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Vertebral Artery Atherothrombosis Workup

  • Author: Mark D Morasch, MD, RPVI; Chief Editor: Brian H Kopell, MD  more...
Updated: Jan 16, 2016

Imaging Studies

A precise diagnosis of vertebrobasilar ischemia begins with an accurate assessment of the presenting symptom complex. This must be followed by efforts to exclude other causes for patient symptoms. These other medical conditions include inappropriate use of antihypertensive medications, cardiac arrhythmias, anemia, brain tumors, and benign vertiginous states. A thorough investigation generally includes work up for inner ear pathology, and ruling out cardiac arrhythmias, internal carotid artery stenosis/occlusion, and the inappropriate use of medications as causes.

Any systemic mechanism that decreases the mean pressure of the basilar artery may be responsible for hemodynamic symptomatology. Affected individuals may or may not have concomitant vertebral artery stenosis or occlusion. Certain prescription medications can mimic vertebrobasilar ischemia; as such, patient medications require thorough review. Excessive use of antihypertensive medications is the most common cause of posterior circulation symptoms and can also cause hemodynamic posterior circulation ischemia by decreasing the perfusion pressure and inducing severe orthostatic hypotension.

The evaluation of patients with posterior circulation ischemia should include numerous specific steps. The precise circumstances associated with development of symptoms should be ascertained. Symptoms often appear on standing in older individuals with poor sympathetic control of their venous tone, which causes excessive pooling of blood in the veins of the leg. This is particularly common in patients with diabetes who have diminished sympathetic venoconstrictor reflexes. A 20 mm Hg systolic pressure drop on rapid standing is criterion for a diagnosis of orthostatic hypotension causing low-flow in the vertebrobasilar system. In these cases, the pressure drop triggers the symptoms of posterior circulation ischemia.

A cardiac abnormality is another common cause of brainstem ischemia, especially in the elderly, and thorough evaluation should include monitoring for arrhythmias and a thorough assessment heart valve function. An ambulatory 24-hour electrocardiogram (Holter monitor) should be performed in patients with hemodynamic ischemia because arrhythmias are a common cause for symptomatology due to decreased cardiac output associated with the arrhythmia. Patients with ischemia secondary to arrhythmias often report the association of palpitations with the appearance of symptoms. Echocardiography is useful to rule out significant valvular pathology that could cause brainstem hypoperfusion.

Investigation must be undertaken to exclude inner ear pathology including rare cerebellar-pontine angle tumors. In addition, neurological evaluation to rule out benign vertiginous states should be considered.

Because patients often present with a combination of cerebral hemispheric and posterior symptoms, investigation of the great vessels and the carotid circulation is usually warranted. An important aspect of the history is identifying triggering events such as positional or postural changes. This is followed by a thorough physical examination, which includes palpation, auscultation, pulse exam, and comparative arm blood pressures (recumbent and standing).

Physical examination can alert the physician to the possibility of a subclavian steal in patients with brachial pressure differences greater than 25mmHg or with diminished or absent pulses in one arm. The diagnosis of reversal of vertebral artery flow can be made accurately by noninvasive indirect methods and demonstrated directly by duplex imaging of the reversal of flow in the vertebral artery.

Patients may relate their symptoms to turning or extending their heads. Frequently, the mechanism is extrinsic compression of the vertebral artery, usually the dominant or the only one, by arthritic bone spurs.[7] To differentiate this mechanism from dizziness or vertigo secondary to labyrinthine disorders that appear with head or body rotation, the patient should attempt to reproduce the symptoms by turning the head slowly and then repeating the maneuver, but this time briskly, as when shaking the head from side to side. In labyrinthine disease, the sudden inertial changes caused by the latter maneuver result in immediate symptoms and nystagmus. Conversely, in extrinsic vertebral artery compression, a short delay occurs before the patient fears for his or her balance.

Once a suspicion of vertebrobasilar ischemia has been entertained, only a few studies clearly ascertain vertebral anatomy.

