Skull Base Lesions: Extracranial Origins Kristine M. Mosier, DMD, PhD* A number of extracranial anatomical sites, including the nasopharynx, paranasal sinuses, and masticator space, may give rise to lesions involving the skull base. Implicit in the nature of an invasive lesion, the majority of these lesions are malignant. Accordingly, for optimal patient outcomes and treatment planning, it is imperative to include a search pattern for extracranial sites and to assess accurately the character and extent of these diverse lesions. Of particular importance to radiologists are lesions arising from each extracranial site, the search patterns, and relevant information important to convey to the referring clinician. Semin Ultrasound CT MRI 34:436-444 C 2013 Elsevier Inc. All rights reserved.
n spite of varied origins, extracranial lesions breaching the skull base create diverse diagnostic challenges while sharing similar characteristics. Contiguous with critical neurovascular structures, extracranial lesions that penetrate beyond traditionally observed anatomical borders to reach the skull base demand critical observation of their site of origin, biological behavior, and imaging characteristics to optimize treatment planning.
Nasopharynx Nasopharyngeal malignancies account for most invasive skull base lesions arising from extracranial sites and are most commonly nasopharyngeal carcinomas (NPCs) with lymphoma occurring less commonly.1-3 To appreciate skull base involvement from nasopharyngeal lesions, it is necessary to understand the anatomical relationship of the nasopharynx to the skull base. The roof of the nasopharynx is formed by the basisphenoid (the ﬂoor of the sphenoid sinus), basiocciput (clivus), and the anterior aspect of the vertebral bodies of C1 and C2 (Fig. 1).4 Deep to the mucosal layer of the nasopharynx lies the pharyngobasilar fascia, a dense aponeurotic sheet forming the superﬁcial layer of the deep cervical fascia. The middle layer of deep cervical fascia, the buccopharyngeal fascia, bounds the pharyngobasilar fascia posteriorly. The Project Editor: Suzanne Byan-Parker. Tel.: +1-205-934-4274; +1-205-4823229 (mobile). E-mail: [email protected]
*Department of Radiology, Section of Neuroradiology, Indiana University, School of Medicine, Indianapolis, IN. Address reprint requests to Kristine M. Mosier, DMD, PhD, Department of Radiology, Section of Neuroradiology, Indiana University, School of Medicine, 355 W. 16th St. Goodman Hall Suite 4100, Indianapolis, IN 46202-7176. E-mail: [email protected]
0887-2171/$-see front matter & 2013 Elsevier Inc. All rights reserved. http://dx.doi.org/10.1053/j.sult.2013.08.003
buccopharyngeal fascia is loosely apposed to the subjacent deep layer of deep cervical fascia, the alar fascia, thus creating a space, the retropharyngeal space, whose origin is at the skull base. The alar fascia lies interposed between the retropharyngeal space and another deep layer of deep cervical fascia, the preverterbral fascia, creating the danger space. These fascial layers act as a barrier to spread of infection or neoplasm; transgression indicates the malignant or aggressive nature of the process (Fig. 2). Tumor penetration through the layers of the deep cervical fascia in the nasopharynx provide the most direct access to the skull base; however, an anatomical avenue in the buccopharyngeal fascia provides an additional means for tumor extension. The sinus of Morgagni is a notch at the posterior superior margin of the buccopharyngeal fascia and the superior aspect of the superior constrictor through which the levator palatini muscle and eustachian tube pass from the skull base to the pharyngeal mucosal space of the nasopharynx (Fig. 3). Note the intimate relationship of the fossa of Rosenmüller to the sinus of Morgagni. This allows NPCs arising from within the fossa of Rosenmüller to access the skull base. NPCs arise from the squamous epithelium of the nasopharynx in the pharyngeal mucosal space. During infancy and childhood, the epithelium is predominately composed of columnar ciliated respiratory epithelium, which is gradually replaced by stratiﬁed squamous epithelium during adolescence and adulthood.4 Hence NPCs are typically squamous cell carcinomas, although rarely, minor salivary glands in the mucosa may give rise to adenoid cystic carcinoma or adenocarcinomas.5-8 The World Health Organization classiﬁes NPC into 3 categories based on histology: type I NPCs are wellto-moderately differentiated keratinizing squamous cell carcinomas, most common in North American (Caucasian) populations; type II NPCs are non-keratinizing, transitional
Skull base lesions
Figure 1 Sagittal, T1-weighted MR image shows the mucosa of the nasopharynx (arrow) abutting the ﬂoor of the sphenoid sinus and clivus.
