British Journal of Radiology 74 (2001),662-667 © 2001 The British Institute of Radiology
Imaging of giant tumours involving the anterior skull base
S E J Connor, MRCP, FRCR1,
N Umaria, MRCP, FRCR2 and
S V Chavda, FRCR2
1Department of Neuroimaging, King's College Hospital, Denmark Hill, London SE5 9RS and 2Department of Radiology, City Hospital NHS Trust, Birmingham B18 7QH, UK
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Abstract
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Tumours involving the anterior skull base are a challenge in diagnosis and treatment. They may arise from the bony skull base itself, intracranially or from the sinonasal tract and orbit. It is often difficult to determine the site of origin of giant tumours as anatomical boundaries are frequently breached. Accurate imaging evaluation is useful in planning treatment and may help in the differential diagnosis. We review those CT and MRI features of giant anterior cranial fossa tumours which may be helpful in identifying a pre-operative diagnosis.
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Introduction
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Tumours involving the anterior skull base encompass a variety of benign and malignant lesions which may arise inferiorly (paranasal sinuses, nasal cavity, orbit), superiorly (meninges, olfactory pathway), anteriorly (skin, frontal sinus), posteriorly (sphenoid bone, sella, parasellar region) or from the bone itself. Giant anterior cranial base tumours are defined as those with a "tumour equivalent diameter" of greater than 4.5 cm. The tumour equivalent diameter is calculated as (X x Y x Z)1/3 where X, Y and Z are the maximum diameters in each plane [1].
The role of imaging in these giant tumours is principally to assess the tumour extent. The presence of dural and perineural invasion influences both prognosis and surgical planning [2]. Although operative biopsy is normally required to reach a definite diagnosis in these tumours, it is also helpful to consider a pre-operative diagnosis based on the imaging appearances. The aim of this pictorial review is to discuss the CT and MRI appearances of these giant tumours involving the anterior skull base.
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Epithelial sinonasal malignancy
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These are the commonest malignant tumours to invade the anterior skull base, accounting for 39% of cases requiring craniofacial resection. While most of these carcinomas invade the skull base by direct extension, adenocystic carcinoma has a tendency to spread along neurovascular bundles. These tumours are of soft tissue CT attenuation. Contrast enhancement may show areas of central necrosis. Tumoral calcification is rare. There is aggressive bone destruction of the anterior cranial base and wherever the tumour has spread beyond the confines of the sinonasal tract. Since epithelial tumours are highly cellular they tend to be relatively homogeneous and of intermediate signal on both T1 and T2 weighted sequences (Figures 1a,b
). There may be focal signal inhomogeneity in areas of necrosis or haemorrhage. The degree of gadolinium enhancement varies with tumour vascularity and is mild to intense [3]. The epicentre of these tumours is likely to be the ethmoid air cells or nasal cavity from where there may also be extension through the medial orbital wall to the infratemporal fossa or to the middle cranial fossa via the superior orbital fissure. The surface of the intracranial extension tends to be broad based and flat, although expansive "dumbbell tumours" have been described.
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Figure 1. Coronal (a) and sagittal (b) T1 weighted spin echo MR images post-gadolinium demonstrate a large, intermediate signal squamous cell carcinoma which is centred on the ethmoid sinus. It extends into orbits, upper nasal cavity, right maxillary antrum and into the upper clivus. There was very limited enhancement following gadolinium administration.
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Meningioma
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Meningiomas of the anterior cranial fossa floor arise most frequently from the olfactory groove or tuberculum sella and account for 12–22% of all meningiomas. Anterior cranial fossa meningiomas are greater than 4 cm in diameter in 73% of cases. On CT most giant meningiomas are hyperdense, well demarcated and lobulated lesions. Calcification is detected in 15–20% of cases. Anterior skull base penetration may be associated with marked thickening of the bone (Figures 2a,b), corticated pressure erosion or occasionally bony lysis. On T1 weighted MRI, 60% of meningiomas are isointense and 30% are hypointense compared with grey matter. There is intense gadolinium enhancement of meningiomas (Figure 3), and a linear enhancing "tail" extending away from the tumour mass is a characteristic feature in 60% of cases. On T2 weighted imaging, 50% of tumours are isointense and 40% hyperintense to grey matter. T2 weighted sequences are frequently more heterogeneous, owing to the presence of cysts and calcification. Hyperintensity on T2 weighted sequences is associated with aggressive meningiomas [4].
