Cavernous Hemangioma

Incidence peaked in during third and fourth decades (6 cases, 31.57%; 19 cases, 50%; age range: 5–65 years; mean = 36.42 years; M:F = 1:2.8]). Clinically, features of raised intracranial pressure were common and included headache (75%), blurring of vision (37.5%), followed by ptosis (60%), diplopia (33.3%), facial numbness (33.3%), and dystonia (6.6%) with a mean duration of symptoms being 1 year. Multiple cranial nerve palsies (total ophthalmoplegia = 33.3%, third and sixth nerve palsy = 20%, isolated fifth nerve palsy = 13.3%, and isolated third nerve palsy = 20%] were frequent. On cranial computed tomography (CT) and magnetic resonance imaging (MRI), most were well circumscribed. On MRI, all lesions were iso-hypointense on T1-weighted imaging (WI) and brilliantly hyperintense on T2WI and fluid-attenuated inversion recovery (FLAIR) showing exuberant enhancement on contrast administration (Fig. 1A–D). Few lesions showed early central nonenhancing areas which enhanced in the delayed images. These lesions insinuated the surrounding structures without causing destruction. On CT scans, bony remodeling was seen with the lesion appearing hyper- to isodense. On neuroimaging, four cases of cavernous hemangiomas were mistaken for meningioma (three cases) or schwannoma (one case). Histologically, the lesions appeared partially circumscribed by a collagenous capsule drawn from the cavernous sinus dural wall (Fig. 1E). Microscopically showed vascular channels of varying caliber arranged back to back in a lobular manner (Fig. 1E). The channels were lined by prominent endothelium. The lumina were widely patulous and lacked thrombosis, calcification, and was devoid of hemosiderin. A single case that showed a sudden increase in the size of the lesion following pregnancy was positive for progesterone receptor in the lining endothelial cells but failed to express estrogen receptor.

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Fig. 1 Cavernous angioma. MR imaging shows left cavernous regional well-circumscribed lesion displaying brilliantly hyperintensity on T2WI and FLAIR image, iso to hypointense on T1WI (A, B) with exuberant enhancement on contrast administration (C, D) reminiscent of a meningioma. However central non-enhancing areas in the early phase (C) which enhanced in the delayed phase are characteristic of cavernous angioma. Histology revealed circumscribed, smooth-surfaced lesion (E) with characteristic back-to-back arranged thin venous channels with flattened endothelium (F) separated by thin fibrous stroma (G). (E, MAT × 8; F: H&E × Ob. ×10; G, MAT × Obj. ×10). H&E, hematoxylin and eosin; MAT, Masson's trichrome; MR, magnetic resonance; WI, weighted imaging.

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Fig. 1 Cavernous angioma. MR imaging shows left cavernous regional well-circumscribed lesion displaying brilliantly hyperintensity on T2WI and FLAIR image, iso to hypointense on T1WI (A, B) with exuberant enhancement on contrast administration (C, D) reminiscent of a meningioma. However central non-enhancing areas in the early phase (C) which enhanced in the delayed phase are characteristic of cavernous angioma. Histology revealed circumscribed, smooth-surfaced lesion (E) with characteristic back-to-back arranged thin venous channels with flattened endothelium (F) separated by thin fibrous stroma (G). (E, MAT × 8; F: H&E × Ob. ×10; G, MAT × Obj. ×10). H&E, hematoxylin and eosin; MAT, Masson's trichrome; MR, magnetic resonance; WI, weighted imaging.

