Anatomy

The sphenoid sinus (SS) is one of the four paired PNSs within the sphenoid bone body divided by the septum. The sphenoid sinus ostium is placed in the cranial part of the intranasal surface. The spheno-ethmoid recess (SER) is the drainage pathway of the posterior ethmoidal air cells and sphenoid sinuses into the superior nasal meatus. The sphenoid sinus is antero-superior-laterally related to the optic nerve, laterally to the cavernous sinus, inferiorly to the nasopharynx, and superiorly to sella turcica (Fig. 1).

Fig. 1
figure 1

Anatomy of sphenoid sinus and sella: Axial unenhanced CT image (A), sagittal unenhanced CT image (B), sagittal T2-weighted image (C), coronal un-enhanced CT images (D, E), and coronal T2-weighted image (F) reveal anatomy of SS. Abbreviations: SS: sphenoid sinus, EC: ethmoidal air cells, VN: vidian nerve canal, FR: foramen rotundum, SER: spheno-ethmoidal recess, AC: anterior clinoid process, OC: optic canal, ON: optic nerve

Full size image

Imaging modalities

Computed tomography (CT) is the modality of choice for imaging PNS in acute recurrent or chronic sinusitis, non-invasive fungal sinusitis, sinonasal polyposis, suspected mucocele, patients not responding to treatment, pre-functional endoscopic sinus surgery (FESS) workup or bony involvement in masses. CT has limited soft tissue resolution. Contrast-enhanced MRI is performed in acute sinusitis with suspected extra-sinus, orbital or intracranial complications, invasive fungal sinusitis, or suspected mass. CT in this study was performed on a GE Dual-energy scanner. MRI was performed on GE Artist & Signa HD XT 1.5 Tesla scanner in this study using a head coil [1].

Development and pneumatization

SS is non-pneumatized at birth; pneumatization starts at age 2–3 years, with some variability, with a development period of pneumatisation of 3–5 years or 6–10 years [2].

Classification proposed by Hammer and Radberg, the SS shape can be divided into different groups, recognizable on the sagittal planes, and based on the relation to the anterior and posterior walls of sella:

  • Conchal type: A small pneumatised space in front of the anterior wall of the sella.

  • Presellar type: SS ends anteriorly to the anterior edge of sella

  • Sellar type: posterior wall of the SS is between the anterior and posterior walls of the sella.

  • Post-sellar type: posterior wall of the SS is located behind the posterior wall of the sella (Fig. 2) [3].

Fig. 2
figure 2

Unenhanced CT sagittal MPR reconstructions: different types of sphenoid sinus in relation to sella: A conchal, B presellar, C sellar, D post-sellar type

Full size image

Non-pneumatized and conchal types are less favourable for a transsphenoidal approach to sellar and parasellar lesions, as it requires thick bone perforation and long operative times [3].

Anatomical variants

Arrested pneumatization

If the process of pneumatization of sinus does not occur, bones atypically contain yellow marrow into adulthood, described as arrested pneumatization. The criteria for arrested pneumatisation are as follows: The lesion is located at a site of normal pneumatisation, non-expansile with sclerotic, well circumscribed margins with fatty content and shows internal curvilinear calcifications and preserved skull base foramina (Fig. 3) [4].

Fig. 3
figure 3

Variants: Coronal un-enhanced CT image (A): pneumatization of lateral recesses of sphenoid sinuses (arrows in A) and right anterior clinoid process (dashed arrow in A). Coronal un-enhanced CT image (B): Onodi cell (arrow). Arrested pneumatisation: coronal un-enhanced CT images (C, D) reveal a non-expansile intra-osseous with curvilinear calcifications and no cortical breach in the right sphenoid bone (arrows)

Full size image

Pneumatization of the lateral recess

Pneumatisation can extend into greater wing of sphenoid (beyond a vertical line crossing the foramen rotundum), or pterygoid plates (extending horizontal plane crossing Vidian canal). Pneumatisation of anterior or posterior clinoid processes can also be seen (Fig. 3) [5].

Other variants

Internal carotid artery, optic nerve, Vidian nerve, or maxillary nerves can protrude into the sphenoid sinus. Vidian or maxillary nerve protrusions are associated with neuralgia in sphenoid sinus disease [3]. When the inter-sphenoid septum is deflected to one side, attaching to the bony wall, mainly covering the carotid artery, avulsion of septum during surgery can lead to arterial injury. In some cases, the artery may bulge into the sinus or in 4–8% of cases, dehiscence or absence of the thin bony part separating the artery and the sinus may be seen [5]. Other variants include accessory septae or spheno-ethmoid cell/Onodi cell (Fig. 3) [5].

