Unlike the common cerebral ischemia caused by carotid artery lesions, obstructive lesions of the vertebrobasilar artery cause cerebellar ischemia, which manifests as inadequate blood supply to the vertebrobasilar artery. Treatment includes drugs, surgery and endoluminal stenting. I. Etiology and diagnosis Two mechanisms are thought to cause vertebrobasilar artery insufficiency: low blood flow and microembolism. Obstructive lesions of the vertebral artery and its proximal arteries are clearly the most important, followed by embolization. Insufficient blood supply to the vertebral basilar artery can be caused by microemboli from the heart or, more often, the emboli are from vessels supplying blood flow to the basilar artery (innominate artery, proximal subclavian artery, and vertebral artery). The importance of embolic mechanisms as a cause of symptomatic vertebral basilar artery lesions has been confirmed by clinical and pathological studies. These facts have been derived from biopsies and magnetic resonance images confirming microinfarcts in the brainstem and cerebellum, which in the past were often not visualized on CT. They are derived from lesions in the proximal subclavian or vertebral arteries shown on selective arteriography. Patients with vertebrobasilar insufficiency due to embolism can progress to multiple infarcts in the brainstem, cerebellum, and occasionally in the posterior cerebral artery region, resulting in a high incidence of stroke. Nearly 30% of the etiologies are microemboli resulting in vertebrobasilar insufficiency. Mechanisms of low blood flow are better understood and are more common than embolic mechanisms. Patients with TIA episodes due to vertebrobasilar insufficiency have low flow in the basilar region because they lack adequate blood supply from the vertebral artery and adequate compensation from the carotid region. This is usually caused by stenosis or occlusion of the vertebral arteries, although most of the lesions are atheromatous plaques. Vertebral artery stenosis can also be caused by extrinsic compression caused by a bony bulge close to the vertebral artery. In patients with low blood flow due to vertebrobasilar artery insufficiency, it is essential to rule out systemic causes of vertebrobasilar artery insufficiency prior to action pachymetry. In elderly patients, vertebral artery stenosis is not uncommon on arteriography, and dizziness is a common complaint. However, the coexistence of the two in a patient is not necessarily considered to be causally related. Systemic causes of low blood flow in vertebrobasilar insufficiency generally include upright hypotension, hyporegulation on antihypertensive therapy, arrhythmias, heart failure, pacemaker malfunction, and anemia. Evaluation of patients with vertebrobasilar artery insufficiency requires several specific steps. The first step is to determine the precise, detailed condition associated with the progressive symptoms. In elderly patients with sympathetic dysregulation that does not control venous tone, their symptoms usually appear after standing, which causes overfilling of the leg veins. This is particularly common in diabetic patients because their sympathetically innervated venous sphincter reflexes are diminished. We use a 20 mmHg drop in systolic blood pressure during rapid uprightness as a criterion for diagnosing upright hypotension resulting in reduced blood flow to the vertebrobasilar system. In these patients the fall in blood pressure caused symptoms of inadequate blood supply to the vertebrobasilar artery. Patient onset is associated with head rotation or extension. These dynamic symptoms usually appear when the head is turned to the other side. The mechanism is often caused by extrinsic compression of the vertebral artery, with osteoarthritis generally being the primary or sole cause. To differentiate the different pathogenesis of vertigo due to vestibular disorders, this vertigo symptom appears when the head or body is rotated and the patient can try to make the symptom appear by slowly turning the head and repeating this movement. In vestibular disorders, sudden inertial changes caused by the latter approach can lead to immediate symptoms and nystagmus. In contrast, in patients with extrinsic vertebral artery compression, a transient lag occurs before discomfort with their balance is experienced. Evidence of extrinsic vertebral artery compression, usually due to osteophytes, needs to be confirmed by arteriography. This procedure either requires the patient to be in a seated position with contrast injected bilaterally by the brachial artery, or supine in a head-down (Trendelenburg) position with the head stationary and the drug injected through the femoral artery. In these positions, axial compression is applied to the cervical spine, allowing the acquisition of arterial flow maps that induce symptoms during head rotation or extension. When the patient becomes symptomatic, an arteriogram will show extrinsic compression due to rotation or extension of the head. The reason for a seated or 25-degree head-down/foot-up position is to minimize the gravitational effect of the head on the spine. When the weight of the head