Vertebrobasilar insufficiency

The history and presentation of this patient who may present to a neurotology or otolaryngology clinic should alert the clinician to the possibility of vertebrobasilar ischemia, or cerebrovascular disease. Reasons for a heightened suspicion include (1) spontaneous vertigo spells that last a few minutes in duration (2) accompanying focal neurological symptoms including numbness and visual disturbance (3) risk factors of age, hyperlipidemia, hypertension, cardiovascular disease, and tobacco abuse. The recent worsening of symptoms should trigger an expedited workup, referral to experts in cerebrovascular disease, and in some cases such as transient ischemic attacks within the last 72 hours, hospitalization is warranted. In this review, the first section addresses the anatomy and vascular supply of the posterior cerebral circulation and inner ear, with particular attention to major branches and labyrinthine circulation. Topics addressed include the causes of cerebrovascular/vertebrobasilar ischemia and infarcts related to symptoms of vertigo and dizziness. The natural history of posterior circulation ischemic attacks and strokes is discussed. Particular stroke syndromes and their presentation are described in detail. The common presentation to the neurotologist of vertebrobasilar infarct or ischemia is discussed, as well as ways to identify and evaluate the patient at risk for stroke. Critical components and key questions of the clinical examination are addressed, and guidelines for direction of evaluation are presented. Lastly, the relationship between migraine, migrainous stroke, and migraine-related stroke are discussed.

Brief summary of the anatomy of the posterior circulation

The vertebrobasilar vascular system feeds the posterior region of the brain, which includes the brainstem, cerebellum, and inner ear. The vertebrobasilar system represents about 20% of cerebral blood flow. When vertigo is the presenting symptom of a transient ischemic attack or cerebrovascular stroke, the cerebrovascular region involved is the vertebrobasilar system. Ischemic attacks in the anterior circulation, that is, carotid system, may present with lightheadedness, but will not present with rotational vertigo. Vertigo can result from ischemia of the inner ear, brainstem, or cerebellar structures served by the posterior circulation. Posterior circulation transient ischemic attacks (TIAs) and strokes represent about 20% of all TIAs and strokes.

The vertebral arteries originate from the subclavian arteries, which branch from the thoracic aorta. The two vertebral arteries are only rarely the same size, and in 72% of subjects in an anatomic study, one vertebral artery is at least double the size of the other. The vertebral artery is designated into 4 sections: V1, which includes the origin and is the extracranial prevertebral portion; V2, which is the extracranial foraminal or cervical artery; V3, which is the extracranial postforaminal artery at the atlanto-axial region; and V4, which is the intracranial artery and includes the junction with the basilar artery. The most common sites of stenosis are at V1 and V4, particularly at the origin of the vertebral artery as it comes off of the subclavian, and at the vertebrobasilar junction.

The posteroinferior cerebellar artery (PICA) is the largest branch of the vertebral artery. It generally originates 1 to 2 cm below the basilar artery, but in angiograms has been shown to sometimes originate below the level of the foramen magnum. PICAs supply the lateral medulla including the vestibular nuclei and the posteroinferior cerebellum. The two vertebral arteries merge to form the midline basilar artery, which courses along the ventral surface of the pons. The basilar artery gives off penetrating median, paramedian, and short circumferential branches.

The largest circumferential branches are the anterior inferior cerebellar arteries (AICAs), which arise from the proximal third of the basilar artery. In addition to supplying the labyrinth, AICAs supply the lateral pontine tegmentum, brachium pontis, flocculus, and part of the anterior cerebellum. An AICA infarct typically involves the middle cerebellar peduncle. There is often a close relationship between the PICA and ipsilateral AICA; if one PICA is hypoplastic, the ipsilateral AICA may be large, and the contralateral PICA small.

The vascular anatomy of the inner ear has been studied in multiple species. The inner ear consists of the auditory and vestibular end organs for hearing and balance, respectively. The vestibular labyrinth is composed of the 3 semicircular canals (SCCs) and 2 otolith organs, the saccule and utricle. The vestibular end organs are involved in sensing head movement and position; the cristae ampullares sense angular acceleration. The cristae ampullares contain vestibular hair cells that act as mechanoelectrical receptors, transducing the mechanical bending of the stereocilia bundle to an electrical transduction current. Inner ear vascular supply is provided by the internal auditory artery (also known as the labyrinthine artery), arising most commonly as a branch of the ipsilateral AICA. Within the internal auditory canal, the internal auditory artery branches into two arteries:

• 1.
  