Aspergilloma

Clinically, three cases presented with features of facial pain while one patient, in addition, had MCA infarct, ptosis, and visual loss (five cases, 13.51%; age range: 25–53 years, mean = 39.4 years). The mean duration of symptoms was 1 month. Total ophthalmoplegia was seen in one, and sensory loss in trigeminal nerve distribution area in two patients. Radiographically, the tumor appeared heterogeneously hyperdense on CT scan (Fig. 2A), heterogeneously hyperintense on T2WI, and FLAIR images with hypointense areas within, hypointense on T1WI, with heterogeneous postcontrast enhancement (Fig. 2B–E). Narrowing and stretching of the internal carotid artery (ICA) were noted. Bone destruction was evident in few lesions with no blooming seen on susceptibility weighted imaging (SWI) images. Histologically, the lesion revealed abundant necrotic debris, enclosed by broad fibrotic zones highlighted on Masson's trichrome stain (Fig. 2F) with dense lymphohistiocytic infiltrate and multinucleate giant cells (Fig. 2G) that contained ingested fragments of septate acute-angled branching hyphal forms on periodic acid schiff and gomeri methenamine silve staining, morphologically resembling Aspergillus spp. (Fig. 2H).

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Fig. 2 Aspergilloma. CT scan plain (A), T1WI, T2WI and postcontrast images showing heterogeneous hyperdensity (A) at left cavernous sinus without bony destruction (A, B). It is hypointense on T2WI (C) with heterogenous postcontrast enhancement. Note the presence of edema in the left temporal parenchyma (D). The imaging diagnosis was meningioma. The lesion on histology revealed a granulomatous lesion extending along the dural wall (F) of the cavernous sinus. The giant cells had engulfed characteristic septate acute angled branching hyphae of Aspergillus spp. demonstrated by periodic acid–Schiff (PAS) (G) and Gomori's methenamine silver stains (GMS) (H). (F, MAT × Obj. ×4; G, PAS stain × Obj. ×20; H, GMS stain × Obj. ×20). CT, computed tomography; MAT, Masson's trichrome; WI, weighted imaging.

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Fig. 2 Aspergilloma. CT scan plain (A), T1WI, T2WI and postcontrast images showing heterogeneous hyperdensity (A) at left cavernous sinus without bony destruction (A, B). It is hypointense on T2WI (C) with heterogenous postcontrast enhancement. Note the presence of edema in the left temporal parenchyma (D). The imaging diagnosis was meningioma. The lesion on histology revealed a granulomatous lesion extending along the dural wall (F) of the cavernous sinus. The giant cells had engulfed characteristic septate acute angled branching hyphae of Aspergillus spp. demonstrated by periodic acid–Schiff (PAS) (G) and Gomori's methenamine silver stains (GMS) (H). (F, MAT × Obj. ×4; G, PAS stain × Obj. ×20; H, GMS stain × Obj. ×20). CT, computed tomography; MAT, Masson's trichrome; WI, weighted imaging.

Meningioma

Majority of the patients presented with ptosis and diplopia (80%) of 2 years' duration (five cases, 13.51%; age range: 44–67 years; mean = 49.2 years, all-female patients). Raised intracranial pressure, headache, visual disturbances, third nerve palsy, and left ophthalmic branch of trigeminal nerve causing hypoesthesia were noted in one case each. Radiographically, the tumor showed T1 hypointense (Fig. 3A) and T2 hyperintense, well-circumscribed, and solid with uniform contrast enhancement (Fig. 3D). Narrowing and stretching of the ICA was seen when the ICA was encased by the lesion (Fig. 3E). Few lesions also revealed a dural tail. Extension of the lesion along the nerve roots of the trigeminal nerve was evident. On neuroimaging, all four cases were concordant with histological diagnosis. Microscopically, various histological subtypes were noted (fibrous, meningothelial, chondroid, and angiomatous). The tumor showed meningothelial cells in lobules demarcated by predominant small to medium-sized thin-walled vascular channels (Fig. 3F). The tumor cells were largely uniform, with oval benign nuclei and delicate chromatin that showed occasional mitosis and expressed globally expressed epithelial membrane antigen (EMA) positivity (Fig. 3F inset).