Onodi cell is an anatomical variant first described by Adolf Onodi in 1903, consisting of the most posterior ethmoid air cell which extend into sphenoid sinuses superiorly and laterally, near to or abut the optic nerve. If Onodi cell abuts the optic nerve and when excision of this cell is to be performed, the nerve is at risk [5].

Understanding anatomy and recognising anatomical variant is necessary for endoscopic skull base surgeons [3] (Table 1).

Table 1 Anatomical variants and pathologies affecting sphenoid sinuses
Full size table

Pathologies

Inflammatory disease

Bacterial sinusitis

The inflammation of the sinus mucosa is accompanied by inflammation of nasal mucosa. A clinical diagnosis and imaging are required in complicated acute sinusitis or chronic/recurrent sinusitis. It is acute if less than 4 weeks, subacute if between 4 and 12 weeks, and chronic if it takes longer than 12 weeks. Imaging findings of acute sinusitis are mucosal thickening, submucosal edema, air-fluid levels, or sinus secretions interspersed with air bubbles. In the spheno-ethmoid recess pattern of sinonasal inflammatory disease, the obstruction is at spheno-ethmoid recess with inflammatory changes seen in sphenoid sinus and posterior ethmoid air cells (Fig. 4) [6].

Fig. 4
figure 4

Sphenoidal sinusitis: Axial T2-weighted and unenhanced T1-weighted images (A, B) reveal opacified sphenoid sinus. Axial DWI image (C) shows restricted diffusion in the left sphenoid sinus (arrow) and shows peripheral mucosal enhancement seen on axial contrast-enhanced T1-weighted image (D)

Full size image

The imaging features of chronic sinusitis include mucosal thickening, sinus opacification, intra-sinus calcifications, and sclerosis in their bony walls. Chronic sinusitis with inspissated secretions can mimic normal sinus on MR imaging (Fig. 5). Yoon et al. described round or egg-shell calcifications in chronic inflammatory rhinosinusitis [7]. Retention cysts in the sphenoid sinus are rare.

Fig. 5
figure 5

Sphenoidal sinusitis mimicking aerated sinus on MRI (T2W): Axial and sagittal T2W images (A, B) reveal a hypointense signal in the right sphenoid sinus. Axial unenhanced T1W image (C) shows hyperintense signal in the right sphenoid sinus (arrow) which is mildly hyperintense on axial DWI (arrows in D) representing inspissated secretions

Full size image

Sphenoid sinus mucocele is a rare entity comprising only 1–2% of paranasal sinus mucoceles [8]. These are benign, encapsulated lesions filled with mucus and lined by epithelium. Paranasal mucocele is reported as a complication in children with cystic fibrosis (CF) in up to 4% of patients [9]. Accumulating and retaining mucoid secretions within the sinus can lead to thinning with distension and erosion of its bony walls. Mucoceles may have variable densities on CT and signal intensities on MRI depending on their protein content, inspissation and possible superinfection and do not show contrast enhancement (Fig. 6) [8].

Fig. 6
figure 6

Mucocele: 32-year-old male presented with right optic neuropathy. Coronal T2- and T1-weighted images (A, B) reveal expansion with opacification of the right sphenoid sinus (arrows), appearing hyperintense on T1-weighted image, representing inspissated secretions (arrow in B). Coronal contrast-enhanced T1-weighted image (C) reveals no significant enhancement (arrow). Coronal un-enhanced CT image (D) reveals areas of cortical thinning and bony breach of right sphenoid sinus (arrows). Axial and coronal short tau inversion recovery sequence (STIR) images (E, F) show thinning of the right optic nerve (dashed arrow)

Full size image

They can occur either in isolation or in combination with other paranasal sinus mucoceles.

Fungal sinusitis

Fungal rhinosinusitis includes various conditions that can present acutely in severely immunocompromised patients or chronically in patients with mild immunosuppressive states such as diabetes mellitus or chronic corticosteroid use.

Fungal sinusitis is broadly classified into invasive and non-invasive forms. The non-invasive form includes allergic fungal sinusitis and mycetoma. Invasive forms include acute and chronic invasive fungal sinusitis and chronic granulomatous conditions.

