(A) Causes
There are many causes of cerebral hemorrhage. The most common cause is hypertensive atherosclerosis, followed by congenital cerebrovascular malformation or aneurysm, hematologic disease, traumatic brain injury, anticoagulation or thrombolytic therapy, amyloid angiopathy, and other causes of cerebral hemorrhage.
The classification according to the etiology is as follows
1.According to vascular pathology, there are microaneurysm or microangioma, cerebral arteriovenous malformation (AVM), amyloid cerebrovascular disease, cystic hemangioma, intracranial venous thrombosis, meningeal arteriovenous malformation, atopic arteritis, fungal arteritis, smoker’s disease and arterial anatomical variation, etc.
2.According to hemodynamics There are hypertension and migraine, hematological factors such as anticoagulation, antiplatelet or thrombolytic therapy, Haemophilus infection, leukemia, thrombotic thrombocytopenia
3.Other Intracranial tumor, alcoholism and sympathetic excitatory drugs, etc.
4.Understood causes such as idiopathic cerebral hemorrhage
In addition, some factors have a certain relationship with the occurrence of cerebrovascular disease and may be the cause of cerebrovascular disease.
① blood pressure fluctuations: such as hypertensive patients who have not taken antihypertensive drugs recently or angry and anxious, etc., causing an increase in blood pressure, especially systolic blood pressure.
(ii) short-tempered or emotional tension: common after anger and quarrel with others.
③ bad habits: such as smoking, alcohol abuse, excessive salt, excessive weight.
④ Excessive fatigue: such as excessive physical and mental labor, bowel movements, and exercise.
(II) Pathogenesis
1, the mechanism of cerebral hemorrhage
In terms of the mechanism of occurrence, in fact, each case of cerebral hemorrhage is not caused by a single factor, but may be caused by a combination of several factors. There are many theories on the mechanism of cerebral hemorrhage formed by hypertension. The more recognized theory is the microaneurysm theory, which generally believes that the simple increase in blood pressure is not enough to cause cerebral hemorrhage.
(1) Rupture of microaneurysm: Because the wall of small arteries in the brain is affected by the tension caused by hypertension for a long time, aneurysms are formed in the weak parts of the vessel wall. When the blood pressure suddenly rises, these saccular vessels are prone to rupture and cause cerebral hemorrhage.
(2) Fatty vitreous degeneration or fibrous necrosis: Long-term hypertension damages the intima of the wall of small penetrating arteries of 100-300 μm in diameter in the brain parenchyma. Lipids in the plasma enter the subintima through the damaged intima, causing thickening of the wall and infiltration of plasma cells, resulting in fatty vitreous degeneration and finally necrosis of the wall. When blood pressure or blood flow changes drastically, it is easy to rupture and bleed.
(3) Cerebral atherosclerosis: Most patients with hypertension have a variety of intimal lesions, including localized fat and complex glycogen accumulation, hemorrhage or thrombosis, fibrous tissue growth, and calcium deposits.
Patients with cerebral atherosclerosis are prone to cerebral infarction, and arteries in large areas of cerebral ischemia and softening are prone to rupture and bleeding, forming hemorrhagic necrotic lesions.
(4) The outer membrane and middle layer of cerebral arteries are structurally weak: the middle cerebral artery is at right angles to its deep penetrating branch, the doublestem artery. This anatomical structure is prone to rupture and bleeding when the blood pressure rises abruptly due to factors such as forceful excitement.
2.Pathophysiological mechanism of cerebral hemorrhage
(1) The main pathophysiological changes: the blood vessel ruptures to form a hematoma, and the surrounding tissues appear spongy degeneration 30 min after the formation of the hematoma; 6 h later, there are spongy degeneration and edema in the adjacent brain parenchyma with the change of necrotic layer and hemorrhagic layer from near to far with time. In addition to mechanical compression, these changes in the brain tissue around the hematoma are mainly due to plasma, blood cell components such as hemoglobin and other vasoactive substances play an important role.
The increase in intracranial volume after hemorrhage destabilizes the intracranial environment and the resulting cerebral edema leads to a further increase in intracranial pressure and also affects local cerebral blood flow and the function of the coagulation and fibrinolytic system.
In addition to the occupational damage of the hematoma itself, cerebral hemorrhage is associated with impaired circulation in the surrounding brain tissue, metabolic disorders (e.g. acidosis), vasomotor paralysis
Damage to cerebral tissue caused by damage to the blood-cerebrospinal fluid barrier and the release of various bioactive substances from blood breakdown products.
①Macromolecular substances: Albumin in plasma Cleavage of membranous components of cells and intracellular release of macromolecular substances can be involved in brain edema formation.
(2) Vasoactive substances in the hematoma: Vasoactive substances in the hematoma can diffuse into the brain tissue causing vasospasm, vasodilation or changes in vascular permeability.
