With the rapid socio-economic development and the improvement of national living standards, the society and families have a strong desire to know more about their health and show unprecedented concern and demand for health protection. One of the most important causes of sudden death diseases that threaten human health is the acute onset of cerebrovascular disease, including cerebral aneurysms, cerebral arteriovenous malformations, cerebral infarction caused by carotid and intracranial artery stenosis, and cerebral venous thrombosis complicated by hemorrhage. The application of high field strength MR and high speed spiral CT can provide a more accurate basis for the diagnosis and treatment of stroke cerebrovascular diseases other than hypertensive cerebral hemorrhage, making it possible for modern medicine to effectively intervene in different stroke pathologies.
Cerebral aneurysm
Cerebral aneurysm is the main lesion of hemorrhagic cerebrovascular disease, and its risk of causing more than 30% mortality after hemorrhage is also a factor that attracts high clinical attention in neurology. As the public gradually pays attention to their health, the number of cases of intracranial aneurysms found during general checkups is gradually increasing; the annual bleeding rate seen in aneurysms that have ever bled is generally considered to be 23-25%, while the annual bleeding incidence rate of these unbleeding aneurysms is generally considered to be around 5-10% per 100,000. Although patients may benefit from the elimination of the potential risk of bleeding if more aggressive treatments such as surgery or embolization are used for these unbleeding aneurysms, the 1-5% risk of complications such as intraoperative bleeding or infarction that accompanies the treatment makes careful clinical consideration impossible. A study in Europe and the United States showed that because of the significantly increased probability of bleeding in cerebral aneurysms larger than 6 mm in diameter, surgical intervention or endovascular embolization should be given even if no bleeding has occurred. From domestic clinical observation, cerebral aneurysms do not bleed after they are larger than 6 mm, and more and more cases confirm that the bleeding detection rate of aneurysms smaller than 5 mm and even tiny aneurysms less than 2.5 mm in diameter is increasing year by year.
Since most aneurysms accompany the human body for life without dangerous conditions, it is not possible to determine when a single individual with an aneurysm may bleed; therefore, the authors suggest two options for the management of asymptomatic cerebral aneurysms that are found incidentally: 1) to treat asymptomatic cerebral aneurysms that have not experienced intracranial hemorrhage, but have irregular aneurysm growth or even daughter aneurysm formation, or are associated with heart valve disease, coronary artery disease, and cerebral blood supply deficiency that require For cases that require anticoagulation and antiplatelet aggregation, if the receiving physician can master more proficient embolization techniques and the medical unit has the corresponding medical equipment and conditions, it is basically guaranteed that no intraoperative complications will occur, the less invasive intravascular embolization treatment or even craniotomy clamping should be selected as early as possible, with the aim of eliminating the risk of cerebral hemorrhage and contributing to The aim is to eliminate the risk of cerebral hemorrhage and improve the quality of life of patients and the safety of treating coexisting ischemic cardiac and cerebral lesions.
For individuals with small aneurysms and regular growth patterns and patients who have difficulty with any prophylactic treatment, conservative treatment with symptomatic management and stricter restrictions on lifestyle habits is a conditional option. According to the basic condition of aneurysm rupture and bleeding which is characterized by abnormal hemodynamic changes, good control of blood pressure in body circulation, adjustment of nervous stress, taking suitable blood pressure lowering drugs, etc. are required; avoiding heavy physical strength or excessive exercise as much as possible in daily life, ensuring 6-8 hours of sleep daily, maintaining a tolerant and generous mind and preventing constipation, etc.; medical observation It is confirmed that these basic requirements are effective measures to prevent aneurysm rupture and bleeding. It is also important to ensure annual checkups to understand the trend of aneurysm and general health condition, so that proper intervention can be made in time if necessary.
Cerebral arteriovenous malformation
The majority of asymptomatic AVMs can often live with the patient for the rest of his or her life without threatening, and some AVMs are not seen until hemorrhage and seizure induction occurs in the malformed brain lesion. This is why we call AVMs at risk for hemorrhage or seizures high-risk arteriovenous malformations. The risk of high-risk AVMs usually consists of the following high-risk factors: the presence or absence of intra-, pre-focal, or parafocal AVM aneurysms, the presence of narrow deep venous drainage or intracerebroventricular growth in the AVM, and the high-flow, high-obstructive characteristics of the AVM. Since high-risk AVMs are life-threatening to patients, when incidental or hemorrhagic findings with cerebral AVMs are made, they should be advised to undergo whole brain angiography as soon as possible for meticulous imaging analysis and judgment.
