eMedicine Specialties > Neurology > Neuro-vascular Diseases

Basilar Artery Thrombosis

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
Coauthor(s): Sombat Muengtaweepongsa, MD, Faculty, Department of Neurology, Thammasat University, Pathumthani, Thailand
Contributor Information and Disclosures

Updated: Aug 18, 2009

Introduction

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.

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.

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.

Clinical

History

A stuttering and progressive course of symptoms or transient ischemic attacks in the vertebrobasilar territory is seen in patients with atherosclerotic occlusion.

  • As many as 50% of patients experience transient ischemic attacks or a waxing and waning course for several days to weeks prior to the occlusion.
  • The most common heralding symptoms include the following:
    • Motor deficits such as hemiparesis or tetraparesis and facial paresis - 40-67% of cases
    • Dysarthria and speech impairment - 30-63% of cases
    • Vertigo, nausea, and vomiting - 54-73% of cases
    • Headache - 40-42% of cases
    • Visual disturbances - 21-33% of cases
    • Altered consciousness - 17-33% of cases
  • In a few cases, convulsive-like movements along with hemiparesis (herald hemiparesis) may be the only diagnostic clues.
  • Occasionally, patients may present with isolated vertigo or dizziness with no other neurological symptoms, but this situation is very rare. The presence of vascular risk factors, headache, and the inability to walk may suggest the diagnosis of vertebrobasilar insufficiency. Any associated neurological signs of brainstem dysfunction also support the diagnosis of vertebrobasilar insufficiency.
  • Based on the temporal profile of the symptoms, basilar artery thrombosis may manifest in at least these 3 different ways, as follows:
    • Sudden onset of severe motor and bulbar symptoms with impaired consciousness
    • Gradual or stuttering course of a combination of symptoms described above that end with disabling motor and bulbar symptoms, impaired consciousness, or both
    • Prodromal symptoms that may include loss of vision, diplopia, dysarthria, vertigo, hemiparesis, paresthesias, imbalance, and convulsive-like movements (These symptoms may precede monophasic basilar artery thrombosis by several days or even months.)

Physical

  • An abnormal level of consciousness and motor signs, such as hemiparesis or quadriparesis (usually asymmetric), are seen in more than 70% of patients.
  • Bulbar and pseudobulbar signs are the most common findings in one series, reportedly affecting 74% of patients.
  • Pupillary abnormalities, oculomotor signs, and pseudobulbar manifestations (ie, facial weakness, dysphonia, dysarthria, dysphagia) are seen in more than 40% of patients.
  • The signs described can be present in different combinations. The recognized syndromes more commonly associated with basilar artery occlusion are:
    • Locked-in syndrome: It is caused by infarction of the basis pontis secondary to occlusive disease of the proximal and middle segments of the basilar artery, which leads to quadriplegia. Because the tegmentum of the pons is spared, the patient has a spared level of consciousness, preserved vertical eye movements, and blinking. Coma associated with oculomotor abnormalities and quadriplegia also indicates proximal basilar and midbasilar occlusive disease with pontine ischemia.
    • Top-of-the-basilar syndrome: This is the manifestation of upper brainstem and diencephalic ischemia caused by occlusion of the rostral basilar artery, usually by an embolus. Patients present with changes in the level of consciousness. They may experience visual symptoms such as hallucinations and/or blindness. Third nerve palsy and pupillary abnormalities are also frequent. Motor abnormalities include abnormal movements or posturing.
  • Oculomotor signs are common and can be associated with the syndromes described above. They usually reflect involvement of the vertical gaze center in the midbrain and/or the abducens nucleus, the horizontal gaze center located in the paramedian reticular formation contiguous to the abducens nucleus, and/or the medial longitudinal fasciculus. Lesions to these structures result in the following:
    • Ipsilateral abducens palsy
    • Ipsilateral conjugate gaze palsy
    • Internuclear ophthalmoplegia
    • One-and-a-half syndrome caused by a lesion simultaneously affecting the paramedian reticular formation and the medial longitudinal fasciculus, resulting in ipsilateral conjugate gaze palsy and internuclear ophthalmoplegia
    • Ocular bobbing, which localizes the lesion to the pons: This is characterized by a brisk downward movement of the eyeball with a subsequent return to the primary position.
    • Skew deviation
  • Other reported signs of pontine ischemia include limb shaking, ataxia (usually associated with mild hemiparesis), facial weakness, dysarthria, dysphagia, and hearing loss.

Causes

  • The risk factors are those seen in patients with stroke. The most common risk factor is hypertension, which is seen 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 mid segment 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.

More on Basilar Artery Thrombosis

Overview: Basilar Artery Thrombosis
Differential Diagnoses & Workup: Basilar Artery Thrombosis
Treatment & Medication: Basilar Artery Thrombosis
Follow-up: Basilar Artery Thrombosis
Multimedia: Basilar Artery Thrombosis
References
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Further Reading

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Keywords

basilar artery occlusion, anterior inferior cerebellar artery, AICA, posterior cerebral artery, PCA, atherothrombosis, embolism, arterial dissection, atherosclerotic occlusion, vertebrobasilar insufficiency, VBI, stroke, hypertension, partial basilar artery occlusion, intravenous thrombolysis, atherosclerotic basilar artery stenosis, occlusion of the distal basilar artery, pontine ischemia, locked-in syndrome, top-of-the-basilar syndrome, stroke, neck injury, chiropractic manipulation, atrial fibrillation.

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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 Medical Association, American Society of Neuroimaging, American Stroke Association, National Stroke Association, Neurocritical Care Society, and Society of Critical Care Medicine
Disclosure: NovoNordisk Grant/research funds clinical trial; Photothera INC Grant/research funds clinical trial; IMRX therapeutics Inc Grant/research funds clinical trial; Coaxia Inc Grant/research funds clinical trial; Neurobiological Technologies Inc Grant/research funds clinical trial

Coauthor(s)

Sombat Muengtaweepongsa, MD, Faculty, Department of Neurology, Thammasat University, Pathumthani, Thailand
Disclosure: Nothing to disclose.

Medical Editor

Draga Jichici, BSc, MD, FRCP, Associate Clinical Professor, Department of Medicine, Division of Neurology and Critical Care Medicine, McMaster University, Canada
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

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: Boehringer Ingelheim Honoraria Speaking and teaching; BMS/Sanofi Honoraria Speaking and teaching; Novartis Honoraria Speaking and teaching

CME Editor

Selim R Benbadis, MD, Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, University of South Florida School of Medicine, Tampa General Hospital
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: Nothing to disclose.

Chief Editor

Helmi L Lutsep, MD, Professor, Department of Neurology, Oregon Health & Science University; 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; Talecris Consulting fee Review panel membership; AGA Medical Consulting fee Review panel membership; Boehringer Ingelheim Honoraria Speaking and teaching; Concentric Medical Consulting fee Review panel membership; Abbott Consulting fee Consulting; Sanofi  Consulting

 
 
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