I. Understanding of posterior circulation ischemia and its definition and significance
The posterior circulation, also known as the vertebrobasilar system, consists of the vertebral artery, the basilar artery and the posterior cerebral artery, which mainly supplies blood to the brainstem, cerebellum, thalamus, occipital lobe, part of the facial lobe and the superior crista. Posterior circulation ischemic drought, a common ischemic cerebrovascular disease, accounts for about 20% of ischemic strokes.
1. History of recognition of ischemia in the posterior circulation.
In the 1950s, it was found that some patients with transient ischemic attack (TIA) of the carotid system had severe stenosis or occlusion of the extracranial segment of the carotid artery, which was presumed to be caused by the relative ischemia of the tissue in the vascular distribution area supplied by the collateral circulation only. By extending this concept to the posterior circulation, the concept of “vertebrobasilar insufficiency” (VBI) was developed. The classical concept of VBI has two meanings: clinically, it refers to TIA in the posterior circulation, and etiologically, it refers to hemodynamic hypoperfusion due to severe stenosis or occlusion of the great arteries.
After the 1970s, it became clear that the only two forms of ischemia in the carotid system were TIA and infarction, and the concept of “carotid insufficiency” was no longer used. However, due to the lag in the understanding of posterior circulation ischemia, the concept of VBI is still widely used and has given rise to some inaccurate perceptions: for example, dizziness/vertigo is often attributed to VBI; cervical spine osteophytes are considered as an important cause of VBI; and the concept of VBI has been generalized to a state that is neither normal nor ischemic. These situations are especially serious in China, leading to unclear concepts, unclear diagnostic criteria and irregular disposition of VBI.
2. Current state of awareness of posterior circulation ischemia.
After the 1980s, with the deepening of clinical research and the development of research techniques, several important understandings of the clinical and etiology of posterior circulation ischemia have been made.
(1) The main etiology of posterior circulation ischemia is atherosclerosis, while cervical spine osteophytes are only a rare case;
(2) The predominant mechanism of posterior circulation ischemia is embolism;
(3) Neither clinical nor imaging examinations can reliably define a state that is neither normal nor ischemic;
(4) Although dizziness/vertigo is a common symptom of posterior circulation ischemia, the common cause of dizziness/vertigo is not posterior circulation ischemia.
Based on the above understanding, the concept of VBI has been replaced by the concept of posterior circulation ischemia internationally, and VBI is no longer used in the International Classification of Diseases.
3. Definition of posterior circulation ischemia: It refers to TIA and cerebral infarction in the posterior circulation.
Its synonyms include ischemia of the vertebrobasilar system, masticatory A and cerebral infarction of the posterior circulation, vertebrobasilar artery disease, and vertebrobasilar artery thromboembolic disease. Given that MRI diffusion-weighted imaging (DWI) finds that about half of posterior circulation πA has definite infarct changes and the boundary between TIA and cerebral infarction is becoming increasingly ambiguous, the use of posterior circulation ischemia to cover TIA of the posterior circulation and cerebral infarction is beneficial for clinical operation.
II. Pathogenesis and risk factors of posterior circulation ischemia
1. The main etiology and pathogenesis of posterior circulation ischemia.
(1) Atherosclerosis is the most common vascular pathological manifestation of posterior circulation ischemia. The mechanisms leading to posterior circulation ischemia include: low perfusion due to large artery stenosis and occlusion, thrombosis and arterial-derived embolism. Atherosclerosis occurs in the beginning and intracranial segments of the vertebral arteries.
(2) Chalazion is the most common pathogenesis of posterior circulation ischemia, accounting for about 40% of emboli, which mainly originate from the heart, aorta and vertebral basilar artery. The most common sites of embolism are the intracranial segment of the vertebral artery and the distal basilar artery.
(3) Penetrating small artery lesions, including vitreous lesions, microaneurysms and atherosclerotic lesions at the initiation of small arteries, occurring in the pontine brain, midbrain and thalamus.
2. Major risk factors for posterior circulation ischemia.
Similar to carotid system ischemia, in addition to non-adjustable age, gender, race, genetic background, family history, and personal history, the main factors are lifestyle (diet, smoking, lack of activity, etc.), obesity and multiple vascular risk factors, the latter including hypertension, diabetes, hyperlipidemia, heart disease, history of stroke ITIA, carotid artery disease and peripheral vascular disease.
3. Cervical spondylolisthesis is not a major cause of posterior circulation ischemia.
It was previously thought that turning the head/neck could cause compression of the vertebral artery by the osteophytes, resulting in posterior circulation ischemia and dizziness/vertigo because the vestibular nucleus is sensitive to ischemia. This model of hypothesis instead of evidence is a major cause of confusion in the diagnosis of VBI. In contrast, clinical studies have demonstrated that cervical osteophytes are never a major risk factor for posterior circulation ischemia, as there is no significant difference in the degree of cervical osteophytes between middle-aged and older adults with or without posterior circulation ischemia, but only in vascular risk factors; serial dynamic vertebral arteriograms only show isolated arterial compression due to osteophytes; Doppler ultrasonography after cervical rotation is not seen between those with or without posterior circulation symptoms The rate of extracranial segment compression of the vertebral artery was different.
