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Vertebrobasilar Atherothrombotic Disease

  • Author: Eddy S Lang, MDCM, CCFP(EM), CSPQ; Chief Editor: Robert E O'Connor, MD, MPH  more...
 
Updated: Sep 09, 2014
 

Background

Vertebrobasilar atherothrombotic disease (VBATD) describes a wide spectrum of clinical entities with a common pathophysiology. Transient ischemic attacks (TIAs) in this vascular territory are also referred to as vertebrobasilar insufficiency (VBI). This more commonly used term was developed in the 1950s when Fisher introduced the term carotid insufficiency to describe TIAs of the anterior circulation. These, in turn, frequently serve as the prodrome to carotid branch infarcts. Although carotid insufficiency has been dropped from common medical jargon, vertebrobasilar insufficiency persists as the term that encompasses all TIA syndromes of the posterior circulation. In this article, vertebrobasilar atherothrombotic disease describes both transient and permanent ischemic deficits as they affect posterior cerebral circulation.

Vertebrobasilar atherothrombotic disease (VBATD) deserves special attention among emergency physicians because it is difficult to diagnose and important not to misdiagnose. Signs and symptoms of VBATD overlap those of other more common benign entities (eg, labyrinthitis, vestibular neuronitis, benign paroxysmal positional vertigo).

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Pathophysiology

Vertebrobasilar (posterior) circulation constitutes the arterial supply to the brainstem, cerebellum, and occipital cortex. The image below shows the vascular territories of the brain.

Vascular territories of the brain. Vascular territories of the brain.

Any interruption in blood flow to these areas may manifest in a myriad of symptoms. These symptoms are determined by which particular branch or branches of the vertebrobasilar circulation have been compromised, extent of any collateral circulation, and degree of occlusion.

The brainstem is an intensely concentrated area of neurologic activity, housing cranial nerves, the reticular activating system, and a series of ascending and descending neurosensory tracts. As a result of impaired blood flow, this compact area of neurologic activity malfunctions and results in several different but overlapping clinical syndromes.

Embolic phenomena cause infarction in vertebrobasilar territory in 9-40% of reported cases. The vertebrobasilar bed appears less susceptible than carotid circulation to embolic occlusion.

The vertebral artery is often classified into intracranial and extracranial segments; the atherosclerotic process tends to affect vertebrobasilar circulation at specific intracranial and extracranial sites. The extracranial site is defined as the initial segment of the vertebral artery just proximal to its take-off from the subclavian. The intracranial site is defined as the proximal portion of the basilar artery, just after the joining of the 2 vertebral arteries or just distal to the pontomedullary junction.

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Epidemiology

Frequency

United States

Approximately one fourth of strokes and transient ischemic attacks (TIAs) occur in the vertebrobasilar distribution.[1]

  • Brainstem infarctions have been reported in autopsy series at a rate of 2 per 1000 cases. One clinical study has suggested that the disease occurs 25% as frequently as occlusions of the carotid artery and its branches.
  • Recent developments in neuroimaging provide new perspectives about the disease's prevalence. Some studies using MRI suggest that 40% of patients with vertebrobasilar TIAs have evidence of brainstem infarction.

Mortality/Morbidity

Vertebrobasilar ischemic disease encompasses a vast spectrum of clinical syndromes, extending from subclinical to lethal brainstem infarctions.

  • Of patients who suffer infarctions in the vertebrobasilar territory, 50% report TIAs in the days or weeks (rarely months) prior to onset of the permanent deficit. A systematic review suggests that although overall mortality is no different than anterior territory ischemia, the early risk (within 7 d) of recurrent stroke or TIA progression to stroke is higher with VBATD. [1]
  • Basilar artery syndrome, which presents as a locked-in state, is caused by complete occlusion of the intracranial portion of vertebrobasilar circulation. It is a devastating disease with a mortality rate of 75-85%.

Race

Intracranial atherosclerosis is more common among black African[34] or East Asian ethnicities.[33]

Sex

As with atherosclerosis, this disease affects men twice as often as it does women.

Age

Vertebrobasilar ischemic disease occurs in the late decades of life (eg, 70s and 80s).

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Contributor Information and Disclosures
Author

Eddy S Lang, MDCM, CCFP(EM), CSPQ Associate Professor, Senior Researcher, Division of Emergency Medicine, Department of Family Medicine, University of Calgary Faculty of Medicine; Assistant Professor, Department of Family Medicine, McGill University Faculty of Medicine, Canada

Eddy S Lang, MDCM, CCFP(EM), CSPQ is a member of the following medical societies: American College of Emergency Physicians, Society for Academic Emergency Medicine, Canadian Association of Emergency Physicians

Disclosure: Nothing to disclose.

Coauthor(s)

Marc Afilalo, MD, FACEP, FRCPC MCFP (EM), CSPQ, Director, Emergency Department, Associate Professor, Faculty of Medicine, Section of Emergency Medicine, The Sir Mortimer B Davis-Jewish General Hospital

Marc Afilalo, MD, FACEP, FRCPC is a member of the following medical societies: American College of Emergency Physicians, Royal College of Physicians and Surgeons of Canada, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Ryan Wilkie University of Calgary Faculty of Medicine, Canada

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.

J Stephen Huff, MD, FACEP Professor of Emergency Medicine and Neurology, Department of Emergency Medicine, University of Virginia School of Medicine

J Stephen Huff, MD, FACEP is a member of the following medical societies: American Academy of Neurology, American College of Emergency Physicians, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Chief Editor

Robert E O'Connor, MD, MPH Professor and Chair, Department of Emergency Medicine, University of Virginia Health System

Robert E O'Connor, MD, MPH is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Association for Physician Leadership, American Heart Association, Medical Society of Delaware, Society for Academic Emergency Medicine, Wilderness Medical Society, American Medical Association, National Association of EMS Physicians

Disclosure: Nothing to disclose.

Additional Contributors

Richard S Krause, MD Senior Clinical Faculty/Clinical Assistant Professor, Department of Emergency Medicine, University of Buffalo State University of New York School of Medicine and Biomedical Sciences

Richard S Krause, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

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Vascular territories of the brain.
Diffusion-weighted MRI images showing a right cerebellar infarct.
Magnetic resonance angiography demonstrating the absence of flow in the vertebrobasilar system.
Right vertebral artery angiography showing an occlusion with no flow in the basilar artery.
Angiography performed after intra-arterial thrombolysis and angioplasty showing recanalization and perfusion of the basilar artery and its branches.
Hyperdense basilar artery (arrow).
 
 
 
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