Non-ischemic cerebral enhancing (NICE) lesions

Last revised by Bálint Botz on 29 Nov 2022

Non-ischemic cerebral enhancing (NICE) lesions are an uncommon delayed complication of cerebrovascular procedures, including aneurysm coiling, thrombectomy and placement flow-diverting stent placement 1,2,4.

As NICE lesions are seen following endovascular procedures most commonly for aneurysm treatment, the epidemiology of cases mirrors that of cerebral aneurysms. Reported cases vary in age from 31 to 71 years 1.

The incidence of NICE lesions in patients who have undergone aneurysm coiling is reported as approximately 0.5% 1,2 although, given the low number of reported cases and the potential for many cases being unrecognised, the true incidence is unknown.

There appears to be a female predilection 1.

NICE lesions are a delayed phenomenon and typically present many days to weeks following the procedure; reported range: 2 weeks to 12 months 1,2,4. Symptoms are variable depending on the location and number of lesions 1.

CSF examination is usually bland or demonstrates mild elevation of protein and white cells 1,2.

The cause of NICE lesions remains somewhat controversial with most authors believing that they represent a granulomatous reaction to foreign body emboli occurring at the time of intervention 1,2. An alternative theory is that they are the result of nickel hypersensitivity 1.

In some reported cases where biopsy was undertaken, histology demonstrated foreign-body granulomatous reaction surrounding sterile microabscess containing fragments of the hydrophilic coating of many catheters, polyvinylpyrrolidone (PVP) 2. Similar reactions have been identified in other parts of the body (e.g. the wrist from radial puncture in coronary angiograms) 1.

It has been postulated that the risk of developing NICE lesions is related to tight-fitting catherter/guidewire/device combinations, where the risk of sheering off the PVP lining is theoretically higher 2. This may also explain why the use of flow-diverting stents, which are relatively stiff and bulky, is over-represented in reported cases 2.

Of note, it has been theorized that the same mechanism may be responsible for delayed ipsilateral parenchymal hemorrhage (DIPH) following aneurysm repair 3.

NICE lesions are typically only seen in the territory corresponding to the vessel that was the target of endovascular therapy 1. Variations in circle of Willis anatomy can therefore influence the distribution of lesions.

Non-contrast CT may be normal or demonstrate small areas of hypodensity 1.

NICE lesions appear as multiple punctate or small ring enhancing foci. They can involve the white matter, cortex or leptomeninges 1. They have the following signal characteristics 1.

  • T1: hypointense

  • T2

    • central iso- to hypointense

    • peripheral hyperintensity due to vasogenic edema

  • DWI/ADC: variable

  • SWI/T2*: variable, some normal other show signal loss

No angiographic features have been described 1,2.

The natural history of NICE lesions remains to be established. Corticosteroids can reduce edema and enhancement, however, recurrence may occur and thus followup with MRI is recommended 1.

  • subacute infarcts: may appear similar, however, would be expected to appear immediately following the procedure and will undergo expected evolution

  • cerebral microabscesses: may appear similar on imaging but are usually encountered in a different clinical scenario and would not be expected to be confined to the vascular territory of prior treatment

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Cases and figures

  • Case 1: FLAIR
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  • Case 1: T1 C+
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