is applied to the cervical spine in the standing position it changes its flexion and reduces the distance between the cervical spine 1-7. This compression of the longitudinal spine often increases the result of extrinsic compression in osteoarthritis. In patients with vertebrobasilar artery insufficiency, MRI scans of the head are more appropriate than CT to rule out brain tumors and to evaluate brain integrity. Brainstem infarcts are often missed by CT scans because of their small lesions and the poor resolution of brainstem CT. In patients preparing for vertebral artery reconstruction, preoperative MR brain scans can determine whether infarction has occurred in the region of the vertebrobasilar artery. Overuse of antihypertensive medications can cause basilar artery insufficiency by decreasing filling pressures and causing severe upright hypotension. 24-hour ambulatory electrocardiography can be used to evaluate low blood flow due to basilar artery insufficiency. Sometimes patients with vertebrobasilar insufficiency due to arrhythmias may recognize a relationship between palpitations and symptoms of vertebrobasilar insufficiency, which are associated with reduced cardiac output due to the arrhythmia. Physical examination can alert the physician to the possibility of subclavian artery steal when the patient has a pressure difference between the brachial arteries of more than 25 mmHg or a diminished or absent pulse in one upper extremity. The diagnosis of vertebral artery flow reversal can be accurately determined by noninvasive indirect methods and can be directly demonstrated by multispectral flow of the reversed vertebral artery. Any systemic cause that decreases the mean pressure of the basilar artery can cause symptoms of vertebral basilar artery insufficiency. Affected individuals may or may not have concomitant vertebral artery stenosis or occlusion. In some patients, the cause of the lowered mean arterial pressure can be corrected by adjusting the dose of antihypertensive medication, antiarrhythmic drugs, or placing a pacemaker. Some patients with upright hypotension may be ineffective for pharmacologic treatment or reconstruction of only the diseased or occluded vertebral artery, the cause of which is a persistent fluctuation of blood pressure due to reduced sympathetic venous tone. Rheological factors, such as increased blood flow viscosity (erythrocytosis) and reduced oxygen-carrying capacity (anemia), can exacerbate or cause the development of vertebrobasilar insufficiency in patients with severe vertebral artery occlusion. Currently, the principles of medical drug therapy are basically the same as those for secondary prevention of ischemic stroke or transient ischemic attacks (TIAs). It mainly includes antithrombotic therapy, statins for lipid lowering, and treatment for risk factors. Antithrombotic therapy includes antiplatelet and anticoagulation therapy. The latest American Stroke Association prevention guidelines consider aspirin, aspirin plus extended-release disulfiram, and poliovir as options for initial treatment. Anticoagulation is effective in preventing vertebrobasilar stenosis. The results of the study showed that warfarin anticoagulation (international normalized ratio 1.4 to 2.8) did not increase the risk of severe bleeding but was not superior to aspirin (325 mg/d) in preventing ischemic stroke recurrence and reducing morbidity and mortality. Anticoagulation may be considered in patients with TIA episodes despite taking antiplatelet agents. Statins significantly reduce the risk of ischemic stroke and stabilize atherosclerotic plaques. They are recommended when imaging shows unstable plaques, unless the patient’s LDL cholesterol level is <1.81 mmol/L. In addition, medical therapy includes treatment of risk factors such as hypertension, diabetes, obesity, smoking, and hyperhomocysteinemia, as well as necessary In addition, medical treatment includes treatment of risk factors such as hypertension, diabetes, obesity, smoking and hyperhomocysteinemia and necessary lifestyle changes. Arteriography is necessary to evaluate the pathological changes in the vertebral arteries, to show the course of the system, the outflow tract, and to evaluate the system from the beginning to the end of the basilar artery. The vertebral artery is described in four segments, each with unique imaging and pathologic features. The arteriogram begins with the aortic arch, which can be examined for the presence or absence of bilateral vertebral arteries. to see if one vertebral artery is the dominant artery (usually the left) and if the vertebral artery has a normal origin. The most common variant is the left vertebral artery originating from the aortic arch (6%). The least common variant is a right vertebral artery originating from the innominate or common carotid artery. Aortic arch images should have at least right and left anterior oblique projections. Usually, these two images clearly demonstrate the first segment of the vertebral artery from the opening of the vertebral artery to the sixth cervical cross-section. Occasionally, other oblique projection images are required. The most common atherosclerotic lesion