Abstract

A 58-year-old male with hypertension, hyperlipidemia, diabetes mellitus, and obesity had abrupt left leg weakness and gait imbalance. Four hours later, left arm weakness, numbness, and dysarthria developed, and he presented to the hospital. Computed tomographic angiogram of the head and neck showed no acute hemorrhage, large vessel occlusion, or significant stenosis of the intracranial or extracranial arteries. He was treated with aspirin and clopidogrel. Thirteen hours later, he developed double vision, with a new right 6th nerve palsy and dysconjugate gaze. Brain magnetic resonance (MR) imaging showed an acute right basal paramedian pontine infarction on diffusion-weighted imaging (DWI) without hemorrhage (Fig A). Intracranial vessel wall MR imaging was performed using time-of-flight magnetic resonance angiography (MRA) and pre- and post-contrast black-blood imaging optimized to visualize the vessel walls. The basilar artery at the level of the pontine infarction showed subtle irregularity of the lumen, with low-grade stenosis (<30% stenosis) (Fig B). Vessel wall MR imaging showed eccentric vessel wall thickening and enhancement along the right basilar artery wall ipsilateral to the side of infarction, as shown in the coronal and sagittal planes (Fig C, D). Orthogonal planes of the pre- and postcontrast imaging confirmed an enhancing plaque along the right lateral surface of the basilar artery (Fig E, F). No other intracranial arteries, including the dominant right intradural vertebral artery, showed stenosis, vessel wall thickening, or wall enhancement. Taken together, the imaging findings implicate a mid-basilar atherosclerotic plaque occluding right pontine perforators as the stroke etiology. This is also consistent with the patient's stuttering, stepwise deterioration over the initial 24 hours. Perforator disease, also known as branch atheromatous disease, is a common mechanism for paramedian pontine infarctions with plaque occluding the perforator ostia.1, 2 Owing to the ability of the vessel wall to accommodate plaque formation by outwardly remodeling, the artery may not show significant luminal stenosis on lumen-based imaging. Vessel wall MR imaging highlights vessel wall pathology, such as atherosclerotic plaque, that is not otherwise detected by conventional computed tomography or MR angiography. The technique can be of particular diagnostic value for stroke subtyping by identifying non-stenotic plaque, as shown in this illustrative case.3 Given that about 20% of cardiac emboli can flow anterograde into the posterior circulation, cardioembolism could be considered a cause of this stroke.4 Upon the exclusion of other potential sources of stroke mechanism, such as cardioembolism, vessel wall MR imaging can be used to support intracranial atherosclerotic plaque as the underlying cause of stroke and provide greater precision in diagnostic care. J.W.S., S.R.E., and B.L.C. contributed to the conception and design of the study; B.L.C. and J.W.S. contributed to acquisition and analysis of the data. J.W.S., S.R.E., and B.L.C. contributed to drafting of the text. J.W.S. prepared the figure. Nothing to report.

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