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Figure 2. (a) Post-gadolinium coronal T1 weighted spin echo MR image demonstrates a giant anterior cranial base meningioma. The non-enhancing intermediate signal in the ethmoid air cells (arrowheads) did not enhance and represented hyperostosis. (b) Hyperostosis of the anterior skull base is confirmed on the axial CT image in the same patient.
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Figure 3. Post-gadolinium sagittal T1 weighted spin echo MR image demonstrates giant recurrent (note craniotomy, arrowheads) anterior cranial base meningioma which extends into the ethmoid sinus and upper nasal cavity. There is intense gadolinium enhancement.
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Esthesioneuroblastoma
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Esthesioneuroblastomas are rare, slow growing malignant neoplasms which usually arise from the basal layer of olfactory mucosa in the region of the olfactory plate or superior nasal cavity. As the symptoms and signs are non-specific, patients tend to present with advanced disease, with intracranial extension occurring in 25% of cases. As the histological diagnosis of this tumour is difficult and since it may be confused with several other giant anterior cranial fossa tumours such as squamous cell carcinoma, meningioma and lymphoma, the possibility of an esthesioneuroblastoma must be appreciated at pre-operative imaging. CT shows a homogeneous soft tissue mass with relatively uniform enhancement. One distinguishing feature is occasional focal calcification, which makes CT particularly useful in the presence of a superior nasal mass [5]. There is usually bony remodelling and rarely hyperostosis. These lesions are of variable T1 weighted and T2 weighted signal with some heterogeneity and minimal to moderate gadolinium enhancement (Figure 4) [6]. Although esthesioneuroblastomas are initially unilateral within the upper nasal cavity, they subsequently expand the nasal cavity and ethmoid air cells bilaterally, before penetrating the orbit and cribriform plate. There is a broad base of bony destruction when the tumour extends into the anterior cranial fossa. The presence of cysts at the intracranial margin of a sinonasal mass is suggestive of esthesioneuroblastoma.
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Figure 4. Post-gadolinium coronal T1 weighted spin echo MR image shows a heterogeneously enhancing esthesioneuroblastoma, which is centred on the cribiform plate, and extends in to the anterior cranial fossa and to the nasal cavity.
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Haemangiopericytoma
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Haemangiopericytomas are vascular neoplasms and comprise less than 1% of skull base tumours. They are commonly very large, multilobulated masses which may invade the skull base. The mass and the pattern of spread depends on whether they have a sinonasal or intracranial origin and thus anterior skull base invasion may result from either inferior or superior extension of these tumours. On CT haemangiopericytomas are moderate to intensely enhancing, well defined hyperdense masses. Although they may resemble meningiomas, these tumours tend to erode bone instead of inducing hyperostosis and they rarely contain calcification. MR images demonstrate low to intermediate T1 signal and intermediate to high T2 signal intensities. There may be some T2 heterogeneity and there is always marked gadolinium enhancement (Figures 5a,b) [7].
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Figure 5. Coronal T1 weighted spin echo MR images (a) pre- and (b) post-gadolinium, demonstrating a bilateral mixed cystic and solid giant haemangiopericytoma extending into both frontal lobes from the ethmoid sinus. The solid portion intensely enhances. A cystic component is a recognized but atypical feature of a haemangiopericytoma.
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Benign fibro-osseous lesions
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In benign fibro-osseous lesions, bone is replaced with benign fibrous tissue containing varying proportions of mineralized structure. The term encompasses both fibrous dysplasia and ossifying fibroma. Histological differentiation of these two entities is difficult and they are indistinguishable on imaging criteria. In the skull, fibrous dysplasia commonly involves the ethmoid, sphenoid, frontal and temporal bones in decreasing order. Extensive fibrous dysplasia of the frontoethmosphenoid region is uncommon but is more aggressive than that confined to the ethmoid sinus. CT characteristics include expansion of the medullary space with an appearance ranging from ground glass to scattered foci of bone formation, or a primarily non-ossified matrix (Figure 6a). The cortical margins are intact with minimal thickening. Three-dimensional CT reconstructions may aid surgical planning. MRI demonstrates intermediate to low signal on T1 weighting and there is heterogeneous T2 signal owing to the mixture of matrix, haemorrhagic and cystic elements. There is moderate gadolinium enhancement (Figures 6b, c) [8]. High clinical and pathological activity may correlate with increased intensity on both T1 and T2 weighted sequences.
