What Is Cerebral Thrombosis?

Cerebral thrombosis is the most common type of cerebral infarction. It is caused by atherosclerosis of the cerebral arterial trunk or cortical branch leading to thickening of blood vessels, stenosis and occlusion of the lumen, and thrombosis, resulting in reduced cerebral blood flow or interruption of blood supply, cerebral ischemia and hypoxia leading to softening and necrosis and focal neurological symptoms .

Basic Information

nickname
Cerebral thrombosis
English name
cerebralthrombosis
Visiting department
Neurology
Multiple groups
Middle-aged and older people over 50 years old, rheumatic heart disease patients, hypertension patients, etc.
Common causes
Atherosclerosis, endovascular emboli shedding, etc. are the basic causes of this disease
Common symptoms
Sudden symptoms of numbness in the upper and lower limbs, skewed eyes and eyes

Cerebral thrombosis epidemiology

A large-scale population survey from 1986 to 1990 in China showed that the incidence of stroke was 109.7 / 100,000 to 217 / 100,000, the prevalence was 719 / 100,000 to 745.6 / 100,000, and the mortality rate was 116 / 100,000 to 141.8 / 100,000. The incidence rate is higher in males than in females: 1.3: 1 to 1.7: 1 for males and females.

Causes of cerebral thrombosis

1. Atherosclerosis is the basic cause of this disease, leading to atherosclerotic cerebral infarction, often accompanied by hypertension, and cause and effect of atherosclerosis. Diabetes and hyperlipidemia can also accelerate atherosclerosis process.
2. Rare blood cells such as erythrocytosis, thrombocytosis, thromboembolic thrombocytopenic purpura, diffuse intravascular coagulation, sickle cell anemia, etc .; cerebral amyloid angiopathy, Moyamoya disease, muscular fiber dysplasia and skull Internal and external (carotid, intracranial, and vertebral) dissection aneurysms are rare.
3. Although some cases of cerebral infarction are confirmed by imaging examination, it is difficult to find the exact cause. Possible causes include cerebral vasospasm, microemboli of unknown origin, abnormalities of antiphospholipid antibody syndrome protein C and protein S, and anticoagulation. Deficiency of serum enzyme III, incomplete release of plasminogen activator accompanied by hypercoagulable state, etc.

Clinical types of cerebral thrombosis

1. According to the evolution of symptoms and signs
(1) The symptoms and signs of neurological deficits after ischemic stroke are more serious and progress rapidly after complete stroke , often reaching a peak within a few hours (<6h).
(2) After the onset of ischemic stroke, the symptoms of neurological deficits are mild, but they gradually increase until severe neurological deficits appear. The literature reports that the incidence is 16% to 43%. Family members of some patients do not understand this feature of cerebral infarction, and mistakenly believe that the disease is aggravated by the drug.
2. Based on clinical manifestations, especially neuroimaging evidence
(1) Large-scale cerebral infarction is usually a complete stroke of the internal carotid artery trunk, middle cerebral artery trunk, or cortical branch, showing complete hemiplegia on the opposite side of the lesion, hemiplegia and paralysis on the opposite side of the lesion. Vertebro-basal artery infarction shows progressive increase in consciousness disturbance, quadriplegia, and most cerebral nerve palsy, with obvious signs of cerebral edema and increased intracranial pressure, and even cerebral hernia, a critical condition, may be life-threatening.
(2) Watershed Cerebral Infarction (CWSI) is ischemia at the border or watershed of the adjacent blood supply division, also known as peripheral cerebral infarction. Mostly due to hemodynamic disorders, which typically occur when the internal carotid artery is severely narrowed or occluded with a decrease in systemic blood pressure, and can also originate from cardiogenic or arterial embolism.
(3) Hemorrhagic cerebral infarction is arterial necrosis of the cerebral infarction area causing blood to leak out or secondary blood, which is common after large-scale cerebral infarction.
(4) Multiple cerebral infarction is a cerebral infarction caused by the simultaneous occlusion of two or more cerebral blood vessels of different blood supply systems.

Clinical manifestations of cerebral thrombosis

Cerebral thrombosis often develops during quietness or sleep. In some cases, there are precursor symptoms of transient ischemic attack (TIA), such as limb numbness, and sudden symptoms of numbness in the upper and lower limbs, skewed mouth and eyes, and slurred speech.

