M Alain Babi, Salman Al Jerdi and Mark Gorman
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".