  The common cochlear artery, which feeds most of the cochlea, and a branch, the posterior vestibular artery, which feeds the inferior saccule and posterior SCC

  
  
• 2.
  

  The anterior vestibular branch, which feeds the horizontal and anterior SCC, utricle, and a small portion of the saccule.

The labyrinthine arteries are end-arteries; they do not anastomose with other major arterial branches. Therefore, if blood flow is interrupted for as little as 15 seconds, the auditory nerve fibers become unexcitable. By contrast, there are richer anastomoses in the brainstem and overlying territories in the cerebellum, and thus the inner ear appears to be more vulnerable to interruption of blood flow than the brainstem or cerebellum.

Age-related atrophy of inner ear structures may be secondary to relative ischemia, that is, microvascular ischemia, a well-studied phenomenon in human temporal bone studies. There is a significant (11.7%) loss of spiral ligamental volume and a 32% loss of stria vascularis volume in subjects older than 60 years compared with those younger than 40 years. In the aging Fisher rat, there is a significant age-related 75% decrease in blood flow in the capillaries of the posterior crista. Cells in the inner ear, especially strial marginal cells and the auditory and vestibular hair cells, may be exceptionally vulnerable to ischemia because of the high volume density of mitochondria, which is associated with high energy demand.

Before dividing into the two posterior cerebral arteries (PCAs), the basilar artery gives off the superior cerebellar arteries (SCAs). The cerebellum is fed by the AICAs, PICAs, and SCAs with prominent anastomoses between these arterial arcades on the cerebellar surface. These arteries feed areas of the brainstem related to wakefulness and consciousness, and there is a high degree of collateralization in this critical area. By contrast, there is little significant collateralization within the inner ear. This fact may explain why vertebrobasilar insufficiency can present with isolated labyrinthine infarctions and cochlear hearing loss.

The cause of vertebrobasilar insufficiency or ischemia (VBI) is usually atherosclerotic disease of the subclavian, vertebral, or basilar arteries. However, clinicians should realize that it has been estimated that 1 in 5 posterior circulation infarcts is cardioembolic, and another 1 out of 5 occurs from intra-arterial emboli from extracranial and intracranial vertebral arteries. Emboli will travel to the distal arterial branches, often causing isolated cerebellar infarction in the distribution of the superior cerebellar artery, AICA, or PICA. Therefore, patients with isolated cerebellar infarctions should be evaluated for an embolic source. The evaluation should include looking for a cardiac source of emboli, and assessment of the intracranial and extracranial vertebrobasilar arteries, including the origin of the vertebral artery. There may be a tendency for cardiac catheterization embolic events to involve the posterior vertebrobasilar system.

The extracranial vertebral arteries are also susceptible to dissection, which refers to a tear in the arteries, involving the medial coat. Sudden neck movements such as neck manipulations, or trivial motions such as bending the neck back to take medications, can be the inciting event. There is a predilection for development of atherosclerotic plaques at sites with turbulent flow, such as bifurcation points and at the origin of arteries.

By contrast, dissections usually occur in portions of extracranial arteries that are mobile rather than at the origins of arteries, for example, at the distal extracranial vertebral artery V3. The extracranial and intracranial vertebrobasilar system is well visualized using present-day noninvasive imaging modalities. There are heritable disorders of connective tissue disease, such as Ehlers Danlos type IV associated with arterial dissection, which can occur in multiple sites ; however, transient emboli often are not seen, and very small infarcts in communicating areas may not be seen on magnetic resonance imaging (MRI). Therefore, the diagnosis of a posterior circulation TIA or stroke is sometimes made on a clinical basis.

Brief summary of the anatomy of the posterior circulation

The vertebrobasilar vascular system feeds the posterior region of the brain, which includes the brainstem, cerebellum, and inner ear. The vertebrobasilar system represents about 20% of cerebral blood flow. When vertigo is the presenting symptom of a transient ischemic attack or cerebrovascular stroke, the cerebrovascular region involved is the vertebrobasilar system. Ischemic attacks in the anterior circulation, that is, carotid system, may present with lightheadedness, but will not present with rotational vertigo. Vertigo can result from ischemia of the inner ear, brainstem, or cerebellar structures served by the posterior circulation. Posterior circulation transient ischemic attacks (TIAs) and strokes represent about 20% of all TIAs and strokes.

