Cerebral thrombosis

Introduction to cerebral thrombosis Cerebral thrombosis (CT) is the most common type of cerebral infarction. It is the cerebral artery or cortical atherosclerosis leading to vascular thickening, stenosis and thrombosis, causing local blood flow reduction or blood supply interruption, brain tissue ischemia and hypoxia leading to softening and necrosis, focal neurological system Symptoms and signs, and therefore clinically known as "atherosclerotic cerebral thrombosis", or "thrombotic cerebral infarction." basic knowledge The proportion of illness: 5% (the incidence of cerebral thrombosis can account for 50% of systemic arterial embolism, the elderly are higher.) Susceptible people: middle-aged and elderly. Mode of infection: non-infectious Complications: Acne Depression

Causes of cerebral thrombosis

Atherosclerosis (45%)

Lead to atherosclerotic cerebral infarction, often accompanied by hypertension, and atherosclerosis are causal, diabetes and hyperlipidemia can also accelerate the progression of atherosclerosis, cerebral atherosclerosis mainly occurs in the diameter of the tube Aorta above 500 m. Atherosclerotic plaque leads to stenosis and thrombosis, which can be seen in any part of the internal carotid artery and vertebrobasilar system. It is more common in the bifurcation of the arteries, such as the common carotid artery and the neck, the bifurcation of the external artery, and the front of the brain. At the beginning of the middle artery, the vertebral artery is at the beginning of the subclavian artery, the vertebral artery enters the intracranial segment, the initial segment of the basilar artery and the bifurcation.

Other factors (35%)

Although some cases of cerebral infarction have been confirmed by imaging examination, it is difficult to find the exact cause. Possible causes include cerebral vasospasm, microembolics of unknown origin, antiphospholipid antibody syndrome, abnormal protein C and protein S, anticoagulation Enzyme III deficiency, incomplete release of plasminogen activator accompanied by hypercoagulable state.

Pathogenesis

A variety of causes of cerebral artery trunk or cortical atherosclerosis, which leads to thickening of the intima, stenosis of the lumen and thrombosis, and sudden decrease or stop of blood supply to the local blood supply artery of the brain tissue, resulting in the blood supply area of the blood vessel. Brain tissue ischemia, hypoxia, the result is brain tissue necrosis, softening, accompanied by clinical symptoms and signs of the corresponding parts, such as hemiplegia, aphasia and so on.

The incidence of cerebral infarction accounts for about 4/5 of the internal carotid artery system and about 1/5 of the vertebral-basal artery system. The occluded blood vessels are the internal carotid artery, the middle cerebral artery, the posterior cerebral artery, the anterior cerebral artery and the vertebrobasilar artery. Wait.

Occlusion of atherosclerosis or vasculitis, thrombosis or embolus, cerebral ischemia generally forms white infarction, brain tissue softening and necrosis in infarct area, with cerebral edema and punctiform hemorrhage around the bulb, large area cerebral infarction Hemorrhagic infarction can occur, ischemia, hypoxia damage can occur in two ways of neuronal necrosis and apoptosis.

1. Pathological staging of cerebral ischemic lesions

(1) Ultra-early (1~6h): The changes of brain tissue were not obvious. Some vascular endothelial cells, nerve cells and astrocytes were swollen, and mitochondria were swollen and cavitation.

(2) Acute phase (6-24h): The brain tissue in the ischemic area was pale and mildly swollen, and the nerve cells, glial cells and endothelial cells showed obvious ischemic changes.

(3) Necrotic phase (24-48h): a large number of nerve cells disappeared, glial cells deteriorated, neutrophils, lymphocytes and macrophages infiltrated, and brain tissue was obviously edematous.

(4) Softening period (3 days to 3 weeks): The liquefaction of the lesion area becomes soft.

(5) Recovery period (after 3 to 4 weeks): The liquefied necrotic brain tissue is cleared by the lattice cells, the brain tissue is atrophied, the small lesions form glial scars, and the large lesions form a stroke capsule, which lasts for several months to 2 years.

2. Pathophysiology

Brain tissue is very sensitive to ischemia and hypoxia damage. Cerebral artery occlusion leads to cerebral infarction after ischemia for more than 5 minutes. Neuronal injury is selective after ischemia. Only some neurons are lost during mild ischemia. Various neurons, glial cells and endothelial cells were necrotic in the ischemic region during ischemia.

