Insufficient blood supply to the vertebrobasilar artery and vertigo is one of the more common diseases in clinical practice. The disease is insidious, fast-changing, heavy, and has many complications, causing a great psychological burden to patients, and is also a difficult disease for clinicians to treat. The incidence of this disease has been increasing in recent years, and the social risk is also increasing year by year, but it has not been clinically treated in a reasonable and standardized way. This article will elaborate on this aspect, aiming to promote more reasonable and effective diagnosis and treatment of vertebrobasilar insufficiency and vertigo in clinical work. The vertebral artery originates from the subclavian artery, passes upward through the transverse foramen of the upper six cervical vertebrae, and then enters the skull through a hole in the occipital bone. The vertebral artery travels in the neck and has no branches. The vertebral artery is extremely closely related to the position of each cervical vertebra. Therefore, its blood flow is easily influenced by the activity of the cervical vertebrae. After the approach, the two vertebral arteries converge along the ventral aspect of the medulla oblongata forward and inward to the inferior border of the cerebral bridge to become a single basilar artery. Both the vertebral artery and the basilar artery give off branches into the brain, collectively referred to as the vertebrobasilar system. The blood of this system mainly supplies the medulla oblongata, pons, midbrain, inner ear, mesencephalon, occipital lobe, and the vestibular system at the base of the temporal lobe, all of which are supplied by branches of the vertebrobasilar system. Therefore, ischemic lesions of the vertebrobasilar system must lead to vertigo. Clinical manifestations of vertebrobasilar artery insufficiency Most of the patients with insufficiency of vertebrobasilar artery supply occur in middle age or above, and most of them have a history of atherosclerosis or cervical spondylosis. The main clinical manifestations are functional deficits in its blood supply area. Common symptoms include vertigo, visual impairment, ataxia, headache, impaired consciousness, and brainstem localization disorder. The clinical manifestations of vertebrobasilar artery insufficiency include: vertigo: often the first symptom, which can be rotational or mobile in nature; or bilateral lower extremity tenderness and unsteadiness in standing. Visual impairment: manifested as transient blackout or visual field defects, mainly due to the blood supply of the posterior cerebral artery. If the occipital lobe ischemia is not too severe, vision can still be preserved, but it is often accompanied by color vision and flashing golden flowers in front of the eyes, very similar to the migraine attack. Ataxia: This is manifested as a disorder of balance in body position and gait. Tilting, positive Romberg’s sign, which is due to vestibular and cerebellar dysfunction. Headache: Headache attacks are present in approximately 30-50% of cases. The headache is mainly located in the posterior and parieto-occipital regions and is throbbing and distending in nature. It is accompanied by nausea, vomiting, cold sweats and other symptoms of vegetative dysfunction. Disorders of consciousness: syncope or even coma may occur when the upward activating system of the reticular structures is involved due to brainstem ischemia. Brainstem localization signs: Ischemia affects the brain nuclei and the sensory and motor conduction bundles that travel through the brainstem, resulting in brainstem localization signs. The main manifestations are: ball palsy, crossed paresis or quadriplegia, numbness or hypesthesia of the face and limbs. When multiple oculomotor nuclei are affected, oculomotor weakness and diplopia also occur. When thrombosis of the vertebrobasilar system occurs, these symptoms are more severe and difficult to recover from, and localization symptoms are more pronounced. The main cause of insufficient blood supply or thrombosis in the vertebrobasilar artery is atherosclerosis, which not only narrows the blood vessels and reduces blood flow, but also causes wall thrombosis and embolism if a sclerotic plaque or embolus is dislodged. Secondly, trauma to the cervical spine, fracture or dislocation of the cervical spine, as well as cervical spondylosis, cervical fusion, flattened skull base, and herniation of the greater occipital foramen may affect or compress the vertebral artery and cause ischemia of the vertebral artery. Special syndromes of ischemia of the vertebrobasilar system include the following: III. First is the subclavian artery steal syndrome. The proximal subclavian artery is narrowed or occluded due to atherosclerosis, infection, congenital anomalies, trauma, etc. When the upper limb on that side is strained or moved, blood from the vertebral artery on the healthy side can flow backwards into the vertebral artery on the affected side and then into the distal end of the subclavian artery on the affected side. This is a compensatory mechanism of blood circulation to compensate for the blood supply to the affected upper extremity. However, the blood supply is still inadequate and can