(3) Some vasoactive substances outside the hematoma: such as histamine, 5-hydroxytryptamine, kinin, bradykinin, arachidonic acid and its metabolites can increase the damage to brain tissue.
④Free radicals: extravasation of erythrocytes destroys hemoglobin and releases iron ions and heme, which can induce the production of large amounts of free radicals and aggravate brain damage.
⑤Release of active enzymes: Nerve cells contain a large number of lysosomes, and various hydrolytic enzymes are released into the cytoplasm, causing further damage or necrosis of nerve cells.
(6) Endothelin release: endothelin produced by vascular endothelial cell injury can lead to intracellular calcium ion overload, resulting in vasoconstriction and increased cerebral ischemia.
(7) Excitatory neurotoxic amino acids: increased excitatory amino acids in the injury area can contribute to neuronal cell necrosis.
(8) Involvement of various immune reactions: various chemokines promote the transfer of neutrophils to the lesion and produce active substances, enzymes and free radicals, which cause direct and severe damage to local brain tissue.
(2) Brain edema formation: edema is most severe around the hemorrhagic foci ipsilateral cerebral cortex, contralateral cortical and basal nucleus areas also have edema. Brain edema distant from the lesion is the result of diffusion of cerebral edema of vascular origin. Experimentally, autologous blood injection into the caudate nucleus of mice showed that the edema in the ipsilateral basal nucleus peaked within 24 h and remained constant until it started to subside on day 5.
(3) The effect of cerebral hemorrhage on coagulation, anticoagulation, and fibrinolytic status: It is generally believed that the release of tissue thrombin after acute brain tissue injury increases coagulation activity in the blood, decreases antithrombin depletion, and increases fibrinolytic activity compensatively. Studies of the coagulation process have found that the release of thrombin during clot formation in the first 24 h after hemorrhage causes adjacent cerebral edema, blood-cerebrospinal fluid barrier disruption, and cytotoxic effects.
In addition, erythrocyte lysis, which peaks about 3 days after the initial bleeding, is another mechanism of brain edema formation, which may be related to the release of free hemoglobin and its degradation products. Recent studies have shown that free radical excitatory amino acids and membrane permeability to calcium are important factors in ischemic brain injury. The release of trivalent iron contributes to the conversion of peroxides and hydrogen peroxide to the more toxic hydroxyl radicals, a more important transmitter of ischemic cerebral edema. The ability of blood and brain parenchyma to produce superoxide negative ions is probably related to the fact that blood breakdown products include trivalent iron.
In conclusion, although the pathophysiological mechanism of cerebral hemorrhage is very complex, understanding and mastering the pathological process of brain damage during cerebral hemorrhage will help in drug treatment and promote the absorption of hematoma and recovery of neurological function. At the same time, the understanding of the pathophysiological mechanism of cerebral hemorrhage needs to be further developed.
3.The main pathological changes of cerebral hemorrhage
(1) Hemorrhage site: about 70% of hypertensive cerebral hemorrhage occurs in the basal nucleus region; the brain lobes, brain stem and cerebellar dentate nucleus each account for about 10% of the deep penetrating arteries of the brain are often seen as small cornual aneurysms. Supratentorial branch (12%) Parietal-occipital and temporal lobe white matter branches (10%), etc. Shell nucleus hemorrhage often invades the internal capsule and breaks into the lateral ventricles Blood fills the ventricular system and subarachnoid space; thalamic hemorrhage often breaks into the third ventricle or lateral ventricles Outward injury to the internal capsule; pontine or cerebellar hemorrhage directly breaks into the subarachnoid space or the fourth ventricle Non-hypertensive cerebral hemorrhage is mostly located in the subcortex Commonly caused by cerebral amyloid angiopathy Arteriovenous malformation Moyamoya disease and other causes.
(2) Pathological examination: swelling and congestion of the hemisphere on the side of the hemorrhage, blood flowing into the subarachnoid space or breaking into the ventricle; irregular cavity in the center of the hemorrhage foci filled with blood or purple grape pulp-like clots surrounded by necrotic brain tissue bruised with hemorrhagic softening and obvious inflammatory cell infiltration pressure on the brain tissue around the hematoma, marked edema, large hematoma can cause displacement of brain tissue and ventricles deformation and brain herniation formation hemorrhage in the supratentorial hemisphere hematoma downward The hematoma may cause displacement of the inferior thalamus and brainstem. Deformation and secondary hemorrhage often result in herniation of the cerebellar ventricles; central herniation may occur when the midline structures such as the inferior thalamus and supratentorial brainstem are displaced; occipital foramen herniation may occur if the intracranial pressure is extremely high or if there is massive bleeding in the inferior brainstem and cerebellum; cerebral herniation is the most common direct cause of death from cerebral hemorrhage.
After the acute phase, clots dissolve and phagocytes remove iron-containing heme and necrotic brain tissue Gliosis Small hemorrhagic foci form glial scars Large hemorrhagic foci form stroke sacs.