Subarachnoid hemorrhage pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Syed Ahsan Hussain, M.D.[2] Sara Mehrsefat, M.D. [3]

Overview[edit | edit source]

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[edit | edit source]

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[edit | edit source]

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[edit | edit source]

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]

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

• Hypertension
• Cigarette smoking
• Connective tissue disease
  • Ehlers-Danlos syndrome
  • Pseudoxanthoma elasticum
• Familial aldosteronism type I

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[edit | edit source]

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]

• Technical errors
• Hematoma
• Aneurysm thrombosis
• Vasospasm
• Small aneurysm size
• Aneurysm obscuration

Histopathologic findings[edit | edit source]

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]

Nonaneurysmal subarachnoid hemorrhage[edit | edit source]

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 [edit | edit source]

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]}

• Hypertension
• Acute lacunar infarctions
• Physical exertion

Vascular malformations[edit | edit source]

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]}

• 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[edit | edit source]

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[edit | edit source]

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