of the vertebral artery is a stenosis at its origin. This lesion may be missed in standard aortic images because of the overshadowing of the subclavian artery above the first segment of the vertebral artery. An additional oblique projection is necessary to "cut out" the subclavian artery to obtain a clear image of the beginning of the vertebral artery. If there is a post-stenotic dilatation at the beginning of the vertebral artery, this indicates that there is a significant stenosis at the beginning of the vertebral artery hidden behind the subclavian artery. Vertebral artery origin redundancy and kinking are also common, but only very severe kinking originating from post-stenotic dilatation is associated with symptoms of low blood flow. The second segment of the vertebral artery (V2) is visualized from C6 to the top of the C2 transverse process and can be visualized by combined oblique aortic arch imaging and selective subclavian arteriography. The vertebral artery opening within the spine is confirmed, and an abnormal low arterial opening at the level of C7 rather than the plane of C6 should be noted. This is associated with a short V1 segment, suggesting that it does not have sufficient length to perform a possible end-lateral anastomosis from the vertebral artery to the common carotid artery. The level of the arterial opening into the spine is best shown by non-subtracted imaging. Extrinsic compression due to tendinous structures is common in anomalous high convergence of the vertebral artery into the spine, particularly C4 or C5. this is due to the sharp angle of entrapment caused by the anomalous entrance. The most common lesion in the V2 segment is extrinsic compression caused by a bony bulge. In patients with dynamic symptoms induced by cervical rotation, rotation of the cervical artery to the right or left with head weight or equivalent forces acting on the cervical spine may reveal the V2 segment. The vertebral artery may appear normal in one projection and be obstructed by extrinsic compression in the other. The V2 and V3 segments are the site of traumatic or spontaneous arteriovenous fistulae because the epicardium of the artery and the periosteal fixation of the vertebral artery foramen make the former vulnerable to dislocation or subluxation of the vertebral joint or to fracture in the transverse region. The close proximity of the artery to the surrounding venous plexus leads to arteriovenous fistulas in cases of persistent injury to both arteries and veins. Extension injuries caused by rapid neck rotation or high neck tension can cause complete or incomplete lacerations (entrapment) of the vertebral artery. The V3 segment crosses over the C2 transverse process to reach the atlanto-occipital plane. After passing this side it passes through the foramen magnum at the base of the skull into the dura mater. The two atlanto-axial vertebrae are the most mobile of the spinal column. Fifty percent of cervical motion occurs in C1 and C2. The vertebral artery is long enough in this segment to accommodate the arc of atlantoaxial transverse process rotation (approximately 80 degrees). The most common problems in this segment are arterial entrapment, arteriovenous fistulas, and arteriovenous aneurysms. The entrapment is associated with muscle fiber dysplasia or minor trauma to the normal artery. Vertebral artery entrapment leads to stenosis, thrombosis, distal embolism, and pseudoaneurysmal dilatation. Arteriovenous fistulas occur when the arterial wall ruptures into the surrounding venous plexus. In long-standing fistulas, the pulsating mass consists of a fistula and an enlarged venous channel called an arteriovenous aneurysm. The V3 segment between the occipital ridge and the atlantoaxial arch becomes compressed. In these patients, the ischemic symptoms can come on suddenly during head extension or rotation. An anatomical finding that is critical to the choice of surgical approach is that when the proximal vertebral artery is occluded it usually reestablishes collateral circulation with the occipital artery at the level of the third segment. Because of this collateral circulation network, the distal vertebral arteries (V3 and V4) and the basilar artery usually remain open, and the V4 segment rarely becomes atherosclerotic. The basilar artery can be clearly visualized in the lateral projection. Digital subtraction in the lateral projection should remove temporal bone density. In Towne's projection (Towne) anterior-posterior images, which are routinely performed using neuroradiological methods, the basilar artery is shown to be poorly resolved in the distal and proximal methods. Progressive basilar artery atherosclerotic lesions are inappropriate for vertebral artery reconstruction. 