There are imaging features on CT and MR that suggest fungal sinusitis. On CT, opacified sinus is hyperdense due to calcium and magnesium salts. MR imaging better evaluates disease into adjacent soft tissues, orbit, and intracranial compartments [9, 10].

Non-invasive forms

1. Allergic fungal sinusitis is the most common in young, atopic, and immunocompetent patients. Plain CT shows central hyperdense areas.MR signal depends on the contents of material ranging from isointense to hypointense signal on T1- and T2-weighted images (Fig. 7).

Fig. 7
figure 7

Allergic fungal sinusitis: A 26-year-old male with nasal polyposis. Axial and coronal un-enhanced CT images (A, B) reveal complete opacification of paranasal sinuses with areas of hyperdensity representing inspissated secretions and fungal concretions (dashed arrows)

Full size image

2. Fungus ball: Single sinus is affected and there is usually thickening and sclerosis of the sinus walls with central areas of high-density calcification [9, 10].

Invasive forms

1. Acute invasive fungal sinusitis: this fungal infection has rapid progressive time course (< 4 weeks). The unique feature is the lack of enhancement of areas that generally enhance, like nasal mucosa and turbinates. MR imaging better evaluates the disease extension into adjacent soft tissues, orbit and intracranial compartment (Fig. 8) [10, 11]. Mucormycosis occurred in COVID-19 patients, especially with poor glycaemic control, injudicious use of corticosteroids and broad-spectrum antibiotics, and invasive ventilation [12].

Fig. 8
figure 8

Invasive fungal sinusitis: Top row: skull base involvement: coronal STIR (A), coronal contrast-enhanced T1-weighted (B), and axial contrast-enhanced T1-weighted (C) images reveal sphenoidal sinusitis and altered marrow signal showing heterogeneous peripheral enhancement and central hypointensity in the left pterygoid bone (arrows in A, B), maxilla and hard palate (thin arrow in C) and marked enhancement of the left masticator space (dashed arrow in C). bottom row: right orbital intraconal abscess: axial STIR image (D) reveals ethmoidal sinusitis (white arrow). An intraconal lesion of the right orbit medially (dashed arrow in D) which shows central restricted diffusion on the axial DWI (arrow in E). Axial contrast-enhanced T1-weighted image (F) reveals thick peripheral enhancement. Biopsy revealed mucormycosis

Full size image

2. Chronic invasive fungal sinusitis: This has an indolent course of disease (4–12 weeks). The imaging features are similar to acute form. Calcification is dense and coarse.

3. Chronic granulomatous form: Imaging findings are similar to other invasive fungal sinusitis with soft tissue opacification of the involved sinus, and involvement of surrounding tissue [10, 11].

Osteomyelitis

Skull base osteomyelitis is a life-threatening condition seen in elderly diabetics or immunocompromised patients and common bacterial organisms are Staphylococcus aureus and Pseudomonas aeruginosa. Atypical central skull base osteomyelitis does not involve external auditory canal. CT shows erosions of skull base with soft tissue collections. Fungal infections like Aspergillosis can involve skull base which are hypointense on T1W and T2W [13].

Tumors

Benign tumors

These are rarely found in the sphenoid sinus. These include fibrous dysplasia, aneurysmal bone cyst, and hemangioma.

Fibrous dysplasia

Common sites affected by fibrous dysplasia are the skull base and facial bones. It can involve a single bone (monostotic) or more than one bone (polyostotic). CT reveals expanded medullary bone with ground-glass opacity (Fig. 8). Three patterns have been described: (a) ground-glass (56%), (b) homogeneously dense (23%), and (c) cystic pattern (21%). MRI shows a low to intermediate signal on T1W. On T2W, signal is variable, lesions with mineralised matrix show low signal and lesions with fibrous content appear hyperintense on T2W and show avid enhancement (Fig. 9) [14, 15].

Fig. 9
figure 9

Fibrous dysplasia: monostotic type – coronal unenhanced CT (A) shows expansion with sclerosis/ground glass density involving walls of the right sphenoid sinus and lesser wing of sphenoid surrounding right optic canal (arrow in A). Polyostotic type in another patient: coronal unenhanced CT (B, C) reveal expansion with ground glass densities involving the left sphenoid sinus (arrow in C), the left middle turbinate, lesser and greater wing of left sphenoid bone, left frontal bone and left half of mandible

Full size image

Hemangioma

It is a slow-growing hamartoma of blood vessels. CT shows a well circumscribed lytic lesion with thickened and coarse trabecular pattern. On MRI, it is usually hyperintense on T1W and T2W images but may show atypical low signal on T1W and T2W [16].