(1) The central necrotic area and the surrounding ischemic penumbra consist of: the necrotic area causes brain cell death due to complete ischemia, but there is still a collateral circulation in the ischemic penumbra, and part of the blood supply is available. There are still a large number of viable neurons. If the blood flow is rapidly restored, the brain metabolism is improved, the damage is still reversible, and the nerve cells can still survive and restore function. Therefore, protecting these reversible injured neurons is the key to the treatment of acute cerebral infarction.

(2) Reperfusion damage: The study confirmed that the time window for early treatment of cerebral ischemia is within 6 hours. If the cerebral blood flow recanal exceeds the time window, brain damage can continue to increase and reperfusion injury occurs.

At present, the mechanism of reperfusion injury mainly includes: excessive formation of free radicals and free radical "fall" chain reaction, calcium overload in nerve cells, cytotoxicity of excitatory amino acids and acidosis, leading to nerves. Cell damage.

The concept of ischemic penumbra and reperfusion injury has updated the clinical concept of acute cerebral infarction. The key to rescue the ischemic penumbra is super-early thrombolytic therapy. The core of reperfusion injury is actively taken to protect the brain.

Cerebral thrombosis prevention

Preventive treatment

Prophylactic treatment for risk factors such as hypertension, diabetes, atrial fibrillation and carotid stenosis with clear ischemic stroke, antiplatelet drug aspirin 50 ~ 100mg / d, ticlopidine 250mg / d, It has a positive effect on secondary prevention of stroke, and is recommended for application; there should be a discontinuous period in long-term medication, and those with bleeding tendency should be used with caution.

2. Active prevention against possible causes

(1) For patients with hypertension, the blood pressure should be controlled at a reasonable level, because the blood pressure is too high, it is easy to cause microvascular hemangioma and atherosclerotic small artery rupture and hemorrhage; and low blood pressure, cerebral blood supply insufficiency, microcirculation stasis When it is easy to form cerebral infarction, it should prevent various factors such as sudden decrease in blood pressure, slow blood flow to the brain, increased blood viscosity, and increased blood coagulation.

(2) Active treatment of transient ischemic attacks.

(3) pay attention to mental health, many episodes of cerebral infarction, are related to emotional excitement.

(4) Pay attention to changing bad habits, moderate physical activity is good for health, avoid bad habits such as smoking, alcoholism, overeating, overeating, mainly low-fat, low-calorie, low-salt diet, and have enough high-quality protein, Vitamins, cellulose and trace elements, foods that are not conducive to health, mildew, salted fish, cold foods, do not meet the requirements of food hygiene, fasting.

(5) When the temperature changes suddenly, the air pressure, and the temperature change significantly, most of the elderly, especially the frail and sick, are sick and sick, especially in the cold and summer, the elderly have poor adaptability, reduced immunity, and the incidence rate and The mortality rate is higher than usual, so be careful.

(6) Pay attention to the signs of cerebrovascular disease in time, such as a sudden side of the face or upper and lower limbs suddenly feel numb, weak and weak, mouth sputum, drooling; suddenly feel dizzy, shaking; short-term confusion or lethargy, etc. .

Cerebral thrombosis complications Complications, acne depression

Pulmonary infection

Pulmonary infection is one of the major complications, and patients with severe bedridden often have pulmonary infections.

2. Upper gastrointestinal bleeding

It is one of the serious complications of cerebrovascular disease, namely stress ulcer, which is caused by the inferior colliculus and brain stem lesions. It is now considered to be associated with the anterior and posterior part of the hypothalamus, the gray nodules and the vagus nerve in the medulla oblongata. Related to the autonomic nerve center in the lower part of the hypothalamus, but its high-level center in the frontal lobe, hippocampus and limbic system, the mechanism of gastrointestinal bleeding is related to the primary or secondary lesions of the above-mentioned sites.

Hemorrhoids

Mainly because the body does not change body position for a long time, and the local skin and tissues are subjected to excessive compression for a long period of time, and a series of manifestations of ischemia and necrosis occur. Patients with cerebrovascular disease have more limbs, limb paralysis, prolonged bed rest, and inconvenient activities. It is easy to compress the bone bulge and other parts, causing local tissue ischemia and hypoxia.

4. Post-cerebral vascular disease depression and anxiety response

Post-cerebral vascular disease depression is a common emotional disorder of cerebrovascular disease, which should be highly valued in clinical practice.

(1) Characteristic symptoms of depression response:

1 The mood is bad, the mood is pessimistic, and the self feels bad.

2 sleep disorders, insomnia, dreams or wake up early.

