Basilar Artery Infarct

Excerpt

The basilar artery (BA) is formed over the surface of the pons by two vertebral arteries to supply the critical areas of the brain and brainstem. Anatomically, it is subdivided into three arbitrary segments: proximal from the vertebral artery (VA) to anterior inferior cerebellar arteries (AICA), middle from AICA to the origin of superior cerebellar arteries (SCA), and finally, the distal segment from SCA to the terminal posterior cerebral arteries (PCA). Basilar artery infarct or occlusion (BAO) results from the obliteration of blood supply to the posterior circulation or vertebrobasilar system of arteries to the brain. BAO was first described in 1828 by Scottish physician John Abercrombie.

The most common causes are atherosclerosis and thromboembolism from large vessel occlusion (LVO) or the heart. The clinical presentation can be very mild as nausea, dizziness, headache, confusion, and vertigo to severe symptoms like aphasia, dysarthria, dysphagia, hemiparesis/quadriparesis, loss of consciousness, coma, cranial nerve abnormalities, vision loss, and even cardiac or respiratory compromise which is usually lethal unless immediately identified to achieve revascularization.

Reduced consciousness is the hallmark of basilar artery occlusion. A patient presenting with these brainstem symptoms and signs qualifies for rapid evaluation, consult with the stroke and endovascular teams, and an urgent imaging confirmation with computed tomography (CT) scan of the head, CT angiography of the head and neck, and/or magnetic resonance imaging (MRI) with or without perfusion imaging are usually done. The whole process should not delay the administration of intraarterial thrombolytics like alteplase (tPA) or tenecteplase and transfer to the angiography suite for mechanical thrombectomy (MT) in eligible patients to achieve potentially good clinical outcomes.