Vasculogenic vertigo is a type of vertigo that is mainly caused by cerebrovascular disease and accounts for more than 50% of all types of vertigo. Vascular vertigo can come from the anterior circulation, but most of it comes from the posterior circulation, i.e., the vertebrobasilar system. The main branches of the vertebrobasilar system are: (1) posterior cerebral artery; (2) superior cerebellar artery; (3) anterior inferior cerebellar artery (AICA); (4) posterior inferior cerebellar artery (PICA); (5) internal auditory artery, mostly from AICA (85%), a few from basilar artery (15%), and some from PICA (2%-4%). PICA (2%-4%). The most frequent vertigo occurs in the internal auditory artery, AICA, and PICA. Classical vertigo of vascular origin, with neurological signs, is generally not difficult to diagnose. In contrast, non-classical vasogenic vertigo is not accompanied by neurological signs, and most of these patients are seen in vertigo clinics, making the diagnosis more difficult. How to identify this kind of vasogenic vertigo at an early stage and reduce the serious consequences of malignant vertigo has attracted a lot of attention from scholars in the field of vertigo in recent years, which is reviewed as follows. Main types and characteristics of vasogenic vertigo Vertebrobasilar artery-transient ischemic attack (VA-TIA) ①TIA simple vertigo attack. TIA simple vertigo attacks can be very brief, ranging from one minute to several minutes, and can occur several times a day. The diagnosis is not difficult to make if accompanied by other neurological signs, but it is difficult to distinguish between vertigo of central origin and peripheral origin when no signs are present. The imaging study of frequent TIA attacks of simple vertigo found that among patients with no abnormalities on cranial magnetic resonance imaging (MRI), cerebral angiography showed lesions of the basilar artery in 7 patients (6 with atherosclerotic stenosis and occlusion and 1 with pyknotic angiomatous wall changes) and 6 with stenosis formed by vertebral arteriosclerosis, resulting in little or no blood flow in the basilar artery. or absent, relying on collateral circulation for blood supply. This study concluded that although no infarct foci were seen on MRI, the sclerotic stenosis of the vessel wall caused hypoperfusion, and the hypercoagulable state promoted emboli generation, which further reduced the perfusion pressure in the occluded vessel in a typical vertebrobasilar insufficiency (VBI) state. Under certain triggers (e.g., excessive neck rotation), this eventually leads to ischemia in vertigo-sensitive structures such as the vagus, brainstem, and cerebellum, causing transient vertigo attacks. Ischemic attacks with involvement of the internal auditory artery are also a cause of vertigo. Braun et al. reported 12 cases of cerebral infarction misdiagnosed as peripheral vestibular disorders, in which patients complained of episodic vertigo with no neurological signs and no abnormalities on computed tomography (CT) scan, and only 9 cases had spontaneous nystagmus. Neurological signs gradually appeared 1-10 d after onset, and infarct foci were visible on cranial MRI 1-7 d later. A similar study found that 42% of recurrent VA-TIA simple vertigo attacks eventually resulted in cerebral infarction, but the duration varied from 1-10 d after the onset of cerebral infarction in short cases to 2 years after the onset of cerebral infarction in long cases. Therefore, TIA simple vertigo attacks are an early warning of cerebral infarction, and if treated promptly during this period, the incidence of cerebral infarction can be effectively reduced. Silent brain stroke About 79% of silent strokes are ischemic strokes and about 4% are small hemorrhages. Most strokes occur distal or terminal to branches of the basilar artery and are dominated by episodes of vertigo with no obvious signs of neurological deficit. Much like peripheral vestibular disorders, the following forms of presentation are common: ① Positional vertigo can be the only symptom of vertebrobasilar stroke and is seen in patients with acute infarction of the dorsolateral aspect of the four ventricles, infarction of the cerebellar vomeronasal tubercle, and small hemorrhages in the cerebellar earthworms. The symptoms are similar to benign paroxysmal positional vertigo (BPPV), which presents with recurrent episodes of position-related transient vertigo and positional nystagmus on Dix-Hallpike testing. The difference is that BPPV is due to stimulation of a hallux valgus by a dislodged otolith, and the direction of the nystagmus must be consistent with the ocular muscle innervated by the stimulated hallux valgus. In contrast, positional nystagmus of central origin can induce nystagmus that is not innervated by a specific semicircular canal, such as rotational nystagmus or vertical nystagmus. ② Isolated vertigo alone is characterized by simple vertigo episodes without clear signs, and is called isolated vasogenic