Aneurysmal bone cyst

An aneurysmal bone cyst (ABC) is extremely rare in sinuses. It can be diagnosed by specific radiographical findings containing an eccentric lytic lesion with an expanded and remodelled “ballooned” bony contour of the affected bone. On CT and MRI, it appears benign multi-cystic expansile lesion with blood-fluid levels. MRI may reveal an expansile non-homogenous lesion. Between solid parts, there may be multiple variable sized cystic lesions. On contrast study, substantial enhancement may be seen (Fig. 10) [17].

Fig. 10
figure 10

Aneurysmal bone cyst: A 18-year-old male presented with headache and nasal obstruction. Coronal STIR (A), coronal un-enhanced T1-weighted (B), and axial un-enhanced T1-weighted (C) images reveal expansile cystic lesions with thin internal septations, some cystic areas showing hyperintensity on T1-weighted images representing blood–fluid levels involving the ethmoidal air cells and the sphenoid sinus (white arrows in B, C) with extension into the anterior cranial fossa and left orbit. Coronal contrast-enhanced T1-weighted image (D) shows peripheral enhancement in this lesion with thin enhancing septations. Axial gradient echo image (E) shows peripheral and central blooming areas representing hemorrhage. Axial un-enhanced CT (F) reveals expansile lesion with areas of bony breach (dashed arrow)

Full size image

Ossifying fibroma

It is a benign fibro-osseous tumor in which normal bone is replaced by dense fibrous tissue and foci of mineralisation [18]. CT shows an expansile lesion with a sclerotic shell, variable intralesional calcification and heterogeneous contrast enhancement. On MRI, central fibrous component is hypointense on T1W images and mixed low to high signal on T2W images and ossified rim is hypointense on T1W and T2W images and shows heterogenous contrast enhancement [18]. It is frequently associated with aneurysmal bone cyst [19].

Epidermoid

It is a rare, slow-growing, benign lesion of ectodermal origin. PNS is rare site for epidermoid. On CT, it appears hypodense, usually do not enhance but sometimes show rim enhancement. On MRI, epidermoid is isointense to CSF or may show high signal intensity on T1W (white epidermoid) with restricted diffusion [20].

Malignant tumors

Chordoma

Chordoma is a slow-growing, relatively rare malignant tumor arising from remnants of the primitive notochord. They may occur at any age but usually seen in adults with peak prevalence in the 4th decade of life. The classic CT appearance of chordoma is that of a centrally located, well-circumscribed lytic lesion with a hyper-attenuating expansile soft-tissue mass which is often disproportionately large compared to bony destruction. It shows irregular intra-tumoral calcifications. On MRI, chordoma is hyperintense on T2-weighted images reflecting high fluid content of vacuolated cellular component, intermediate to low signal on T1-weighted images with small foci of hyperintensity on T1-weighted IMAGES.On susceptibility-weighted images, it shows blooming due to intralesional hemorrhage. On contrast administration, the chordomas show moderate to marked enhancement and occasionally enhancement is slight or even absent. Sometimes enhancement pattern of the tumor has honeycomb appearance with intra-tumoral areas of low signal intensity [21]. Thumb sign is seen in midline sagittal images as indentation on pons (Fig. 11) [22]. A chordoma can be treated by surgical resection along with adjuvant radiation therapy. The main differential diagnosis of chordoma is chondrosarcoma which is off-midline, arises along the petro-occipital fissure and shows linear, globular or arc-like calcification [21].

Fig. 11
figure 11

Chordoma: A 58-year-old male. Axial T2-weighted (A) and axial un-enhanced T1-weighted (B) images reveal heterogeneous mass lesion involving posterior ethmoids, sphenoid sinus and clivus with retro-clival component (arrows) which compresses the pons: “thumb-sign” (arrow in sagittal T2-weighted image (C). The lesion is heterogeneously hyperintense on axial T2-weighted image (A) with small foci of hyperintensity on axial T1-weighted image (B) which show blooming on axial gradient-echo image (arrows in D). Axial and sagittal contrast-enhanced T1-weighted images (arrows in E, F) show heterogeneous enhancement of the mass lesion. Post-biopsy changes are seen in the posterior nasal cavity on sagittal images (C, F)

Full size image

Squamous cell carcinoma, adenocarcinoma, and melanoma

Primary sinonasal neoplasms are rare. Squamous cell carcinoma (SCC) is by far the commonest, accounting for 80% of all the neoplasms in this region, and maxillary sinus most frequently involved. Primary involvement of the sphenoidal sinus has been reported to occur in only 1 to 2% of all paranasal sinus tumors [23, 24].

