Subarachnoid hemorrhage pathophysiology

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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

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.[1] Excluding head trauma, sub arachnid hemorrhage mainly results from spontaneous rupture of a saccular aneurysm.[2] 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. One of the most common subtype is called perimesencephalic nonaneurysmal subarachnoid hemorrhage (PM NASAH). It is characterized as localized specific blood  pattern on computed tomography (CT), normal cerebral angiography, and less sever symptoms and course of the condition.[3]

Pathophysiology

Subarachnoid hemorrhage

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.[1] Excluding head trauma, sub arachnid hemorrhage mainly results from spontaneous rupture of a saccular aneurysm.[2]

Aneurysmal subarachnoid hemorrhage

Spontaneous subarachnoid hemorrhage can be a result of the aneurysmal rupture:[1][2][4][5]

  • 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:[2]

  • 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.[4][6]

The most common sites of saccular aneurysms[7]

Common associated conditions may include:[8][9][10]

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.[9][10] Additionally, it is thought concurrent hypertension may play a role in patient with autosomal dominant polycystic kidney disease (PKD).[11]

Occult aneurysm

It is thought that negative angiogram following subarachnoid hemorrhage can be observed in almost 25% of all cases. As a result even two negative angiograms result can not exclude aneurysmal subarachnoid hemorrhage.[12][13][14]

Common reasons for having negative result in aSAH may include:[12][14][15]

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:[16]

Histological types Consecutive stages of aneurysm walls Chance of aneurysmal rupture
Type A
  • Endothelialized wall
  • Linearly organized smooth muscle cell
  • 41%
Type B
  • Thickened wall
  • Disorganized smooth muscle cells
  • 55%
Type C
  • 64%
Type D
  • Extremely thin thrombosis-lined hypocellular wall
  • 100%

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.[3][17][18]

The exact pathogenesis of perimesencephalic nonaneurysmal subarachnoid hemorrhage (PM NASAH) is not fully understood. However the three possible hypothesis may be as following:[17][19][20]

  • 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:[21][20][22][23]

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.[24][25]

Vascular malformations may include:[24][25][26][27]

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 into thrombus formation, and thromboembolic stroke. If dissection extends through the adventitia, it may result in subarachnoid hemorrhage.[24][28][29]

References

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  2. 2.0 2.1 2.2 2.3 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. 
  3. 3.0 3.1 van Gijn J, van Dongen KJ, Vermeulen M, Hijdra A (1985). "Perimesencephalic hemorrhage: a nonaneurysmal and benign form of subarachnoid hemorrhage.". Neurology. 35 (4): 493–7. PMID 3982634. 
  4. 4.0 4.1 Schievink WI, Karemaker JM, Hageman LM, van der Werf DJ (1989). "Circumstances surrounding aneurysmal subarachnoid hemorrhage.". Surg Neurol. 32 (4): 266–72. PMID 2675363. 
  5. Patel RL, Richards P, Chambers DJ, Venn G (1991). "Infective endocarditis complicated by ruptured cerebral mycotic aneurysm.". J R Soc Med. 84 (12): 746–7. PMC 1295527Freely accessible. PMID 1774755. 
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  7. Wikimedia, Subarachnoid_hemorrhage https://commons.wikimedia.org/wiki/Category:Subarachnoid_hemorrhage#/media/File:Wikipedia_intracranial_aneurysms_-_inferior_view_-_heat_map.jpg
  8. 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 3845363Freely accessible. PMID 23713738. 
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  16. 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. PMID 15322297. doi:10.1161/01.STR.0000140636.30204.da. 
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  19. Alén JF, Lagares A, Lobato RD, Gómez PA, Rivas JJ, Ramos A (2003). "Comparison between perimesencephalic nonaneurysmal subarachnoid hemorrhage and subarachnoid hemorrhage caused by posterior circulation aneurysms.". J Neurosurg. 98 (3): 529–35. PMID 12650424. doi:10.3171/jns.2003.98.3.0529. 
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  22. Tatter SB, Buonanno FS, Ogilvy CS (1995). "Acute lacunar stroke in association with angiogram-negative subarachnoid hemorrhage. Mechanistic implications of two cases.". Stroke. 26 (5): 891–5. PMID 7740585. 
  23. Matsuyama T, Okuchi K, Seki T, Higuchi T, Murao Y (2006). "Perimesencephalic nonaneurysmal subarachnoid hemorrhage caused by physical exertion.". Neurol Med Chir (Tokyo). 46 (6): 277–81; discussion 281–2. PMID 16794347. 
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  25. 25.0 25.1 Cordonnier C, Al-Shahi Salman R, Bhattacharya JJ, Counsell CE, Papanastassiou V, Ritchie V; et al. (2008). "Differences between intracranial vascular malformation types in the characteristics of their presenting haemorrhages: prospective, population-based study.". J Neurol Neurosurg Psychiatry. 79 (1): 47–51. PMID 17488785. doi:10.1136/jnnp.2006.113753. 
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