vertigo episodes. In recent years, there have been a large number of clinical reports related to it, which has attracted attention. Approximately 52% of patients with pure isolated vertigo of uncertain etiology have posterior circulation abnormalities that persist for more than 24 h and become acute vertigo syndrome. The lack of other signs after infarction and clinical presentation similar to vestibular neuronitis or vagotomy are commonly associated with cerebellar infarction, brainstem infarction, AICA infarction, and PICA infarction, requiring attention to differential diagnosis. (iii) Vagal ischemic infarction. The blood supply of the labyrinth comes from the internal auditory artery, which is the terminal artery and lacks collateral circulation, and is easily involved once there is an ischemic attack. Ischemic infarcts in the labyrinth often cause benign peripheral vertigo or sudden hearing impairment, with no abnormal findings on cranial MRI and no signs of neurological deficits. However, many times the ischemic attack is not limited to the internal auditory artery, but often involves other branches of the vertebrobasilar system, and several days later, MRI examination may reveal the infarct foci. Thus, an ischemic attack or vagus infarction in the internal auditory artery may be a precursor or early warning of infarction in the vertebrobasilar system. When vagal ischemia appears as a precursor of posterior circulation ischemia, it is difficult to confirm the diagnosis by MRI. Pathological studies have found that the vagus and cochlea become necrotic after inner ear infarction, and fibrosis leads to sometimes only simple vertigo attacks. An autopsy pathology report of a typical case found:significant atherosclerosis in the union of the vertebrobasilar artery, resulting in pallor of the internal auditory artery branches on both sides, fibrotic scarring and multiple degenerative areas in the right vestibular vagus branch, and significant degenerative changes in the right cochlea and vestibular vagus. These patients often present with typical BPPV-style positional vertigo episodes for months or years during the recovery period after the acute phase. This positional vertigo, originating from ischemic necrosis of the ellipsoidal saccule capsule, leads to the release of the otolith after dislodgement into the long arm of the posterior semicircular canal. Thus, ischemic necrosis of the inner ear end organs due to vascular lesions is one of the common causes of BPPV. Microangiopathies White matter disease (WMD) is a condition of microangiopathies caused by processes such as hypertension, diabetes mellitus, and aging, and is named for the predominant involvement of the white matter. The vitreous degeneration of the tiny arteries causes a reduction in their internal diameter, tissue ischemia, and massive loss of axons and myelin sheaths leading to gliosis. The resulting disruption of the blood-brain barrier leads to the entry of serum proteins into the extracellular fluid and activation of astrocytes. The astrocytes release endothelin and other vasoactive peptides, causing microinfarcts and further disruption of the blood-brain barrier. Deep brain tissue is mostly perfused by tiny arteries with small diameters, and these small-diameter arteries are the first places where microinfarcts occur, i.e., WMD occurs at the border of the microinfarct perfusion zone. WMD is focally or diffusely distributed and occurs mainly in the peripheral regions of the lateral ventricles, the subcortex and the white matter of the brainstem. The clinical manifestations are balance dysfunction in addition to cognitive dysfunction and mood disorders, with a high risk of falls, which causes great clinical concern. Due to the involvement of the motor system, there is a significant slowing of gait speed, reduced coordination and reduced strain. Due to the involvement of the brainstem, it leads to significant balance disorders and unstable gait. This may be related to the fact that brainstem WMD involves the vestibulospinal tract, corticospinal tract, spinal cerebellar tract, medial longitudinal tract, and the conduction pathways between the vestibulocerebellum and cerebellar vestibule that traverse the brainstem. WMD increases with age and is a predictor of stroke recurrence in people at high risk for hypertension and small vessel stroke. With the National Action Plan of The Fall Free Coalition, WMD has become a major reason for visits to fall prevention clinics. Diagnosis and treatment Vertigo faces two major diagnostic and treatment tasks: (1) timely identification of malignant vertigo to save lives; and (2) diagnosis and treatment of benign vertigo to improve quality of life. Since most malignant vertigo is a central disorder and most benign vertigo is a peripheral disorder, it is crucial to distinguish between central and peripheral vertigo. Early diagnosis History of vertigo – routine examination of vertigo – vertigo screening tools is the main process