Cerebral thrombosis test

Laboratory inspection
(1) Cerebrospinal fluid examination of lumbar puncture : Cerebrospinal fluid is a clear liquid circulating on the surface of the brain and spinal cord. It is only performed when CT cannot be performed clinically and it is difficult to distinguish between cerebral infarction and cerebral hemorrhage, and cerebral pressure and cerebrospinal fluid are usually normal.
(2) Biochemical examination is mainly to find the risk factors of cerebrovascular disease, such as lipid metabolism disorders, hyperglycemia, hyperhomocysteinemia, and so on.
2. Auxiliary inspection
(1) Neuroimaging examination CT scans of heads in most cases show low-density infarcts 24 hours later. 2 to 15 days after the onset, obvious low-density lesions with uniform flaky or wedge shape can be seen. Large-scale cerebral infarction with cerebral edema and mass effect hemorrhagic infarction are mixed density. However, sometimes CT does not show smaller infarcts of the brainstem and cerebellum. Head MRI MRI can clearly show venous sinus thrombosis of the brain stem and cerebellar infarction in early ischemic infarction. T1 low-signal and T2-high-signal lesions appeared several hours after the infarction, and hemorrhagic infarction showed mixed T1 high-signal. Functional MRI diffusion-weighted imaging (DWI) can diagnose ischemic stroke early, showing ischemic lesions within 2 hours of onset provides important information for early treatment. Cerebral angiography (DSA) can find vascular stenosis and occlusion sites, showing arteritis, moyamoya disease (also known as Moyamoya disease), aneurysms and arteriovenous malformations.
(2) Transcranial Doppler (TCD) can detect carotid and internal carotid artery stenosis, atherosclerotic plaque or thrombosis. Echocardiography revealed mural thrombus, atrial myxoma, and mitral valve prolapse.
(3) Local plaques and stenosis can be found in color Doppler ultrasound of the carotid and subclavian arteries . Strong echoes and isoechoic plaques are unstable plaques, and low echoes and mixed echo plaques are unstable plaques. Unstable plaques can easily lead to cerebral infarction. The nature of the plaque is more important than the size of the plaque and the degree of stenosis of the lumen. The thickness of the plaque is more important than the length of the plaque. Thicker plaques have a greater effect on blood flow.

Cerebral thrombosis diagnosis

Diagnosis basis
Middle-aged or older with history of hypertension or arteriosclerosis or family history, sudden onset, symptoms and signs of focal brain damage within one to several days, and can be attributed to an intracranial artery occlusion syndrome Infarction is possible.
2.CT or MRI examination
Finding an infarct can confirm the diagnosis. Young patients with a significant history of infection or inflammatory disease need to consider the possibility of arteritis.

Differential diagnosis of cerebral thrombosis

Cerebral hemorrhage or subarachnoid hemorrhage: Cerebral infarction sometimes resembles the clinical manifestations of a small amount of cerebral hemorrhage, but onset of activity, rapid disease progression, history of hypertension, and headache often suggest cerebral hemorrhage or subarachnoid hemorrhage, CT Inspections are generally distinguishable. When sometimes a small amount of subarachnoid hemorrhage has no obvious abnormalities in CT, a lumbar puncture examination is needed to identify it.

Cerebral thrombosis complications

Lung infection
It is one of the main complications. Severe bedridden patients often have pulmonary infections.
2. Upper gastrointestinal bleeding
It is one of the serious complications of cerebrovascular disease, that is, stress ulcer. The pathogenesis of the hypothalamus and brainstem is now thought to be related to the gray and white nodules in the anterior and posterior part of the hypothalamus and the medulla vagal nucleus. The autonomic nerve center is in the lower part of the optic mast, but its high-level center is in the hippocampal gyrus and limbic system of the frontal orbital surface. The mechanism of gastrointestinal bleeding is related to the involvement of cerebral infarction.
3. Pressure ulcer
That is, skin pressure ulcers, which are mainly a series of manifestations of local body and tissues that have been compressed for a long time and have suffered ischemia and necrosis, are mainly caused by the body's body not changing for a long time. Cerebrovascular disease patients, because there are many elderly patients, limb paralysis is bedridden for a long time, inconvenience, easy to pressure on the bone and other parts of the pressure to force local tissue ischemic necrosis ulceration and form pressure ulcers.
4. Emotional abnormalities
Includes depression and anxiety.