3 loss of appetite, do not think about diet.

4 Loss of interest and pleasure, lack of motivation for anything, lack of vitality.

5 life can not take care of themselves, self-blame and sin, and passively want to die.

6 weight dropped rapidly.

7 low sexual desire, not even sexual desire.

(2) Characteristic symptoms of anxiety response:

1 Sustained tension and anxiety.

2 There are also psychological symptoms, such as inattention, memory loss, sensitivity to the sound and easy irritability.

3 At the same time there are physical symptoms, including sympathetic excitability symptoms, such as elevated blood pressure, rapid heartbeat, chest tightness, rapid breathing, irritability, restlessness, and symptoms of parasympathetic excitation, such as polyuria, increased gastrointestinal activity and diarrhea .

Symptoms of cerebral thrombosis Common symptoms Inability to swallow dysphagia Hypersensitivity Sensory disturbance Slow response Blood viscosity increased high fever

Examination of cerebral thrombosis

Laboratory inspection

1. Cerebrospinal fluid examination: lumbar puncture can only be performed without CT examination, clinically difficult to distinguish between cerebral infarction and cerebral hemorrhage, usually brain pressure and CSF routinely normal.

2. routine and biochemical examination of hematuria: mainly related to risk factors of cerebrovascular disease such as hypertension, diabetes, hyperlipidemia, heart disease, atherosclerosis.

Film degree exam

1. Neuroimaging

(1) CT examination should be performed routinely: in most cases, low-density infarcts are gradually displayed after 24 hours of onset, and uniform lamella or wedge-shaped low-density lesions can be seen 2 to 15 days after onset, large-area cerebral infarction with brain edema and mass effect. Hemorrhagic infarction is mixed density. It should be noted that the infarction absorption period is 2 to 3 weeks after the disease, the edema disappears and the phagocytic infiltration can be equal to the density of brain tissue. It is difficult to distinguish on CT, which is called fuzzy effect. Significance, 5 to 6 days after infarction, enhanced phenomenon, the most obvious 1 to 2 weeks, about 90% of infarcts showed uneven lesions, but sometimes CT can not show brain stem, cerebellum smaller infarct.

(2) MRI: can clearly show early ischemic infarction, brain stem and cerebellar infarction, venous sinus thrombosis, etc., T1 low signal, T2 high signal lesions appear within hours after infarction, hemorrhagic infarction shows mixed T1 high signal , enhanced MRI is more sensitive than plain scan, functional MRI diffusion-weighted imaging (DWI) can early diagnosis of ischemic stroke, ischemic lesions within 2 hours of onset, providing important information for early treatment, DSA can find vascular stenosis and occlusion , showing arteritis, Moyamoya disease, aneurysm and arteriovenous malformations.

2. Transcranial Doppler (TCD): carotid and internal carotid artery stenosis, atherosclerotic plaque or thrombosis, echocardiography can be found in the wall of the wall thrombus, atrial myxoma and mitral valve prolapse .

Diagnosis and diagnosis of cerebral thrombosis

diagnosis

1. Diagnostic basis: middle-aged and above, history of hypertension and arteriosclerosis, sudden onset, symptoms and signs of focal cerebral damage within one to several days, and can be attributed to an intracranial artery occlusion syndrome, clinical considerations Acute thrombotic cerebral infarction may be.

2. CT or MRI examination found that infarct can be diagnosed, young patients with a history of obvious infection or inflammatory disease need to consider the possibility of arteritis.

Differential diagnosis

1. Cerebral hemorrhage: Cerebral infarction is sometimes similar to the clinical manifestations of small amount of cerebral hemorrhage, but the onset of activity, the disease progresses rapidly, the history of hypertension often indicates cerebral hemorrhage, CT examination can confirm the diagnosis.

2. Cerebral embolism: rapid onset, focal signs reach a peak in seconds to minutes; often have cardiac emboli sources, such as rheumatic heart disease, coronary heart disease, myocardial infarction, subacute bacterial endocarditis, and merger Atrial fibrillation, etc., common middle cerebral artery embolism caused a large area of cerebral infarction, leading to cerebral edema and increased intracranial pressure, often accompanied by seizures.

3. Intracranial lesions: intracranial tumors, subdural hematoma and brain abscess may be stroke-like episodes, and there are focal signs such as hemiplegia. When the signs of increased intracranial pressure are not obvious, they are easily confused with cerebral infarction. , CT or MRI examination can confirm the diagnosis.

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