3.2. Indications Two types of patients are indicated for surgical treatment of vertebral artery stenosis or occlusion: (1) patients with inadequate blood supply to the basilar artery in order to increase blood flow to the basilar region or to prevent further embolization; (2) patients with extensive and severe symptomatic extracranial lesions who require increased cerebral blood flow. The latter patients often have extensive extracranial lesions with one or both internal carotid arteries obstructed and with full manifestations of cerebral ischemia. In these patients, the carotid artery may be occluded or severely stenosed, making direct internal carotid artery reconstruction impossible, and vertebral artery reconstruction may be the best option to obtain adequate cerebral blood supply. In patients with cerebral ischemia, the vertebral artery is an important route for cerebral revascularization when the cerebral vessels are severely stenosed or occluded. They often establish distal blood flow in the cranial region. A posterior communicating artery of normal canal size increases the likelihood of successful correction of cerebral ischemic symptoms. The minimum anatomic requirement for performing vertebral artery reconstruction in patients with hemodynamic symptoms is a bilateral vertebral artery stenosis of greater than 60% or the same degree of stenosis in the dominant vertebral artery and hypoplasia (terminating in the posterior inferior cerebellar artery) or occlusion of the contralateral vertebral artery. In addition, normal vertebral arteries can adequately perfuse the basilar artery, independent of whether the contralateral vertebral artery is stenosed or not. In those cases where the basilar artery is insufficiently supplied by microembolism and the lesion happens to be proximal to the vertebral or subclavian artery, the possible source of the embolus needs to be excluded, regardless of the condition of the contralateral vertebral artery. In a selection of partially reported vertebral artery reconstruction cases, 96% of patients have neurological symptoms (TIA or stroke) and 4% are asymptomatic. 4% of patients have neurological symptoms related to the cerebral hemisphere, 60% to the vertebrobasilar system, and 30% to the whole brain. 3.3. Surgical techniques Most vertebral artery reconstructions are performed to relieve stenosis at the opening of the vertebral artery (V1), but also stenosis, entrapment or occlusion of parts of the vertebral canal (V2 and V3). Although in the 1970s Berguer and his colleagues advocated correction of proximal vertebral artery lesions by subclavian artery-vertebral artery bypass, this technique is now rarely used and is only considered in anomalous anatomic situations, such as (1) occlusion of the contralateral carotid artery increases the risk of blocking the carotid artery during a vertebral artery-carotid bypass and (2) V1 segments are short and enter the C7 transverse foramen. This anatomic variation leaves the vertebral artery without sufficient length for vertebral artery-common carotid artery bypass grafting. For lesions involving the origin of the vertebral artery, we routinely perform vertebral artery-common carotid artery bypass, which is a simple and perfect approach compared to vertebral artery-subclavian artery bypass. Exposure of the common carotid artery is easier than the subclavian artery, and this procedure requires only one anastomosis and no venous grafts. For lesions involving the C6 transverse plane or above, we routinely perform reconstruction at the C2-C1 level (V3 segment). This reconstruction is usually performed with a distal vertebral artery-common carotid artery bypass, although other techniques may be used in exceptional cases (see below). Reconstruction of the V2 segment (C6-C2) is extremely difficult because this segment is more difficult to expose than the V3 segment. In addition, it is important to note that bypass at the C2-C1 level is the area with the greatest potential for extrinsic compression due to osteophytes. 3.3.1, Vertebral artery to common carotid artery end-lateral anastomosis If the vertebral artery procedure is performed as a separate operation, the incision should be made via the supraclavicular to reveal the vertebral artery between the heads of the sternocleidomastoid muscles (Figure 2). The scaphoid hyoid muscle is dissected. The jugular vein and vagus nerve are drawn laterally to open the carotid sheath. The proximal end of the carotid artery is exposed as much as possible. After the carotid artery is freed, the sympathetic trunk can be seen parallel to its posterior aspect. On the left side, the thoracic duct is cut and double ligated avoiding sutures that could cause lymphatic leakage. The accessory lymphatic ducts commonly found on the right side should also be identified and dissected and ligated. The entire dissection is limited to the medial aspect of the incision to the fat pad overlying the anterior oblique angle muscle and the anterior phrenic nerve. The tissue located lateral to this area does not need to be dissected. The inferior thyroid artery crosses this area and needs to be cut and ligated. The vertebral vein emanates from the angle between the longissimus dorsi and anterior oblique muscles and lies in front of the vertebral artery and the subclavian artery below the operative field. Unlike its eponymous artery, the vertebral vein has geniculate branches. It often needs to be cut and ligated, and the vertebral vein is posterior to the vertebral artery. It is very important to identify and avoid injury to the sympathetic trunk. The vertebral