Role of Plaque Morphology in Recurrent Stroke Risk
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A 74-year-old woman with past medical history of hypertension and hyperlipidemia developed transient left arm weakness and slurred speech. Computed tomography (CT) of the head was unremarkable, and the patient was referred for outpatient workup. Magnetic resonance imaging (MRI) a few days later showed numerous small diffusion positive lesions in the right middle cerebral artery distribution. Magnetic resonance angiography revealed bilateral carotid bulb stenosis (35% to 40% stenosis on the left and 50% stenosis on the right). CT angiogram (CTA) was ordered to clarify the percentage stenosis and need for intervention. In the meantime, her aspirin dose was increased from 81 to 325 mg. She was not on a statin. Five days after the MRI, the patient awoke complaining of pixilated vision. In the emergency room, a CT of the head showed a small subacute right parietal infarct. Immediately after CT, she developed a flaccid left hemiparesis (National Institutes of Health Stroke Scale score of 7). She was not given tPA (tissue-type plasminogen activator) because of her recent stroke and was transferred to a Comprehensive Stroke Center for possible endovascular intervention. On arrival at the Stroke Center, she had a National Institutes of Health Stroke Scale score of 15 with forced gaze deviation, left homonymous hemianopsia, left hemiparesis, dysarthria, left sensory loss, and neglect. Emergent MRI/magnetic resonance angiography of the brain showed a large right middle cerebral artery infarct and an occluded right internal carotid artery. There was no significant penumbra, and therefore, revascularization was not attempted. Her hospital course was complicated by cerebral edema, which was treated with hypertonic saline and aspiration pneumonia requiring prolonged intubation. She required a gastrostomy tube for feeding and was discharged to a skilled nursing facility with a National Institutes of Health Stroke Scale score of 12. At 3 months, she had a modified …