Vertebrobasilar artery dolichoectasia manifesting as Millard-Gubler syndrome in a young acute ischemic stroke

January 28, 2022 Nephrology & Neurology No Comments

Introduction: Vertebrobasilar dolichoectasia (VBD) is an arterial disease characterized by
dilatation, elongation, and tortuosity of the vertebral and basilar arteries. VBD can generate
intracranial hemorrhage, compression of the brainstem, and ischemic stroke as the most
common presentation. Millard-Gubler syndrome (MGS) is a pontine-crossed syndrome
affecting the pons at the level of the facial nerve nucleus. We present an unusual case of
posterior circulation ischemic stroke presenting as MGS due to VBD.
Observation: A 50-year-old man, with a medical history of high blood pressure, was
hospitalized after 20 hours of transient dizziness, left facial numbness, and diplopia. On
examination, he had a right hemiparesis with right Babinski. Deep tendon reflexes were
present. Cranial nerves examination showed left abducens paresis with left peripheral facial
nerve palsy. Cranial computed tomography (CT) imaging showed left pontine infarct with
dilated basilar artery. Brain MRI showed a tortuous and dilated vertebrobasilar system
touching the left acoustico-facial complex nerves with a high signal intensity involving the
left anterolateral pons with a small right cerebellar hemorrhage. Paraclinical tests showed
high blood total cholesterol and bilateral carotid artery atherosclerosis without stenosis. The
patient received aspirin, atorvastatin with anti-hypertensive agents. Two weeks after his
admission, there was a resolution of the left abducens nerve paresis with mild residual left
peripheral facial paresis and left hemiparesis.
Discussion: VBD is a complex arteriopathy with unknown etiology. Clinical symptoms
in patients with VBD are various including brainstem and cranial nerve compression,
intracranial hemorrhage, and ischemic stroke. MGS is an uncommon pontine-crossed
syndrome occurring due to a lesion in the pons at the level of the facial nerve nucleus. MGS
can be caused by brainstem tumor, cavernous angioma, neurocysticercosis, and cerebral
infarction. The coexistence of MGS and VBD is rarer.
Conclusion: Our case provides evidence that VBD may be presented as MGS secondary
to a posterior circulation ischemic stroke. Therapeutic management of patients with VBD
requires a careful balancing of the benefits and risks.

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