artery is separated beyond the tendon of the longissimus carotidus muscle and medial to the vertebral artery at the beginning of the subclavian artery. The vertebral artery and sympathetic trunk are sufficiently freed to lie anterior to the vertebral artery to avoid injury to the sympathetic trunk or branches of the ganglion. In order to preserve the sympathetic trunk and stellate or intermediate ganglion located on the surface of the artery, it is usually required to free the vertebral artery from these structures, which are moved anterior to the sympathetic trunk after dissection at the origin. Once the vertebral artery is visualized intact, the next step is to select a suitable location for bypass with the common carotid artery. The distal end of the V1 segment is clamped vertically at the edge of the long carotid muscle by a small vessel clamp, taking care to avoid twisting the vertebral artery at an angle during grafting. 5-0 polyethylene sutures are used to close the proximal end of the vertebral artery. The vertebral artery is moved to the common carotid artery, and the free end is appropriately cut for anastomosis. The common carotid artery is blocked and an oval incision of approximately 5 x 7 mm in size is made in the posterior lateral wall. 6-0 or 7-0 polyethylene sutures are used for continuous anastomosis in the open position to avoid excessive tension on the vertebral artery that could easily rupture. Before completion of the anastomosis, the relaxed sutures are tightened with moderate tension using a nerve hook and knotted to restore blood flow. If carotid endarterectomy is performed concurrently, a standard carotid artery incision should be made in the vertebral artery and extended below the head of the clavicle. Through this route, the sternocleidomastoid muscle is located laterally, and the operative field may be slightly narrower than through the sternocleidomastoid head route. 3.3.2. Distal vertebral artery reconstruction Distal vertebral artery reconstruction is usually performed at the C1-C2 level. Rarely is a posterior route via the C1-C0 level performed. Although several techniques are available to reconstruct the V3 segment (between the C1-C2 transverse processes), the reconstruction methods are similar. The incision anterior to the sternocleidomastoid muscle is the same as the carotid procedure, and just below the earlobe the internal jugular vein and the sternocleidomastoid muscle are retracted on each side, freeing the paraspinal nerve located 3-4 cm below the mastoid process, which can be reached by the operator's fingers. It is necessary to pull the diastasis muscle upward or cut it off. Once the anterior border of the scapular raphe is identified, the surgeon can locate the anterior branch of C2. The anterior branch is a marker and a right angle forceps is slid over the surface of the anterior branch to lift the scapular raphe that has been transected (Figure 3 left). The proximal end of the scapularis raphe is severed up to the portion of the C1 transverse process that is attached. The vertebral artery travels below the C2 branch, in close proximity to it and perpendicular to it. After cutting it off, the underlying vertebral artery is revealed (Figure 3 middle) and the final anastomosis is completed (Figure 3 right). The vertebral artery is freed at this level for reconstruction using binocular magnification. Extra care should be taken to free the artery from the peripheral veins, as bleeding is difficult to control here. The location of the saphenous vein anastomosis with the common carotid artery should not be chosen too close to the bifurcation, where clamping will often fragment the underlying atheromatous plaque present. Prepare the appropriate length of the grafted saphenous vein, paying attention to the direction of the valve. After total heparinization, the vertebral artery is gently lifted by a glue ring and blocked with a J-clamp, separating this portion out for end-lateral anastomosis. The vertebral artery is incised longitudinally for sufficient length to fit the opening of the graft, and the 7-0 polyethylene thread and fine needle are sutured continuously to perform an end-lateral anastomosis to restore blood flow to the vertebral artery, with intraoperative attention to prevent the occurrence of embolism. 3.3.3. Anastomosis of the vertebral artery to the external carotid artery The distal vertebral artery can also be reestablished via the external carotid artery, either by anastomosing the external carotid artery directly to the distal vertebral artery or by anastomosing the proximal end of the graft to the external carotid artery. Anastomosis of the external carotid artery to the distal vertebral artery requires the absence of lesions in the bifurcation of the carotid artery and a long external carotid trunk. The external carotid artery often branches early and is too thin to match the diameter of the vertebral artery. The external carotid artery is ligated so that the trunk has sufficient diameter and length to reach the vertebral artery. The external carotid artery is then rotated over the internal carotid artery to perform an end-to-end anastomosis with the distal vertebral artery at the C1-C2 level via the inferior internal carotid vein. After completion of the anastomosis, the proximal vertebral artery is ligated below the anastomosis. 