Effectiveness of Infliximab for Refractory Non-ischemic Cerebral Enhancing Foreign-body Granulomatous Lesions Following Endovascular Therapy
Albert Aboseif1, Farris Taha2, Nathan Tagg3, Andrew Smith4, Eoin Flanagan1, Robert Brown1, Sean Pittock1, Gina Perez-Giraldo5, Andrew McKeon1
1Department of Neurology, Mayo Clinic, 2Department of Neurology, Washington University in St. Louis, 3Duke Eye Center, Duke University Medical Center, 4Neurology Clinic, UCHealth, 5Department of Neurology, Medical University of South Carolina
Objective:

To highlight the novel use of tumor necrosis factor (TNF)-α inhibition in treating refractory non-ischemic cerebral enhancing (NICE) lesions.

Background:
NICE foreign-body granulomatous lesions are an immune-mediated complication of endovascular therapy (EVT). No single immunotherapy has demonstrated consistent effectiveness. 
Design/Methods:

This multi-center case series describes three patients with refractory NICE lesions (recurrent seizures, persistent MRI enhancement, and/or steroid dependence with failure of ≥ 1 maintenance immunotherapy) treated with infliximab. Their clinical course, evaluation, and outcomes are detailed.

Results:

Patients were female (median age 57 years [range 56-58]), presenting with headache and seizures within six months of EVT for intracranial aneurysm (n=2) or carotid stenosis (n=1). MRI (n=3) revealed unilateral nodular enhancement with vasogenic edema, and brain biopsy (n=2) revealed foreign-body granulomatous inflammation. All patients developed refractory disease and steroid dependence despite ≥1 immunotherapy including mycophenolate (n=3), rituximab (n=1), and/or cyclophosphamide (n=1). Infliximab treatment resulted in significant clinical and radiological improvement in all three patients.

Conclusions:

TNF-α inhibition may be an effective targeted treatment strategy for NICE foreign-body granulomatous lesions, expanding treatment options for patients with refractory disease. Larger prospective studies are needed to establish treatment guidelines aimed at improving outcomes in individuals with refractory disease.

10.1212/WNL.0000000000215791
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