alexa Bilateral Borderzone Infarcts in Hypereosinophilic Leukemia without Proximal Vessel Stenosis | OMICS International | Abstract
ISSN: 2155-9562

Journal of Neurology & Neurophysiology
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Case Report

Bilateral Borderzone Infarcts in Hypereosinophilic Leukemia without Proximal Vessel Stenosis

M Alain Babi1,2*, Salman Al Jerdi1 and Mark Gorman1

1Department of Neurological Sciences, University of Vermont College of Medicine, Burlington, Vermont 05405, USA

2Division of Neuro-critical care, Department of Neurology, Duke University Hospital, Durham NC 27713, USA

*Corresponding Author:
M Alain Babi
Duke University Hospital DUMC 2900 Durham
NC 27710, USA
Tel: (802) 777 2880
Fax: 802-847-5690
E-mail: [email protected]

Received date: December 21, 2015 Accepted date: January 19, 2016 Published date: January 26, 2016

Citation: Babi MA, Al Jerdi S, Gorman M (2016) Bilateral Borderzone Infarcts in Hypereosinophilic Leukemia without Proximal Vessel Stenosis. J Neurol Neurophysiol 7:349. doi:10.4172/2155-9562.1000349

Copyright: © 2016 Babi MA, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Objective: We describe border-zone territory infarctions without evident hypotension or vascular stenoses in a case of hypereosinophilic syndrome (HES). We review the spectrum of neurological changes associated with HES and explore about its relationship with the observed infarction pattern.
Methods: This is a case report. A PubMed literature search was conducted searching clinico-radiographic findings of neurological complications associated with HES.
Results:
A previously healthy 47 year old man presented with progressive encephalopathy, weight loss and general malaise over three weeks. MRI head revealed bilateral hemispheric watershed infarcts at the junction of the anterior and posterior circulations. No intracranial or extracranial vascular stenoses were found and cardiac evaluation via transesophageal echocardiography, telemetry, and cardiac computed tomography (CT revealed no clear cardiac source of emboli. Persistently elevated eosinophil (>5,000/ μL) led to a bone marrow biopsy and diagnosis of eosinophilic leukemia with CHIC-2 mutation. Treatment with Imatinib and high dose prednisone was undertaken with significant clinical improvement.
Conclusion: This case highlights a very rare cause of bilateral watershed cerebral infarction in non-hemodynamic stenoses. We hypothesize that the particular pattern of infarct observed in this setting may be explained on the basis of the lower capacity of hypoperfused vessel (borderzone) to eliminate emboli related to in situ-thrombosis from degranulation of eosinophils: "Impaired Wash-Out Theory".

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