Table 2 Summary of the imaging findings in meningiomas and their mimics
| Â | Summary of typical imaging findings | Useful distinguishing features |
|---|---|---|
Meningioma | CT: hyperdense, wide base, often with intratumoural calcification. T1WI: isointense. T2WI: isointense. Other features: avid enhancement with enhancing dural tail, adjacent hyperostosis, ECA blood supply. | Intratumoural calcification. Hyperostosis of adjacent skull. May have sunburst enhancement due to internal vessels. High choline:Cr ratio, low NAA peak on MRS. Alanine peak, if present, is characteristic. High rCBV compared with most mimics |
Metastasis | CT: hyperdense, diffuse thickening or mass like. T1WI: hypointense but variable. T2WI/FLAIR: hypointense but variable. Other features: strongly enhancing. Local invasion with destruction of the bone. Hypervascular metastases (renal and melanoma) can have similar rCBV to meningiomas. | Can be hypointense on T2WI. Multivessel blood supply from ICA and ECA. Invasion of adjacent skull and soft tissue structures. Low NAA:Cr and high lipid:Cr ratio on MRS. |
Low-grade SFT | CT: iso- to hyperdense. Well circumscribed. Can contain calcification. T1WI: isointense T2WI: mixed signal due to hypointense regions of collagen. Other features: solitary. Even hypointense areas on T2WI enhance. Separate regions of different T2 signal can cause Yin-Yang sign. May have high rCBV similar to meningiomas. | May have ‘fluffy’ contrast enhancement rather than sunburst. Enhancement of regions of hypointensity on T2WI (collagen). High myo-inositol with lipid and lactate peaks on MRS. |
High-grade SFT | CT: hyperdense. May ‘mushroom’ away from the dura with due to a narrow dural base T1WI: heterogeneous, with areas of haemorrhage. T2WI/FLAIR: heterogeneous with areas of cystic change and necrosis. Other features: heterogeneous strong enhancement. Higher grades are more likely to cause bone destruction and cross the midline. A dural tail is common but less so in the highest-grade lesions. Multiple flow voids. Solitary. May have high rCBV similar to meningiomas. | No calcification. Destruction of the bone rather than hyperostosis. Often a narrow dural base. Highly vascular with supply from ICA and ECA. High myo-inositol on MRS. |
Lymphoma | CT: hyperdense. T1WI: hypointense. T2WI/FLAIR: iso- to hypointense. Other features: may be lobulated with indistinct ‘fluffy borders’. Strong enhancement and prominent perilesional oedema. Secondary leptomeningeal disease can cause meningeal thickening and enhancement. | No calcification and no hyperostosis. Lobulated Fuzzy tumour-brain interface |
Melanotic tumours | CT: iso- to hyperdense. May be diffuse or mass like. T1WI: contain areas of hyperintensity due to haemorrhage and high melanin content. T2WI/FLAIR: iso- to hypointense. Other features: strongly enhancing. Lack of primary systemic melanotic lesion is suspicious for primary CNS disease. | No calcification and no hyperostosis. Usually contain areas of T1 hyperintensity due to melanin and haemorrhage |
Gliosarcoma | CT: heterogeneous mass with hyperdense soft tissue components T1WI: isointense but may contain areas of haemorrhage T2WI: heterogeneous with areas of necrosis Other features: heterogeneous or peripheral strong enhancement, small amount of perilesional oedema. | High lipid and high lipid-choline ratio on MRS Some lesions have peripheral enhancement. No calcification and no hyperostosis. |
Rosai-Dorfman disease | CT: hyperdense. Well circumscribed with no calcification. T1WI: isointense T2WI/FLAIR: iso- to hypointense. Other features: erosion of adjacent bone with slight vasogenic oedema. Arise from meninges or endocranium. | More likely to have bone erosion with no calcification or hyperostosis. Lesions are hypovascular. |
Erdheim-Chester disease | CT: hyperdense. Nodular or diffuse meningeal thickening. T1WI: isointense. T2WI/FLAIR: iso- to hypointense. Other features: strong, homogenous enhancement that can persist for up to 8 days. Most patients have diffuse calvarial thickening or paranasal sinus wall osteosclerosis. | Patients with intracranial disease will almost always have facial bone or calvarial sclerosis or thickening. Persistent dural enhancement. |
Tuberculosis | CT: iso- to hyperdense. Focal nodular or diffuse dural thickening. T1WI: isointense. T2WI/FLAIR: isointense. Other features: strong enhancement without calcification. Parenchymal tuberculomas can also attach to dura and can have solid or ring-enhancement. | Meningitis preferentially affects the basal meninges. No calcification in acute phase. Erosion of the bone instead of hyperostosis. Peripheral parenchymal lesions may have ring-enhancement rather than solid. Decreased NAA:Cr and NAA:choline ratios. |
Granulomatosis with polyangiitis | CT: isodense diffuse or focal dural thickening. T1WI: isointense. T2WI/FLAIR: isointense. Other features: moderate uniform enhancement. Focal nodular disease typically affects the skull base and tends to be contiguous with paranasal sinus involvement. Ischaemic changes in the brain due to vasculitis. Longstanding disease may calcify. | Characteristically located at the skull base. Contiguous invasive inflammatory soft tissue in adjacent paranasal sinuses. Secondary features of cerebral vasculitis. |
Epstein–Barr virus-associated smooth muscle tumour | CT: hyperdense dural masses. T1WI: iso- to hypointense. T2WI/FLAIR: iso- to hypointense. Other features: avid enhancement. Multifocal. | Patients are immunosuppressed, most commonly due to AIDS or after solid organ transplantation. Typically multifocal with additional CNS and systemic lesions arising in many tissues. |
IgG4-related disease | CT: hyperdense. Focal nodular or diffuse linear dural thickening. T1WI: hypointense. T2WI/FLAIR: hypointense. Sometimes additional foci of hyperintensity Other features: avid homogeneous enhancement. Typically causes remodelling of adjacent bone but infiltration also very rarely occurs. Avid FDG and methionine PET tracer uptake. | Often found in the presence of other IgG4-related diseases, and patients characteristically have raised serum IgG4. Lesions are low signal on T1WI and T2WI due to fibrosis. |