This article provides a summary of how to approach the imaging analysis of lesions of the anterior, central, and posterior skull base. The primary focus is tumors and tumor-mimickers, and representative examples are shown to differentiate the features of lesions that can occur in the same location.
Key Points
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A specific diagnosis is not always possible based on imaging alone; however, a systematic approach to the imaging of skull base lesions can allow the rapid formation of a concise and logical differential diagnosis.
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CT of the skull base provides excellent anatomic detail of osseous structures.
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MRI provides excellent soft tissue detail, although no single “routine” MRI protocol exists that will work for all skull base pathology.
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Positron emission tomography (PET)/CT is an important tool for the diagnosis and follow-up of head and neck malignancies.
Introduction
Lesions of the skull base can be challenging to diagnose and treat because of the complex anatomy, proximity to cranial nerves and important vasculature, and wide variety of pathology that may be infrequently encountered. Modern imaging techniques can help characterize skull base lesions, determine a diagnosis, and formulate a plan for tissue diagnosis and/or subsequent treatment.
Imaging considerations for skull base
CT
CT of the skull base provides excellent anatomic detail of osseous structures. CT is a widely available technique that can be performed quickly. When using a helical acquisition technique, the raw data can be processed within the scanner to provide reconstructions in any imaging plane from a single acquisition. Although orthogonal axes are most commonly used (axial, sagittal, and coronal), oblique planes can be used to correct for head tilt or provide optimal visualization of a specific structure (eg, simulated Stenvers or Pöschl views).
CT source data can be rendered into images of varying thicknesses, with thinner sections providing higher anatomic detail at the expense of more image noise. CT source data can also be subjected to sharpening algorithms to enhance osseous detail. Soft tissue–optimized images (“soft tissue algorithm”) can be adjusted to show osseous detail (“bone window”), however, with less osseous resolution than the dedicated bone algorithm images.
When tumor, infection, or a vascular lesion is suspected, intravenous iodinated contrast may be a helpful adjunct. If the CT images are obtained during the initial arterial phase after administering contrast, the study provides excellent vascular detail (ie, CT angiography). CT images performed 1 to 3 minutes after contrast administration provide less angiographic detail; however, tumors with capillary/venous pooling and hyperemic tissue associated with an infectious process will become more conspicuous. When evaluating cerebrospinal fluid (CSF) leaks, intrathecal iodinated contrast can be administered via lumbar puncture and then used to diagnose and localize a leak.
Given the ionizing radiation required for CT examinations, carefully identifying the diagnostic question before the scan helps maximize utility of the study while minimizing excess radiation. Efforts to reduce radiation dose, possibly through use of alternative imaging modalities, may be especially important in children.
MRI
MRI provides excellent soft tissue detail; however, no single “routine” MRI protocol exists that will work for all skull base abnormalities. The imaging protocol required will be based on the suspected abnormality, the available imaging equipment, and local imaging expertise.
T1- and T2-weighted sequences are the 2 basic MR pulse sequences that can be performed in different planes and with different slice thicknesses. Typically, fat, proteinaceous material, and some blood products (particularly methemoglobin) have a hyperintense (or “bright”) appearance on T1-weighted imaging. Fat and water tend to be hyperintense on T2-weighted imaging. Note that subtle variations between sequences on different protocols, at different field strengths, and using equipment from different manufacturers can significantly vary the appearance of structures, and thus familiarity with locally used protocols is important for proper interpretation of images.
Intravenous administration of gadolinium chelates serves a similar contrast-enhancement role for MR that iodinated contrast does for CT. Enhancing lesions will be hyperintense, or “bright,” on postcontrast T1-weighted sequences; however, 2 pitfalls can occur if one is not careful. A finding that has intrinsic hyperintense signal on T1-weighted images (T1 hyperintense appearance) will be hyperintense on postcontrast sequences even in the absence of enhancement, and therefore comparison with precontrast T1-weighted imaging is important. As fat has a hyperintense appearance on T1-weighted images, a small enhancing lesion surrounded by fat can be difficult to detect. For this reason, special MR sequences in which the signal of fat is nulled (fat suppression) can improve conspicuity of lesions surrounded by fat. Often, however, using non–fat-suppressed imaging at the skull base is preferred because of the image degradation and artifacts that can occur with fat suppression techniques. Moreover, because of its intrinsic bright signal, fat provides excellent contrast with low-intensity structures, such as nerves and vessels. Diffusion-weighted imaging is a technique commonly used in the brain to detect stroke; however, it has recently become recognized for its ability to characterize abscesses and head and neck tumors, and to differentiate cholesteatoma from granulation tissue.
