the majority of patients with CVT. Increased venous pressure due to the occlusion of the cerebral vein causes cytotoxic edema and venous infarction,blood brain barrier disruption associated vasogenic edema and parenchymal hemorrhage due to venous and capillary rupture.
<img src="https://www.ahajournals.org/cms/asset/01aa1024-5777-4e2b-8efb-f1b93ffed164/zhc0131205700002.jpg" alt="Figure 2."/>[1]
The veins of the brain, both the superficial veins and the deep venous system, empty into the dural venous sinuses, which carry blood back to the jugular vein. In cerebral venous sinus thrombosis, blood clots usually form both in the veins of the brain and the venous sinuses. The thrombosis of the veins themselves causes cerebral edema (both vasogenic and cytotoxic edema) through back pressure, and small petechial hemorrhages that may merge into large hematomas. Thrombosis of the sinuses is the main mechanism behind the increase in intracranial pressure due to decreased resorption of cerebrospinal fluid (CSF). Because this process is generalized, the condition does not lead to hydrocephalus.[2]
Any blood clot forms due to an imbalance between coagulation (the formation of the insoluble blood protein fibrin) and fibrinolysis. The three major mechanisms for such an imbalance are enumerated in Virchow's triad: alterations in normal blood flow, injury to the blood vessel wall, and alterations in the constitution of blood (hypercoagulability). Most cases of cerebral venous sinus thrombosis are due to hypercoagulability.[2]
It is possible for the clot to break off and migrate (embolism) to the lungs, causing a pulmonary embolism.[2][3] An analysis of previous case reports concludes that this occurs in about 10% of cases, but has a very poor prognosis.[4]
References
- ↑ Piazza, Gregory (2012). "Cerebral Venous Thrombosis". Circulation. 125 (13): 1704–1709. doi:10.1161/CIRCULATIONAHA.111.067835. ISSN 0009-7322.
- ↑ 2.0 2.1 2.2 Stam J (2005). "Thrombosis of the cerebral veins and sinuses". N. Engl. J. Med. 352 (17): 1791–8. doi:10.1056/NEJMra042354. PMID 15858188.
- ↑ Einhäupl K, Bousser MG, de Bruijn SF; et al. (2006). "EFNS guideline on the treatment of cerebral venous and sinus thrombosis". Eur. J. Neurol. 13 (6): 553–9. doi:10.1111/j.1468-1331.2006.01398.x. PMID 16796579.
- ↑ Diaz JM, Schiffman JS, Urban ES, Maccario M (1992). "Superior sagittal sinus thrombosis and pulmonary embolism: a syndrome rediscovered". Acta Neurol. Scand. 86 (4): 390–6. PMID 1455986.