cause two groups of symptoms. One group is the symptoms of inadequate blood supply to the vertebrobasilar artery due to the backflow of blood from the vertebrobasilar system into the subclavian artery. The other group is due to symptoms of inadequate blood supply to the affected upper extremity, where the patient experiences numbness and weakness of the upper extremity. The symptoms are significantly aggravated during exercise. On examination, cerebral artery fluctuations in the affected limb may be found to be diminished or absent. Blood pressure is unequal between the two sides, and the systolic pressure can differ by more than 20 mm Hg. A vascular murmur may be heard in the subclavian fossa. Symptoms of vertebrobasilar artery insufficiency and vertigo, as well as visual disturbances are the most common, followed by syncope. Most of these symptoms are transient in nature. The next most common syndrome is dorsolateral medullary syndrome. The main clinical manifestations of dorsolateral medullary syndrome are: first, due to damage to the vestibular nucleus, the patient presents with vertigo, nausea, vomiting and nystagmus. Second, due to damage to the nucleus suspensus and the linguopharyngeal vagus nerve, the clinical manifestations are paralysis of the soft palatopharyngeal muscles on the side of the lesion, manifested by dysphagia, dysarthria, ipsilateral soft palate hypoplasia and loss of pharyngeal reflex. Thirdly, due to damage to the cordiform body as well as the cerebellar tract and part of the cerebellar hemisphere of the spinal cord. The clinical manifestation is ataxia on the side of the lesion. Fourth, Horner’s syndrome is clinically present because the lesion damages the sympathetic downward fibers. Fifth, damage to the trigeminal spinal tract nucleus results in crossed sensory deficits, i.e., loss of ipsilateral lateral pain and temperature, and loss of contralateral eccentric pain and temperature. Dorsolateral medullary syndrome is commonly associated with ischemic damage to the posterior inferior cerebellar artery, vertebrobasilar artery, or lateral medullary artery. Ischemic specific syndromes of the vertebrobasilar system also include spasm of the internal auditory artery: the internal auditory artery originates from the basilar artery, runs perpendicular to the basilar artery, and goes horizontally to the temporal bone rock to enter the internal auditory meatus together with the posterior auditory nerve. The internal auditory artery has a very small diameter and sends branches to supply the local auditory nerve, as well as the vestibular organs of the inner ear. With spasm of this artery, acute progressive tinnitus and deafness develop on the affected side, the latter quickly turning into hearing loss and sudden onset of severe vertigo. The hearing gradually improves after a few hours of duration and the vertigo improves. (I) Clinical manifestations of vertebrobasilar system TIA vertebrobasilar system TIA vertebrobasilar system TIA: The most common manifestations are vertigo, balance disorders, abnormal eye movements and diplopia. There may be unilateral or bilateral facial and perioral numbness, alone or with contralateral limb hemiparesis and sensory deficits, presenting a typical or atypical brainstem ischemia syndrome. The following clinical syndromes with specific manifestations may also be manifested: fall attack: manifested as a sudden loss of tension in the lower limbs and fall without loss of consciousness when the patient turns his head or tilts his head, often standing up on his own soon, caused by ischemia of the lower brainstem reticular formation. Transient global amnesia: The episodes of transient temporal memory loss, in which the patient has self-awareness, last for several minutes or tens of minutes, or even hours or even tens of hours in individual patients, with disorientation to time and place, but normal ability to talk, write and calculate. Bilateral episodes of visual impairment: bilateral ischemia of the talar branch of the posterior cerebral artery leads to involvement of the occipital visual cortex and causes temporary cortical blindness. (B) Auxiliary examination and diagnosis of vertebrobasilar system TIA Auxiliary examination and diagnosis of vertebrobasilar system TIA: Most of the CT or MRI examinations are normal, some cases (those with an attack time of more than 1 hour) can be seen as lamellar ischemic foci on diffusion-weighted MRI; CTA, MRA and DSA examinations can reveal vascular stenosis and atherosclerotic plaques; TCD examination can reveal intracranial arterial stenosis. Diagnosis: Most of the clinical symptoms have disappeared when TIA is seen, so the diagnosis mainly relies on medical history. The sudden onset of focal cerebral impairment in middle-aged and elderly patients, consistent with the manifestation of ischemia in the vertebrobasilar system and its branches, and complete recovery of symptoms within a short period of time, should highly suspect TIA. (C) Differential diagnosis of TIA in the vertebrobasilar system Partial seizures of epilepsy, especially simple partial seizures, often manifest as twitching or numbing pins and needles sensation in the limbs lasting from a few seconds to several minutes, starting