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Fig. 3 Meningioma. T2WI, T1WI, FLAIR, postcontrast and MRA showing right cavernous sinus hyperintense lesion on T2WI and FLAIR (A–C), isointense on T1WI (B) with uniform post-contrast enhancement (D) characteristic of meningioma. Note right cavernous ICA is stretched and narrowed on MRA (A–D). Histology reveals an angiomatous meningioma with several thick hyalinized vessels (E). The tumor cells reveal membranous labeling for EMA (E, inset). (E, H&E × Obj. ×40; F, EMA × Obj. ×40). H&E, hematoxylin and eosin; FLAIR, fluid-attenuated inversion recovery; MRA, magnetic resonance angiogram; WI, weighted imaging.

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Fig. 3 Meningioma. T2WI, T1WI, FLAIR, postcontrast and MRA showing right cavernous sinus hyperintense lesion on T2WI and FLAIR (A–C), isointense on T1WI (B) with uniform post-contrast enhancement (D) characteristic of meningioma. Note right cavernous ICA is stretched and narrowed on MRA (A–D). Histology reveals an angiomatous meningioma with several thick hyalinized vessels (E). The tumor cells reveal membranous labeling for EMA (E, inset). (E, H&E × Obj. ×40; F, EMA × Obj. ×40). H&E, hematoxylin and eosin; FLAIR, fluid-attenuated inversion recovery; MRA, magnetic resonance angiogram; WI, weighted imaging.

Schwannoma

Patients presented with features of raised intracranial pressure with headache and diplopia (2 cases) of 2 years duration (three cases, 7.8%; age range: 19–28 years, mean = 22.3 years; M:F = 2:1). Clinical evaluation showed involvement of multiple cranial nerve (left third, fourth, and sixth nerves) causing palsy. Radiologically, the tumor showed heterogeneous signal intensity on T2WI and FLAIR images, with grossly hyperintense cystic areas and solid isointense areas on T2WI and FLAIR and heterogeneous postcontrast enhancement (Fig. 4A–D). CT scan showed trigeminal nerve root involvement and enlargement of nerve root foramen. On neuroimaging, the diagnosis was accurate in two, whereas one was mistaken for meningioma. Microscopically, the tumor was highly vascular with spindle cells arranged in characteristic hyper- and hypocellular Antoni A and B areas (Fig. 4E). Tumor cells expressed S-100 (Fig. 4F) positivity on immunohistochemistry confirming its Schwannian origin.

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Fig. 4 Schwannoma. Left parasellar lesion hypointense on T1WI, T2WI, SWI, and postcontrast T1WI shows a heterogeneously hyperintense lesion on T2WI with cystic areas (A, B), and heterogenous post-contrast enhancement (D). SWI images are showing microbleeds (C) within the lesion characteristic of schwannoma (A–D). Histology reveals schwannoma with characteristic spindled cells with wavy nuclei arranged in compact and loose zones (E) with strong diffuse S-100 positivity confirming Schwannian origin (F). (E, H&E × Obj. ×10; F, S-100 × Obj. ×20). H&E, hematoxylin and eosin; SWI, susceptibility weighted imaging; WI, weighted imaging.

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Fig. 4 Schwannoma. Left parasellar lesion hypointense on T1WI, T2WI, SWI, and postcontrast T1WI shows a heterogeneously hyperintense lesion on T2WI with cystic areas (A, B), and heterogenous post-contrast enhancement (D). SWI images are showing microbleeds (C) within the lesion characteristic of schwannoma (A–D). Histology reveals schwannoma with characteristic spindled cells with wavy nuclei arranged in compact and loose zones (E) with strong diffuse S-100 positivity confirming Schwannian origin (F). (E, H&E × Obj. ×10; F, S-100 × Obj. ×20). H&E, hematoxylin and eosin; SWI, susceptibility weighted imaging; WI, weighted imaging.

