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Challenge of Identifying the Cause of Intracranial Artery Stenosis in Patients With Ischemic Stroke
Author(s) -
Sylvain Lanthier,
Céline Odier,
Sophia Sundararajan,
Daniel Strbian
Publication year - 2014
Publication title -
stroke
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.397
H-Index - 319
eISSN - 1524-4628
pISSN - 0039-2499
DOI - 10.1161/strokeaha.114.007419
Subject(s) - medicine , neurovascular bundle , stroke (engine) , neurology , university hospital , stenosis , family medicine , general surgery , surgery , psychiatry , mechanical engineering , engineering
A 49-year-old white, right-handed, nonmigraineur woman sought medical attention at a secondary-level hospital because of an unusual headache that has lasted 3 days. She was a cigarette smoker and had a history of depression, for which she was treated with trazodone. She had a previous episode 2 years before presentation of transient right facial palsy, and brain MRI at the time showed multifocal chronic infarcts in the middle cerebral artery (MCA) territory bilaterally, and an acute watershed infarct on the left MCA (Figure 1). Blood tests and cerebrospinal fluid analysis had been unremarkable. She was then lost to follow-up.Figure 1. Brain MRI 2 years before presentation. A , Fluid attenuation inversion recovery sequences showing bilateral chronic infarcts in the middle cerebral artery (MCA) territories (white arrows), on the left . B , Diffusion-weighted sequences showing recent watershed infarcts in the left MCA territory (black arrows).During the current admission, she reported asthenia and lack of attention for the previous 6 months. After lifting heavy boxes, she developed a mild occipital headache that gradually worsened >3 days to become severe and pulsatile. Other than an asymmetrical blood pressure, which was lower on the right arm than on the left, her vital signs were normal. Her neurological examination revealed memory impairment, ideational apraxia, visual agnosia, left homonymous hemianopia, facial asymmetry, sensory ataxia, and sensory extinction. Systemic examination was unremarkable. Brain MRI (Figure 2) showed the chronic changes that were seen on her previous MRI, 2 years earlier and a new acute right posterior cerebral artery infarct with mass effect, and no crescent sign on T1-weighted imaging with fat saturation. Computed tomographic angiography and catheter angiography documented occlusion of the right posterior cerebral artery, severe stenosis of the left, and occlusion of the right distal M1 segments of the …

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