from one part of the torso CT/MRI may reveal focal lesions in the brain. Meniere’s disease: Episodes of vertigo, nausea and vomiting are similar to vertebrobasilar TIA, but the duration of each episode often exceeds 24 hours, accompanied by tinnitus, a sense of ear obstruction, hearing loss after repeated episodes, and no other neurological localization signs other than nystagmus. Cardiac diseases: A-S syndrome with severe heart rate arrhythmias such as supraventricular tachycardia, multi-source ventricular precontraction, ventricular tachycardia or ventricular fibrillation, pathological sinus node syndrome, etc. Dizziness, fainting and loss of consciousness may occur due to paroxysmal total cerebral hypoperfusion, but there are often no focal neurological signs and symptoms, and there are often abnormal findings on ambulatory electrocardiographic monitoring and echocardiography. Others: intracranial tumors, abscesses, chronic subdural hematomas, and intracerebral parasites may also present with symptoms similar to TIA episodes. Primary or secondary autonomic insufficiency may also present with transient whole brain hypoperfusion and episodic disorders of consciousness due to rapid changes in blood pressure or heart rate. Basilar artery type migraine, which often has posterior circulation ischemic attacks, should be excluded with care. (iv) Treatment of TIA in vertebrobasilar system The treatment of TIA attacks aims to eliminate the cause, reduce and prevent recurrence, and protect brain function. First, etiological treatment should be carried out. Patients with a clear etiology should be treated for the etiology as much as possible. For example, patients with hypertension should have their hypertension controlled. Patients with diabetes should control hyperglycemia. Patients with dyslipidemia should have their blood lipids controlled. Patients who smoke should quit smoking. Correct lifestyle, etc. For patients with some bad habits, they should be properly guided to quit smoking and alcohol. Second, preventive drug therapy includes: first of all, anti-platelet drugs. Anti-platelet drugs can reduce the occurrence of microemboli and reduce the recurrence of TIA. Commonly used clinically are aspirin, the dose of which is 75-150 mg per day, taken after a meal. However, it is often taken clinically after dinner. Because patients are at night, blood pressure is low and blood flow is slow, in which case they are most likely to have thrombosis and TIA episodes. Therefore, antiplatelet drugs should be recommended to be taken at night. The main adverse effects of aspirin are gastrointestinal reactions. Aspirin can also be used in small doses, which is 25 mg per day. It is combined with bimatoprost 200 mg per dose. Bimatoprost is 200 mg per dose, twice a day. Aspirin 25 mg once a day. Clopidogrel is also an antiplatelet drug and the dose is usually used 75 mg per day. Adverse effects are significantly less than with aspirin and are recommended for people at high risk, or for patients who are intolerant to aspirin. Ozagrel may also be used. Ozagrel is an intravenous antiplatelet agent and there is still a lack of large scale clinical observations and efficacy has not been established. Currently, there is no clinical trial evidence to support anticoagulation as a routine treatment for TIA. However, it may be considered in patients with TIA who have frequent clinical episodes of atrial fibrillation. These include mainly heparin, low molecular heparin and warfarin. Oral anticoagulant therapy is recommended for patients with cardiogenic embolic TIA with atrial fibrillation and coronary artery disease. The goal of treatment is to achieve an international normalized ratio of 2-3 or a prothrombin time of 1.5 times the normal value. When clinically encountering frequent episodes of TIA, or patients with TIA of the vertebrobasilar system, anticoagulant therapy may be considered in cases where antiplatelet aggregation agent therapy is ineffective. For patients with TIA treated with adequate oral anticoagulant after valve replacement, a combination of low-dose aspirin or bimatoprost may also be added. During the administration of oral anticoagulants such as warfarin and neomidacromol, the coagulation function should be monitored dynamically and the dose of medication should be adjusted according to the results of the coagulation function. This is antiplatelet therapy and anticoagulation. In patients with TIA with hyperfibrinogenemia, fibrin-lowering enzyme therapy is available. For elderly TIA with contraindications to antiplatelet aggregation agents, or resistant ones, blood-activating herbal treatment can be used. Third, surgical treatment of TIA. For patients with TIA who have severe stenosis of carotid artery or vertebrobasilar artery, the stenosis rate should be greater than 70%. After antiplatelet aggregation treatment and anticoagulation therapy is not effective, or the condition has a tendency to deteriorate, endovascular intervention, endarterectomy or arterial bypass therapy can be selected as appropriate. The prognosis is that some untreated or ineffective cases will progress to cerebral infarction, some will continue to have attacks, and some patients with TIA will resolve on their own.