Subarachnoid hemorrhage pathophysiology: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
Subarachnoid hemorrhage (SAH) is the result of the bleeding within the subarachnoid space, which is filled with [[cerebrospinal fluid]]. It is a bleeding which is accumulated between the arachnoid and pia mater and can spread into [[Intraventricular|intraventricular space]], brain parenchyma and [[subdural space]]. | |||
===Aneurysmal subarachnoid hemorrhage=== | ===Aneurysmal subarachnoid hemorrhage=== | ||
Aneurysmal subarachnoid hemorrhage is a result of : | Aneurysmal subarachnoid hemorrhage is a result of : | ||
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===Nonaneurysmal subarachnoid hemorrhage=== | ===Nonaneurysmal subarachnoid hemorrhage=== | ||
The exact pathogenesis of nonaneurysmal SAH (NASAH) is not fully understood. It is though that the mechanism of the bleeding in this type of subarachnoid hemorrhage is diverse. | |||
==== Perimesencephalic nonaneurysmal subarachnoid hemorrhage ==== | |||
The exact pathogenesis of perimesencephalic nonaneurysmal subarachnoid hemorrhage (PM NASAH) is not fully understood. It is thought that there is association between lacunar infarct and this type of (NASAH). | |||
==References== | ==References== | ||
Revision as of 22:46, 5 December 2016
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sara Mehrsefat, M.D. [2]
Overview
Pathophysiology
Subarachnoid hemorrhage (SAH) is the result of the bleeding within the subarachnoid space, which is filled with cerebrospinal fluid. It is a bleeding which is accumulated between the arachnoid and pia mater and can spread into intraventricular space, brain parenchyma and subdural space.
Aneurysmal subarachnoid hemorrhage
Aneurysmal subarachnoid hemorrhage is a result of :
- Saccular aneurysms (responsible for most SAHs)
- Fusiform aneurysms (dilatation of the entire circumference of the vessel that may in part be formed due to atherosclerosis)
- Mycotic aneurysms (infected emboli due to infective endocarditis)
Saccular aneurysms
Saccular (berry) aneurysms are responsible for most cases of subarachnoid hemorrhage (SAH). Multiple factors play a role in formation of a saccular aneurysms. Saccular aneurysms usually results from degenerative change in the vessel wall following:[1]
- Hemodynamic stress (turbulent blood flow) which it may result in excessive tear and breakdown of the internal elastic lamina which it progress to lack of elastic lamina.
It is also thought that inflammatory process is also play a role in pathogenesis of aneurysms.[2]
Common associated conditions may include:[3][4][5]
The role for genetic factors in pathogenesis of aneurysmal formation has been approved. However, the exact pathogenesis remains unknown. It is thought that some connective tissue disease may result in arterial wall weakness and non-laminar flow pattern of blood, which is then progress to tear and breakdown of the wall.[4][5] Additionally, it is thought concurrent hypertension may play a role in patient with autosomal dominant polycystic kidney disease (PKD).[6]
Histopathologic findings
Unruptured aneurysms wall may present with complete absence of endothelial lining.
However, ruptured aneurysm walls may present with Inflammatory cells (T cell and macrophage infiltration) in addition to complete absence of endothelial lining.
Histological types of aneurysm walls may be identified as follow:[7]
| Histological types | Consecutive stages of aneurysm walls | Chance of aneurysmal rupture |
|---|---|---|
| Type A |
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| Type B |
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| Type C |
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| Type D |
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Nonaneurysmal subarachnoid hemorrhage
The exact pathogenesis of nonaneurysmal SAH (NASAH) is not fully understood. It is though that the mechanism of the bleeding in this type of subarachnoid hemorrhage is diverse.
Perimesencephalic nonaneurysmal subarachnoid hemorrhage
The exact pathogenesis of perimesencephalic nonaneurysmal subarachnoid hemorrhage (PM NASAH) is not fully understood. It is thought that there is association between lacunar infarct and this type of (NASAH).
References
- ↑ Austin G, Fisher S, Dickson D, Anderson D, Richardson S (1993). "The significance of the extracellular matrix in intracranial aneurysms". Ann Clin Lab Sci. 23 (2): 97–105. PMID 7681275.
- ↑ Aoki T, Nishimura M (2010). "Targeting chronic inflammation in cerebral aneurysms: focusing on NF-kappaB as a putative target of medical therapy". Expert Opin Ther Targets. 14 (3): 265–73. doi:10.1517/14728221003586836. PMID 20128708.
- ↑ Starke RM, Chalouhi N, Ali MS, Jabbour PM, Tjoumakaris SI, Gonzalez LF; et al. (2013). "The role of oxidative stress in cerebral aneurysm formation and rupture". Curr Neurovasc Res. 10 (3): 247–55. PMC 3845363. PMID 23713738.
- ↑ 4.0 4.1 Pepin M, Schwarze U, Superti-Furga A, Byers PH (2000). "Clinical and genetic features of Ehlers-Danlos syndrome type IV, the vascular type". N Engl J Med. 342 (10): 673–80. doi:10.1056/NEJM200003093421001. PMID 10706896.
- ↑ 5.0 5.1 Neil-Dwyer G, Bartlett JR, Nicholls AC, Narcisi P, Pope FM (1983). "Collagen deficiency and ruptured cerebral aneurysms. A clinical and biochemical study". J Neurosurg. 59 (1): 16–20. doi:10.3171/jns.1983.59.1.0016. PMID 6864273.
- ↑ Vlak MH, Algra A, Brandenburg R, Rinkel GJ (2011). "Prevalence of unruptured intracranial aneurysms, with emphasis on sex, age, comorbidity, country, and time period: a systematic review and meta-analysis". Lancet Neurol. 10 (7): 626–36. doi:10.1016/S1474-4422(11)70109-0. PMID 21641282.
- ↑ Frösen J, Piippo A, Paetau A, Kangasniemi M, Niemelä M, Hernesniemi J; et al. (2004). "Remodeling of saccular cerebral artery aneurysm wall is associated with rupture: histological analysis of 24 unruptured and 42 ruptured cases". Stroke. 35 (10): 2287–93. doi:10.1161/01.STR.0000140636.30204.da. PMID 15322297.