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Incheon St. Mary’s Hospital, College of Medicine, The Catholic University of Korea, Departments of Rehabilitation Medicine1, Incheon St. Mary’s Hospital, College of Medicine, Departments of Cardiology2 |
Introduction
Bilateral medial medullary infarction (MMI) is a rare, limited subtype of stroke, which occasionally represents progressive quadriplegia, dysarthria, dysphagia or impaired sensation. A 49-year-old female patient was admitted with chief complaint of left hemiparesis and dizziness. She suffered from dyspnea requiring oxygen supply, and was diagnosed silent myocardial ischemia (MI) with abnormal wall motion on echocardiogram and normal cardiac enzyme. The coronary angiography (CAG) unveiled stenosis at all three major coronary arteries, and percutaneous coronary intervention (PCI) improved patient’s dyspnea. This case report highlights that dyspnea in a bilateral medial medullary infarction could be caused not by respiratory failure, but by silent MI. Early cardiac evaluation for the silent MI could be essential for dyspnea patients in medullary infarction.
Case Report
A 49-year-old female patient, without any prior medical or family history, visited emergency room with chief complaint of left hemiparesis, dizziness and dysarthria. The patient showed quadriplegia, dysarthria, dysphagia and dizziness. Magnetic resonance imaging revealed acute infarction on bilateral anteromedial medullas, accompanied by hypoplasia of the right vertebral artery and stenosis of both distal internal carotid arteries and anterior cerebral arteries (Fig 1). Blood pressure was high since the onset. Oxygen saturation was under 95% since the 6th day from onset. She complained dyspnea at the 7th day from onset (Table 1). There was no structural abnormality on laryngoscopy that might cause upper airway problems. Transthoracic echocardiogram (TTE) revealed akinesia of basal inferior septal wall and base-to-mid inferior wall, suggesting ischemic insult of right coronary artery (RCA) territory at 7th day from onset. The cardiac enzyme level was within normal. The HbA1C was 8.4%, the diabetes mellitus was diagnosed.
The CAG disclosed diffuse stenosis up to 70% on mid left anterior descending artery, diffuse irregular stenosis up to 50% on left circumference artery, discrete eccentric 20% stenosis on proximal RCA and diffuse irregular stenosis up to 90% on mid-distal RCA at 9th day from the onset. After immediate PCI dyspnea was improved and 4 days after and blood pressure were stabilized. Without any complications of PCI, she was brought back to general ward and restarted neuro-rehabilitation. Modified Rankin scale were 5 initially and improved to 4 at 3 months after the onset.
Conclusion
This case report highlights that dyspnea in bilateral MMI is due to silent MI rather than respiratory failure, and emphasizes significance of early cardiac work up in bilateral MMI. Early diagnosis of disease by immediate diagnostic imaging study and thorough evaluation of etiologic studies helps detection of underlying ischemic heart disease. Additional studies are needed for better understanding of pathophysiology, etiology, frequency of silent MI in the bilateral MMI.
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Table 1. The change of blood pressure, oxygen saturation and dyspnea before and after the percutaneous coronary intervention. * PCI: Percutaneous coronary intervention; **SpO2:O2 saturation measured by pulse oximetry
Figure 1. A. Axial diffusion-weighted image shows hyperintense ‘heart appearance’ signal in the bilateral anteromedial medulla. B. MRA showed hypoplasia of the right vertebral artery and stenosis of both distal internal carotid arteries and anterior cerebral arteries.
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