Adenocarcinoma

Three cases of metastatic carcinoma were diagnosed (three cases, 7.89%; age range: 25–73 years, mean = 51 years, M:F = 2:1). Clinically the patients presented with features of raised intracranial pressure like headache, visual blurring, cranial nerve palsies (second–fifth and 7th), and recurrent memory loss of 2 months' duration. Radiologically, the tumor was hypointense on T2WI and FLAIR images and isointense on T1WI showing uniform enhancement (Fig. 5A–E). Extension and destruction of the adjacent structures including orbit, pituitary fossa, and petrous bone were evident. On neuroimaging, two of the three cases were mistaken for meningioma. Microscopically, the tumor was seen in lobules forming characteristic acini and solid nest of cells exhibiting moderate anaplasia with brisk mitosis and areas of necrosis (Fig. 5F) and expressed cytokeratin positivity on immune staining (Fig. 5F, inset).

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Fig. 5 Adenocarcinoma. CT plain and contrast study shows a mildly hyperdense enhancing lesion in right parasellar lesion (A, B). On MRI, the lesion is hypointense on T2WI, isointense on T1WI showing uniform contrast enhancement (C–E). Imaging possibility considered was meningioma Histopathology revealed features of adenocarcinoma with neoplastic epithelial cells arranged in tubules and acini. (F, H&E × Obj. ×4) Immunostaining was strongly pan cytokeratin positive (F) and negative for pituitary adenoma markers (images not shown). (F, H&E × Obj. ×20; F, inset: pan-cytokeratin × Obj. ×20). CT, computed tomography; H&E, hematoxylin and eosin; WI, weighted imaging.

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Fig. 5 Adenocarcinoma. CT plain and contrast study shows a mildly hyperdense enhancing lesion in right parasellar lesion (A, B). On MRI, the lesion is hypointense on T2WI, isointense on T1WI showing uniform contrast enhancement (C–E). Imaging possibility considered was meningioma Histopathology revealed features of adenocarcinoma with neoplastic epithelial cells arranged in tubules and acini. (F, H&E × Obj. ×4) Immunostaining was strongly pan cytokeratin positive (F) and negative for pituitary adenoma markers (images not shown). (F, H&E × Obj. ×20; F, inset: pan-cytokeratin × Obj. ×20). CT, computed tomography; H&E, hematoxylin and eosin; WI, weighted imaging.

Chondrosarcoma

Two cases were diagnosed (two cases, 5.26%; age range: 48–56 years, mean = 52 years). Clinically, the patients presented with diplopia, visual impairment, and one of the cases showed cranial nerve involvement (third–fifth). Neuroimaging revealed heterogeneously hyperintense on T2WI and FLAIR (not so hyperintense) with the appearance of septations within it, hypointense on T1WI with heterogenous enhancement with more nonenhancing areas (Fig. 6A–F). Extension into foramen rotundum noted along the left maxillary nerve. No areas of blooming as noted. On neuroimaging, it was mistaken for schwannoma. Histologically the lesion showed lobulated chondroid lesion (Fig. 6G) with low-grade malignant chondrocytes (Fig. 6H), showing hyperchromasia, binucleation, and mitotic activity. The tumor was positive for S-100 (Fig. 6I) and negative for EMA and cytokeratin. Ki-67 / MIB-1 mindbomb E3 ubiquitin lprotein ligase 1 labeling index was low.

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Fig. 6 Chondrosarcoma. CT scan and bone windows show hypodense lesion with calcification and destruction of the left side of the clivus and sellar floor (A, B). The lesion is hypointense on T1WI (C), Hyperintense on T2WI with calcification with Postcontrast Enhancement.T2WI, VenoBOLD and postcontrast images of right cavernous sinus lesion (A–F). The possibility of schwannoma was considered on imaging. Histology revealed a chondroid neoplasm with chondrocytes within lacunae (G), displaying increased cellularity and mild atypia but low mitotic activity characteristic of low-grade chondrosarcoma (H). Tumor cells exhibiting strong S-100 positivity confirming chondroid origin (I). (G, H&E × Obj. ×10; H, H&E × Ob. ×20; I, S100 × Obj. ×20). CT, computed tomography; H&E, hematoxylin and eosin; WI, weighted imaging.

