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Arrested Pneumatization of the Skull Base: Imaging Characteristics

¹ Department of Radiology, Division of Neuroradiology, Mayo Clinic, 200 First St. SW, Rochester, MN 55905.

Received September 10, 2007; accepted after revision January 2, 2008.

 
Address correspondence to K. M. Welker (welker.kirk{at}mayo.edu).

Abstract

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OBJECTIVE. Arrested skull base pneumatization is a benign developmental variant that can be confused with significant skull base disease processes. This study reviews the imaging findings in 30 suspected cases of arrested skull base pneumatization.

CONCLUSION. When encountering a nonexpansile lesion with osteosclerotic borders, internal fat, and curvilinear calcifications in the basisphenoid bone or adjacent skull base, radiologists should strongly consider the diagnosis of arrested pneumatization.

Keywords: arrested pneumatization • congenital anomalies • craniofacial lesions • head and neck imaging • skull base • sphenoid sinus

Introduction

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The process of paranasal sinus, mastoid, and accessory skull base pneumatization begins in utero and continues through adolescence [1-3]. In a given individual, sinus and air cell development may proceed stereotypically or diverge from the norm and manifest as developmental variants [4]. Accessory pneumatization is a frequent, easily recognizable developmental variant of the skull base [5]. Similarly, absent or hypoplastic sinuses are occasionally encountered [6, 7]. Another departure from normal development is arrested pneumatization.

Arrested pneumatization is less recognized among radiologists and can create significant diagnostic confusion. It is known that the sphenoid bones undergo early fatty marrow conversion antecedent to normal pneumatization [8, 9]. However, for unclear reasons, some individuals experience failure of pneumatization before respiratory mucosa has fully extended into sites of early fatty marrow conversion. These individuals are then left with persistent atypical fatty marrow adjacent to the sinus that persists into adulthood. If unrecognized, arrested pneumatization may create diagnostic difficulty in the interpretation of skull base CT and MR scans.

The purpose of our study was to define the CT and MRI characteristics of arrested pneumatization in an effort to provide a basis for prospective diagnosis.

Materials and Methods

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Subjects
This study was performed with institutional review board approval. The CT and MRI studies and charts of 30 patients with suspected arrested skull base pneumatization were retrospectively reviewed. The subjects, identified between August 2004 and August 2006, included all the cases we encountered during routine clinical practice and all the cases referred to us by other radiologists at the same institution. The patients included were required to have an asymptomatic, incidentally discovered region of abnormal skull base marrow mineralization on CT or MR examination (or both) performed for unrelated purposes. In addition, these regions of bone were required to be nonaerated and to correlate with recognized sites of normal or accessory pneumatization. Patients with known potentially confounding abnormalities such as osseous meta stases, osteomyelitis, or fibrous dysplasia were excluded. Clinical data that were evaluated included patient age, sex, symptoms, major medical diagnoses, and indications for imaging. The results of any potentially related imaging studies, such as technetium bone scans or FDG PET scans, were reviewed.

Using these inclusion criteria, we identified 30 cases of suspected arrested pneumatization. The patients ranged in age from 14 to 75 years with a mean and median age of 44 years. Seventeen patients were male and 13 were female. The indications for scanning included sinonasal symptoms or sinus disease (10/30), headache (6/30), dizziness or vertigo (3/30), and multiple sclerosis (2/30). There were single instances of the following indications: hearing loss, tinnitus, trauma, dysarthria, eyelid droop, dysphagia, vomiting, fever, neuropathies, oligo dendroglioma, meningioma, cavernous mal formation, seizure, syncope, calvarial protuber ance, and cerebral ischemia.

Imaging Technique
The imaging studies were performed using a variety of techniques dictated by the clinical indications that prompted evaluation. All CT scans were obtained on helical scanners without contrast material. Slice thickness ranged from 1 to 5 mm. Images were reviewed in bone and soft-tissue windows. Imaging planes varied with clinical indication but were most often coronal or axial.

Most MR examinations were acquired at 1.5 T and included sagittal spin-echo T1 sequences (TR/TE, 583/14; number of excitations [NEX], 0.5) with a 5-mm slice thickness and 1-mm interslice gap. Most examinations also included an axial dual spin-echo T2 sequence (TR/first-echo TE, second-echo TE, 2,200/30, 80; NEX, 1) using a 5-mm slice thickness and a gap of 2.5 mm. Axial or coronal FLAIR images (11,000/141; inversion time, 2,600 milliseconds) were acquired with a 5-mm slice thickness and no interslice gap. Some examinations included axial fast spin-echo T2-weighted images (4,350/100; NEX, 1; echo-train length, 8) at a 4-mm slice thickness and no gap. A subset of examinations included axial gadolinium-enhanced T1-weighted images (400/21; NEX, 2) with a 5-mm slice and 2.5-mm gap or, alternatively, coronal gadolinium-enhanced T1 images with a 4-mm slice and no gap. The use of fat saturation on gadolinium-enhanced images was variable.

