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    Home > Active Ingredient News > Study of Nervous System > This article explains the etiology of subarachnoid hemorrhage thoroughly!

    This article explains the etiology of subarachnoid hemorrhage thoroughly!

    • Last Update: 2021-11-05
    • Source: Internet
    • Author: User
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    *It is only for medical professionals to read for reference.
    Concise and detailed, it is worth a look! Subarachnoid hemorrhage (SAH) is a common hemorrhagic cerebrovascular disease with a high mortality and disability rate, and the causes of this disease are diverse
    .

    At the 24th National Neurology Conference of the Chinese Medical Association, Professor Qin Chao from the Neurology Department of the First Affiliated Hospital of Guangxi Medical University gave a wonderful report entitled "The Etiology of Subarachnoid Hemorrhage".
    Come and see Bar! Subarachnoid hemorrhage refers to the spontaneous rupture of blood vessels at the base of the skull or on the surface of the brain, and blood flows into the subarachnoid space, causing corresponding clinical symptoms
    .

    The causes are diverse and the clinical evolution is intricate, so some scholars call SAH a clinical syndrome
    .

    There are many causes of SAH.
    Intracranial aneurysms are the most common cause of SAH (85%).
    Other causes include non-aneurysmal perimedullary hemorrhage, cerebral arteriovenous malformations (AVM), moyamoya disease (MMD), scleroderma Meningeal arteriovenous fistula (DAVF), vasculitis, intracranial venous system thrombosis, connective tissue diseases, intracranial tumors, hematological diseases, coagulopathy and complications of anticoagulation therapy, etc.
    , some patients have unknown causes
    .

    Figure 1: Aneurysm prone site (picture source from Professor Qin Chao's PPT) Intracranial aneurysm Intracranial aneurysms best occur in the circle of Willis and its bifurcations, 90% are located in the anterior circulation, and the most common site is the anterior traffic Arteries (40%~45%), followed by the junction between the posterior communicating artery and the internal carotid artery (30%~35%), and the first major branch of the middle cerebral artery in the lateral fissure (10%~15%)
    .

    Posterior circulation aneurysms account for about 10%, most commonly at the tip of the basilar artery or the junction of the vertebral artery and the posterior inferior cerebellar artery
    .

    According to the size, intracranial aneurysms are divided into small (<5mm), medium (5-10mm), large (11-25mm), and huge (>25mm)
    .

    According to the shape, it is divided into saccular aneurysm, pseudoaneurysm, blood alveolar aneurysm, and fusiform aneurysm
    .

    Figure 2: Classification according to the size of aneurysm (pictured by Professor Qin Chao, PPT) Figure 3: Diversity of aneurysm morphology (pictured by Professor Qin Chao, PPT) What are the causes of aneurysm rupture? 1.
    The mural ducts of the intracranial cerebral arteries are dysplasia and lack the muscle layer or elastic layer
    .

    2.
    Microscopic examination shows that the wall of the saccular aneurysm is very thin or missing.
    For example, the muscle layer is missing or only fragments remain, the intima is thickened, and the tumor wall is only composed of the inner and outer membranes, with a small number of fibers in between.
    Degeneration or hyaline degeneration
    .

    3.
    Immunohistochemical analysis showed that type I collagen and fibronectin were mixed, the expression of type 3 and 4 collagen and conversion factor was reduced, and the globulin heavy chain subtype was not expressed
    .

    4.
    Inducing factors: smoking, fatigue, emotional agitation, high blood pressure and so on
    .

    Intracranial dissecting aneurysm occurs in the arterial media layer, between the media and adventitia, the arterial wall bulges, aneurysm-like expansion occurs, the incidence rate is 2.
    5-4/10 million
    .

    Prevalent parts: C1, V3, and V4 are the most common
    .

    MRI is highly sensitive to intracranial dissecting aneurysms.
    It can show changes in the arterial lumen and inter-wall hemorrhage, and the signal changes with the absorption of hematoma.
    The observation of the double-lumen sign and intimal valve is the basis for direct diagnosis
    .

    Treatment methods: 1.
    Drug therapy; 2.
    Surgery: Patients who have failed drug therapy, have persistent ischemic symptoms, persisted dissecting aneurysms, especially SAH, can choose surgery or interventional therapy
    .

    Non-aneurysmal subarachnoid hemorrhage (PNSH) around midbrain was first proposed in 1980 by Dutch neurologist Van Gijn and radiologist AnDongen
    .

    The center of the hemorrhage is immediately in front of the midbrain, with or without hemorrhage extending to the base of the cistern
    .

    The anterior part of the longitudinal fissure cistern is not completely filled, generally does not extend to the outside of the lateral fissure cistern, and there is no obvious intraventricular hematoma
    .