A sinonasal soft tissue mass with bony destruction is seen on CT. MRI shows intermediate signal on T1WI and hypointense signal compared to fluid on T2WI and variable enhancement on contrast-enhanced study. It is homogeneous in smaller lesions and heterogeneous in larger lesions with areas of necrosis and hemorrhage. Imaging features of adenocarcinoma are indistinguishable from those of squamous cell carcinoma [23, 24]. Diffusion-weighted MR imaging (DWI) shows restricted diffusion and low apparent diffusion coefficient values. In the maxillary sinus, the ADC values of SCC (0.95 × 10−3 mm2/s) were higher than those of non-Hodgkin’s lymphoma (NHL) (0.61 × 10−3 mm2/s) [25].

Primary melanoma of the sphenoid sinus is also extremely rare. CT reveal isodense to hyperdense mass with bony destruction. MR imaging shows iso-hyperintense on T1-weighted images and hypointense on T2-weighted images with homogenous enhancement on postcontrast scans [26].

Sinonasal undifferentiated carcinoma

Sinonasal undifferentiated carcinoma (SNUC) is a very rare and aggressive malignancy, accounting for approximately 5% of all sinonasal cancers. The median age at presentation is fifth to the sixth decade of life, with a male-to-female ratio is around 2–3:1. SNUC commonly arises from the ethmoid sinus and superior nasal cavity. SNUC mostly presents as a rapidly enlarging tumor, and most patients have stage IV disease. Nodal involvement, orbital BS intracranial invasion and distant metastasis are frequent findings. Most SNUCs are more than 4 cm in maximal diameter at presentation and have ill-defined margins. The tumor has highly aggressive nature with bony destruction and invasion of adjacent structures, including paranasal sinuses, orbit, pterygopalatine fossa, parapharyngeal space, and cavernous sinuses. On CT, SNUCs usually appear as noncalcified mass and shows variable contrast enhancement and areas of central necrosis. On MRI, SNUCs show iso intensity on T1WI, iso- to hyper-intensity on T2WI, and heterogeneous enhancement on contrast-enhanced T1WI [27,28,29].

Rhabdomyosarcoma

Rhabdomyosarcoma (RMS) is a malignant neoplasm derived from primitive mesenchymal tissue. It has bimodal age distribution, with first peak during the first decade of life and a second during adolescence with a slight male predilection [30]. CT reveals a poorly defined enhancing soft-tissue mass with aggressive destruction of bone. On MRI, head and neck RMS shows isointensity relative to muscle on T1WI, and moderate hyperintensity relative to muscle on T2WI and moderate homogeneous enhancement [30, 31].

Lymphomas

The head and neck region are the second most prevalent site for extra-nodal lymphomas after the gastrointestinal tract. Non-Hodgkin’s lymphoma (NHL) is the subsequent most common malignancy in the sinonasal tract after SCC. Patients classically present in the seventh to eighth decades of life with a reported male-to-female ratio is 2:1. Diffuse large B-cell lymphoma (DLBCL) most commonly arises from the paranasal sinuses, with the maxillary sinus being the most common site of involvement [28]. On CT, sino-nasal lymphomas may show infiltrative or permeative bony invasion, leading to regional bony destruction. NHL with permeative-type tumor invasion typically cross the sinus wall and exhibit remnants of the sinus wall as a linear structure within the tumor (Fig. 12).

Fig. 12
figure 12

Lymphoma: A 75-year-old male with headache. Coronal T1-weighted (A) and coronal T2-weighted (B), coronal contrast-enhanced T1-weighted (C), and sagittal contrast-enhanced T1-weighted (D) images reveal a large enhancing sellar-suprasellar mass lesion involving pituitary gland, clivus with extension into the sphenoid sinus (arrows). Axial DWI (E) and ADC maps (F) show restricted diffusion (arrows)

Full size image

In contrast, bone sclerosis may be associated with bony resorption or remodelling caused by lymphoma. Lymphoma usually shows isointense signal on T1WI and slightly hyperintensity on T2WI [28] (Fig. 13). Restricted diffusion is seen with very low ADC values (≤ 0.60 × 10–3 mm2 /s) [32].