Image Evaluation
All cases were reviewed jointly by two board-certified neuroradiologists who openly discussed the findings. Common consensus was reached for any differences in interpretation. Each lesion was reviewed with respect to the following characteristics, subject to the availability of appropriate imaging: The size of the lesion was measured along its longest dimension, and the anatomic location was recorded. On CT, the margins of the lesions were evaluated for the presence or absence of circumscription and a sclerotic border. The matrix of each lesion was evaluated on CT for attenuation and the presence of calcification. Matrix attenuation was initially assessed by visual comparison of the lesion with the internal standards of subcutaneous fat, muscle, and skull base bone for each study. For those cases in which visual evaluation of matrix attenuation was ambiguous, Hounsfield units were measured using a CT workstation. Each lesion was assessed for evidence of associated osseous expansion. The margins of neural foramina passing through or adjacent to the lesions were evaluated for evidence of bone destruction.

For those subjects who underwent MRI, the signal characteristics on T1- and T2-weighted images were recorded. Gadolinium-enhanced images were re viewed for evidence of enhancement.

For the subjects with serial imaging studies, all such studies were reviewed and compared for evidence of significant interval change.

Results

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Of 30 subjects, 12 had both CT and MR scans, 13 had only CT scans, and five had only MR scans. The imaging findings from these scans are summarized in Table 1.

All but one lesion occurred in regions of normal or accessory sphenoid sinus pneumatization including the basisphenoid bone, pterygoid processes, and clivus. Contiguous involvement across multiple sphenoid subsites was common. A single lesion was identified in the right occipital bone in a location analogous to accessory pneumatization occurring in that same patient's left occiput. Lesions ranged in size from 7 to 63 mm in maximal diameter with an average size of 20 mm.

Of the lesions evaluated on CT, all had predominantly well-circumscribed osteosclerotic margins (Figs. 1A, 1B, 1C and 1D). These margins converged with normal cortex in subcortical lesions and occasionally had small gaps. None of the lesions was osteoexpansile. Most had internal curvilinear calcifications that morphologically differed from the ringlet pattern commonly described in chondroid tumors and the ground-glass pattern typical of fibrous dysplasia. Eighty percent of lesions had varying amounts of internal fat density on CT. An identical percentage of lesions showed regions of internal soft-tissue density. Fat and soft-tissue densities were commonly interspersed. In 22 of the cases with CT in which there was passage of one or more neural foramina through or immediately adjacent to the lesion, there was no evidence of foraminal cortical destruction or bone occlusion (Fig. 2). The most commonly associated neural foramina were the foramen rotundum and the vidian canal.

View larger version (151K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 1A —46-year-old woman referred for evaluation of possible chordoma. However, unenhanced CT showed findings of arrested pneumatization. Coronal CT image through sphenoid shows bilateral abnormal marrow trabecular pattern involving basisphenoid bone in location that often corresponds to lateral recesses of sphenoid sinus. Lesion has narrow sclerotic margins (arrows) and occasional internal curvilinear calcifications (arrowheads).

View larger version (148K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 1B —46-year-old woman referred for evaluation of possible chordoma. However, unenhanced CT showed findings of arrested pneumatization. Same CT image as A displayed with soft-tissue windows shows multiple foci of fat density within lesion (arrows).

View larger version (139K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 1C —46-year-old woman referred for evaluation of possible chordoma. However, unenhanced CT showed findings of arrested pneumatization. Axial CT image shows that lesion extends into pterygoid processes bilaterally (asterisks). Note that margins of lesion have merged with cortex of sphenoid bone at this level.

View larger version (122K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 1D —46-year-old woman referred for evaluation of possible chordoma. However, unenhanced CT showed findings of arrested pneumatization. Axial CT image shows additional extension inferoposteriorly into clivus (arrow) with preservation of sphenoid bone cortex.

View larger version (77K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 2 —Coronal CT image in 50-year-old man shows arrested pneumatization of left basisphenoid bone occurring in association with prominent sphenoid sinus lateral recess on right. Left vidian canal (black arrow) passes directly through region of arrested pneumatization; however, bone cortex of canal is preserved. Right vidian canal passes through sphenoid sinus (white arrow).

