Basilar Artery Thrombosis
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Acute basilar artery thrombosis is associated with a poor prognosis. [1] However, the advent of high-quality, reliable, and noninvasive technology (eg, magnetic resonance imaging [MRI]) has made its diagnosis possible even in subjects with mild symptoms (see the image below). This has illustrated that some patients have an acute partial occlusion or a slow progressive occlusion with limited ischemic injury and, therefore, a better prognosis. (See Etiology and Workup.)
Although outcomes continue to be poor in patients with basilar artery thrombosis, advances in pharmacologic and mechanical thrombolysis and in endovascular therapy may reduce the mortality and disability rates associated with this disease. (See Prognosis, Treatment, and Medication.)
Vertigo is one of several common presenting symptoms associated with basilar artery occlusion. See Vertigo: 5 Case-Based Diagnostic Puzzles, a Critical Images slideshow, to help recognize diagnostic clues in vertigo cases.
Complications of basilar artery thrombosis can include the following (see Prognosis, Presentation, and Workup):
Aspiration pneumonia
Myocardial infarction
Deep vein thrombosis and pulmonary embolism
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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 the 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 third 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 of basilar artery thrombosis depend on the location of the occlusion, the extent of the 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 has 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 risk factors for basilar artery thrombosis are the same as those seen generally in stroke. The most common risk factor is hypertension, which is found in as many as 70% of cases. It is followed by diabetes mellitus, coronary artery disease, peripheral vascular disease, cigarette smoking, and hyperlipidemia.
The mechanism of stroke in basilar artery occlusion differs depending on the segment of the vessel involved. Atherosclerotic occlusive disease predominantly affects the midsegment of the basilar artery, followed by the vertebrobasilar junction.
Embolism, either from a cardiac or arterial source, is much more frequent in the distal third of the basilar artery and the vertebrobasilar junction.
Arterial dissection is much more common in the extracranial vertebral artery. It has been associated with a previous neck injury or chiropractic manipulation. Intracranial dissections are very uncommon.
The frequency, incidence, and prevalence of basilar artery occlusion are not known. Although basilar artery occlusion has been reported in 2 per 1000 autopsy cases, basilar artery thrombosis may, in stroke registries, explain as many as 27% of ischemic strokes occurring in the posterior circulation.
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. The male-to-female ratio for basilar artery thrombosis is 2:1.
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.
Patients with acute basilar artery occlusion have a mortality rate of greater than 85%, although the mortality rate may be as low as 40% in patients with recanalization. Good functional outcomes can be expected in as many as 24-35% of patients treated with intravenous (IV) or intra-arterial thrombolysis, respectively. For symptomatic patients who survive, the risk of recurrent stroke is 10-15%.
The prognosis for basilar artery occlusion is generally poor, with the mortality rate for this condition consistently reported at greater than 70%. However, the prognosis depends on several factors, including the following [2] :
Decreased level of consciousness
Dysarthria
Pupillary abnormalities
Bulbar symptoms
Diplopia
Bilateral cerebellar lesions
Tetraplegia
Cardiac cause of embolism
Up to 90% of patients with no such factors have a good functional outcome, while in one study, all patients with such factors either died or had severe disability. [2]
Recanalization is an important requisite for a good functional outcome. [3] A Barthel index of 85 can reportedly be achieved in as many as 58% of patients with vessel recanalization. Recanalization may decrease the mortality rate from basilar artery thrombosis by 50%, although the outcome in a series of patients with the condition who were treated with antithrombotics was similar to that reported in the available series of patients treated with thrombolytic therapy.
A study by Schonewille et al involving 82 patients with symptomatic basilar artery occlusion found that conventional therapy with antiplatelets, anticoagulation, or both was associated with a poor outcome in almost 80% of patients. The case fatality are in the study was 40%, with 65% of survivors remaining dependent (Rankin score 4-5). [4]
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Salvador Cruz-Flores, MD, MPH, FAHA, FCCM, FAAN, FACP, FANA Professor and Founding Chair, Department of Neurology, Paul L Foster School of Medicine, Texas Tech University Health Sciences Center
Salvador Cruz-Flores, MD, MPH, FAHA, FCCM, FAAN, FACP, FANA 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, Society of Critical Care Medicine
Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Novo Nordisk, DUke University.
Sombat Muengtaweepongsa, MD, MSc Associate Professor, Department of Neurology, Faculty of Medicine, Thammasat University, Thailand
Sombat Muengtaweepongsa, MD, MSc is a member of the following medical societies: American Academy of Neurology, Royal College of Physicians of Thailand
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: Received salary from Medscape for employment. for: Medscape.
Helmi L Lutsep, MD Professor and Vice Chair, Department of Neurology, Oregon Health and Science University School of Medicine; Associate Director, OHSU Stroke Center
Helmi L Lutsep, MD is a member of the following medical societies: American Academy of Neurology, American Stroke Association
Disclosure: Medscape Neurology Editorial Advisory Board for: Stroke Adjudication Committee, CREST2; Executive Committee for the NINDS-funded DEFUSE3 Trial; Physician Advisory Board for Coherex Medical.
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.
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.
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
Basilar Artery Thrombosis
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