Vertebral Artery Atherothrombosis

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The most common disease affecting the vertebral artery is atherosclerosis. Less commonly, the extracranial vertebral arteries can be affected by pathologic processes including trauma, fibromuscular dysplasia, Takayasu disease, osteophyte compression, dissections, and aneurysms. True extracranial aneurysms are virtually always found in the setting of a connective tissue disorder (CTD) whereas false aneurysms may or may not be related to a CTD but usually follow arterial dissection.

Crawford and coworkers first described the technique of trans-subclavian endarterectomy of the vertebral artery. ^[1] Transposition of the proximal vertebral artery to the common carotid was described by Clark and Perry in 1966 through a similar approach. ^[2] During the 1970s, the saphenous vein was first used to bypass vertebral artery origin stenoses. ^[3] Eventually, transposition techniques were found to be superior solutions for proximal vertebral disease and have supplanted endarterectomy and bypass as the reconstruction options of choice.

The approach to the distal vertebral artery was first described by Matas and Henry and was used for the treatment of traumatic injury. ^{[4, 5]} During the late 1970s, venous bypass and skull base transposition procedures to revascularize the distal vertebral artery were developed using a similar approach. ^{[6, 7]}

Ischemia affecting the temporo-occipital areas of the cerebral hemispheres or segments of the brain stem and cerebellum characteristically produces bilateral symptoms. The classic symptoms of vertebrobasilar ischemia are dizziness, vertigo, diplopia, perioral numbness, alternating paresthesia, tinnitus, dysphasia, dysarthria, drop attacks, ataxia, and homonymous hemianopsia. Ischemia affecting the temporo-occipital areas of the cerebral hemispheres and segments of the brainstem and cerebellum characteristically produces bilateral symptoms. See the image below.

When patients present with two or more of these symptoms, vertebrobasilar ischemia is likely the cause. Nevertheless, symptoms associated with posterior circulation ischemia are often dismissed as nonspecific findings. Because of the oftentimes vague nature of patient presentation, clinicians may be reluctant to pursue pathologic diagnosis or to recommend treatment for potentially correctable vertebral artery lesions.

Numerous medical conditions may cause or mimic vertebrobasilar ischemia, thus confounding the selection of patients in need of posterior circulation treatment. These include inappropriate use of antihypertensive medications, cardiac arrhythmias, anemia, brain tumors, benign vertiginous states, basilar artery migraine, and postsubarachnoid hemorrhage vasospasm. See the image below.

In general, the ischemic mechanisms can be broken down into those that are hemodynamic and those that are embolic. Hemodynamic symptoms occur as a result of transient “end-organ” (brainstem, cerebellum, and/or occipital lobes) hypoperfusion and can be precipitated by postural changes or transient reduction in cardiac output. Ischemia from hemodynamic mechanisms rarely results in tissue infarction. Symptoms from hemodynamic mechanisms tend to be short lived, repetitive, almost predictable and more of a nuisance than a danger.

For hemodynamic symptoms to occur in direct relation to the vertebrobasilar arteries, significant occlusive pathology must be present in both of the paired vertebral vessels or in the basilar artery. In addition, compensatory contribution from the carotid circulation via the Circle of Willis must be incomplete. Alternatively, hemodynamic ischemic symptoms may follow proximal subclavian artery occlusion and the syndrome of subclavian/vertebral artery steal (subclavian-vertebral steal phenomenon).

In later years of life, vertebral artery stenosis is a common arteriographic finding and dizziness is a common complaint. The presence of both cannot necessarily be assumed to have a cause-effect relationship. Surgical reconstruction is not indicated in an asymptomatic patient with stenotic or occlusive vertebral lesions. These patients are well compensated, usually from the carotid circulation through the circle of Willis.

The minimal anatomic requirement to justify vertebral artery reconstruction for a patient with hemodynamic symptoms is stenosis of more than 60% diameter in both vertebral arteries if both are patent and complete or the same degree of stenosis in the dominant vertebral artery if the opposite vertebral artery is hypoplastic, ends in a posteroinferior cerebellar artery (PICA), or is occluded. A single, normal vertebral artery is sufficient to adequately perfuse the basilar artery, regardless of the patency status of the contralateral vertebral artery.