3.3.4. Variations in surgical technique The proximal external carotid artery can be used as an inflow channel for the graft if the patient has a suitable diameter saphenous vein but does not have sufficient length to create a bridge between the common carotid artery and the distal vertebral artery; or this technique appears particularly valuable when the contralateral internal carotid artery is occluded to avoid blocking the common carotid artery, the only blood supply. If the vein graft is used for bypass of the external carotid artery and the distal vertebral artery, it should have appropriate tension and be considered not to twist when the neck is rotated back to a neutral position postoperatively. If the patient is younger than 35 years of age and does not have atherosclerosis, the cause of vertebral artery occlusion is usually trauma (subluxation injury), myofibrillar dysplasia, or intentional ligation (Blalock-Taussig procedure). These patients usually have collateral branches to the distal vertebral artery established by the patent internal and external carotid artery branches (occipital artery), but these collateral branches are very thin and do not provide sufficient blood to the basilar artery. In this case, if the occipital artery is large enough, it can be anastomosed directly to the distal vertebral artery. This approach can also be used in patients who do not have a suitable saphenous vein. If the patient is at risk for atherosclerosis, it should be ensured that there is no stenosis at the origin of the external carotid artery. Other methods of reconstructing the distal vertebral artery are to anastomose the graft vein to the distal internal carotid artery below the level of the C1 transverse process. This technique is particularly suitable for patients who do not have a suitable saphenous vein and in whom the external carotid artery cannot be utilized because of anatomic malposition or lesions at the carotid bifurcation. This is the most direct end-lateral anastomosis between the distal vertebral artery and the distal internal carotid artery. However, it is contraindicated in patients with occlusion of the contralateral internal carotid artery. A small percentage of patients have lesions above the C1 level that require reconstruction of the last extracranial portion of the vertebral artery. In order to achieve it, the vertebral artery must be exposed to the atlantoaxial spine, where the artery travels alongside the atlantoaxial pedicle before entering the greater occipital foramen. The distal portion of the suboccipital vertebral artery is reached via a posterior pathway. The patient is placed in a prone position. The incision is racket-shaped and runs from the lateral aspect of the horizontal portion of the midline below the occiput to the sternocleidomastoid muscle, with the incision running diagonally and along the posterior ventral aspect of the sternocleidomastoid muscle. The superficial layers of the dorsal cervical muscles (cephalicus and semispinalis) are cut. The paraspinal nerve below the sternocleidomastoid muscle is freed to the lateral side. The C1 transverse process is localized by palpation. The short posterior muscles between the atlantoaxial and occipital bones (the posterior main part of the cephalic oblique and rectus muscles) are dissected. The artery is encircled by a dense venous plexus, which is freed by bipolar electrocoagulation and microligation of the vein. The arteries are visualized from the beginning of the vertebral artery above C1 to the dural location. From the same posterior approach, the internal carotid artery is freed posteriorly and medially from the sternocleidomastoid muscle after distraction of the subglottis and vagus nerve. The distal anastomosis of the vein graft is completed first, and the graft can be extended over the atlantoaxial pedicle and into the anastomosis of the posterior wall of the internal carotid artery. IV. Outcomes and complications 4.1. Proximal vertebral artery reconstruction For patients undergoing proximal vertebral artery reconstruction, the incidence of death and stroke is low (less than 1%). When proximal vertebral artery reconstruction is combined with carotid surgery, the rate of death and stroke increases to 5.7%, a condition that can be partially attributed to their extensive arterial lesions. The proximal vertebral artery reconstruction patients reported in the literature have a better prognosis than those with carotid artery reconstruction because some of them are due to external compression of the vertebral artery stenosis, and these patients are young and do not have cardiovascular disease. When performing venous bypass between the vertebral artery and the common carotid artery, it is important to avoid torsion of the graft vein leading to thrombosis in the short postoperative period. Adequate attention is given to the protection of the sympathetic trunk to avoid the development of Horner's syndrome. Lymphatic leak is also a common early complication. It is important to avoid penetrating sutures and to carefully ligate the thoracic duct and other geniculate branches to eliminate this complication. 