Basilar Artery Thrombosis 

  • Author: Salvador Cruz-Flores, MD, MPH; Chief Editor: Helmi L Lutsep, MD   more...
 
Updated: Feb 3, 2012
 

Background

Acute basilar artery occlusion is associated with poor prognosis.[1] However, the advent of high-quality, reliable, and noninvasive technology (eg, MRI) has made its diagnosis possible even in subjects with mild symptoms. This has illustrated that some patients may have an acute partial occlusion or a slow progressive occlusion with limited ischemic injury and, therefore, a better prognosis. Although outcomes continue to be poor, advances in pharmacological and mechanical thrombolysis and in endovascular therapy may increase the survival and limit the disability rate.

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Pathophysiology

The basilar artery is the most important artery in the posterior circulation. It is formed at the pontomedullary junction by the confluence of both vertebral arteries. It lies on the ventral surface of the pons and, throughout its course, gives off its median, paramedian, short, and long circumferential branches.

The branch of the basilar artery with the larger circumference is the anterior inferior cerebellar artery. It normally arises at the junction of the proximal and middle thirds of the basilar artery and supplies the lateral pontine tegmentum, brachium pontis or middle cerebellar peduncle, flocculus, and a small part of the anterior cerebellum. The internal auditory artery usually arises from the anterior inferior cerebellar artery; however, it may also arise as a direct branch of the basilar artery.

The terminal branch of the basilar artery is the posterior cerebral artery (PCA); it supplies the midbrain, the thalamus, and the medial aspect of the temporal and occipital lobes. Proximal to its bifurcation into the terminal branches (ie, PCA), the basilar artery gives off the superior cerebellar arteries that supply the lateral aspect of the pons and midbrain and the superior surface of the cerebellum.

Given the anatomy of the posterior circulation and the circle of Willis, the clinical manifestations depend on the location of the occlusion, the extent of thrombus, and the collateral flow. Normally, the blood flows in an anterograde fashion from the vertebral arteries to the basilar artery up to its terminal branches. This pattern of flow may vary. If the proximal segment of the basilar artery is occluded and the occlusion resulted from a slowly progressive stenosis, collateralization occurs within the cerebellum into the circumferential branches of the basilar artery. Additionally, flow can be reversed from the PCAs into the distal basilar artery.

The mechanism of basilar artery occlusion is different depending on the segment of the vessel that is occluded. On one hand, most cases of distal (top of the basilar) or proximal (vertebrobasilar junction) occlusions are due to embolism either from a cardiac or an arterial source. On the other hand, midbasilar artery occlusion is typically the result of atherothrombosis. Arterial dissections are very rare and usually involve the vertebral artery and occasionally extend to the basilar artery.

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Epidemiology

Frequency

United States

The actual frequency, incidence, and prevalence of basilar artery occlusion are not known; basilar artery occlusion was reported in 2 cases per 1000 autopsy cases. However, in stroke registries, basilar artery thrombosis may explain as many as 27% of ischemic strokes occurring in the posterior circulation.

Mortality/Morbidity

  • The prognosis of basilar artery occlusion is generally poor, although it depends on several factors that include decreased level of consciousness, dysarthria, pupillary abnormalities, bulbar symptoms, diplopia, bilateral cerebellar lesions, tetraplegia, and a cardiac cause of embolism.[2] Up to 90% of patients with no such factors have a good functional outcome, while all patients with such factors either died or had severe disability in one study.[2]
  • The mortality rate is consistently reported at greater than 70%. Recanalization may decrease the mortality rate by 50%. However, the outcome in a recent series of patients with basilar artery thrombosis treated with antithrombotics was similar to the reported outcome in the available series of patients treated with thrombolytic therapy.
  • Recanalization is an important requisite for a good functional outcome.[3] Reportedly, a Barthel index of 85 can be achieved in as many as 58% of patients with vessel recanalization.
  • Conventional therapy for symptomatic basilar artery occlusion with antiplatelets, anticoagulation, or both is associated with a poor outcome in almost 80% of patients. The case fatality was 40%. Among survivors, 65% remained dependent (Rankin score 4-5).[4]

Race

  • Atherosclerotic basilar artery stenosis, like stenosis of any other intracranial artery, is more frequent in the African American and Asian populations than in white populations.