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Fig. 6 Chondrosarcoma. CT scan and bone windows show hypodense lesion with calcification and destruction of the left side of the clivus and sellar floor (A, B). The lesion is hypointense on T1WI (C), Hyperintense on T2WI with calcification with Postcontrast Enhancement.T2WI, VenoBOLD and postcontrast images of right cavernous sinus lesion (A–F). The possibility of schwannoma was considered on imaging. Histology revealed a chondroid neoplasm with chondrocytes within lacunae (G), displaying increased cellularity and mild atypia but low mitotic activity characteristic of low-grade chondrosarcoma (H). Tumor cells exhibiting strong S-100 positivity confirming chondroid origin (I). (G, H&E × Obj. ×10; H, H&E × Ob. ×20; I, S100 × Obj. ×20). CT, computed tomography; H&E, hematoxylin and eosin; WI, weighted imaging.

Chordoma

A single case (2.63%) was recorded in a 30-year-old female presenting with dropping of the eyelid, vision impairment due to involvement of cranial nerves (third, fourth, and sixth). The tumors were hypodense on CT with punctate calcification, heterogeneously hyperintense on T2WI showing few cystic areas within, and partially inverting on FLAIR images. It was hypointense on T1WI with areas of hyperintensity within showing mild heterogenous postcontrast enhancement (Fig. 7A–E). Foci of blooming were seen on SWI images. CT scan revealed destruction of the apex of the right petrous bone with superior clivus. On neuroimaging, both the cases were diagnosed as schwannoma. Histologically, a lobulated lesion composed of cells with epitheloid morphology arranged in characteristic chords separated by bubbly mucoid stroma was seen with scattered physaliphorous cells with abundant multivacuolated cytoplasm(Fig. 7F). Immunohistochemistry revealed positivity for S-100 (Fig. 7G), EMA, and cytokeratin (Fig. 7H) confirming the diagnosis.

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Fig. 7 Chordoma. Left parasellar lesion on CT scan appears hypodense. Note the absence of any bony destruction (A, B). On MRI it is hyperintense on T2WI (C), hypointense on T1WI (D) with heterogenous post-contrast enhancement (F). Based on these features, the possibility of schwannoma was suspected. Histology revealed a lobulated tumor showing distinctive cells with epitheloid morphology arranged in chords separated by bubbly mucoid stroma and characteristic physaliphorous cells with abundant multivacuolated cytoplasm. (F), tumor cell express S-100 (G) and strong cytokeratin confirming the diagnosis of chordoma (H). (F, H&E × Ob.40x; G, S100 × Obj.20; H, pan-cytokeratinxObj.20). CT, computed tomography; H&E, hematoxylin and eosin; MRI, magnetic resonance imaging; WI, weighted imaging.

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Fig. 7 Chordoma. Left parasellar lesion on CT scan appears hypodense. Note the absence of any bony destruction (A, B). On MRI it is hyperintense on T2WI (C), hypointense on T1WI (D) with heterogenous post-contrast enhancement (F). Based on these features, the possibility of schwannoma was suspected. Histology revealed a lobulated tumor showing distinctive cells with epitheloid morphology arranged in chords separated by bubbly mucoid stroma and characteristic physaliphorous cells with abundant multivacuolated cytoplasm. (F), tumor cell express S-100 (G) and strong cytokeratin confirming the diagnosis of chordoma (H). (F, H&E × Ob.40x; G, S100 × Obj.20; H, pan-cytokeratinxObj.20). CT, computed tomography; H&E, hematoxylin and eosin; MRI, magnetic resonance imaging; WI, weighted imaging.