    The clinical features are also different from those of aneurysmal SAH, which are rarely accompanied by disturbances of consciousness and focal neurological symptoms, and the prognosis is good
    .

    Causes of PNSH 1.
    The cause is not clear, such as cerebral venous hemorrhage, rupture of cerebral artery perforating branch, telangiectasia, occult cavernous hemangioma or bleeding from arteriovenous malformation
    .

    It is currently believed that PNSH is caused by venous hemorrhage in the front of the midbrain.
    The bleeding pressure is low, the area is limited, and it is easily diluted by cerebrospinal fluid, so the symptoms after hemorrhage are relatively mild
    .

    The sources of venous hemorrhage are mostly interfoot veins, prepontine veins, posterior communicating veins, ventricle striatal veins and thalamic perforating veins
    .

    2.
    There is a relationship between PNSH and the reflux mode of the deep cerebral venous system.
    Intracranial venous hypertension plays a vital role in the occurrence of PNSH: Transverse sinus thrombosis can lead to the occurrence of PNSAH
    .

    3.
    The predisposing factors cause increased intracranial venous pressure or venous dilation, which in turn leads to rupture and bleeding of veins and capillaries around the midbrain
    .

    Dural Arteriovenous Fistula (DAVF) is an arteriovenous shunt that is partially or completely located in the dura
    .

    They are rare acquired lesions
    .

    DAVF accounts for 5%-15% of intracranial vascular malformations
    .

    The clinical manifestations of DAVF range from asymptomatic to potentially fatal intracranial hemorrhage
    .

    The clinical manifestations and natural course of the disease depend on the venous drainage mode, which is also the most important factor in determining the prognosis of patients
    .

    In the dural arteriovenous fistula with a benign natural history, the drainage does not involve the cerebral veins, and tinnitus or ocular symptoms are the most common manifestations
    .

    Fistulas with a high risk of bleeding are characterized by retrograde cortical venous drainage, which can manifest as intracranial hemorrhage, SAH, progressive neurasthenia, dementia, epilepsy, or intracranial hypertension
    .

    Figure 4: Example of DAVF (pictured by Professor Qin Chao from the PPT) Cerebral Arteriovenous Malformation Cerebral Arteriovenous Malformation (AVM) is a relatively rare vascular malformation that may cause intracranial hemorrhage, and may cause devastating nerve damage or death
    .

    They are composed of abnormally formed blood vessels, and are generally considered to be a lesion with low resistance, high flow, connected between arteries and veins, and without capillary beds
    .

    The AVM detection rate is approximately 1.
    3/100,000 per year
    .

    These lesions have a high risk of intracranial hemorrhage.
    About half of the newly discovered AVMs have hemorrhage.
    The estimated rupture risk in AVM patients without rupture is 1%-3%/year
    .

    Figure 5: AVM example (Tuyuan Qin Chao's PPT) Figure 6: AVM example (Tuyuan Qin Chao's PPT) The bleeding factors of AVM Previous bleeding history, location, vascular structure, AVM size and genetic factors
    .

    The AVM is mostly located in the deep part of the brain tissue, especially the AVM around the basal ganglia and ventricles is more prone to bleeding
    .

    The size of AVM: AVM with a diameter of <3cm is easy to bleed or AVM with a diameter of >5cm is easy to bleed.
    Generally speaking, the pressure of the blood supply artery of a small AVM is higher than that of a large AVM, and may be more likely to bleed
    .

    What are the treatment methods for AVM? 1.
    Microsurgical resection; 2.
    Interventional embolization; 3.
    Reflex surgery (small size, located in the functional area)
    .

    Choosing an appropriate, safe, effective and individualized treatment is critical to the prognosis of patients
    .

    Moyamoya disease (MMD) is an abnormal vascular network at the base of the skull
    .

    Clinically, it can cause cerebral hemorrhage, cerebral infarction, and SAH
    .

    Reports in the literature only account for 0.
    2%-1.
    0% of subarachnoid hemorrhage
    .

    The cause of bleeding is the rupture of fragile smoke-like blood vessels due to constant hemodynamic pressure
    .

    Figure 7: Example of moyamoya disease (pictured by Professor Qin Chao) Summary: 1.
    The most common cause is the rupture of an intracranial aneurysm, which should be taken seriously
    .

    2.
    Uncommon but not uncommon causes such as non-aneurysmal hemorrhage around the midbrain
    .

    AVM, Moyamoya disease, MMD, intracranial vascular dissection, meningeal arteriovenous fistula DAVF, intracranial venous tumor are worthy of attention
    .

    3.
    Rare or rare causes such as blood system diseases and intracranial venous sinus thrombosis should not be taken lightly
    .

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