Fig. 13
figure 13

Plasmacytoma: Axial T2-weighted (A), axial un-enhanced T1-weighted (B), coronal T2-weighted (C), and sagittal T2-weighted images (D) reveal expansion with soft tissue lesion in the right sphenoid sinus (arrows). Axial DWI (E) and ADC maps (F) show restricted diffusion (dashed arrows). Axial contrast-enhanced T1-weighted (G) and sagittal contrast-enhanced T1-weighted images (H) show intense enhancement (arrows). The left sphenoid sinus shows mild mucosal thickening. Histopathology revealed plasma cell neoplasm

Full size image

Extramedullary plasmacytomas

Extramedullary plasmacytomas (EPMs) are characterized by monoclonal plasma cell proliferation with no obvious evidence of multiple underlying myelomas. EPMs usually occur in the sixth decade of life, with a male-to-female ratio of 3–4:1. Most EPMs involve the head and neck region in which the nasal cavity and paranasal sinuses are most commonly affected, followed by the nasopharynx, oropharynx, and larynx. Local recurrence or spread to other nearby osseous sites may occur. Some of the patients develop multiple myeloma [33]. The prognosis depends on the tumor size and the nodes' involvement. On CT scan, EMPs typically appear as well-defined, polypoid soft-tissue masses, which show homogenous enhancement. A large tumor may show internal areas of necrosis, adjacent bony destruction with infiltration into the adjacent structures, and vascular encasement [33, 34] (Fig. 13).

Neuroendocrine tumors

Neuroendocrine tumors (NETs) are epithelial neoplasms with predominant neuroendocrine differentiation. Although they can be found almost anywhere in the body, the most frequent sites are the gastrointestinal tract and respiratory system. In the head and neck region, neuroendocrine tumors most commonly appear in the larynx. Sinonasal tract NET is rare accounting for 5% cases. An MRI provides detailed information on the relationships between the tumor and the surrounding structures; therefore, this technique is superior in assessing dural invasion and perineural and arterial encasement. CT scans with multiplanar reconstructions, on the other hand, are more helpful in characterizing the degree and extent of bony erosion [35, 36] (Fig. 14).

Fig. 14
figure 14

Neuroendocrine tumor: A 65-year-old male. Coronal T2-weighted and T1-weighted images reveal a large soft tissue lesion in posterior ethmoids, sphenoid sinus and sella involving the pituitary gland, cavernous sinuses (arrow in A) and compressing optic chiasm (arrow in B). Coronal contrast-enhanced T1-weighted (C), sagittal contrast-enhanced T1-weighted images (D) reveal mild heterogeneous enhancement (arrows in C, D). Axial DWI (E) reveals restricted diffusion (arrows) and hypointense on ADC maps (not shown). Sagittal un-enhanced CT image (F) shows partial erosions of walls of sphenoid sinus and clivus (dashed arrows)

Full size image

Secondary involvement /invasion of the sphenoid sinus

Juvenile nasopharyngeal angiofibroma (JNA)

It is a locally aggressive, highly vascular soft tissue mass in a young male with a typical imaging appearance because of its consistent location near the sphenopalatine foramen, causing the pterygopalatine fossa to expand with anterior bowing of the ipsilateral posterior maxillary sinus wall. When the tumor grows it involves sphenoid bone- sphenoid sinus and may invade middle cranial fossa. It can also extend into the orbit and the intracranial compartment via the superior and inferior orbital fissures. MRI shows intermediate to high T1 and T2 signal intensity with multiple flow voids. Angiography is mostly useful in both evaluating the feeding vessels and in preoperative embolization (Fig. 15). The blood supply of these tumors is generally via branches of an external carotid artery like the internal maxillary and ascending pharyngeal arteries. Less commonly, branches of the internal carotid artery are involved [37].

Fig. 15
figure 15

Juvenile nasopharyngeal angiofibroma: A 21-year-old male with epistaxis. Coronal T2-weighted image (A), coronal contrast-enhanced T1-weighted (B), and axial contrast-enhanced T1-weighted (C) images reveal a large enhancing soft tissue lesion in the left sphenopalatine foramen, pterygopalatine fossa, and left sphenoid sinus (arrows). Coronal contrast-enhanced CT (D) reveals erosion of the floor of the left sphenoid sinus with an enhancing soft tissue lesion in this sinus. Frontal left external carotid artery angiogram (E) shows a hypervascular mass supplied by branches of the left external carotid artery, mainly the internal maxillary artery (dashed arrow). Mass was embolized preoperatively (dashed arrows in F)

Full size image

Invasive pituitary adenoma

The pituitary gland lies in the pituitary fossa, bound anteriorly by the tuberculum sellae and by the dorsum sellae posteriorly. Pituitary adenomas are common intracranial lesions and represent approximately 15% of all intracranial neoplasms. Tumors with a diameter less than 1 cm are microadenomas, and those with a diameter greater than 1 cm are macroadenomas. In pituitary tumors, suprasellar growth is the most common when it extends past its bony boundaries, whereas intrasellar and intra-sphenoidal extension is present in approximately 2% of cases [38] (Fig. 16).