Figure 3 Coronal, enhanced T1-weighted MR image. Long arrow ¼ sinus of Morgagni, short arrow ¼ superior constrictor, arrowhead ¼ levator veli palatine muscle, dashed arrow ¼ fossa of Rosenmüller.
carcinoma or lymphoepileliomas; and type III NPCs are undifferentiated carcinomas. Types II and III are more common in Asian populations and are associated with Epstein-Barr virus.9,10 Small or early-stage NPC presents as an asymmetric fullness in the pharyngeal mucosal space of the nasopharynx, typically with effacement of the fossa of Rosenmüller (Fig. 4). The normal nasopharyngeal mucosa, even in the presence of adenoid hypertrophy, appears bilaterally symmetric, hence, the presence of asymmetry warrants consideration of a malignant process. In the most recent American Joint Committee on Cancer Staging Manual (seventh edition, 2010), NPCs conﬁned to the pharyngeal mucosal space, even with extension to the oropharynx or nasal cavity, are staged as T1. Figure 4 Axial, contrast-enhanced CT scan shows asymmetric fullness in the right nasopharynx in this patient with a T1 nasopharyngeal carcinoma (white arrow) that displaces the torus tubarius (T) laterally. Note the preservation of the fat plane at the levator veli palatini muscle (arrowhead) and the parapharyngeal fat (black arrow).
Figure 2 Axial, T1-weighted MR image. The mucosa of the nasopharynx (white arrow) is bound posteriorly by the hypointense signal of the longus capitis muscles. The pharyngobasilar, buccopharyngeal, and alar fascia are compressed sheets lying between the deep margin of the mucosa and the longus capitis muscle (short white arrow). The buccopharyngeal fascia extends laterally (black arrow).
Extension into the parapharyngeal space, however, upstages NPC to T2. This reﬁnement of the staging reﬂects the recognition that extension to the parapharyngeal space occurs only with transgression of the pharyngobasilar fascia (Fig. 5). Patients with small, T1 lesions are often asymptomatic, may complain of vague, mild eustachian tube symptoms or hearing loss. Indeed, these patients may be imaged initially for middle ear etiology. Thus, any asymmetric middle ear or mastoid effusion in the absence of otologic etiology should prompt close inspection of the nasopharynx.11 The pattern of spread from larger NPCs breeching the pharyngobasilar fascia is most commonly posterolateral or posterior extension into the sphenoid rostrum, basisphenoid, and or clivus. This is best appreciated on T1-weighted magnetic resonance imaging, which demonstrates loss of the normally bright signal (Fig. 6). As most NPCs arise from off midline, lesions extending into the clivus often extend to, and
Figure 5 Axial, T1-weighted contrast-enhanced MR image shows an inﬁltrating mass (short white arrow) in the right nasopharynx, which proved on biopsy to be squamous cell carcinoma. Inﬁltration through the parapharyngeal fat (white arrow) upstages this to T2. Note the breach of the pharyngobasilar fascia (black arrow) at the sinus of Morgagni compared with the contralateral side. This ﬁnding, as well as inﬁltration of the longus capitis muscle posteriorly (*), demonstrates the typical lateral and posterior spread pattern of these lesions.
widen, the petroclival ﬁssure (Fig. 6B).12 This is an important feature to recognize, as the presence of adenoidal hypertrophy in both pediatric population and adult populations may obscure a nasopharyngeal primary tumor.12,13 More extensive NPCs may erode through the sphenoid and sphenoid sinus and extend to the cavernous sinus (Fig. 7A). A key feature to examine when there is involvement of the sphenoid is extension of the mass through the sinus of Morgagni and laterally to the ptyergopalatine fossa (Fig. 7B). Extension to the pytergopalatine fossa may occur via the sphenopalatine foramen, or via extension along the vidian or palatovaginal canals.14,15 Note, however, that in the current American Joint Committee on Cancer Staging Manual staging system, extension to the sphenoid sinus (or any of the paranasal sinuses) and skull base only upstages the lesion to T3. Advanced (T3-T4) lesions often obliterate the bone of the skull base; nevertheless, rapidly advancing NPCs may leave ossiﬁed fragments of the skull base, creating an appearance that may mimic the chondroid matrix of chordoma or chondrosarcomas (Fig. 8). NPCs are upstaged to T4 when there is extension into the orbit, intracranial extension or extension along cranial nerves, or extension to the infratemporal fossa (masticator space) (Fig. 9).