Cerebral thrombosis treatment

Drug treatment
Principles of Acute Drug Therapy.
(1) Ultra-early treatment firstly enables the public to increase the awareness of emergency and emergency treatment of stroke to understand the importance and necessity of ultra-early treatment. Seek medical treatment immediately after the onset, if there is no contraindication, strive to thrombolytic therapy within 3 to 6 hours of treatment time window, and reduce cerebral metabolism to control cerebral edema and protect brain cells, and save the ischemic penumbra;
(2) Individualized treatment takes the most appropriate treatment according to the age of the patient, the type of ischemic stroke, the degree of illness, and the underlying disease;
(3) Prevention and treatment of complications such as infection, cerebral heart syndrome, hypothalamic injury, post-stroke anxiety or depression, abnormal antidiuretic hormone secretion syndrome, and multiple organ failure;
(4) Holistic treatment adopts supportive symptomatic treatment and early rehabilitation treatment; timely preventive intervention for stroke risk factors such as hypertension, diabetes, and heart disease is used to reduce the recurrence rate and reduce the disability rate.
2. Surgical treatment
For patients with large-scale cerebral infarction with severe cerebral edema occupying effect and signs of cerebral hernia, craniotomy can be performed; patients with cerebellar infarction causing brain stem compression to worsen the condition, inhale cerebellar tissue and posterior cranial fossa by aspiration Decompression can save lives.
3. Rehabilitation
It should be carried out early, and short-term and long-term treatment plans should be formulated in accordance with the principle of individualization, and treatment methods should be selected in stages and according to local conditions. Target patients with physical fitness and skills training to reduce the disability rate, improve the recovery of neural function, improve the quality of life, and return to society.

Prognosis of cerebral thrombosis

Cerebral thrombosis has a lower mortality rate and a higher disability rate than cerebral hemorrhage. The mortality rate has increased significantly with age, with an average mortality rate of about 25%. Common causes of death are cerebral hernia, multiple organ failure, secondary infections, and heart and lung insufficiency. Survival rates are also higher among survivors, about 20% of survivors. Recurrence within 1 to 2 years. So once you get cerebral thrombosis, you must take medicine for life to prevent recurrence, and you must take the medicine under the guidance of a professional doctor.

Cerebral thrombosis prevention

Cerebral thrombosis mostly occurs in middle-aged and older people over 50 years old, and is often accompanied by diseases such as hypertension, hyperlipidemia, hyperglycemia, and obesity.
1. Pay attention to controlling blood pressure
Keep your blood pressure at a certain level, but be careful not to lower your blood pressure too low. Because hypotension can cause insufficient blood supply to the brain, it can easily lead to cerebrovascular embolism.
2. Actively treat basic diseases
For those who have hyperlipidemia, diabetes, transient ischemic attack and history of coronary heart disease, long-term preventive treatment should be performed.
3. Do not smoke or drink as much as possible.
4. Periodic inspection
It is best to check cholesterol and blood lipids and carotid ultrasound every six months.
5. Healthy eating
Such as obese people should limit the intake of staple foods, control weight; eat or not eat animal fats and internal organs, such as fatty meat, fat intestines, belly, because these foods contain high cholesterol and saturated fatty acids, it is easy to increase arteriosclerosis ; Eat high-quality protein appropriately, such as milk, duck, fish, eggs (eat less yolk), soy products, eat less pork, beef, lamb, and lean meat is better; eat more foods rich in vitamins, such as rich Fresh fruits, tomatoes, hawthorn, etc. containing vitamin C; soy products, milk, and eggs rich in vitamin B 6 ; green leafy vegetables, beans, etc. rich in vitamin E; diet should be mainly light and avoid too salty, It's better not to eat pickles. Because eating too salty can easily cause high blood pressure.
6. Others < br Avoid tiring and staying upset and keep your stools open. Exhausting and getting angry easily lead to constipation. You can eat bitter gourd and other foods, and you can also take Chinese medicine intermittently.

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