Fig. 16
figure 16

Invasive pituitary adenoma: A 38-year-old male with blurred vision. Coronal T2-weighted (A), sagittal T2-weighted (B), coronal contrast-enhanced T1-weighted (C), and sagittal contrast-enhanced T1-weighted (D) images reveal a large enhancing sellar-suprasellar soft tissue lesion with extension into sphenoid sinus, cavernous sinuses, and compressing the optic chiasm (arrows). Axial gradient-echo images (E, F) reveal hemorrhage within the lesion (arrow in E) with subarachnoid hemorrhage (dashed arrow in F). Coronal and sagittal un-enhanced CT images (G, H) show the expansion of sella with partial erosions of its walls and soft tissue within sphenoid sinus (white arrows)

Full size image

Nasopharyngeal carcinoma

Nasopharyngeal carcinoma (NPC) is uncommon with a unique geographical distribution. They are of squamous cell origin and some types are strongly associated with the Epstein-Barr virus (EBV). According to 8th edition of the UICC/ AJCC staging system, T0 is added for Epstein-Barr virus-positive, unknown primary lesions with cervical lymph node involvement. Nasopharyngeal carcinoma can be confined to nasopharynx and /or extent into oro-pharynx is T1 category and adjacent soft tissue involvement is T2 category. The T3 category includes bony structures at skull base, cervical vertebra, pterygoid structures, and/or paranasal sinuses (Fig. 17). King et al. showed that the incidence rates of invasion of sphenoid sinus was more (27%) than maxillary sinus and ethmoid sinus (5% and 14%, respectively) [39]. Intra-cranial extension, involvement of cranial nerves, hypopharynx, orbit, parotid gland, and/or extensive soft tissue infiltration beyond lateral surface of the lateral pterygoid muscle is included in T4 category [40].

Fig. 17
figure 17

Nasopharyngeal carcinoma: A 62-year-old male. Axial un-enhanced T1-weighted (A) and axial contrast-enhanced T1-weighted (B) images reveal soft tissue thickening (arrows in A) with enhancement involving the left lateral nasopharyngeal wall (arrows in B). Axial contrast-enhanced T1W (C) and coronal contrast-enhanced T1W images (D, E) show erosion of floor and extension of soft tissue into the left sphenoid sinus (arrow in D) and left cavernous sinus and Meckel’s cave (C, E). Coronal un-enhanced CT (F) reveals erosion of the floor of the left sphenoid sinus with soft tissue along the floor of the left sphenoid sinus (arrow)

Full size image

Metastatic tumors to the paranasal sinuses

Metastatic tumors of the paranasal sinuses are rare. Major locations of the primary tumors include kidney (renal cell carcinoma), breast, lung, testis (seminoma), gastrointestinal tract, prostate, and thyroid gland which gives origin to these metastases [41]. The sphenoid sinus is most frequently involved among them, followed by the maxillary sinus. Even though a metastatic presentation of an occult prostatic carcinoma is not uncommon, axial skeleton is commonly involved. Metastasis of the sphenoid sinus is an infrequent event, with less than ten documented cases reported in the literature [42].

CT scans and MRI are essential for diagnosing metastases within the paranasal sinuses, as they reveal the size of the lesion and its extension to the adjacent structures, such as the orbit or the brain [41] (Fig. 18).

Fig. 18
figure 18

Metastasis in right sphenoid sinus in a known case of invasive ductal carcinoma of the right breast (NOS GRADE-II): A 52-year-old lady presented with a reduced vision in the right eye. Coronal T2-weighted (A), coronal un-enhanced T1-weighted (B), and coronal contrast-enhanced T1-weighted (C) images show altered signal with soft tissue involving walls of the right sphenoid sinus (A, B) which show mild enhancement (arrows in C). Coronal un-enhanced CT reveals erosion of walls of the right sphenoid sinus (dashed arrow in D). PET CT shows a heterogeneous soft tissue with increased FDG uptake in the upper outer quadrant of the right breast involving skin (arrow in E) with right axillary lymphadenopathy (arrows in F)

Full size image

Miscellaneous

Ecchordosis physaliphora

Ecchordosis physaliphora (EP) is one of the rare congenital benign hamartomatous lesions considered ectopic notochordal remnants. This is generally histopathologically indistinguishable from chordoma, so imaging plays a crucial role in diagnosis.