Sex

  • The male-to-female ratio is 2:1.

Age

  • Basilar artery occlusion secondary to atherosclerosis is most prevalent in the sixth and seventh decades of life.
  • Occlusion of the distal basilar artery is usually secondary to embolism and is most frequent in the fourth decade.
  • Women with basilar artery occlusion are typically older than men.
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Contributor Information and Disclosures
Author

Salvador Cruz-Flores, MD, MPH  Professor of Neurology, Director of Souers Stroke Institute, Department of Neurology and Psychiatry, St Louis University School of Medicine; Director, Mid-America Stroke Network and Neuroscience Critical Care Unit, St Louis University Hospital

Salvador Cruz-Flores, MD, MPH is a member of the following medical societies: American Academy of Hospice and Palliative Medicine, American Academy of Neurology, American College of Physicians, American Heart Association, American Society of Neuroimaging, American Stroke Association, National Stroke Association, Neurocritical Care Society, and Society of Critical Care Medicine

Disclosure: Axio inc Honoraria Review panel membership; Roche Honoraria Review panel membership; Lilly Honoraria Review panel membership

Coauthor(s)

Sombat Muengtaweepongsa, MD  Faculty, Department of Neurology, Thammasat University, Pathumthani, Thailand

Sombat Muengtaweepongsa, MD is a member of the following medical societies: American Academy of Neurology and Royal College of Physicians of Thailand

Disclosure: Nothing to disclose.

Specialty Editor Board

Draga Jichici, MD, FRCP, FAHA  Associate Clinical Professor, Department of Neurology and Critical Care Medicine, McMaster University School of Medicine, Canada

Draga Jichici, MD, FRCP, FAHA is a member of the following medical societies: American Academy of Neurology, Canadian Congress of Neurological Sciences, Canadian Congress of Neurological Sciences, Canadian Congress of Neurological Sciences, Canadian Critical Care Society, Canadian Medical Protective Association, Canadian Neurocritical Care Society, Neurocritical Care Society, Royal College of Physicians and Surgeons of Canada, and Society of Critical Care Medicine (USA)

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

Howard S Kirshner, MD  Professor of Neurology, Psychiatry and Hearing and Speech Sciences, Vice Chairman, Department of Neurology, Vanderbilt University School of Medicine; Director, Vanderbilt Stroke Center; Program Director, Stroke Service, Vanderbilt Stallworth Rehabilitation Hospital; Consulting Staff, Department of Neurology, Nashville Veterans Affairs Medical Center

Howard S Kirshner, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Neurology, American Heart Association, American Medical Association, American Neurological Association, American Society of Neurorehabilitation, National Stroke Association, Phi Beta Kappa, and Tennessee Medical Association

Disclosure: Nothing to disclose.

Selim R Benbadis, MD  Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, Tampa General Hospital, University of South Florida College of Medicine

Selim R Benbadis, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Sleep Medicine, American Clinical Neurophysiology Society, American Epilepsy Society, and American Medical Association

Disclosure: UCB Pharma Honoraria Speaking, consulting; Lundbeck Honoraria Speaking, consulting; Cyberonics Honoraria Speaking, consulting; Glaxo Smith Kline Honoraria Speaking, consulting; Pfizer Honoraria Speaking, consulting; Sleepmed/DigiTrace Honoraria Speaking, consulting

Chief Editor

Helmi L Lutsep, MD  Professor and Vice Chair, Department of Neurology, Oregon Health and Science University School of Medicine; Associate Director, Oregon Stroke Center

Helmi L Lutsep, MD is a member of the following medical societies: American Academy of Neurology and American Stroke Association

Disclosure: Co-Axia Consulting fee Review panel membership; AGA Medical Consulting fee Review panel membership; Concentric Medical Consulting fee Review panel membership

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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).
Spiral CT angiography showing occluded basilar artery.
 
 
 
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