Acute basilar artery occlusion

Case contributed by Juan Martín Leguízamo-Isaza
Diagnosis certain

Presentation

A patient with no prior medical history presented to the emergency department with a 3 hour history of horizontal gaze paresis, loss of postural tone, and reduced consciousness.

Patient Data

Age: 25 years
Gender: Female

There is increased attenuation of the basilar artery, also referred to as the hyperdense basilar artery sign.

CTA MIP and 3D Reconstruction

ct

There is a contrast filling defect of the the proximal, middle, and distal segments of the basilar artery.

DWI image showing an increase in signal intensity in the pons and the left cerebellar hemisphere, as well as an ADC map showing correspondingly low values in the pons and the left cerebellar hemisphere suggesting restricted diffusion. 

This study depicts a filling defect at the proximal segment of the basilar artery.

After mechanical thrombectomy

dsa

This study after arterial recanalization depicts now patent basilar and posterior cerebral arteries. 
 

After mechanical thrombectomy

ct

There are pontine and left cerebellar hypodensities in keeping with cytotoxic edema causing obstruction of the fourth ventricle and secondary non-communicating hydrocephalus.

Case Discussion

The presence of neurological clinical manifestations suggestive of a posterior cerebral circulation stroke in association with the finding of areas of restricted diffusion on MRI of vertebrobasilar vascular distribution, as well as a contrast media filling defect of the basilar artery on DSA are the most important findings to support an acute basilar artery occlusion (BAO). 

However, other findings favoring acute BAO such as the hyperdense basilar artery on non-contrast CT, as well as contrast filling defects of the basilar artery on CTA and DSA in the presence of an unremarkable anterior cerebral circulation were also in keeping with acute BAO.

Lastly, acute BAO has been described to be tied to a very high mortality and poor functional outcome, even when successful arterial rencalization is achieved. The fact that this patient went on to develop significant cytotoxic edema, obstructive hydrocephalus, and brain herniation leading to her death despite having been adequately treated via mechanical thrombectomy is also in keeping with the clinical course of acute BAO.

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