III. Clinical manifestations and diagnosis of posterior circulation ischemia
1.Main clinical manifestations of posterior circulation ischemia.
Common symptoms of posterior circulation ischemia: dizziness/vertigo, limb/head and face numbness, limb weakness, headache, vomiting, diplopia, transient loss of consciousness, visual disturbance, unstable walking, or fall. Common signs of posterior circulation ischemia: oculomotor disturbances, limb paralysis, sensory abnormalities, gait/limb ataxia, dysarthria/swallowing, visual field defects, hoarseness, and Homer’s syndrome. The presence of crossover of neurological damage on one side of the brain and motor-sensory damage on the other side is a characteristic manifestation of posterior circulation ischemia.
Common syndromes of posterior circulation ischemia: posterior circulation mastication A, cerebellar infarction, lateral delayed brain syndrome, basilar artery acinar syndrome, Weber syndrome, atresia syndrome, posterior cerebral artery infarction, lacunar infarction (motor light hemiparesis, ataxia light hemiparesis, dysarthria-clumsy hand syndrome, pure sensory stroke, etc.) .
2. Clinical manifestations that are often mistaken for posterior circulation ischemia.
The dense structure of the brainstem and the non-one-to-one correspondence between vascular innervation and neural structure determine that the majority of posterior circulation ischemia presents as a variety of overlapping clinical manifestations, rarely as a single symptom or sign. Simple dizziness/vertigo, syncope, fall episodes or transient loss of consciousness are rarely caused by posterior circulation ischemia.
Evaluation and diagnosis of posterior circulation ischemia: A detailed history, physical examination and neurological examination are the basis for diagnosis.
It is important to carefully understand the history, especially the occurrence, form, duration, concomitant symptoms, evolution and possible precipitating factors of symptoms; to pay attention to various vascular risk factors; to focus on the examination of cerebral nerves (vision, oculomotor, facial sensation, Xin sensation, vestibular function) and ataxia. For those with dizziness/vertigo as the main complaint, be sure to perform Dix-Hallpike examination to exclude benign episodic positional vertigo.
Neuroimaging, mainly MRI, should be performed in all patients with suspected posterior circulation ischemia, with DWI being the most diagnostic for acute lesions. Cranial CT examination is susceptible to bone artifacts and has little diagnostic value, and is only applicable to exclude bleeding and patients who cannot undergo MRI examination.
Various vascular examinations should be actively carried out. Digital subtraction angiography, CT angiography, MRI angiography and vascular Doppler ultrasonography can help to detect and clarify large intracranial and extracranial vascular lesions. Each examination has its own characteristics, and there is a lack of correlation studies between different examinations. Transcranial Doppler ultrasonography (TCD) can reveal stenosis or occlusion of the vertebral artery: however, it cannot be the only basis for the diagnosis of posterior circulation ischemia. Various cardiac examinations can help to identify emboli from the heart or aortic arch. Imaging of the cervical spine is not the preferred or important test.
IV. Prevention and treatment of posterior circulation ischemia
1.Acute phase treatment.
There is still a lack of results from large randomized controlled studies specifically on posterior circulation ischemia, so the acute phase management of posterior circulation ischemia is the same as that of anterior circulation ischemic stroke. An organized treatment model for stroke units should be actively pursued. Intravenous thrombolysis with recombinant tissue-type fibrinogen activator (this-PA) can be performed in appropriate patients within 3 h of onset. The treatment time window can be relaxed for those who are eligible for intravenous thrombolysis. For all those who are not suitable for thrombolytic therapy and have no contraindication, they should be treated with aspirin 100-300 mg/d. Other therapeutic measures can refer to the relevant treatment guidelines at home and abroad.
2. Prevention.
Refer to the relevant domestic and foreign prevention and treatment guidelines to control various vascular risk factors. In view of the prevalence of embolism, etiological examination should be actively carried out. Antithrombotic therapy should be carried out for those with a clear diagnosis. The use of antiplatelet agents alone or in combination has an important preventive role. The efficacy of angioplasty stenting should be explored.
3. Missionary education.
Continuing re-education of posterior circulation ischemia, especially for physicians, is actively carried out to update the concept and knowledge, and the concept of VBI is no longer used. Propaganda should be strengthened to correctly grasp the early manifestations of posterior circulation ischemia to achieve early detection and early diagnosis. The risk factors of posterior circulation ischemia should be correctly understood, and a scientific view of prevention should be established.
V. Clinical research of posterior circulation ischemia
Clinical research in this field should be actively promoted in China, and a national or regional registration system and database should be established. The diagnostic criteria and prevention measures of posterior circulation ischemia should be standardized.
VI. Several important understandings about posterior circulation ischemia
1, posterior circulation ischemia includes white A and cerebral infarction in the posterior circulation.
2. The main etiology of posterior circulation ischemia is the same as that of anterior circulation ischemia, and cervical spondylosis is not the main etiology.
3.Dizziness/vertigo is a common manifestation of posterior circulation ischemia, but the common cause of dizziness/vertigo is not posterior circulation ischemia.
4. The diagnosis, treatment and prevention of posterior circulation ischemia should be consistent with that of anterior circulation ischemia.