Subarachnoid hemorrhage pathophysiology: Difference between revisions
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==== Vascular malformations ==== | ==== Vascular malformations ==== | ||
Spinal or intracranial [[Vascular malformations of the brain|vascular malformations]] may also result in subarachnoid hemorrhage. Instead of a brain [[parenchyma]] where normally [[vascular malformation]] occurs. Vascular lesion may also primarily occurs in the [[subarachnoid space]] and result in subarachnoid hemorrhage. | Spinal or intracranial [[Vascular malformations of the brain|vascular malformations]] may also result in subarachnoid hemorrhage. Instead of a brain [[parenchyma]] where normally [[vascular malformation]] occurs. Vascular lesion may also primarily occurs in the [[subarachnoid space]] and result in subarachnoid hemorrhage.<ref name="pmid8362440">{{cite journal| author=Rinkel GJ, van Gijn J, Wijdicks EF| title=Subarachnoid hemorrhage without detectable aneurysm. A review of the causes. | journal=Stroke | year= 1993 | volume= 24 | issue= 9 | pages= 1403-9 | pmid=8362440 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8362440 }}</ref> | ||
Vascular malformations may include: | Vascular malformations may include: | ||
Revision as of 18:25, 6 December 2016
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Subarachnoid Hemorrhage Microchapters |
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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
perimesencephalic nonaneurysmal subarachnoid hemorrhage (PM NASAH) is characterized as localized specific blood pattern on computed tomography (CT), normal cerebral angiography, and less sever symptoms and course of the condition.[8]
The exact pathogenesis of perimesencephalic nonaneurysmal subarachnoid hemorrhage (PM NASAH) is not fully understood. However the three possible hypothesis may be as following:[8]
- Perforating artery disease: Because of the specific location which PM NASAH occurs, rupture of perforating artery arising from the posterior circulation can be a possible theory.
- Venous source: Because of a low rate of rebleeding and low pressure bleeding, It is thought that PM NASAH happens in the setting of of venus leakage.
- Basilar artery abnormalities: It can be secondary to intramural hematoma or possible vasospasm
Possible associated conditions may include:[9]
- Hypertension
- Acute lacunar infarctions
- Physical exertion
Vascular malformations
Spinal or intracranial vascular malformations may also result in subarachnoid hemorrhage. Instead of a brain parenchyma where normally vascular malformation occurs. Vascular lesion may also primarily occurs in the subarachnoid space and result in subarachnoid hemorrhage.[10]
Vascular malformations may include:
- Arteriovenous malformation (AVM): Abnormal connection between arteries and veins in the brain and can result in vessels break and bleed into the brain.
- Dural arteriovenous fistulae
Intracranial arterial dissection
Dissection of an intracranial artery begins as a tear in the arterial wall. It is usually transverse and extends through the intima and halfway through the media and then create the false-lumen. In this setting, it usually result in to thrombus formation, and thromboembolic stroke. If dissection extends through the adventitia, it may result in subarachnoid hemorrhage.
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.
- ↑ 8.0 8.1 Schwartz TH, Solomon RA (1996). "Perimesencephalic nonaneurysmal subarachnoid hemorrhage: review of the literature". Neurosurgery. 39 (3): 433–40, discussion 440. PMID 8875472.
- ↑ Schwartz TH, Solomon RA (1996). "Perimesencephalic nonaneurysmal subarachnoid hemorrhage: review of the literature". Neurosurgery. 39 (3): 433–40, discussion 440. PMID 8875472.
- ↑ Rinkel GJ, van Gijn J, Wijdicks EF (1993). "Subarachnoid hemorrhage without detectable aneurysm. A review of the causes". Stroke. 24 (9): 1403–9. PMID 8362440.