High-resolution fluid-sensitive balanced steady state free precession sequences, often referred to by manufacturers proprietary acronyms, such as CISS (constructive interference in the steady state; Siemens AG, Munich, Germany) or FIESTA (fast imaging employing steady state acquisition; GE, Fairfield, CT) can provide submillimeter resolution and are excellent for detecting cranial nerve abnormalities and finding fluid communications in suspected meningoceles/encephaloceles.
Intrathecal gadolinium to detect skull base CSF leaks has been described in several reports, although this technique is not currently approved by the U.S. Food and Drug Administration and therefore is not discussed in this report. However, this technique may emerge as an important problem-solving tool in the future.
Angiography
Angiography remains an important tool for confirming the diagnosis of vascular lesions of the skull base, and can serve as a therapeutic option in many cases, either on its own or for presurgical embolization.
Nuclear Medicine
Although PET/CT is an important tool for the diagnosis and follow-up of head and neck malignancies and metastases, it is not significantly discussed in this article. Radionuclide cisternography can be helpful for confirming a CSF leak, but it has less spatial resolution than either CT or MR cisternography. Nuclear medicine studies can also help confirm whether a tumor has a neuroendocrine origin, such as in glomus tumors/paragangliomas.
Anterior skull base
Anatomy
The anterior skull base includes the pterygopalatine fossa, cribriform plate, and planum sphenoidale, and thus abnormalities can have an intracranial, neurovascular, or sinonasal origin ( Table 1 ). Traumatic and congenital abnormalities are also commonly encountered.
| Neoplasms | Sinonasal carcinoma Metastatic lesions Sinonasal undifferentiated carcinoma Juvenile nasal angiofibroma Sinonasal melanoma Hemangiopericytoma Non-Hodgkin’s lymphoma, sinonasal Nerve sheath tumor Esthesioneuroblastoma Meningioma |
| Congenital | Sincipital encephalocele |
| Infection/other | Empyema of sinonasal origin Mucocele Fibrous dysplasia Sinonasal osteoma |
The pterygopalatine fossa is a crossroads of nerves and vessels that communicates with the intracranial contents via foramen rotundum posteriorly ( Fig. 1 C, G, J), the central skull base/carotid canal via the vidian canal posteriorly ( Fig. 1 D, G), the orbit via the infraorbital foramen superiorly ( Fig. 1 J), the paranasal sinuses via the sphenopalatine foramen medially ( Fig. 1 C), the masticator space via the pterygomaxillary fissure laterally ( Fig. 1 C, D), and the hard palate via the greater and lesser palatine foramina inferiorly. Therefore, the pterygopalatine fossa is often involved in perineural spread of head and neck neoplasms and should be especially scrutinized in patients with head and neck, orbital, and sinonasal abnormalities.
Congenital Lesions
Congenital anomalies of the anterior skull base often present in infancy, and their complexity is rich enough for a dedicated article. Because occasionally patients may present later in childhood or adulthood, it is important to be aware of and exclude these entities before biopsy or excision of an anterior skull base lesion. Sincipital encephaloceles can be subdivided by location into frontonasal, frontoethmoidal, and sphenoid encephaloceles. Embryologic rests of tissue can also result in masses such as a nasal glioma and a nasal dermoid. High-resolution fluid-sensitive sequences (eg, CISS/FIESTA) can help identify CSF/dural extension through the skull base, thereby helping to characterize these lesions.
Tumors
Many types of neoplastic processes may involve the anterior skull base, including juvenile nasal angiofibroma (JNA), esthesioneuroblastoma, sinonasal malignancies, and meningioma. When the mass is large, the center of the mass may become difficult to accurately localize, and the precise diagnosis may similarly become difficult to determine.
