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Basilar Artery Thrombosis Clinical Presentation

  • Author: Salvador Cruz-Flores, MD, MPH, FAHA, FCCM, FAAN, FACP, FANA; Chief Editor: Helmi L Lutsep, MD  more...
 
Updated: Oct 30, 2015
 

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.

In very rare cases, patients may present with isolated vertigo or dizziness, with no other neurologic symptoms. The presence of vascular risk factors, headache, and the inability to walk may suggest the diagnosis of vertebrobasilar insufficiency. Any associated neurologic 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 the symptoms described above that ends 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 by months)
Next

Physical Examination

An abnormal level of consciousness and motor signs, such as hemiparesis or quadriparesis (usually asymmetrical), 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 and top-of-the-basilar syndrome.

Locked-in syndrome

This is caused by infarction of the basis pontis secondary to occlusive disease of the proximal and middle segments of the basilar artery, resulting in 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.

Pontine warning syndrome

This is the manifestation of motor fluctuation that resembles the so-called capsular warning syndrome. Clinical features cannot definitely distinguish between these 2 syndromes. The most common features are waxing and waning of hemiparesis. The postulate mechanism is the plaque in the basilar artery at the orifice of the branch to the pons, resulting in paramedian pontine infarction.[5]

Oculomotor symptoms

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

Additional symptoms

In addition to those discussed above, reported signs of pontine ischemia include the following:

  • Limb shaking
  • Ataxia - Usually associated with mild hemiparesis
  • Facial weakness
  • Dysarthria
  • Dysphagia
  • Hearing loss
Previous
 
 
Contributor Information and Disclosures
Author

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: Received honoraria from Lilly for review panel membership; Received honoraria from Novo Nordisk for review panel membership.

Coauthor(s)

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: Serve(d) as a speaker or a member of a speakers bureau for: Boehringer.

Chief Editor

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.

Acknowledgements

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

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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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