View larger version (116K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 3A —MRI features of arrested pneumatization in 30-year-old woman imaged for follow-up of oligodendroglioma (not shown) and seizures. Axial T1 image (TR/TE, 550/14; number of excitations [NEX], 1) shows circumscribed region of increased T1 signal involving left basisphenoid (arrow) adjacent to sphenoid sinus (S). Findings suggest fat occurring in association with arrested pneumatization. Note that T1 signal of lesion exceeds T1 signal in adjacent clivus (asterisk).

View larger version (136K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 3B —MRI features of arrested pneumatization in 30-year-old woman imaged for follow-up of oligodendroglioma (not shown) and seizures. Axial contrast-enhanced fast spin-echo T2 image (5,200/98; NEX, 2) of same lesion (arrow) shows heterogeneous T2 signal that is predominantly increased relative to normal clival marrow. Given fast spin-echo T2 technique and corresponding T1 hyperintensity, dominant regions of T2 hyperintensity are consistent with fatty content. S = sphenoid sinus.

A single patient had negative findings on technetium-99 methylene diphosphonate (MDP) bone scanning performed 6 days after MRI showed suspected arrested pneumatization. A single patient who had been evaluated with ¹⁸F-FDG PET/CT for rectal cancer follow-up showed no evidence of increased FDG uptake in the region of suspected arrested pneumatization.

Serial imaging was available for 18 of the patients. None of the suspected regions of arrested pneumatization showed any change over follow-up intervals that ranged from 1 to 103 months and averaged 19 months. Biopsy had previously been performed on one of the lesions because of associated patient anxiety; this yielded respiratory mucosa and fat.

Discussion

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Before the age of 4 months, the basisphenoid contains red bone marrow [10]. As a precursor to pneumatization, sphenoid marrow commences fatty conversion at about 4 months of age [10], with most individuals showing significant fatty marrow conversion by the age of 2 years [8]. This sphenoid marrow conversion precedes age-related fatty marrow conversion in the clivus [11], suggesting an alternate stimulus. However, the exact promoter for sphenoid marrow conversion is unknown. Some authors have proposed that fatty marrow conversion is a reactive response to temperature and circulatory changes brought about by adjacent regions of new aeration [8]. Others have noted that marrow conversion often precedes early aeration and have implicated developmental regional blood flow changes as the stimulus for fatty marrow conversion [12]. Respiratory mucosa subsequently expands into regions of sphenoid fatty marrow conversion as aeration proceeds. With respect to the sphenoid, the most rapid aeration occurs between the ages of 1 and 5 years [1]. However, the sphenoid sinus continues to expand throughout childhood, usually reaching its full size around the ages of 12-14 years [8, 9].

The extent of sphenoid sinus pneumatization varies widely, particularly with respect to the lateral recesses. Common variants are extension of sphenoid pneumatization into the pterygoid and anterior clinoid processes [5]. Arrested pneumatization is a departure from normal aeration of the sphenoid sinus or other skull base regions. In typical pneumatization, there is anatomic congruence between early fatty marrow conversion and the final extent of the sinus. In some individuals, aeration fails to fully replace the sites of fatty converted marrow. These individuals with arrested pneumatization are then left with atypical fatty foci of skull base bone marrow that persist into adulthood.

Based on our observation that regions of arrested pneumatization remain stable on serial imaging, we believe that this developmental variant is benign. However, it is important that radiologists recognize this entity to avoid confusing arrested pneumatization with more serious abnormalities. A number of the cases in our series had originally been assigned varied diagnoses such as chordoma, chronic inflammation, and fibrous dysplasia. Such incorrect diagnoses may lead to unnecessary follow-up imaging, biopsy, or treatment.

Our review suggests that arrested pneumatization can be diagnosed when a lesion fulfills the following criteria: First, the lesion must be located at a site of normal pneumatization or of recognized accessory pneumatization. Second, the lesion must be nonexpansile with sclerotic, well-circumscribed margins. Third, the lesion should show fatty content. On CT, internal curvilinear calcifications should be present, and any associated skull base foramina should retain a normal appearance.

View larger version (107K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 4 —Arrested pneumatization of right occipital bone in 61-year-old man. Axial CT image shows large region of accessory pneumatization in left occipital bone (black arrow). There is arrested pneumatization of analogous portion of right occipital bone (white arrow). Lesion has osteosclerotic border and internal curvilinear calcifications.