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Figure 6. (a) Axial CT scan demonstrates groundglass appearance in fibrous dysplasia of the anterior skull base. Post-gadolinium T1 weighted spin echo coronal (b) and STIR sagittal (c) images demonstrate extensive frontoethmosphenoid fibrous dysplasia. The cortical bone in the anterior cranial base is elevated but intact. The high signal on STIR images represents cystic component and there is marked enhancement of the intervening septae compared with the pre-contrast image (not shown).
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Chondrosarcoma
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Skull base chondrogenic tumours are more commonly malignant than those elsewhere in the head and neck. Since the skull base is formed from a cartilaginous matrix, chondrosarcomas probably originate from embryonal rests in the anterior cranial fossa. Less than 10% of skull base chondrosarcomas are derived from the frontoethmoid region. On CT, a slightly hyperdense mass with clumps of calcification and foci of bone destruction is seen (Figure 7a). There is only moderate contrast enhancement, although gadolinium enhancement on MRI studies may be more pronounced (Figure 7b). The tumour appears isointense to hypointense on T1 weighted images. On T2 weighted sequences the mass shows a high signal intensity that may be isointense to cerebrospinal fluid and is characteristic of this lesion [9].
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Figure 7. (a) Coronal CT scan showing bony destruction of the floor of the anterior cranial fossa by a giant chondrosarcoma which contains clumps of calcification. (b) Contrast enhanced T1 weighted spin echo coronal MR image demonstrating peripheral inhomogeneous enhancement and areas of signal void centrally in keeping with areas of calcification.
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Differential diagnosis of giant tumours involving the anterior skull base
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There are other tumour types which should be considered in addition to the illustrated tumours. Malignant cutaneous tumours, sinonasal plasmacytomas, metastases, giant cell tumours, soft tissue sarcomas and meningosarcomas, lymphomas, subfrontal neuromas and teratomas have all been described or illustrated as giant tumours involving the anterior skull base.
Tumour morphology and enhancement as well as the pattern of bony involvement may be useful in limiting the differential diagnosis. A broad-based interface with the anterior cranial fossa is frequently seen with epithelial sinonasal malignancy, esthesioneuroblastoma and meningioma, and marginal cysts generally indicate esthesioneuroblastoma or rarely meningioma. Diffuse marked contrast enhancement is characteristic of meningioma, haemangiopericytoma or plasmacytoma. Tumoral calcification may be seen in association with chondrosarcoma, teratoma, meningioma and esthesioneuroblastoma. A linear "dural tail" of enhancement is characteristic of meningiomas but is also seen with neuromas, metastases and adenocystic carcinomas. This enhancement is distinct from the nodular or thick (>5 mm) marginal dural enhancement which indicates dural infiltration by tumour and which is important for surgical planning and prognosis [2]. Sclerotic or hyperostotic bone reaction is associated with osteoblastic metastases, meningiomas, fibro-osseous lesions or previous radiotherapy. Bone destruction is more typical of epithelial sinonasal malignancy, sarcomas, metastases and lymphoma, whereas bony remodelling may also be noted with neuromas, meningiomas, plasmacytomas and sarcomas. Since these giant tumours traverse anatomical compartments, the epicentre may not be a helpful feature in determining the differential diagnosis. Apart from soft tissue sarcoma, esthesioneuroblastoma, benign fibro-osseous lesions and teratomas, these giant anterior skull base tumours are rare in children.
These tumours must be distinguished from non-neoplastic lesions which can reach a giant size and invade the anterior skull base, such as frontoethmoid mucoceles, invasive aspergillomas and massive nasal polyposis. In addition, tumour extending anteriorly from the central skull base or suprasellar region may mimic anterior skull base lesions, and sagittal images are useful to confirm the tumour origin (Figure 8).
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Figure 8. Post-gadolinium T1 weighed spin echo sagittal MR image shows a giant pituitary macroadenoma which extends from its suprasellar origin into the anterior fossa where it may mimic an anterior skull base lesion.
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In conclusion, CT and MRI appearances of a tumour may indicate the origin of a giant anterior cranial skull base tumour. The morphology, the presence of cysts and calcification, the pattern of contrast enhancement, including the presence of a dural tail, and the type of bony involvement are some of the features that require assessment.
Received for publication April 5, 2000.
Revision received August 23, 2000.
Accepted for publication September 25, 2000.
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Abstract
Introduction