For small AVMs, the lesion should be eliminated as completely as possible while embolization; for Avm with deep penetrating artery supply or difficult to be completely embolized, the aneurysm can be treated first and the blood flow in the main blood supply area of the malformation should be slowed down as much as possible, one is to reduce the flow and pressure in the AVM, but to create better healing conditions for gamma knife treatment. In large AVMs, after eliminating high-risk factors, overemphasis on reducing or eliminating the size of the malformation often requires greater risk to the patient; because an overly large malformation lesion can involve many functional brain areas while creating an abnormal distribution of localized cerebral perfusion blood flow; when overemphasis is placed on embolization or surgical removal of a larger AVM lesion, it can cause damage to functional brain tissue and create abnormal cerebral overperfusion The chances of damage to brain tissue in functional areas and production of abnormal cerebral overperfusion are significantly increased, which in turn reduces the quality of survival of patients. For AVMs without high-risk factors, especially giant cerebral AVMs, if there are no obvious symptoms, they can be advised to avoid overexertion and be reviewed regularly; possibly and the lesion will accompany the patient through a relatively peaceful life. ,.
Since the nervous system has complex functions not possessed by any other organ, inappropriate management may bring temporary or lifelong disability or even end of life to the patient. Many scholars have argued that more attention should be paid to the quality of survival after treatment for AVM; if there is no absolute safety certainty for embolization of malformed lesions in functional brain areas, it should be stopped when appropriate, and after eliminating the most important aneurysms and other high-risk factors, the residual lesions should be transferred to gamma knife treatment with longer healing time but less relative ischemic damage to finally complete the treatment in line with individualized comprehensive treatment of cerebral AVM.
Carotid artery stenosis
Cerebral infarction caused by carotid stenosis accounts for approximately 60% of the incidence of acute cerebral infarction. The risk level is easily detected and evaluated during routine ultrasound and CTA/MRA examinations of the carotid arteries. Timely detection and proper management of stenoses greater than 80% or with unstable plaques will undoubtedly reduce the chance of cerebral infarction to a great extent.
Carotid atherosclerosis with luminal narrowing of the arteries is part of systemic atherosclerosis, and some authors believe that there is a 60-70% correlation between its severity and coronary stenosis in the heart; carotid stenosis can cause cerebral infarction because of embolism caused by wall clots on the surface of the sclerotic plaque or debris dislodged from the surface of the unstable plaque entering the brain with blood flow; sclerotic plaque The separation of the sclerotic plaque from the vessel wall to form an interlayer or very severe stenosis causes complete blockage of the carotid artery lumen, resulting in massive cerebral infarction; or severe stenosis forms a persistent low blood flow state resulting in cerebral ischemia characterized by watershed infarction.
In such cases, it is recommended to apply lipid-lowering and antiplatelet drugs for long-term conservative treatment under the guidance of a doctor; if the stenosis has obviously caused cerebral ischemic symptoms, or if the stenotic plaque breaks down and becomes unstable, timely medical intervention is a wise choice. If the stenosis has already caused cerebral ischemic symptoms or if the stenotic plaque has broken down and become stable, timely medical intervention is a wise choice.
The treatment of carotid artery stenosis is currently available in the form of intra-arterial stenting and endarterectomy, both of which have achieved positive safety and efficacy in clinical applications. The advantages of stenting are that it is less painful for the patient and relatively easy to perform; it can be performed on severe stenosis of the entire carotid system; therefore, it has a wide range of indications, especially for elderly patients with uncontrollable hypertension, diabetes mellitus, cardiac or renal insufficiency, or for various reasons who cannot tolerate surgical procedures. The carotid endarterectomy can completely remove the atherosclerotic plaque in the stenosis and completely unblock the carotid artery; this procedure has been honed for decades and the effect is certain. The advantages of both procedures complement each other and have developed into a routine treatment for cerebral power insufficiency caused by carotid artery stenosis.
Intracranial artery stenting
Intracranial artery stenosis occurs mostly in the basilar artery and middle cerebral artery, which tend to have more deep penetrating branches. When atherosclerosis is formed, the diameter of the penetrating artery will also be reduced; when foreign emboli and local thrombi are formed, blockage of the stenosis is very likely to occur, accounting for about 20-30% of the cerebral infarction incidence. Anatomically, small cortical arteries often gradually form collateral compensations due to chronic stenosis of the proximal artery, thus relieving the inadequate blood supply to the distal part of the diseased artery; therefore, the indications for treatment of intracranial arterial stenosis should be, on the basis of the diagnosis of symptomatic intracranial arterial stenosis, the need for formal anti-poly, lipid-lowering and symptomatic treatment with poor results, stenosis exceeding 70%, and the absence of uncontrollable hypertension, diabetes mellitus, cardiopulmonary insufficiency, active autoimmune disease, and advanced malignancy.