4.2. Distal vertebral artery reconstruction Distal vertebral artery reconstruction has a higher incidence of stroke and death than proximal vertebral artery reconstruction. mark DM reported 7 strokes and 5 deaths in 141 patients undergoing distal vertebral artery reconstruction. Of these, three had brainstem strokes and died, and two died from massive cerebral infarction. Intraoperative and postoperative arteriography is recommended. mark DM reported 3 strokes or deaths (4.5%) and 11% immediate postoperative thrombosis in 53 patients who did not have routine intraoperative and postoperative arteriography. In 88 distal vertebral artery reconstructions with routine intraoperative arteriography, only 1 stroke (1.1%) and 1 postoperative thrombosis occurred. Although improved outcomes may reflect a learning curve, intraoperative arteriography does correct for complications resulting from technical deficiencies. the cumulative opening rate of 80% for distal vertebral artery reconstruction reported by Mark DM is the same as for patients undergoing standard carotid endarterectomy. 70% of patients undergoing distal vertebral artery reconstruction died at 5-year follow-up, mostly due to cardiac lesions. Stroke did not occur in 97% of the survivors. Of these patients, 71% had complete remission and 16% had improvement. In conclusion, the mortality rate for reconstruction of the proximal portion of the vertebral artery is extremely low, and the chance of stroke or death in the distal portion is less than 1.1 percent. Vertebral artery reconstruction has significant effect on preventing posterior cerebral stroke. V. Interventional treatment 5.1. Indications There is no consensus on the indications for stenting of vertebral artery stenosis. Because the basilar artery is mostly formed by the confluence of two vertebral arteries, many patients do not have symptoms of posterior circulation ischemia even if one vertebral artery is completely occluded, so the indications for intervention of vertebral artery stenosis should be strictly controlled. The following indications are recommended: (1) bilateral vertebral artery stenosis exceeding 70%; (2) one vertebral artery stenosis exceeding 70% and contralateral vertebral artery hypoplasia or occlusion; (3) unilateral vertebral artery stenosis causing arterial-arterial embolism; (4) symptomatic dominant vertebral artery stenosis. 5.2. Related techniques The transfemoral route is usually used. If the vertebral artery is poorly positioned or narrowly angled proximally to the subclavian artery, the route may be via the flexural or well artery. It is important to maintain systemic heparinization. The muscular layer at the beginning of the vertebral artery is well developed, and vascular retraction is evident after simple balloon dilation. Plaque in the subclavian artery is often involved in constituting stenosis at the beginning of the vertebral artery, so for stenosis at the beginning of the vertebral artery, the proximal end of the stent can be left 2 to 3 mm in the subclavian artery, and the distal end should reach the relatively normal vessel wall 3 to 5 mm distal to the lesion. Ball expansion stents are used more often in clinical practice because of their stronger radial force and smaller profile. When the vertebral artery diameter is >5.5 mm, self-expanding stents can be used. Because the plaque surface of vertebral artery stenosis is often smooth, there is less ulceration and bleeding within the plaque. At the same time, the vertebral artery is thin and tortuous, often at an angle to the subclavian artery, so there is less experience with the use of distal cerebral protection devices. However, in some special cases or when the situation at the beginning of the vertebral artery permits, cerebral protection devices can be used. Stenting techniques and microspring-ring embolization are feasible for vertebral artery entrapment aneurysms. Phase II spring-ring embolization can greatly reduce stent displacement due to phase I spring-ring embolization. Coronary stenting is more desirable, but the proximal and distal ends of the coronary stent are not well defined under fluoroscopy, so special care should be taken during release to ensure that the stent length completely spans the full length of the entrapped aneurysm. 5.3. Recent outcomes and complications of interventional treatment There are few reports of vertebral artery stenting and a lack of randomized controlled outcomes. 313 patients were summarized by Eberhardt et al. The technical success rate was 99.0%, the perioperative stroke rate was 1.3%, the TIA rate was 1.6%, and the overall mortality rate was 0.3%. At a mean follow-up of 14.2 months, the incidence of posterior circulation TIA was 9.5% and the incidence of posterior circulation stroke was 0.7%. Overall, the vertebral artery intervention technique has a high success rate, fewer complications, and good near-term outcomes. The problem of high restenosis rate is expected to be solved gradually with the improvement of stent performance.