Vertebral Artery Origin Stenosis With Acute Thrombus

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Vertebral Artery Origin Stenosis With Acute Thrombus
A right-handed woman in her early 60s with history of hypertension and hyperlipidemia was admitted to investigate anemia of unknown etiology. Three days after admission to hospital she developed sudden bilateral visual field defects and a reduction in visual acuity.

Neurological examination revealed a visual acuity of 20/100 OD and 20/70 OS. The patient had right lower quadrantanopsia without facial weakness or abnormality in ocular motility. Muscle tone, strength, rapid alternating movements, cerebellar and sensory examinations, and stance and gait were normal. There were no upper motor neuron findings.

MRI revealed multiple small infarcts in both cerebellar hemispheres, occipital poles, splenium of the corpus callosum and the right thalamus (figure 1A,B). Severe narrowing of the left vertebral artery origin was noted on magnetic resonance angiography (MRA) (figure 1C).



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Figure 1.



(A) Diffusion-weighted image, (B) Apparent Diffusion Coefficient (ADC) map showing restricted diffusion in the occipital poles, splenium of the corpus callosum and right thalamus, (C) magnetic resonance angiogram showing high-grade stenosis of the left vertebral artery origin (arrow).





Digital subtraction angiography (DSA) demonstrated a high-grade stenosis of the left vertebral artery origin with a thrombus just distal to the stenosis (figure 2A). Antegrade flow distal to the thrombus was demonstrated. The risk of distal embolization during percutaneous treatment was deemed high so antithrombotic therapy with aspirin/extended-release dipyridamole (25mg/200mg twice daily) and subcutaneous enoxaparin sodium (80 mg twice daily) was initiated. The lesion was to be re-evaluated in 72 h. However, the patient developed sudden acute memory impairment, confabulation, further decline in visual acuity and worsening of the visual field defects less than 48 h later. Repeat brain MRI showed new areas of infarcts in the right mesiotemporal and left occipital lobes (figure 3A,B).



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Figure 2.



(A) Left subclavian artery digital subtraction angiography showing a high-grade vertebral ostial stenosis with an acute thrombus just distal to the stenosis. (B) Selective right vertebral artery injection showing normal perfusion pattern in the posterior circulation.







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Figure 3.



(A) Diffusion-weighted image and (B) ADC map (performed less than 48 h after initiation of antithrombotic therapy) showing new areas of restricted diffusion in the right mesiotemporal lobe and both occipital regions.





In light of these findings we decided to perform an urgent intervention. Control DSA again showed the high-grade stenosis of the left vertebral artery origin with the previously noted thrombus and a new area of perfusion defect in the distal left posterior cerebral artery territory (figure 4A,B). The lesion was successfully treated with VOAS using a flow reversal technique and distal embolic protection. A significant fragment of the thrombus was successfully aspirated. The patient was discharged to a rehabilitation facility 4 days later without new or worsening neurological deficits.



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Figure 4.



(A) Frontal and (B) lateral projections of the posterior circulation from a right vertebral artery injection showing new area of perfusion defect in the distal left posterior cerebral artery territory.





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