Common hemorrhagic cerebrovascular disease
1.Hypertensive cerebral hemorrhage
2.Subarachnoid hemorrhage
3.Arteriovenous malformation
4.Dural arteriovenous fistula
5.Internal carotid artery cavernous sinus fistula
6.Epidural hemorrhage
7.Subdural hemorrhage
8.Smoke disease (Moyamoya)
9, cerebral amyloid angiopathy
10.Intracranial venous malformation
Hypertensive cerebral hemorrhage risk factors
1, genetic factors – primary hypertension mostly has a family history
2, secondary factors – adrenal hyperplasia, tumors, renal artery stenosis, etc.
3.Environmental factors–geography, latitude, cold, etc.
4, dietary habits – high salt, high fat diet
5.Hormone level – the prevalence of hypertension increases after menopause in women
6.Age
7, gender – pre-menopausal women have a lower prevalence than men
8.Obesity
Control
1, low salt diet, avoid long-term high-fat diet, weight control
2, primary hypertension – drug system to lower blood pressure (ACEI, ARB, CCB)
3, antihypertensive goals: young and middle-aged people <130/80mmHg, high-risk patients <140/90mmHg, combined with diabetes or chronic kidney disease <130/80mmHg, more than 50 years old stressed SBP <140mmHg
2.Risk factors for subarachnoid hemorrhage
1, vascular lesions – aneurysm, AVM, arterial coarctation, atherosclerosis, hypertension, cerebral thrombosis, vascular amyloidosis, SLE, giant cell arteritis, focal avascular necrosis, polyarteritis nodosa, capillary dilatation, Sturge-Weber syndrome
2, venous thrombosis – pregnancy, contraceptive pills, trauma, infection, coagulation disorders, wasting, dehydration, etc.
3.Allergic diseases – allergic purpura, hemorrhagic nephritis, Hyland-Henno syndrome
4.Infection – meningitis, parasitic diseases, etc. caused by various pathogens
5, poisoning – cocaine, adrenaline, monoamine oxidase inhibitors, morphine, nicotine, etc.
6.Tumor – glioma, meningioma, hemangioblastoma, pituitary tumor, choroidal papilloma, chordoma, hemangioma, ventricular meningioma, choriocarcinoma, etc.
7.Other – VitK deficiency, electrolyte imbalance, heat stroke, etc.
Control
1.Early detection of aneurysm – Because aneurysm accounts for about 80% of SAH, early detection of aneurysm and individualized treatment is an important means to prevent SAH (by CTA, MRA, DSA), and local neurological symptoms have important warning value (such as ptosis).
2.Specific treatment for high-risk factors – control blood pressure, blood sugar, blood lipids, prevent atherosclerosis, abstain from smoking, avoid alcohol, hormone replacement, prevent and control infection, avoid trauma and eliminate toxic factors, etc.
Risk factors of aneurysm
1. saccular aneurysm – (1) Hemodynamics: a. Increased blood flow (AVM, asymmetry of Willis ring, contralateral artery obstruction, etc.); b. Increased blood pressure (aortic stenosis, polycystic kidney, renal artery fibromuscular dysplasia. (2) Vascular wall structure: a. Acquired (endoelastic layer degeneration, sickle cell anemia, inflammation, trauma, tumor); b. Congenital (familial, hereditary, type II collagen deficiency, etc.). (3) Other (smoldering disease, giant cell arteritis).
Arteriovenous malformation risk factors
(1) Embryonic developmental abnormalities – generally considered to occur between embryonic day 45 and 60. In the fourth week of embryonic life, the primitive vascular network of the brain begins to form and primitive blood circulation appears in the procerebrum. Later, the primitive blood vessels then differentiate into arteries, veins and capillaries. If the local vascular differentiation of the brain is impaired during this period, AVM can be formed.
2.With obvious family tendency
3.Age – 20~39 years old, average 25 years old.
4.Gender – male:female ≈ 2:1
Control
1. avoid all factors leading to abnormal vascular differentiation – balanced diet during pregnancy, avoid exposure to radioactive substances 2. strive to intervene before AVM rupture – focus on detection of signs before AVM rupture (seizures, symptoms of blood theft, etc.) as well as after bleeding for clear 3. AVMs with aneurysms, stenosis or obstruction of the draining veins require aggressive management.