It is a retro-clival notochordal remnant in 2% of the autopsy cases. It is usually asymptomatic but, in a few cases, can present with headache and dizziness. CT reveals a well-defined bony clival defect with preserved cortex and a bony or cartilaginous “stalk” projecting from clivus. These lesions are hypointense on T1-weighted images, hyperintense on T2-weighted images and do not show restricted diffusion. In contrast to chordoma, EP does not generally demonstrate contrast enhancement (Fig. 19) [43, 44].

Fig. 19
figure 19

Ecchordosis physaliphora: axial FIESTA (A) with a sagittal reconstructed image (B) through the posterior fossa demonstrate a well-defined, extra-axial, cystic appearing lesion (arrow) in the retro-clival region. DWI reveals no diffusion restriction (not shown)

Full size image

Spontaneous lateral sphenoidal cephalocele

Spontaneous lateral sphenoidal cephalocele (SLSC) occurring from bony defects in the lateral recess of the sphenoid sinus is rare. The predisposing factor for the occurrence of these leaks appears to be raised intracranial pressure. On CT, an SLSC mostly appears as focal dehiscence of bone with soft tissue or fluid attenuation herniating into the defect, often mimicking a mucous retention cyst. The contents of the cephalocele are better demonstrated on MR imaging or CT cisternography. Meninges are seen herniating through the defect as a thin dark line on T2 imaging (Fig. 20) [45].

Fig. 20
figure 20

Spontaneous lateral sphenoidal cephalocele: A 31-year-old male presented with right sided nasal discharge on bending forward. Coronal T2-weighted fat-suppressed (A) and 3D coronal FIESTA coronal images (B) reveal CSF isointense fluid in the lateral recess of the right sphenoid sinus (arrow). 3D FIESTA coronal image (prone position (C) shows herniation of the right temporal lobe into right lateral recess (arrow). Coronal T2-weighted image (D) reveals an empty sella suggesting altered CSF dynamics. Coronal un-enhanced CT images (E, F) reveal a bony defect in the wall of the lateral recess of the right sphenoid sinus (dashed arrows)

Full size image

Key features of some sphenoid sinus pathologies

Pathology

Imaging features

Fungal infection

T2 hypointense, invasive form: shows lack of contrast enhancement

Mucocele

Sinus opacification with variable density contents and may show areas of bony breach

ABC

Multiple fluid–fluid levels

Fibrous dysplasia

Ground-glass density

Expansion of affected bone

Ossifying fibroma

Expansive mass with sclerotic shell

Plasmacytoma

Solitary lesion

T2 iso to hyperintense, T1 isointense

Lymphoma

T2 mildly hyperintense, T1 intermediate with restricted diffusion

Chordoma

T2 hyperintense, T1 iso to hypointense lesion

Heterogeneous “honeycomb” enhancement

Invasive pituitary adenoma

Sellar-suprasellar mass with hemorrhagic contents

Juvenile nasopharyngeal angiofibroma

Young male, centred at sphenopalatine foramen

Metastasis

Rare, lytic or sclerotic lesions

Spontaneous lateral sphenoidal cephalocele

Bony defect in lateral recess of SS

Ecchordosis physaliphora

T2 hyperintense, T1 hypointense with no contrast enhancement and stalk like clival connection on CISS /FIESTA sequence

Conclusion

Clinicians and radiologists come across multiple sphenoid sinus pathologies of various aetiology in their day-to-day practice. Patients may have various complaints, and often, it is tough to locate the pathology, and that's where there is role of radiology. The complaints may vary from minor headaches to neuro-ophthalmic complaints. The radiologist should appreciate the proximity of critical neurovascular structures to the sphenoid sinus and recognize that sphenoid sinus disease can threaten vision. Abnormalities noted on CT and MR in the appropriate clinical context should not be casually dismissed but should be appreciated as the possible cause of the patient’s problem. CT and MRI play a crucial role in assessing the extent of involvement, delineating the spread of disease, and narrow differential diagnosis in lesions involving sphenoid sinuses.