Figure 1. AP view, left vertebral artery injection showing occlusion of the basilar artery (A) distal to the take-off of the anterior inferior cerebellar arteries (B) and occlusion of the right vertebral artery (C).
A woman in her 30s had been feeling slightly dizzy and not “quite right” for a few days. In addition, she had a headache and nausea, and thinking she had COVID-19, she got tested and was found to be negative. She developed a paraparesis and went to the emergency room where she had tonic-clonic activity and deteriorated quickly with difficulty breathing requiring intubation. The CTA showed a basilar occlusion. A cerebral angiogram found a right vertebral artery occlusion and a mid-basilar occlusion just distal to the take-off of the inferior anterior cerebellar arteries (Fig 1). The clot was removed with total clearance of the blood vessels. Postthrombectomy, there was, however, marked hyperemia of the brainstem (Fig 2).
Figure 2. AP view, left vertebral artery injection post-reperfusion therapy with endovascular thrombectomy. Complete opening of the basilar artery (yellow arrow) with marked hyperemia of the brainstem (red arrows). Persistent right vertebral artery occlusion (black arrow)
The presumed diagnosis was a right vertebral artery dissection with an arterio-arterial embolus. This was, however, not confirmed on a fat suppressed MRI of the neck. Furthermore, no source of the emboli could be found. The patient survived but suffered a brainstem stroke (Fig 3).
Figure 3. Post-reperfusion treatment MRI showing infarcts of the right brain stem (yellow arrow) and in the cerebellar hemisphere (blue arrows), with significant brainstem edema, and an open basilar artery.
A basilar artery occlusion can be a condition that is difficult to diagnose and treat as a recent paper by Demel and Broderick has pointed out1. Unlike the acute clinical symptoms seen in anterior circulation occlusions, the symptoms of basilar artery occlusion can mimic other non-stroke causes and can have a prolonged and fluctuating course. Endovascular therapy can add materially to the hope of a good recovery2. The source of this embolus was never confidently determined despite a vigorous search. This frustrating situation is not uncommon and can be seen in 15-40% of strokes3. Marked hyperemia of the reperfused brain tissue is a common phenomenon that is the result of the pathophysiological changes triggered by ischemic stroke4 (Fig 3). Post-reperfusion hyperemia may increase the risk for hemorrhagic transformation and paradoxically, can be worsened by reperfusion therapy (reperfusion injury). Current devices and treatment forms do not address the ischemia-triggered metabolic and structural changes or the challenges arising from reperfusion therapy4.