Figure 6 (A) Axial CECT image shows bilateral enlargement of the nasopharyngeal soft tissues in this adult patient. Note the asymmetry of the left side (long white arrow) with the torus tubarius and fossa of Rosenmüller obscured. The parapharyngeal fat, however, is intact (short white arrow). The longus capitis muscles are difﬁcult to identify on either side but appear larger on the left and are inﬁltrated (black arrow). (B) Axial bone CT scan in the same patient shows a large erosive defect in the clivus (long white arrow) as well as erosion and widening of the petroclival ﬁssure (short white arrow) and petrous apex. (C) Axial, T1-weighted MR image shows the obliteration of the normal bright marrow from the clivus (white arrow). The MR image conﬁrms that the parapharyngeal fat is preserved (black arrow).
Skull base lesions
Figure 7 (A) Axial bone CT scan shows a large mass obliterating the sphenoid sinus and eroding into the greater wing of the sphenoid (open arrow). The malignant nature of the mass is further revealed as complete loss of the bony canal of the vertical petrous carotid (short arrow) and extension through the posterior recess of the sphenoid sinus and clivus to the dural interface (arrow). (B) Coronal, contrast-enhanced CT scan in the same patient shows the bulky, enhancing mass ﬁlling the nasal cavity, sphenoid sinuses, and through the ptyergopalatine fossa to the infratemporal fossa/masticator space (black arrow). Compare this with the normal right ptyergopalatine fossa (white arrow).
Figure 8 (A) Axial bone CT scan shows erosion of the basisphenoid and clivus with scattered ossiﬁed fragments (arrow) in this patient with an NPC that rapidly progressed over 6-8 months. Note that the eustachian tube is both obstructed and expanded (small arrow). (B) Axial, T2-weighted MR image shows the mass to be T2 hypointense and diffusely inﬁltrating through the sphenoid and clivus. The T2 signal characteristics would argue against a chordoma, and the midline location would be less favorable for chondrosarcoma. (C) Sagittal, T1-weighted MR image shows the origin of the mass in the nasopharynx (*) with the vector of spread posteriorly and superiorly through the sphenoid sinus and clivus (long arrow), and a small nodule penetrating the clivus at the prepontine cistern (short arrow).
Figure 9 (A) Sagittal, contrast-enhanced T1-weighted MR image in a patient with a T4 NPC. An extensive necrotic mass obliterates the sphenoid sinus and base of skull and inﬁltrates into the pituitary fossa. Note the extension through the prepontine cistern and compression of the pons (long arrow). Although the mass inﬁltrates to the dura at the planum sphenoidale (short arrow), there is no intracranial extension to the rectus gyrus. (B) Coronal, contrast-enhanced T1-weighted image shows that the mass has inﬁltrated laterally into the cavernous sinus on both sides (arrows). Having gained access to the cavernous sinus, there is extension along V3 (short arrow). (C) Coronal, contrast-enhanced T1-weighted image further demonstrates the T4 extent of this NPC with extension to the orbit (solid white arrow) and the masticator space (short white arrow). In keeping with the insidious but aggressive nature of these neoplasms, note there is diffuse inﬁltration of the sphenoid (black arrow) adjacent to the intact mucosal surface (open white arrow).
Figure 10 Axial, contrast-enhanced CT scan in a patient with nonHodgkin's lymphoma of the nasopharynx. This classic presentation illustrates the bulky exophytic mass inﬁltrating through the fossa of Rosenmüller (long arrow) but displacing the parapharyngeal fat (short arrow).