The vertebral arteries originate from the subclavian arteries, which branch from the thoracic aorta. The two vertebral arteries are only rarely the same size, and in 72% of subjects in an anatomic study, one vertebral artery is at least double the size of the other. The vertebral artery is designated into 4 sections: V1, which includes the origin and is the extracranial prevertebral portion; V2, which is the extracranial foraminal or cervical artery; V3, which is the extracranial postforaminal artery at the atlanto-axial region; and V4, which is the intracranial artery and includes the junction with the basilar artery. The most common sites of stenosis are at V1 and V4, particularly at the origin of the vertebral artery as it comes off of the subclavian, and at the vertebrobasilar junction.

The posteroinferior cerebellar artery (PICA) is the largest branch of the vertebral artery. It generally originates 1 to 2 cm below the basilar artery, but in angiograms has been shown to sometimes originate below the level of the foramen magnum. PICAs supply the lateral medulla including the vestibular nuclei and the posteroinferior cerebellum. The two vertebral arteries merge to form the midline basilar artery, which courses along the ventral surface of the pons. The basilar artery gives off penetrating median, paramedian, and short circumferential branches.

The largest circumferential branches are the anterior inferior cerebellar arteries (AICAs), which arise from the proximal third of the basilar artery. In addition to supplying the labyrinth, AICAs supply the lateral pontine tegmentum, brachium pontis, flocculus, and part of the anterior cerebellum. An AICA infarct typically involves the middle cerebellar peduncle. There is often a close relationship between the PICA and ipsilateral AICA; if one PICA is hypoplastic, the ipsilateral AICA may be large, and the contralateral PICA small.

The vascular anatomy of the inner ear has been studied in multiple species. The inner ear consists of the auditory and vestibular end organs for hearing and balance, respectively. The vestibular labyrinth is composed of the 3 semicircular canals (SCCs) and 2 otolith organs, the saccule and utricle. The vestibular end organs are involved in sensing head movement and position; the cristae ampullares sense angular acceleration. The cristae ampullares contain vestibular hair cells that act as mechanoelectrical receptors, transducing the mechanical bending of the stereocilia bundle to an electrical transduction current. Inner ear vascular supply is provided by the internal auditory artery (also known as the labyrinthine artery), arising most commonly as a branch of the ipsilateral AICA. Within the internal auditory canal, the internal auditory artery branches into two arteries:

• 1.
  

  The common cochlear artery, which feeds most of the cochlea, and a branch, the posterior vestibular artery, which feeds the inferior saccule and posterior SCC

  
  
• 2.
  

  The anterior vestibular branch, which feeds the horizontal and anterior SCC, utricle, and a small portion of the saccule.

The labyrinthine arteries are end-arteries; they do not anastomose with other major arterial branches. Therefore, if blood flow is interrupted for as little as 15 seconds, the auditory nerve fibers become unexcitable. By contrast, there are richer anastomoses in the brainstem and overlying territories in the cerebellum, and thus the inner ear appears to be more vulnerable to interruption of blood flow than the brainstem or cerebellum.

Age-related atrophy of inner ear structures may be secondary to relative ischemia, that is, microvascular ischemia, a well-studied phenomenon in human temporal bone studies. There is a significant (11.7%) loss of spiral ligamental volume and a 32% loss of stria vascularis volume in subjects older than 60 years compared with those younger than 40 years. In the aging Fisher rat, there is a significant age-related 75% decrease in blood flow in the capillaries of the posterior crista. Cells in the inner ear, especially strial marginal cells and the auditory and vestibular hair cells, may be exceptionally vulnerable to ischemia because of the high volume density of mitochondria, which is associated with high energy demand.

Before dividing into the two posterior cerebral arteries (PCAs), the basilar artery gives off the superior cerebellar arteries (SCAs). The cerebellum is fed by the AICAs, PICAs, and SCAs with prominent anastomoses between these arterial arcades on the cerebellar surface. These arteries feed areas of the brainstem related to wakefulness and consciousness, and there is a high degree of collateralization in this critical area. By contrast, there is little significant collateralization within the inner ear. This fact may explain why vertebrobasilar insufficiency can present with isolated labyrinthine infarctions and cochlear hearing loss.