of early diagnosis. In cases of vasogenic vertigo with few or no signs, the following points are of particular interest: ① Identify certain central signs that are not easily detectable. For example, the ocular lateropulsion sign, the skew deviation sign, and some features of nystagmus of central origin. (2) Lack of a standardized vertigo examination routine. Some vertigo-related special tests are not included in the existing physical examination routine, and some abnormal signs cannot be detected in time, such as the head impulse nystagmus test of skew (HINTS) bedside examination and the bedside vestibular function test. (iii) Screening for risk factors for vasogenic vertigo. Patients with no clinical signs and unclear etiology but suspected vasogenic vertigo often have high risk factors for vasogenic lesions, and timely screening of risk factors as an aid to diagnosis is a practical approach. Risk factors usually include the following: age, TIA, hypertension, diabetes, cardiovascular disease, atherosclerosis, hypercoagulable state, hyperlipidemia, high body mass index, smoking, unhealthy lifestyle, emotional stress, and family history of cardiovascular disease. It was found that 85.7% of patients with simple isolated vasogenic vertigo attacks had 3 or more risk factors, with a positive predictive value of 62%. ④ Vestibular autorotational test (VAT) screening. The integrity of the neural reflex arc and central inhibition is an important way to distinguish central from peripheral damage, such as the tendon reflex, which is commonly used in clinical practice. VAT screening is a simple and convenient way to quantify VOR integrity and central inhibition: damage to the reflex circuit itself, resulting in hyporeflexia, is an indication of peripheral damage; damage to the reflex circuit itself, but with reduced central inhibition resulting in hyperreflexia, is an indication of central damage. VAT is one of the screening tests that can distinguish central from peripheral damage, in addition to physical examination. 60% to 70% of patients with vasogenic vertigo show central abnormalities in VAT testing. ⑤ Imaging. It is clearly unnecessary and impractical to perform imaging in all patients without obvious signs or with unclear etiology. However, imaging should be performed promptly in patients with frequent episodes of TIA and no relief with aspirin therapy; in patients with suspected vasogenic vertigo with >3 risk factors; and in patients with acute vertigo syndrome without relief after 48h. For stenosis caused by atherosclerosis, cerebral angiography is still the gold standard, while magnetic resonance angiography (MRA) has a high sensitivity of 94% and transcranial Doppler (TCD) has a relatively low sensitivity of 70%. Infarct foci. ① Establish a screening routine to identify high-risk groups in a timely manner. For people with suspected vasogenic vertigo, routine risk factor screening should be implemented. ②Treat TIA and risk factors as early as stroke. For example, timely treatment of hypertension, weight control, diet moderation, emotional regulation, and timely removal of factors that trigger atherosclerosis, cardiovascular and cerebrovascular to reduce the incidence of vasogenic vertigo. ③ Actively treat and control primary diseases, for example, hypertension, heart disease, diabetes, etc. (iv) Anti-platelet aggregation or other antithrombotic and anticoagulant drugs should be given promptly to those with frequent TIA episodes of vertigo to help reduce or end the frequent episodes. Studies have found that the likelihood of stroke within 2 and 12 months for symptomatic intracranial artery stenosis is 21% and 16%, respectively, 40% of which are triggered by VBI. The risk of stroke is higher in patients with untreated TIA than in those who receive treatment. ⑤ Simple isolated vertigo of unknown etiology with more than 3 risk factors should be treated accordingly as posterior circulation ischemia even if there are no brainstem or cerebellar signs. (6) Vestibular balance dysfunction caused by vasogenic vertigo should be treated with vestibular rehabilitation based on the treatment of risk factors and etiology mentioned above. (7) Those with symptomatic arterial stenosis may be considered for surgery based on the degree of stenosis and weighing the risk to benefit ratio. Vascular pathology is one of the common causes of vertigo attacks. The diagnosis of classical vasogenic vertigo is generally not difficult. There are 3 main forms of non-classical vasogenic vertigo:VA-TIA, nonsignificant stroke, and microangiopathy. The diagnosis of non-classical vasogenic vertigo is more difficult because it is mostly diagnosed without neurological signs. Recognizing the main characteristics of this type of vasogenic vertigo and its mechanism, and mastering the methods of early detection and diagnosis can help to make early diagnosis, improve the diagnosis rate, give targeted treatment, and reduce the serious consequences of malignant vertigo.