Duplex ultrasonography

Duplex ultrasonography is an excellent tool for detecting lesions in the carotid artery, but it has significant limitations when used to detect vertebral artery pathology. Direct visualization of the second portion of the vessel is difficult due to its intraosseous course through the transverse processes of C2 to C6. The usefulness of duplex ultrasound lies in its ability to confirm reversal of flow within the vertebral arteries and detect flow velocity changes consistent with a proximal stenosis. In addition, this imaging may diagnose great vessel pathology and confirm subclavian steal.[17]


Contrast-enhanced magnetic resonance angiography (MRA) with 3-dimensional (3D) reconstruction and maximum image intensity (MIP) imaging techniques provide full imaging of the vessels including the supra-aortic trunks, the carotid and vertebral arteries, and the circle of Willis. MRA does tend to "overcall" stenoses, especially those lesions found at the origin of the vertebral artery in the V1 segment. Recent developments in MRI allow for accurate and noninvasive visualization of the vertebral and basilar arteries as well as the surrounding posterior fossa structures.

Brain stem infarctions are often missed by CT scan because they tend to be small and the resolution of the CT scan in the brain stem is poor. Transaxial MRI is also invaluable in detecting acute and chronic posterior fossa infarcts, as depicted in the 1st image below. This has been enhanced by the development of MRIA with 3D reconstructions and maximum image intensity (MIP) imaging, as depicted in the second image below.

Magnified view of MRI of the brain. The arrow deno Magnified view of MRI of the brain. The arrow denotes the site of a posterior fossa infarction.
Magnetic resonance angiography (MRA) with 3-dimens Magnetic resonance angiography (MRA) with 3-dimensional reconstruction of the extracranial and intracranial vertebral and carotid arterial system. The arrow denotes the right vertebral artery.


Selective subclavian and vertebral angiography remains the best test for preoperative evaluation of patients with vertebrobasilar ischemia. The most common site of disease, the vertebral artery origin, may not be well imaged with ultrasonography, MRA, or CT angiography and catheter angiography may be necessary to prove pathology here. Lesions at the origin of the vertebral artery, oftentimes the result of "spill-over" from the subclavian vessel, can, in some cases, only be displayed using oblique projections that are not part of standard arch evaluation.

Patients with suspected vertebral artery compression, usually by osteophytes, should undergo dynamic angiography, which incorporates provocative positioning. This is performed either with the patient sitting up, by means of bilateral brachial injections, or with the patient supine in the Trendelenburg position with the head resting against a block, mimic the effects of the weight of the head on the spine, if the femoral route is used. In these positions, intended to exert axial compression of the cervical vertebrae, the angiographer should obtain the specific rotation or extension of the head that provokes the symptoms. When the patient is rendered symptomatic, the arteriographic injection demonstrates the extrinsic compression that developed with the head rotation or extension.[18]

Lastly, delayed imaging should be performed in order to demonstrate reconstitution of the extracranial vertebral arteries through cervical collaterals, such as the occipital artery or the thyrocervical trunk.[19] Because of this collateral network, the distal vertebral and basilar arteries usually remain patent despite a proximal vertebral artery occlusion. A patent V3 segment can be exploited as a distal target for reconstruction. See the image below.

Selective angiography of the left subclavian arter Selective angiography of the left subclavian artery demonstrating collateral flow to a patent distal left vertebral artery via the thyrocervical trunk.
Contributor Information and Disclosures

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.

Specialty Editor Board

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.

Chief Editor

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, International Parkinson and Movement Disorder Society, Congress of Neurological Surgeons, American Society for Stereotactic and Functional Neurosurgery, North American Neuromodulation Society

Disclosure: Received consulting fee from Medtronic for consulting; Received consulting fee from St Jude Neuromodulation for consulting; Received consulting fee from MRI Interventions for consulting.

Additional Contributors

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.

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True vertebral artery aneurysm (9 cm).
Magnified view of MRI of the brain. The arrow denotes the site of a posterior fossa infarction.
Magnetic resonance angiography (MRA) with 3-dimensional reconstruction of the extracranial and intracranial vertebral and carotid arterial system. The arrow denotes the right vertebral artery.
Selective angiography of the left subclavian artery demonstrating collateral flow to a patent distal left vertebral artery via the thyrocervical trunk.
An arteriogram following a proximal vertebral to carotid artery transposition.
An arteriogram demonstrating aneurysmal degeneration of a left vertebral artery in the V2 segment.
Selective angiogram of a right vertebral artery pseudoaneurysm.
Symptoms of vertebrobasilar ischemia.
Vertebral stent fracture with in-stent restenosis.
Nonischemic conditions that may mimic vertebrobasilar ischemia.
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