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Vertebrobasilar Atherothrombotic Disease Clinical Presentation

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

History

Vertebrobasilar TIAs typically have shorter duration than attacks involving the carotid territory, lasting 8 minutes on average compared with 14 minutes for carotid TIAs.

Classic symptoms of posterior region ischemia include the following[29] :

  • Vertigo
  • Visual field defects (diplopia, hemianopia)
  • Auditory phenomena (sudden sensorineural hearing loss)
  • Facial numbness or paresthesias
  • Dysphagia, dysarthria, hoarseness
  • Syncope (drop attacks)
  • Hemisensory extremity symptoms (eg, contralateral to facial component)

Vertigo is the hallmark symptom of patients experiencing ischemia in the vertebrobasilar distribution. Many patients describe their vertigo as nonviolent or more of a swimming or swaying sensation. Exact incidence of vertigo is unknown, yet as many as one third of patients with VBI may experience vertigo as the sole manifestation of their illness.

Other symptoms specific to regional infarcts and syndromes include the following:

  • Lateral medullary infarct (Wallenberg syndrome): When VBI progresses to a complete brainstem infarction, a common syndrome is impaired neurologic functioning in the lateral aspect of the medulla, first described by Wallenberg. This is characterized by the following:
    • Ipsilateral facial pain and numbness
    • Ipsilateral ataxia (falling to side of lesion)
    • Vertigo, nausea, vomiting
    • Contralateral pain and thermal impairment over body and occasionally face
  • Medial medullary infarct: Occlusion of a vertebral artery or branch of the lower basilar artery may produce the following symptoms:
    • Contralateral arm and leg weakness (facial sparing)
    • Diplopia
  • Basilar artery syndrome: Caused by complete basilar artery occlusion, this is characterized by the following:
    • Locked-in state (awake quadriplegia)
    • Paralysis or weakness of all extremities
    • Horizontal gaze paresis, stupor, coma
  • Subclavian steal syndrome: This syndrome results from retrograde blood flow down the vertebral artery in response to increased demands from the left upper limb.
    • One of the earliest descriptions of VBI was reported in patients who suffered from stenotic lesions of their left subclavian arteries, just proximal to the take-off of the vertebral artery. Half of these patients reported vertigo symptoms consistent with posterior circulation ischemia when exercising their left arms.
    • Some series suggest that arm claudication and headache are the most prominent features in patients with symptomatic subclavian steal syndrome.
  • Labyrinthine artery occlusion: This artery commonly branches from the anterior inferior cerebellar artery. The resulting ear damage may lead to the following symptoms:
    • Prolonged vertigo
    • Hearing loss[28]
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Physical

Most patients with early stage VBI have only transient episodes of neurologic dysfunction. As a result, most commonly cited physical symptoms may be minimal or nonexistent. Patients with ongoing symptoms, or those who already have incurred an ischemic deficit, demonstrate physical findings that reflect brainstem and cerebellar dysfunction. Crossed signs (eg, contralateral motor and sensory findings) are hallmarks of many types of brainstem strokes.

  • Vertebrobasilar insufficiency
    • Nystagmus
    • Limb ataxia
    • Truncal ataxia (falling to side of lesion)
    • Contralateral deficit in pain and temperature perception
    • Ipsilateral limb and trunk numbness
    • Ipsilateral loss of taste
    • Visual field defects
    • Ipsilateral hearing loss[29]
  • Lateral medullary infarct (Wallenberg syndrome)
    • Contralateral impairment of pain and thermal sensation to the extremities
    • Nystagmus
    • Ipsilateral Horner syndrome (eg, ptosis, miosis, anhydrosis)
  • Medial medullary syndrome
    • Ipsilateral paralysis and atrophy of the tongue
    • Contralateral deficit in proprioception and fine touch (facial sparing)
    • Internuclear ophthalmoplegia
  • Basilar artery syndrome
    • Bifacial and oropharyngeal palsy
    • Horizontal gaze paresis
    • Decreased level of consciousness
  • Subclavian Steal syndrome
    • Differences between systolic blood pressure (> 25 mm Hg) or diminished/absent arm pulses[30]
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Causes

Atherosclerosis is by far the most common cause of VBI, making VBI most common among patients with cardiovascular risk factors such as age, hypertension, diabetes mellitus, smoking, dyslipidemias, and family history of premature coronary artery disease (men < 55 years old, women < 65). VBI may result from any disease process that has an impact on the arterial supply to the posterior fossa, including the following:

  • Fibromuscular dysplasia
  • Rotational occlusion (Bow hunter's stroke) - Mechanical occlusion or stenosis of the vertebral artery at the C1-C2 level caused by lateral flexion
  • Vertebral artery dissection
  • Vertebrobasilar aneurysms
  • Dolichoectasia of basilar artery
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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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