|ECR 2019 / C-3083|
|Arrested pneumatization of the sphenoid sinus in four symptomatic patients: principal diagnostic elements, pitfalls and differential diagnosis.|
Arrested pneumatization of the sphenoid sinus represents a rare benign variant of skull base development. In most cases it’s asymptomatic and an occasional finding during CT or MR examinations performed for other reasons, most frequently neurologic or ENT symptoms. Otherwise, in some patients it can cause headache and obstructive symptoms due to alteration of normal mucosal drainage in the paranasal sinuses . The physiological process of the pneumatization of the sphenoid sinus begins after about 4 months of life to complete during adolescence. In fact, the sphenoid sinus is absent at birth and its body is completely formed by red bone marrow. From the 2ndto 4thmonth of life, a process of conversion in yellow bone marrow and subsequent respiratory epithelium colonization begins  (figure 1). If, for unknown reasons, this process is interrupted, and aeration does not completely replace the yellow marrow, the sphenoid sinus stops its development with incomplete pneumatization and yellow marrow foci persist in adulthood. This phenomenon can also involve the ethmoid and the adjacent paranasal sinuses . We present four cases of symptomatic patients who have performed MRI and CT examinations in which the imaging characteristics and the main differential diagnoses  are summarized (Table 1).
|Diagnosis||CT/CBCT||MRI-T1W||MRI-T2 Fat Saturation||MRI-T1+Contrast|
Non-expansile lesion with internal curvilinear calcification
and foci of overt fat; sclerotic margin;
variable degrees of loss to bonetrabeculae; no cortical breach
|ncreased intensity||Decreased intensity||No enhancement|
Expansile lesion with internal fatty matrix and micro-calcifications partial to complete loss of bonytrabeculae; cortical breach is common
|Increased or mixed signal intensity||Decreased or mixed signal intensity||No enhancement|
|Chordoma and chondrosarcoma||Expansile, destructive lesion with no fat contents; lobulated borders; may contain internal bone particulate matter/chondroid pattern of calcification with amorphous or stippled configuration; cortical breach is possible||Variable (the bulk of tumor is isointense or hypointense with localized areas of hyperintensity)||Increased or mixed signal intensity||Moderate to marked enhancement|
|Fibrous dysplasia and ossifying fibroma||Expansile, non-fat containing lesion; lobulated borders; sclerotic margins; internal foci of mineralization; the matrix may have an amorphous ground-glass appearance; cortical breach is possible||Variable (hypointense to intermediate signal intensity depending on the ratio of mineralized matrix to fibrous tissue)||Variable (hypointensity due to highly mineralized matrix; hyperintensity due to intralesional cystic components; mixed signal patterns due to mixed contents)||Variable|
|Intraosseous hemangioma||Expansile lesion; may or may not have fatty contents; mixed density lesion with a lacelike pattern of bone trabeculae; cortical breach is possible||Signal intensity may be increase (most commonly) or mixed||Increased intensity||Marked enhancement|
|Osteomyelitis and metastatic disease||Expansile; multifocal areas of dense sclerosis, or lytic permeative/erosive changes in the cortical or cancellous bone; cortical breach is possible||Decreased signal intensity||Increased signal intensity||Marked enhancement in the affected marrow space|
|Primary NHL of sphenoid sinus||Solid intrasinusal lesion without walls thickening or expansion; permative bony erosions||Decreased signal intensity||Isointense or increased signal intensity||Moderate homogeneous enhancement|
Table 1. Principal differential diagnosis of sphenoid lesions .