11/27/2014

Vertebral Artery Atherothrombosis

Vertebral Artery Atherothrombosis

Author: Mark D Morasch, MD; Chief Editor: Allen R Wyler, MD more...
Updated: Dec 3, 2013

Background
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.

History Of The Procedure

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]

Problem
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.

Symptoms of vertebrobasilar ischemia.

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.

Nonischemic conditions that may mimic vertebrobasilar ischemia.

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.

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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.

Epidemiology
Frequency
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]

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

Pathophysiology
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.

Selective angiogram of a right vertebral artery pseudoaneurysm.

An arteriogram demonstrating aneurysmal degeneration of a left vertebral artery in the V2 segment.

True vertebral artery aneurysm (9 cm).

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Indications
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.

Relevant Anatomy
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).

Contraindications
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.

Contributor Information and Disclosures

Author
Mark D Morasch, MD Vascular Surgeon, St Vincent's Healthcare Heart and Vascular Center; Professor of
Surgery, Division of Vascular Surgery, John Marquardt Clinical Research Professor in Vascular Surgery,
Northwestern University, The Feinberg School of Medicine
Mark D Morasch, MD is a member of the following medical societies: American College of Surgeons, American
Heart Association, American Medical Association, American Venous Forum, Central Surgical Association,
Midwest Vascular Society, Peripheral Vascular Surgery Society, Society for Clinical Vascular Surgery, Society
for Vascular Surgery, Southern Association for Vascular Surgery, Western Surgical Association, and Western
Vascular Surgical Society
Disclosure: W.L. Gore & Associates Consulting fee Review panel membership
Specialty Editor Board
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, University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School
Michael G Nosko, MD, PhD is a member of the following medical societies: Academy of Medicine of New
Jersey, Alpha Omega Alpha, American Association of Neurological Surgeons, American College of Surgeons,
American Heart Association, American Medical Association, Canadian Congress of Neurological Sciences,
Congress of Neurological Surgeons, New York Academy of Sciences, and Society of Critical Care Medicine

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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: Medscape Salary Employment
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: Congress of Neurological Surgeons
and Polish Society of Neurosurgeons
Disclosure: Nothing to disclose.
Paolo Zamboni, MD Professor of Surgery, Chief of Day Surgery Unit, Chair of Vascular Diseases Center,
University of Ferrara, Italy
Paolo Zamboni, MD is a member of the following medical societies: American Venous Forum and New York
Academy of Sciences
Disclosure: Nothing to disclose.
Chief Editor
Allen R Wyler, MD Former Medical Director, Northstar Neuroscience, Inc
Allen R Wyler, MD is a member of the following medical societies: American Academy of Neurological and
Orthopaedic Surgeons, American Association of Neurological Surgeons, and Society of Neurological Surgeons
Disclosure: Nothing to disclose.

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