The search pattern for NPC begins with identiﬁcation of the nasopharynx as the source of the skull base lesion. As NPCs may not present with an obvious mucosal mass, the submucosal asymmetry (Fig. 4) and associated ﬁndings of eustachian tube obstruction warrant visual inspection and tissue sampling of the nasopharynx. Positron emission tomography-computed tomography (PET/CT) scan has shown to be of limited efﬁcacy in the diagnosis of primary NPC. The wide overlap in 18 F-Fluorodeoxyglucose uptake between carcinoma and adenoidal or palatine lymphoid tissue in response to increased cellular metabolism in the presence of functional demand or inﬂammation limits the diagnostic efﬁcacy of PET/CT for primary NPC.16,17 Moreover, other studies have suggested that PET/CT may underestimate the amount of skull base involvement relative to magnetic resonance (MR).18,19 This is particularly important, given that more recent studies suggest that the degree of hypermetabolism relative to tumor volume may be a better predictor of overall survival and the need for aggressive therapy.20 Accurately delineating the tumor extension and volume is critical for treatment planning, as most lesions are treated with radiation and chemotherapy.10 Importantly, many advanced stage NPCs are now treated with proton beam radiation21,22 necessitating
Skull base lesions
Figure 11 (A) Axial, contrast-enhanced MR image with fat saturation shows an enhancing mass in the right nasopharynx (large arrow) extending deep through the pharyngobasilar fascial layer to the preverterbral space and the parapharyngeal space (small arrow). Adenoid cystic carcinoma. (B) Coronal, contrast-enhanced MR image with fat saturation shows that the mass extends to the skull base at the vidian canal and sphenoid (arrow).
accurate volume determination, particularly with regard to skull base, cavernous sinus, orbital, and intracranial extension. Finally, because the dose proﬁle of proton beam allows higher doses to be delivered with reduced treatment volumes,23–25 the radiation oncologist needs to know whether there is an extension to the brainstem, the optic chiasm or optic nerve, the cavernous sinus, or the carotid. Nasopharyngeal lymphoma accounts for approximately 20% of nasopharyngeal malignancies3,26-28 and most commonly presents as a diffuse but symmetrically exophytic mass conﬁned to the pharyngeal mucosal space, most often with local extension conﬁned to the oropharynx (Fig. 10).27,28 Nasopharyngeal non-Hodgkin's lymphoma less commonly inﬁltrates into the skull base, and when it does so, it typically is limited.27 The MR characteristics of lymphoma, speciﬁcally the T2 hypointensity and lack of signiﬁcant enhancement, are key to differentiating these lesions from NPC. Nasopharyngeal lymphoma when it does inﬁltrate through the skull base may expand rather than destroy bone.28 Minor salivary gland malignancies arising within the nasopharynx are rare but are typically nonspeciﬁc in appearance, presenting as an enhancing mass within the pharyngeal mucosal space of the nasopharynx (Fig. 11). Adenocarcinomas more typically extend into the skull base rather than adenoid cystic carcinomas, which have a greater predilection for perineural spread.
Paranasal Sinuses Skull base extension from the paranasal sinuses typically occurs from lesions involving the cribiform plate, ethmoid, and sphenoid sinus. Lesions arising in the cribiform plate are
Figure 12 (A) Sagittal, contrast-enhanced MR image with fat saturation in a patient with a stage Kadish C esthesioneuroblastoma shows an enhancing mass extending through the cribiform plate to the rectus gyrus (arrow). Note the tiny cystic-appearing nodules at the superior margin. (B) Coronal, contrast-enhanced magnetic resonance imaging with fat saturation at the level of the sphenoid rostrum shows the mass extending into the posterior nasal cavity and sphenoid sinus (white arrow). Laterally the mass inﬁltrates through the lateral sphenoid wall to the pterygoid process and inferior orbital ﬁssure (black arrow). This lateral extension into the pterygoid process upstages the lesion from Kadish B to C.
Figure 13 Axial, contrast-enhanced MR image in a patient with a sinonasal undifferentiated carcinoma. The mass extends from the ethmoid complex into the sphenoid sinus and cavernous sinus on both sides (short arrows), and runs along the trigeminal nerve through the prepontine cistern to the pons (long arrow). This degree of disease extension would be unusual for an esthesioneuroblastoma or sinonasal neuroendocrine carcinoma.
Figure 15 Axial, contrast-enhanced MR image. This large centrally cystic-appearing avidly enhancing mass (arrow) demonstrates a classic appearance of cystic schwannomas, which when large can extend to involve a more signiﬁcant portion of the greater wing of the sphenoid. Note that the ﬂoor of the orbit is pushed anteriorly, reﬂecting its benign character.