Cavernous Angioma

Cavernous angiomas are uncommon in extra-axial locations and the majority of them are located in the intra-axial portion of the middle cranial fossa. Reported cases at extra-axial locations include the optic chiasm, perimesencephalic cistern, internal auditory canal, cerebellar pontine angles. Extra-axial intracranial cavernous hemangiomas at cavernous sinus were representing 0.4 to 2% of all dural-based haemangiomas.14 Shi et al reported female preponderance and mean age of presentation in the fifth decade.15 In our series, it was the most frequent lesion of cavernous sinus (50%) and female predominance was noted, the tumors occurred at a younger age, in the third decade. Secondary involvement of the oculomotor cranial nerve at the lateral wall of the cavernous sinus wall is a frequent manifestation observed in the present study. In MRI, they appear well-circumscribed, exuberantly hyperintense on T2WI and FLAIR and hypointense on T1WI with heterogenous brilliant contrast enhancement in early postcontrast images. Nonenhancing regions in the early phase show enhancement in the delayed images, a feature seen in some of our cases. They tend to scallop the bone without destroying them. At times, they could not be reliably distinguished preoperatively from meningiomas because of homogenous hyperintensity on T2WI which is a characteristic of the angiomatous and microcystic variants of meningiomas. In such scenarios, other features such as a dural tail, narrowing and stretching of the involved cavernous ICA, and angiography (DSA [digital subtraction angiography]) images showing early enhancement are pointers that favor meningioma.16 17 18 In our series, discordance rate was 22.22% (4/18 cases). The majority of them were mistaken for meningioma (three cases) due to dural tail and narrowing of the ICA. The presence of vascular enhancement along the tentorium may be mistaken for the dural tail on MRI. Sometimes when the hemangioma is very large, it can compress and narrow down the ICA and surgical excision becomes difficult due to excessive bleeding; tendency to invade middle cranial fossa, sellar regions, and encase neurovascular structures11 19 20 21 are the other hindering factors for complete excision. Intra- and postoperative excessive bleeding leading to mortality has been documented up to 12.5%.22 Unlike hemangioma, trigeminal schwannoma of the middle fossa tends to be centered slightly more posteriorly16 and displaces carotid artery, cranial nerves inside the cavernous sinus or the petrous bone, rather than ensheathing them; thereby preservation of these structures during surgery is possible. Several surgical approaches can be used to excise the tumor completely for excellent results at the sellar/parasellar area.23 On imaging, there showed heterogeneous signal characteristics on both T1WI and T2WI, appearing hyperintense on T2WI and hypointense on T1WI. They showed cystic areas within with heterogeneous postcontrast enhancement. No delayed enhancement is seen. Microbleeds are evident within the lesion on gradient or SWI images. They have a propensity to spread along trigeminal nerve branches; however, this feature is not a specific feature of nerve sheath tumors. It may be seen in meningioma, fungal granulomas, and metastasis. Prominent cystic degeneration, foamy macrophages, hemorrhage, hemosiderin-laden macrophages, dystrophic calcification, and perivascular hyalinization of vessels are clues for the diagnosis of schwannoma. In our series, there were only three cases of schwannomas arising from the cavernous sinus, and all were accurately diagnosed on imaging and did not pose any difficulty. Meningiomas can arise from the cavernous sinus lateral wall dura or the dura or from dural coverings of sphenoid/petrous bone. Ambiguous imaging findings and mass effect producing lesions necessitate surgical intervention and histological confirmation for definitive management. They appear homogenously hyperintense on T2WI and FLAIR and iso- to hypointense on T1WI showing uniform enhancement. Other features include dural tail, bony remodeling, compression, and narrowing of the cavernous sinus. ICA and angiography detection of “sunburst” pattern with early staining and delayed washout help in differentiating meningiomas from other lesions. Benign nonmeningothelial tumors have got better surgical clearance compared with meningiomas, hence they cause a lower rate of preoperative nerve deficits and postoperative ocular deficits.16 Surgical and radiosurgical interventions are found to be complementary to each other. The deciding factors for the selection of treatment modality are the size and volume of haemangiomas.24

