Basilar Artery Thrombosis Clinical Presentation

Updated: Oct 18, 2017
  • Author: Salvador Cruz-Flores, MD, MPH, FAHA, FCCM, FAAN, FACP, FANA; Chief Editor: Helmi L Lutsep, MD  more...
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Presentation

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)
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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
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