Embolic causes of vertebrobasilar ischemia may not be as well recognized. As many as one third of vertebrobasilar ischemic episodes are caused by distal embolization from plaques or mural lesions of the subclavian, vertebral, and/or basilar arteries. ^{[8, 6]} Arterial-to-arterial emboli can arise from atherosclerotic lesions, from intimal defects caused by extrinsic compression or repetitive trauma, and rarely from fibromuscular dysplasia, aneurysms, or dissections. Although fewer patients suffer from embolic phenomena when compared with those with hemodynamic ischemia, actual infarctions in the vertebrobasilar distribution are most often the result of embolic events. Patients with embolic ischemia often develop multiple and multifocal infarcts in the brain stem, cerebellum, and, occasionally, posterior cerebral artery territory. Patient presentation is dissimilar to those with hemodynamic symptoms.

Patients who experience emboli have varied presentations. In patients with posterior circulation ischemia secondary to microembolism and appropriate lesions in a vertebral artery, the potential source of the embolus needs to be eliminated regardless of the status of the contralateral vertebral. This cohort is considered candidates for surgical or endoluminal correction of the offending lesion regardless of the condition of the contralateral vertebral artery. With the exception of the patient presenting with a vertebral artery aneurysm, surgical or endovascular intervention is not indicated in asymptomatic patients who harbor suspicious radiographic findings.

Treatable vertebral artery disease may be underdiagnosed in comparison to carotid disease. Patients with vertebrobasilar ischemia do represent a significant cohort of patients. Twenty-five percent of all transient ischemic attacks and ischemic strokes involve areas of the brain supplied by the vertebrobasilar circulation. For patients who experience vertebrobasilar transient ischemic attacks, disease identified in the vertebral arteries portends a 30-35% risk for stroke over a 5-year period. ^{[9, 10, 11]} Medical refractory disease of the vertebrobasilar system carries a 5-11% risk of stroke or death at 1 year. ^[12] Consequently, mortality associated with a posterior circulation stroke is high, ranging from 20-30% and this disease entity should not be ignored. ^{[13, 14, 15, 16]}

Atherosclerosis is the primary etiology, although fibromuscular dysplasia (FMD), dissection, compression, and aneurysms can affect the extracranial vertebral artery.

The most common disease affecting the vertebral artery is atherosclerosis. Less common pathologic processes include trauma, FMD, Takayasu disease, osteophyte compression, dissections, and aneurysms. See the images below.

Once the diagnosis of vertebrobasilar ischemia has been confirmed with appropriate imaging, surgical correction may be considered. The mere presence of vertebral artery stenosis in an asymptomatic patient is rarely an indication for surgery. Surgical reconstruction is based on the specific etiology. The indication for surgery in patients with hemodynamic symptoms depends on the ability to demonstrate insufficient blood flow to the basilar artery.

A single normal-caliber vertebral artery can supply sufficient blood flow into the basilar artery regardless of the status of the contralateral vessel. In this particular subset of patients, surgical intervention is indicated only in the presence of a severely stenotic (>75%) vertebral artery and an equally diseased or occluded contralateral vessel. Surgical reconstruction is not indicated in an asymptomatic patient with the aforementioned radiographic findings because these patients are well compensated from the carotid circulation through the posterior communicating vessels.

In contrast, patients with symptomatic vertebrobasilar ischemia due to emboli are candidates for surgical correction of the offending lesion regardless of the condition of the contralateral vertebral artery. As in the hemodynamic group, surgical intervention is not indicated in asymptomatic patients with suggestive radiographic findings.

The posterior circulation, or vertebrobasilar system, supplies blood to the brainstem, cerebellum, and occipital lobes via paired vertebral arteries. The vertebrals converge beyond the base of the skull and form the basilar artery at the base of the pons. The vertebral artery is arbitrarily segmented into the following 4 parts:

V1: This extends from the origin of the vertebral artery, where it arises from the subclavian artery up to the point at which the artery enters the C6 transverse process. The origin of the vertebral from the subclavian is the most common site for a hemodynamically significant atherosclerotic stenosis.

V2: The segment of the artery within the cervical transverse processes (C6-C2) is buried deep within intertransversarium muscle. The V2 segment is the site of a wide variety of disorders. External compression is most likely to occur in this segment because of osteophytes, the edge of the transverse foramina, or the intervertebral joints. Positional changes, such as rotation or extension of the neck, usually trigger compression of the vertebral artery in this segment. The V2 segment is also the most frequent site of true aneurysmal degeneration, fibromuscular diseases, and embolizing atherosclerotic plaques.