The cause of vertebrobasilar insufficiency or ischemia (VBI) is usually atherosclerotic disease of the subclavian, vertebral, or basilar arteries. However, clinicians should realize that it has been estimated that 1 in 5 posterior circulation infarcts is cardioembolic, and another 1 out of 5 occurs from intra-arterial emboli from extracranial and intracranial vertebral arteries. Emboli will travel to the distal arterial branches, often causing isolated cerebellar infarction in the distribution of the superior cerebellar artery, AICA, or PICA. Therefore, patients with isolated cerebellar infarctions should be evaluated for an embolic source. The evaluation should include looking for a cardiac source of emboli, and assessment of the intracranial and extracranial vertebrobasilar arteries, including the origin of the vertebral artery. There may be a tendency for cardiac catheterization embolic events to involve the posterior vertebrobasilar system.

The extracranial vertebral arteries are also susceptible to dissection, which refers to a tear in the arteries, involving the medial coat. Sudden neck movements such as neck manipulations, or trivial motions such as bending the neck back to take medications, can be the inciting event. There is a predilection for development of atherosclerotic plaques at sites with turbulent flow, such as bifurcation points and at the origin of arteries.

By contrast, dissections usually occur in portions of extracranial arteries that are mobile rather than at the origins of arteries, for example, at the distal extracranial vertebral artery V3. The extracranial and intracranial vertebrobasilar system is well visualized using present-day noninvasive imaging modalities. There are heritable disorders of connective tissue disease, such as Ehlers Danlos type IV associated with arterial dissection, which can occur in multiple sites ; however, transient emboli often are not seen, and very small infarcts in communicating areas may not be seen on magnetic resonance imaging (MRI). Therefore, the diagnosis of a posterior circulation TIA or stroke is sometimes made on a clinical basis.

The posterior circulation: mechanisms of stroke and transient ischemic attacks

A large study of 407 consecutive patients with posterior circulation events, of whom 59% had strokes without TIA, 24% had TIAs then strokes, and 16% had only TIAs, demonstrated that embolism was the most common stroke mechanism. A total of 40% of patients suffered embolic stroke, of whom 24% were cardiac, 14% intra-arterial, and 2% were combined cardiac and intra-arterial. In 32%, large artery atherosclerotic occlusive disease caused hemodynamic vertebrobasilar ischemia. Distal infarcts, that is, those within the PCA, SCA, and top of the basilar artery, had a high likelihood of cardiac or artery-to-artery embolism. Areas that commonly demonstrated stenosis (>50%) included the origin of the vertebral artery in 131 (32.2%), intracranial vertebral artery in 132 (32.4%), basilar artery in 109 (26.8%), and PCA in 38 (9.3%). Many patients (14%) had penetrating and branch artery disease, meaning disease of the branch artery without disease of the parent artery. Most PCA infarcts were embolic. Patients with cardiac emboli had a poorer prognosis than patients with other stroke mechanisms. Consistent with prior studies, lateral medullary strokes were most often caused by atherosclerotic vertebral artery disease (see later discussion on PICA territory infarcts). Hypertension was present in 61% and cardiac disease comorbidity was common (64% of those evaluated with thorough cardiac studies). For the neurotologist, the patient with cardiac emboli as the origin of posterior circulation stroke is not likely to present to the outpatient clinic, and more likely would present to the emergency department. However, of relevance to the physician called on to see a patient with acute vertigo in the emergency room, key differences that distinguish the cerebellar stroke may be the nystagmus (often gaze-evoked, direction changing) and subtle cerebellar signs such as eye movement abnormalities.

Dizziness, vertigo, and vertebrobasilar ischemia

The clinician must evaluate the category of dizziness when a patient complains of dizziness. Global cerebral hypoperfusion is likely to present with a sense of lightheadedness and an impending fainting sensation. Presyncopal lightheadedness is somewhat nonspecific and may arise from cardiac arrhythmias, orthostatic hypotension, or vasovagal reactions. In presyncopal lightheadedness, there is no sense of movement of the external environment. By contrast, vertigo, the sensation of movement of the environment, often in a rotational manner, is a common presentation of vertebrobasilar insufficiency. In the case of posterior circulation ischemia, the onset of vertigo is usually abrupt and spontaneous rather than position-induced, and there may be a flurry of spells within a few weeks’ time. Vertebrobasilar ischemia is a common cause of vertigo in the aging population. Therefore, it is critical to distinguish whether the dizziness is vertigo or lightheadedness.

