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Non-ischemic cerebral enhancing (NICE) lesions - foreign body granuloma secondary to pipeline stenting

Case contributed by Ana Brusic
Diagnosis almost certain

Presentation

4/7 right upper limb weakness on background of pipeline stent for left ICA aneurysm 1/12 ago.

Patient Data

Age: 50 years
Gender: Female

Diffuse white matter changes are demonstrated throughout the left cerebral hemisphere with generalized mass effect resulting in effacement of the cortical sulci near the vertex. Multifocal areas of sub-centimeter nodular enhancement, which are confluent in some areas. No diffusion restriction within the areas of enhancement, however there is a punctate region of diffusion restriction in the left middle frontal gyrus, consistent with a recent infarct.

Flow diverter stent across the neck of left cavernous/ophthalmic ICA large aneurysm. Altered signal within the stent characteristic of susceptibility related signal loss. The aneurysm sac measures up to 1.4 cm, not significantly increased compared to pretreatment imaging. Subtle reduced caliber and signal intensity of distal arteries in the left cerebral hemisphere.

Ventricles and midline structures are otherwise satisfactory. No hydrocephalus.

Conclusion: Diffuse left cerebral hemisphere white matter changes and "non-ischemic cerebral enhancing" (NICE) lesions are most compatible with foreign body reaction to microembolisation of the hydrophilic polymer (SHIELD) in this clinical context. Two small left frontal MCA cortical infarcts noted. Persistent filling of left ICA aneurysm.

DWI obtained a month earlier, immediately after stenting showed no abnormal restricted diffusion to suggest an acute procedure related infarct.

The previously seen extensive left cerebral hemisphere white matter T2/FLAIR hyperintensities have reduced in extent/confluence, while maintaining a similar distribution. Punctate areas of enhancement scattered throughout these white matter changes persist but also have significantly reduced in number and size. Minimal foci of mild diffusion restriction in amongst mainly T2 shine through. Tiny scattered foci of susceptibility artefact within the areas of nodular enhancement, in keeping with microhemorrhages, distributed along with slightly prominent parenchymal draining veins.

Flow diverter stent across the neck of left cavernous/ophthalmic ICA large aneurysm. Flow signal is preserved within the stent, unchanged on MRA compared to the prior study. The left ICA aneurysm has become intrinsically T1 hyperintense, with less T2 hypointensity, and new diffusion restriction. The aneurysm sac measures up to 1.4 cm, not increased in size. The previously seen subtle reduced caliber and signal intensity of distal arteries in the left cerebral hemisphere has resolved. Dominant left vertebral artery, with the right vertebral artery terminating as the PICA. Foetal origin of the left PComA.

The ventricular size and sulcal pattern is appropriate for the patient's age.

Conclusion:  The non-ischemic cerebral enhancing (NICE) lesions have markedly improved. Additionally, there are findings in keeping with thrombosis of the pipeline-treated left ICA aneurysm since the previous MRI.

Case Discussion

Non-ischemic cerebral enhancing (NICE) lesions are a rare complication of intracranial aneurysm endovascular therapy. This complication has been attributed either to foreign body emboli and subsequent granulomatous reaction or cerebral hypersensitivity and nickel allergy.

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