V3: The extracranial segment between the transverse process of the C2 and the base of the skull where the artery enters the foramen magnum and penetrates the dura matter. This segment is infrequently affected by atherosclerosis but is vulnerable to direct trauma and stretch injuries.

V4: The intracranial portion beginning at the atlantooccipital membrane and terminating at the formation of the basilar artery. The V4 segment is devoid of adventitia, as such, open or endovascular interventions in this segment should be approached with extreme caution.

Dissections commonly occur at the base of the skull where V3 transitions to V4. This likely occurs because, here, the vertebrae allow for maximal cervical mobility near where the artery loses some of its integrity.

The anterior spinal artery arises from branches off each of the vertebral arteries just prior to their convergence to form the basilar artery. Pontine and cerebellar arteries arise from the basilar artery before it bifurcates into the paired posterior cerebral arteries. One vertebral artery may end in a posterior inferior cerebellar artery rather than join the basilar artery.

The location of disease will dictate the type of surgical reconstruction that is required. With rare exceptions, most reconstructions of the vertebral artery are performed to treat an origin stenosis (V1 segment) or stenosis, dissection, or occlusion of its intraspinal component (V2 and V3 segments).

As discussed previously, a single normal-caliber vertebral artery can supply sufficient blood flow into the basilar artery regardless of the status of the contralateral vessel. In this particular subset of patients, surgical intervention is indicated only in the presence of a severely stenotic (>75%) vertebral artery and an equally diseased or occluded contralateral vessel. Surgical reconstruction is not indicated in an asymptomatic patient with the aforementioned radiographic findings because these patients are well compensated from the carotid circulation through the posterior communicating vessels.

Patients with symptomatic vertebrobasilar ischemia who are not amenable to surgery or investigational endoluminal therapy may be treated medically with long-term anticoagulation to prevent thrombosis.

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Mark D Morasch, MD, RPVI Vascular Surgeon, Section Head of Vascular and Endovascular Services, Billings Clinic; John Marquardt Clinical Research Professor in Vascular Surgery, Division of Vascular Surgery, Northwestern University, The Feinberg School of Medicine

Mark D Morasch, MD, RPVI is a member of the following medical societies: Society for Vascular Surgery, Western Surgical Association, Southern Association for Vascular Surgery, American Venous Forum, Vascular and Endovascular Surgery Society, Society for Clinical Vascular Surgery, Western Vascular Society, Midwestern Vascular Surgical Society, American College of Surgeons, American Medical Association, American Heart Association, Central Surgical Association, Western Vascular Society, Southern Association for Vascular Surgery

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Ryszard M Pluta, MD, PhD Associate Professor, Neurosurgical Department Medical Research Center, Polish Academy of Sciences, Poland; Clinical Staff Scientist, Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health (NIH); Fishbein Fellow, JAMA

Ryszard M Pluta, MD, PhD is a member of the following medical societies: Polish Society of Neurosurgeons, Congress of Neurological Surgeons

Disclosure: Nothing to disclose.

Brian H Kopell, MD Associate Professor, Department of Neurosurgery, Icahn School of Medicine at Mount Sinai

Brian H Kopell, MD is a member of the following medical societies: Alpha Omega Alpha, American Association of Neurological Surgeons, American Society for Stereotactic and Functional Neurosurgery, Congress of Neurological Surgeons, International Parkinson and Movement Disorder Society, North American Neuromodulation Society

Disclosure: Received consulting fee from Medtronic for consulting; Received consulting fee from Abbott Neuromodulation for consulting.

Michael G Nosko, MD, PhD Associate Professor of Surgery, Chief, Division of Neurosurgery, Medical Director, Neuroscience Unit, Medical Director, Neurosurgical Intensive Care Unit, Director, Neurovascular Surgery, Rutgers Robert Wood Johnson Medical School

Michael G Nosko, MD, PhD is a member of the following medical societies: Academy of Medicine of New Jersey, Congress of Neurological Surgeons, Canadian Neurological Sciences Federation, Alpha Omega Alpha, American Association of Neurological Surgeons, American College of Surgeons, American Heart Association, American Medical Association, New York Academy of Sciences, Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Vertebral Artery Atherothrombosis

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