Important questions to ask the patient:

• 
  

  “Do you feel as if you are about to pass out?” This would be consistent with global hypoperfusion.

  
  
• 
  

  “If you are seated still when the dizziness occurs, do you feel as if the world is moving?” This would be consistent with true vertigo.

  
  
• 
  

  “How long is the actual vertigo spell, and is the onset abrupt or gradual?”

  
  
• 
  

  “How often do the spells occur, and is the frequency of the spells increasing?”

  
  
• 
  

  “Are the spells provoked by positional changes of the head?” This may indicate benign paroxysmal positional vertigo (BPPV), but any vertigo can be associated with sensitivity to head movement.

  
  
• 
  

  “Are there accompanying otological signs with the spells of vertigo, such as aural fullness, hearing loss, or tinnitus?” These may indicate Ménière’s disease but can also be seen in basilar migraine and TIAs in the AICA distribution.

  
  
• 
  

  “Are there accompanying focal neurologic signs with the spells of vertigo, or in isolation?” ( Box 1 ). These would indicate vertebrobasilar TIAs.

  
  
  
  

  Box 1

  
  

  
  

  
  

  
  
  • 
    

    Have you experienced any of the following symptoms? Please check yes or no and indicate if constant or in episodes.

    
    
    
    
    • 1.
      

      Double vision, blurred vision, or blindness

      
      
    • 2.
      

      Numbness of the face or extremities

      
      
    • 3.
      

      Weakness in arms or legs

      
      
    • 4.
      

      Clumsiness in arms or legs

      
      
    • 5.
      

      Confusion or loss of consciousness

      
      
    • 6.
      

      Difficulty with speech

      
      
    • 7.
      

      Difficulty swallowing

      
      
    • 8.
      

      Pain in neck or shoulder

    
    

  
  

  
  

  Neurologic review of systems
  
  
  
  
• 
  

  “Is it followed by a headache?” Note that this does not necessarily indicate migraine vertigo, because strokes, TIAs, dissections, and seizures are often characterized by headache.

  
  
• 
  

  “Is there a personal history of hypertension, hyperlipidemia, diabetes mellitus, cancer, coronary artery disease, peripheral vascular disease, migraines with aura or complicated migraine, strokes or TIAs in the past?”

  
  
• 
  

  “Is there a family history of the above risk factors, as well as hearing loss, dizziness, connective tissue diseases, or migraines?”

The importance of the neurologic examination and of imaging evaluations of the vertebrobasilar system

Any patient presenting with vertigo or hearing loss should be evaluated for focal neurologic signs that localize to the brainstem. In addition, patients should be asked if they suffer from spells that would be consistent with vertebrobasilar ischemia. The authors typically include in the patient questionnaire a neurologic review of systems that localizes to the posterior circulation (see Box 1 ).

On examination, the patient presenting with vertigo or hearing loss should be evaluated for:

• 1.
  

  Facial weakness (which in AICA and PICA infarcts can be peripheral or central)

  
  
• 2.
  

  Facial sensory loss: this can be tested using a cold tuning fork, pinprick, or testing the corneal reflex with a cotton tip

  
  
• 3.
  

  Eye movement abnormalities including skew deviation, diplopia, and nystagmus, because gaze-evoked nystagmus or down-beat nystagmus is typical in cerebellar infarct

  
  
• 4.
  

  The visual fields, as most PCA infarcts will exhibit a visual field cut

  
  
• 5.
  

  Crossed sensory loss, a key indicator for brainstem involvement, commonly seen as loss of facial sensation on the ipsilateral side, and loss of extremity sensation on the contralateral side

  
  
• 6.
  

  Horner syndrome, tested in darkness for an ipsilateral smaller pupil, because the anisocoria or asymmetry will be accentuated in darkness. Horner syndrome occurs when there is loss of sympathetic outflow. The sympathetic system is responsible for pupillary dilation and thus there is a miosis, or pupillary constriction in the ipsilateral pupil.

  
  
• 7.
  

  Limb ataxia, testing for cerebellar ataxia with finger-to-nose, finger-to-finger, and heel-to-shin movements

  
  
• 8.
  

  Gait ataxia, which will generally be exhibited by a wide-based gait or inability to walk

  
  
• 9.
  