It is important to differentiate arrested pneumatization from more menacing conditions that may involve the central skull base. Arrested pneumatization can be differentiated from fibrous dysplasia through careful observation of the internal matrix. Whereas fibrous dysplasia usually exhibits a ground-glass marrow pattern on CT [13], the internal matrix pattern of arrested pneumatization is distinct and characterized by curvilinear calcifications and foci of overt fat. Fibrous dysplasia is expansile and may compromise neural foramina [14, 15]. These features are not associated with arrested pneumatization (Figs. 5A, 5B, 5C and 5D).

View larger version (115K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 5A —Arrested pneumatization distinguished from fibrous dysplasia. Axial CT image in 34-year-old man with arrested pneumatization shows arrested pneumatization of left basisphenoid. Note thin osteosclerotic margin (arrowheads) and internal curvilinear calcifications (arrow). Lesion is nonexpansile and does not narrow adjacent inferior orbital fissure (asterisk).

View larger version (92K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 5B —Arrested pneumatization distinguished from fibrous dysplasia. Axial CT image of same patient in A at level of lateral pterygoid plates shows that although arrested pneumatization extends to involve inferior left pterygoid process (arrow), bone is not expanded.

View larger version (97K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 5C —Arrested pneumatization distinguished from fibrous dysplasia. Axial CT image in 72-year-old woman with presumptive fibrous dysplasia of left basisphenoid. Note that diffuse sclerotic matrix pattern of fibrous dysplasia (arrow) differs significantly from pattern of arrested pneumatization. Lesion is expansile, with convex borders (arrowheads) that narrow pterygopalatine fossa.

View larger version (83K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 5D —Arrested pneumatization distinguished from fibrous dysplasia. Axial CT image in same patient as C shows overt expansion of left lateral pterygoid plate (arrows) by fibrous dysplasia.

The diagnosis of chordoma had previously been entertained in a number of the cases in our study. Although often arising in proximity to the sphenoid sinus, chordomas are most commonly expansile and destructive [18]. Moreover, chordomas are not reported to exhibit central regions of fat. Internal bone particulate matter may be seen in a chordoma [19]; however, these small, irregular shards of destroyed bone do not assume the delicate, curvilinear configuration of the calcifications in arrested pneumatization.

Chondrosarcoma is another diagnostic consideration for a central skull base lesion. Although chondrosarcomas are slow growing, they are destructive and expansile [20] and these features distinguish them from arrested pneumatization. As with chordomas, internal fat in chondrosarcomas would be distinctly unusual. Similar observations allow arrested pneumatization to be differentiated from metastases.

Arrested skull base pneumatization can be distinguished from skull base osteomyelitis because it does not cause a permeative pattern of osseous destruction. A significant reduction in T1 marrow signal is almost always seen in skull base osteomyelitis [21] in contrast to the increased marrow T1 signal that is near-ubiquitous in arrested pneumatization.

The limitations of our study include its retrospective nature and the relatively small number of cases identified during the 2-year study period. Biopsy results were available for only one case. However, given the presumptively benign nature of these skull base lesions, a research protocol based on requisite biopsy is both impractical and unethical. The 19-month average follow-up interval may have excluded our ability to detect extremely slow growth in the lesions. Nevertheless, this interval is likely sufficient to exclude an aggressive growth pattern. Follow-up imaging was not available for 12 of the lesions. The fact that the CT and MR scans acquired in our series were obtained using a variety of protocols may have introduced some degree of sample bias to our results. For instance, because of volume-averaging effects, the subset of CT studies obtained using 5-mm slices likely had a lower sensitivity for small amounts of fat than those obtained using a thinner collimation. In addition, relatively few of the patients in our series underwent technetium bone scanning.

In conclusion, arrested skull base pneumatization is an anatomic variant that most commonly occurs in association with the sphenoid sinus. This condition can be diagnosed when a nonexpansile lesion is encountered at a site of normal or accessory sphenoid sinus pneumatization. The lesion should have thin sclerotic margins, internal fatty content, and curvilinear internal calcifications. It should respect the margins of associated neural foramina. If the full constellation of findings is present, arrested pneumatization can be confidently diagnosed, eliminating the need for additional interventions such as biopsy or surgery. Occasionally, regions of arrested pneumatization may not fulfill all these diagnostic criteria. In such cases, serial imaging follow-up is useful to establish benignity.

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This Article Abstract Figures Only Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Welker, K. M. Articles by Gilbertson, J. R. Search for Related Content PubMed PubMed Citation Articles by Welker, K. M. Articles by Gilbertson, J. R. Social Bookmarking                      What's this? Hotlight (NEW!) What's Hotlight?