Figure 14 (A) Axial, contrast-enhanced MR image with fat saturation in a patient with a recurrent T4N1M0 squamous cell carcinoma of the retromolar trigone. Disease extends into the masticator space, inﬁltrating the lateral pterygoid (white arrow). Diffuse enhancement posteriorly in the pterygoid and in the masseter represents a combination of inﬁltration as well as denervation atrophy (black arrows). Denervation atrophy should prompt suspicion of cranial nerve involvement, as local inﬁltration does not typically result in denervation. (B) Axial, contrast-enhanced MR image with fat saturation more superiorly shows an enhancing mass extending through the pterygopalatine ﬁssure to the left sphenoid (long arrow), carotid canal, and petrous apex (short arrow). Inset: note the extension through the cavernous sinus and Meckel cave (long arrow) and along the trigeminal to the pons (short arrow). Note also the dural extension along the anterior temporal lobe.
Skull base lesions
Figure 16 (A) Axial, contrast-enhanced MR image with fat saturation in adolescent male shows an avidly enhancing mass involving the pterygopalatine ﬁssure and vidian canal (arrow) as well as the left sphenoid. Juvenile nasopharyngeal angioﬁbroma. (B) Coronal, contrast-enhanced MR image with fat saturation demonstrates the extension through the left sphenoid lateral to the foramen rotundum (arrow).
most commonly esthesioneuroblastomas. Given their origin at the cribiform plate, the vector of spread for esthesioneuroblastomas is often cranially into the basal frontal lobes; skull base extension for these lesions results from posterior extension through the ethmoid and sphenoid sinuses (Fig. 12). The commonly used Kadish staging system for esthesioneuroblastoma does not differentiate between intracranial and skull base extension; thus any skull base extension with or without intracranial extension is a Kadish stage C. However, if the lesion remains conﬁned to the nasal cavity or paranasal sinuses, these would be staged as Kadish A or B, respectively.29,30 Although any higher-grade sinonasal malignancy may extend to involve the skull base, this occurs more commonly with sinonasal undifferentiated carcinoma or high-grade squamous cell carcinoma (Fig. 13).
Masticator Space In considering skull base involvement from extracranial sites, the masticator space must be assessed. The masticator space consists of the muscles of mastication and the mandible and is commonly referred to as the infratemporal fossa. Any malignancy involving the masticator space has the potential, given the proximity, to extend to the skull base. Thus, the skull base should be carefully assessed with any sarcoma of the masticator space, but it is prudent as well to look for skull base involvement with more extensive squamous cell carcinomas arising from or involving the masticator space. Squamous cell carcinomas involving the retromolar trigone or buccal space, in particular, may run along or through the mandible, or through the muscles of mastication to the skull base (Fig. 14). These patients often present with signiﬁcant trismus; cranial nerve deﬁcits should prompt concern for cavernous sinus or Meckel's cave involvement. Extension into Meckel's cave may result in denervation atrophy, which in the acute phase results in enhancement of the muscles of mastication, potentially complicating the
interpretation of disease extent (Fig. 14B). Nevertheless, any signs of denervation atrophy warrant thorough inspection of the skull base. Although malignant disease accounts for most cases of skull base involvement from the masticator space, some benign lesions may expand or erode into the skull base. Schwannomas involving cranial nerve V may not only expand the foramen but also may remodel or focally inﬁltrate into the greater wing of the sphenoid (Fig. 15). Moreover, juvenile nasopharyngeal angioﬁbromas although classically associated with widening of the pterygopalatine ﬁssure and anterior displacement of the posterior wall of the maxillary sinus, may occasionally inﬁltrate into the skull base (Fig. 16). This is more common with recurrent lesions, but may occur with more aggressive lesions on initial presentation. Recognizing extension of these lesions into the sphenoid, cavernous sinus or intracranially, is important as this complicates the surgical management and increases the probability of recurrence.31
Summary Skull base lesions may arise from a number of extracranial sites including the nasopharynx, paranasal sinuses, and masticator space. Regardless of the myriad sources of these lesions, the presence of skull base extension portends a worse or poor prognosis. It is essential then to not only recognize skull base involvement but also accurately determine the extent of involvement to ensure appropriate management.
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