  Head-thrust test, which can reveal catch-up saccades in purely peripheral disorders such as vestibular neuritis or gentamicin ototoxicity. However, it is also important to note that in cases of AICA infarct, the head-thrust test will demonstrate catch-up saccades in many cases.

Symptoms that may localize to a PICA infarct should be queried including hiccoughs, inability to swallow, facial sensory and motor loss, and limb ataxia. Hearing always should be tested at bedside in patients with vertigo, and when suspicious, a full diagnostic audiogram with or without auditory brainstem responses should be requested.

The role of imaging

An important clinical point to be made is that in patients with large artery atherosclerosis as an etiologic mechanism of TIA are prone to recurrence or early progression to stroke. In a large study of all consecutive cerebrovascular events (strokes and TIAs), events in the posterior (vertebrobasilar) circulation were more likely to be associated with significant stenosis (26.2%) than those in the anterior (carotid) circulation (11.5%). Therefore, imaging studies in this group of patients with posterior circulation events would be high yield. Furthermore, patients with vertebrobasilar TIAs secondary to atherosclerosis are even more likely to suffer early recurrence of a vascular event or progress to a stroke than patients with symptomatic carotid stenosis. Therefore, the possibility of vertebrobasilar TIA should be assessed with a stroke protocol MRI that includes assessment of the intracranial and extracranial anterior and posterior cerebrovasculature. In the past, the only way to assess posterior circulation accurately was to undertake a cerebral angiogram, an invasive procedure with risks.

Fortunately, there are now noninvasive means of imaging the posterior circulation using contrast-enhanced magnetic resonance angiography (MRA) and computed tomographic angiography (CTA). Contrast-enhanced MRA (CE-MRA) has good sensitivity and specificity for the detection of 50% to 99% vertebral or basilar stenosis, better than CTA, ultrasonography, and/or time-of-flight MRA. The CE-MRA should image the great vessels from the aortic arch to the circle of Willis. In a large study of patients presenting with posterior events, 39 patients had both CE-MRA and CTA, with corroborating results in 35 patients. In only 4 cases out of 186 was it necessary to conduct intra-arterial subtraction angiography. Previously it was necessary to conduct traditional angiography to evaluate the V1 segment, in particular the origin or take-off of the vertebral artery, as noncontrast MRA is not able to visualize the origin of the vertebral artery well. With the advent of CE-MRA and CTA, noninvasive means of visualizing this area are possible. In a large British study of consecutive patients with vertebrobasilar ischemia (N = 186), 39 patients (21%) were found to have stenosis. The V1 and V4 areas were the most common sites of stenosis (42.9% and 34.7%, respectively); of those in the V1 area, 12 of the 39 (31%) were at the origin of the vertebral, the most common single site of stenosis of the vertebral artery.

In patients presenting with symptoms attributable to the posterior circulation, a vertebral artery dissection may also be the cause. In the study by Gulli and colleagues, 8 of 216 consecutive patients with posterior circulation cerebrovascular events occurred secondary to vertebral artery dissection. With current modern techniques, vertebral dissections can also be evaluated using noninvasive imaging, CE-MRA, or CTA.

Acute vertebrobasilar occlusion: interventions are possible and in severe cases must be timely

Acute vertebrobasilar occlusion occurs when there is an occlusive or complete blockage of the basilar artery. This entity carries an extremely high morbidity and mortality. In young patients, the cause can be cardiac emboli or progression from vertebral dissection. Dissections may occur with neck trauma, such as in car accidents with whiplash, cervical neck manipulations, or spontaneously with a higher incidence in migraineurs. Local atherothrombosis is more common in elderly patients. Early percutaneous treatment is associated with an improved outcome, with best results observed within a 4-hour interval and a recommended time period of less than 6 hours, although even with recanalization the mortality rate is between 35% and 75%. Without intervention, mortality rates are as high as 80% to 90%.

Percutaneous interventions for vertebral artery stenosis are now possible. Noninvasive testing can identify vertebral artery stenosis, including Doppler studies identifying reversed vertebral artery blood flow. Endovascular treatment using coronary wires and drug-eluting stents have proved successful for vertebrobasilar stenosis in endovascular centers. One study reported that drug-eluting stents may decrease the incidence of restenosis when compared with non–drug-eluting stents for treatment of vertebral artery origin (V1) stenosis.