JNA
JNA is a vascular tumor that arises in the sphenopalatine foramen and extends into the posterior nasal cavity. The classic presentation is that of an adolescent boy with recurrent unilateral epistaxis. Because it arises from the medial recess of the pterygopalatine fossa, it is not unexpected that the arterial supply is predominantly from the internal maxillary artery. CT typically shows an intensely enhancing mass that causes expansion of the sphenopalatine foramen, an imaging hallmark for this neoplasm. MR often shows heterogeneous signal on T1- and T2-weighted imaging and avid contrast enhancement, with internal flow voids confirming the internal vascularity. Larger masses characteristically produce posterior scalloping and mass effect on the posterior wall of the maxillary sinus. Angiography and embolization are often required as preoperative adjuncts.
Esthesioneuroblastoma
Esthesioneuroblastoma, or olfactory neuroblastoma, is a neural tumor arising from branches of the olfactory nerve and is therefore typically centered at the cribriform plate. Differentiation from other abnormalities involving the cribriform plate can be difficult, but esthesioneuroblastoma will often demonstrate peripheral cystic components along the superior (intracranial) margin ( Fig. 2 ).
Nonesthesioneuroblastoma Cribriform Plate Invasion
Cribriform plate invasion can occur from nearly any sinonasal primary malignancy, including sinonasal undifferentiated carcinoma, squamous cell carcinoma, adenocarcinoma, inverted papilloma, melanoma, and metastases. Sinonasal infections can extend through the anterior skull base, including both pyogenic and fungal infections. Pyogenic infections can often be identified through a rim of peripheral enhancement surrounding a fluid collection on CT and MR, and diffusion restriction within the central purulent contents on diffusion-weighted MR imaging. Pyogenic infections may have ill-defined margins, and often induce edema in the adjacent brain parenchyma. In contrast, fungal infections tend to have circumscribed margins and may demonstrate solid enhancement pattern. A high density on unenhanced CT and internal foci of very low signal on T2-weighted MR sequence from high mineral content may be identified in fungal infections and can serve as an important imaging clue.
Intracranial masses, particularly extradural lesions such as a meningioma ( Fig. 3 ), can extend through the cribriform plate. A cribriform plate meningioma will typically have imaging features commonly seen in meningiomas, such as a dural tail (suggesting an extra-axial origin), and the center of the mass will typically be above the cribriform plate.
Trauma/CSF leak
Fractures of the anterior skull base, in particular the lamina papyracea and fovea ethmoidalis, may incompletely heal and can result in CSF leak. CT can show high-resolution osseous detail, but it may be difficult to determine the site of leakage without the help of intrathecal contrast injection (CT cisternogram).
If CSF leak is confirmed with either beta-2-transferrin or nuclear medicine cisternogram, CT cisternography can help localize the leak to allow targeted repair/patching. Intrathecal gadolinium-enhanced MR cisternography may have a greater role in the future, but the safety profile of intrathecal gadolinium has not yet been established.
Perineural spread
Head and neck tumors can often have perineural spread that involves the pterygopalatine fossa, most commonly squamous cell, adenoid cystic, and mucoepidermoid carcinomas. Tumors of the sinonasal cavity, palate, oral cavity, parapharyngeal space, and masticator space can spread via the perineural route to the pterygopalatine fossa and then gain access intracranially or into the orbit.
Central skull base
Anatomy
The primary structure of the central skull base is the sphenoid bone and clivus ( Table 2 ). The clivus ( Fig. 1 I) is composed of the basisphenoid and basiocciput, separated by the sphenooccipital synchondrosis in childhood. The sella turcica is an intracranial “saddle-shaped” concavity along the superior surface of the basisphenoid ( Fig. 1 I). The central skull base also includes the sphenoid wings, which is the location of the carotid canal ( Fig. 1 D, E), and the major skull base foramina, including the foramen rotundum ( Fig. 1 C, G, J), ovale, spinosum, and lacerum ( Fig. 1 E). The internal carotid artery traverses the cavernous sinus, which is lateral to the basisphenoid. Inferolateral to the cavernous sinus is Meckel cave, an extradural compartment containing the gasserian ganglion.
| Neoplasms | Chordoma Chondrosarcoma Ecchordosis physaliphora Pituitary macroadenomas Craniopharyngioma Schwannoma Meningioma Skull base metastasis Hemangiopericytoma Multiple myeloma Non-Hodgkin’s lymphoma |
| Congenital | Sphenoid dysplasia (neurofibromatosis type I) Transsphenoidal cephalocele |
| Infection/other | Fibrous dysplasia Osteomyelitis Tolosa-hunt syndrome Arachnoid granulation Paget disease Fibrous dysplasia |
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