The usual treatment for symptomatic intracranial artery stenosis is in the form of high-flow bypass grafting of the extracranial and intracranial arteries and transvascular stenting. Seeing that the stentoplasty technique is easy to perform, it is now becoming the method of choice when most cases must undergo intervention. Among the requirements of the operation technique, it should be determined that the stenosis is not significantly angular and that there are no new cerebral infarct lesions within 4 weeks; the dilating balloon used should not exceed the diameter of the vessel distal to the stenosis; the stent needs to cover more than 3 mm of the plaque edge; intraoperative care should be taken to avoid puncturing the tiny branch vessels distal to the stenosis with the head end of the fixed micro-guide wire; the treatment of bifurcation stenosis should be done with the certainty of protecting the important branch vessels from being crushed and occluded. Adequate and effective lipid-lowering and anti-polytherapy should be administered during the perioperative period.
Since intracranial artery stenosis, especially basilar artery stenosis in the posterior circulation, has a high probability of occlusion of the perforating vessels during stentoplasty, traumatic interventions for asymptomatic intracranial artery stenosis are, in principle, not necessary; the main focus is on reducing blood viscosity with lipid-lowering and antiplatelet drugs routinely used in neurology. To curb the development of atherosclerosis of blood vessel wall, it is expected to correct the underlying cerebral blood supply deficiency; meanwhile, to control hypertension, diabetes mellitus and other related conditions, and to review regularly and adjust the treatment plan in time.
Cerebral vein and venous sinus thrombosis
Cerebral venous and venous sinus thrombosis is an important cause of benign cranial hypertension or complicating brain parenchymal hemorrhage. The mortality rate after the onset of the disease used to reach more than 20%. In the last decade or so, the clinical knowledge of blood return disorders in the cerebral venous system has gradually deepened, and cerebral venous circulation disorders can be divided into four conditions: small vein thrombosis, deep vein thrombosis, venous sinus thrombosis and venous sinus stenosis. In terms of complexity, there can be simple thrombosis and combined cerebral parenchymal and subarachnoid hemorrhage. Experiments have shown that the degree of clinical symptoms following cerebral venous circulation disorders depends on the availability of reflux channels in the deep and superficial cerebral veins and does not depend exclusively on the patency of the cerebral venous sinuses. In the case of cerebral venous sinus occlusion, common compensatory pathways for venous return include return to the cavernous sinus via the pterygo-parietal sinus and lateral fissure vein; return to the extracranial scalp vein via the conduit vein; and return to the paravertebral plexus via the skull base vein. In many cases where the cerebral venous sinuses are not completely recanalized, the clinical symptoms can be significantly improved during the same period because of the venous collateral compensatory pathways.
Anticoagulation is the most basic option in the treatment of cerebral venous circulation disorders; it not only reduces the formation of new thrombi, but also promotes the fibrinolytic system in the body to dissolve older thrombi. Although the vast majority of patients with milder disease can be relieved or cured by anticoagulation alone, relying on anticoagulation alone and slow adjustment to treat cases with a longer history, more severe disease, higher intracranial pressure, and difficulty forming collateral pathways for intracranial venous return is far from adequate. Moreover, the etiology of cerebral venous system thrombosis is unknown and the recurrence rate is extremely high, so anticoagulation also needs to be long-term. The experience of PLA General Hospital suggests that anticoagulation of severe cerebral venous system thrombosis needs at least 2 years to effectively control the trend of thrombosis recurrence.
Therefore, in terms of treatment, the choice of individualized therapy should be emphasized for different conditions of cerebral venous return disorders. Anticoagulation can be applied in the basic treatment and management of milder cases; selective lysis (fragmentation) in the venous sinus is suitable for cerebral venous sinus thrombosis of short duration; cerebral small and deep venous thrombosis requires multiple thrombolysis via arterial route; and cerebral venous sinus stenosis formed after thrombus mechanization is more suitable for balloon dilation and stenting. For cerebral venous and venous sinus thrombosis with intracranial hemorrhage, moderate anticoagulation plus thrombolysis will have better results when available.
Conclusion
Mr. Schlapner, the former German head coach of the national football team, said that when a player doesn’t know how to play on the field of play, remember to look at the opponent’s door and play. If one wants to protect one’s health before organic diseases are detected, please take care of one’s blood vessels first. To make the body’s blood vessels healthy, there are only a few principles, pay attention to control hypertension, hyperglycemia, hyperlipidemia, high blood viscosity and increased platelet activity, etc. After combining the advantages of conventional internal conservative treatment and neurointerventional endovascular treatment, it is believed that with the in-depth research and exploration of neurology, it will keep the death of sudden stroke away from healthy or subhealthy people and make the society and family more harmonious and happy.