Aspergillosis was the second most frequent lesion on our series of CS lesions (13.5%): cavernous sinus involvement occurs by direct extension or hematogenous spread. The common primary site involvement includes paranasal sinuses, ear cavity, and orbit. Pathogenesis includes necrotizing vasculitis causing thrombosis and infarction in immunocompromised patients favoring the rapid spread of the inflammation to the cranial cavity.21 They show nonenhancing areas with exuberant enhancement. The presence of perilesional edema in the temporal lobe structures, bony destruction, extension, and involvement of the structures of the infratemporal fossa (across various parapharyngeal spaces) assist in imaging diagnosis of fungal infection. Involvement and extension from the paranasal sinuses is an important clue for diagnosis. Paramagnetic elements like iron and magnesium derived from hemorrhage or aspergillus fungal colonies brings about characteristic reduced signal intensity on T1WI and very low signal intensity on T2WI are characteristic findings in paranasal sinus aspergillosis.25 26

Adenocarcinoma

Metastases to the cavernous sinus are uncommon and the incidence of central nervous system (CNS) involvement is approximately 30 to 40% of systemic cancer patients.27 Thomas and Yoss recorded 23% parasellar lesion to be metastatic tumors.27 28 The role of biopsy and surgical resection in known systemic cancer and MRI-confirmed cavernous sinus lesions is unclear.29 Various reported primary tumors in literature includes squamous cell carcinoma (SCC) of the head and neck,30 nasopharyngeal carcinoma,31 oropharyngeal carcinoma,31 melanoma,32 papillary adenocarcinoma,33 rhabdomyosarcoma of the head and neck,34 35 salivary gland duct carcinoma, and SCC of salivary glands.30 34 35 MRI plays an important role in diagnosing and describes the extent of the lesion. They appear hypointense on both T2WI and FLAIR with bony destruction and extension showing uniform postcontrast enhancement. Perineural extension with involvement of various parapharyngeal spaces and loss of normal fat planes are evident. Histopathological evaluation is essential for confirmation of diagnosis.36 In our series, two of three cases were not suspected on imaging due to lack of known primary malignancy, involvement limited to cavernous sinus area and absence of bony destruction.

Cranial chondrosarcomas are slow-growing invasive lesions arising from the skull base, most common at the petrooccipital synchondrosis, and can extend to involve the cavernous sinus. On imaging, these lesions showed high signal intensity on T2W MR images because of the chondroid matrix.37 Regions of low signal intensity can be depicted owing to calcifications. The lesions usually show marked enhancement on gadolinium-enhanced MR images. CT demonstrates matrix calcification in a chondroid pattern (“ring and arc” pattern) and helps in the assessment of bone destruction. In our series, both the cases were misdiagnosed as schwannoma, as there was no bony destruction and revealed septations with marked gadolinium enhancement.38

Chordomas are malignant midline lesions arising from notochord rest cells of the axial skeleton showing local aggressiveness and clival bone involvement in the cranium. They are seen in the fourth decade and may be off-centered in the cavernous sinus region mimicking other mass lesions. In our series, there was one case and misdiagnosed as schwannoma due to its off-center location, absence of bony destruction, and presence of blooming foci on SWI images. On MRI, they mimic the chondrosarcoma appearing heterogeneously hyperintense with cystic areas on T2WI and hypointense on T1WI showing heterogenous mild postcontrast enhancement. They are hypodense on CT scans and show stippled calcifications and bony destruction.39 Differential diagnosis includes chondrosarcoma chordoid meningioma and other look-alike myxoid lesions (extraskeletal myxoid chondrosarcoma, myxoid liposarcoma, and myxopapillary ependymoma). Epithelial markers' positivity (cytokeratin) is a feature of chordoma and absent in other myxoid sarcomas and ependymomas. On histology, presence of physaliphorous cells is a clue for chordoma diagnosis.40 Low-grade chondrosarcoma needs immunohistochemistry assistance, as it lacks pleomorphism, hyperchromasia, and infiltrative features, the other clues include binucleation and clusters of malignant-looking chondrocytes within a single lacuna extensive sampling of the entire specimen is essential for confirmation of grade.39