Risk factors for dural arteriovenous fistula
1. cranial trauma 2. local infection – mastoiditis, pterygoid sinusitis 3. surgical procedures 4. estrogenic changes in the body – childbirth, abortion, menopause
Control
1. Avoid trauma, control inflammation, etc.
2. Avoid taking oral contraceptives
3. Prevention of hypercoagulable blood
Risk factors for internal carotid cavernous sinus fistula (CCF)
1. head trauma (80%) – skull base fracture 2. medical trauma – endovascular treatment, percutaneous puncture of trigeminal ganglion for trigeminal neuralgia, surgical mishap of the internal carotid sinus segment via the butterfly or pterygoid sinus 3. spontaneous –Seen in ruptured aneurysm of the cavernous sinus segment of the internal carotid artery.
Control
1. Avoid trauma
2. Avoid accidental injury to the internal carotid artery during transsphenoidal or pterygoid sinus surgery
3. Pay attention to the early detection of aneurysms in the cavernous sinus segment and treat them appropriately if necessary
Risk factors of Moyamoya disease
1. Geography – high prevalence in Japan, China and Korea 2. Genetics – family history is 42 times higher than normal population 3. Gender – male to female ratio is 1:1.64. Age — seen at any age, with two peaks at about 4 and 34 years of age, the former predominantly ischemic and the latter predominantly hemorrhagic, but there are many adults who start with ischemic attacks.5. Facial and neck infections — the causal relationship is not obvious.
Control
1. Necessary screening (CTA, MRA, DSA) in high-risk groups 2. Selective temporalis muscle patching, dural inversion, superficial temporal artery-middle cerebral artery bypass for different stages and clinical manifestations of Moyamoya and comprehensive evaluation of brain CT or MRI perfusion findings.
Risk factors for cerebral amyloid angiopathy
1, Apolipoprotein E (ApoE) gene polymorphism is an important risk factor for CAA. ApoEε4 promotes amyloid β (Aβ) deposition in the cerebral vascular wall, while ApoEε2 is a risk factor for amyloid deposition vascular hemorrhage
2, Genetic – Aβ and its precursor protein (APP) are associated with dominantly inherited CAA
3, cysteine protease inhibitor cystatinC – concomitant cystatinC and β amyloid deposition make the vessel wall weak, and cystatinC deposition is a strong indication for CAA bleeding
4, Specific heparan sulfate glycoprotein (HSPG) may be involved in Alzheimer’s disease
(AD) and hereditary hemorrhagic amyloidosis of the brain (HCHWA-D) in the pathogenesis of the disease.
Control
1. In high-risk groups with atrial fibrillation, care should be taken to prevent excessive anticoagulation and to limit the use of drugs such as warfarin.
2.Control blood pressure and prevent complications.
Risk factors for ischemic cerebrovascular disease
1.Heredity
2.Age
3.Gender
4.Race
5.Smoking
6.High blood pressure
7.Arteriosclerosis
8.Heavy alcohol consumption
9.Immune disease
10.Hypercholesterolemia.
11.Obesity
12.Atrial fibrillation
13.Low blood pressure
14.Sedentary
15.Oral contraceptive pills
16.Heart mucinous tumor
17.Hyperuricemia
18.Type II diabetes mellitus
19.Homocysteinemia
20.Other factors
Control
1.Control of blood pressure – see the previous section 2.Control of blood lipids – low-fat diet, weight control, strengthening exercise, statin lipid-lowering drugs 3.Control of blood sugar – diet control, exercise weight control, medication to lower glucose4, control immune response – inhibit all types of immune response5, control inflammation – eliminate inflammatory response in the development of atherosclerosis6, for patients with atrial fibrillation – -eliminate atrial fibrillation or regular and effective anticoagulation therapy7, change lifestyle and diet – appropriate activities, quit smoking, avoid alcohol, etc.8, active management of predisposing lesions – cardiac mucinous tumors, etc.