ArticleNeurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology2014
Acute cerebral infarction in watershed distribution in a patient with hypereosinophilic syndrome without cardiac lesion.
Article in Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 6 citations in OpenAlex.
- Literature reviews of stroke with hypereosinophilic syndrome.International journal of cardiology. Heart & vasculature · 2021Review
- Multiple cerebral infarctions associated with lung cancer-induced hypereosinophilia: a case report.BMC neurology · 2021Article
- Dapsone-induced DRESS after infliximab-induced vasculitis: a case of cerebral infarction in the context of multiple drug reactions.BMJ case reports · 2020Article
- Acute progressive stroke with middle cerebral artery occlusion caused by idiopathic hypereosinophilic syndrome: a case report.BMC neurology · 2020Article
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3 authors at 1 institution in 1 country.
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Abstract
We here in describe a case of hypereosinophilic syndrome (HES) with acute cerebral infarction in a watershed distribution with lesions of the carotid artery but no damage to the endocardium or myocardium. A 62-year-old Chinese man complained of left-sided hemiparesis. Brain MR showed multiple areas of acute ischemia. The eosinophil count was 4.84 × 10(9)/L, or 41.7 % of all white blood cells. Doppler ultrasound showed multiple medium-high echo plaques in the bilateral carotid bifurcation with reduction in diameter of 10-15 %. Transthoracic echocardiography was normal. A short course of glucocorticoids and aspirin were administered to the patient, and he was discharged with significant improvement of his neurological symptoms and eosinophil count. The patient refused to take prednisone thereafter; however, 6 months later, his eosinophil count was 1.57 × 10(9)/L, or 15.3 % of all white blood cells. Transthoracic echocardiography continued to be normal, but vascular ultrasound demonstrated many bilateral carotid low-medium echo plaques. This case describes a patient HES with acute cerebral infarction in a watershed distribution with lesions of the carotid artery but no cardiac damage. HES should be considered to be a cause of multiple cerebral infarctions.
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