Sellar, suprasellar, and parasellar masses: Imaging features and neurosurgical approaches

Abstract

The sellar, suprasellar, and parasellar space contain a vast array of pathologies, including neoplastic, congenital, vascular, inflammatory, and infectious etiologies. Symptoms, if present, include a combination of headache, eye pain, ophthalmoplegia, visual field deficits, cranial neuropathy, and endocrine manifestations. A special focus is paid to key features on CT and MRI that can help in differentiating different pathologies. While most lesions ultimately require histopathologic evaluation, expert knowledge of skull base anatomy in combination with awareness of key imaging features can be useful in limiting the differential diagnosis and guiding management. Surgical techniques, including endoscopic endonasal and transcranial neurosurgical approaches are described in detail.

Keywords: Cavernous sinus; parasellar mass; sellar mass; skull base; suprasellar mass.

Figure 1.

Sellar lesions. (A) Dynamic post-contrast T1WI demonstrates sub-centimeter rounded pituitary gland lesion (arrow), consistent with microadenoma. (B,C) Sellar mass with increased signal on pre-contrast T1 images (B) and peripheral enhancement (C), suggestive of pituitary apoplexy in this patient with acute presentation. (D-F) Pituitary mass with cystic component on coronal T2WI (arrow, D), internal calcification on sagittal CT (E), and diffuse enhancement on sagittal post-contrast T1WI (F), consistent with adamantinomatous craniopharyngioma. (G,H) Sagittal images show a sellar lesion with intrinsic T1WI hyperintense nodule (arrow, G), which does not enhance on post-contrast T1WI (H), consistent with Rathke Cleft Cyst. (I,J) Giant aneurysm arising from the anterior communicating artery on sagittal CT angiography MIP reformats (arrow, I), which demonstrates pulsation artifact in the phase encoding direction on axial T2/FLAIR (arrow, J).

Figure 2.

Suprasellar lesions. (A,B) Two separate patients with suprasellar/hypothalamic pilocytic astrocytoma; lesion demonstrates hyperintense signal on sagittal T2WI (A), and peripheral enhancement on sagittal post-contrast T1WI (B). (C) Sagittal post-contrast T1WI demonstrates synchronous masses in the hypothalamus and pineal gland (arrows), consistent with germinoma. (D) Sagittal post-contrast T1WI demonstrates tuberculum selle meningioma (arrow) with CSF fluid cleft (chevron) between the lesion and normal pituitary gland. (E) Sagittal T1WI demonstrates ectopic posterior pituitary gland (arrow) and absent anterior pituitary gland/infundibulum, consistent with pituitary stalk interruption syndrome on sagittal T1WI. (F,G) Infundibular thickening/enhancement on coronal post-contrast T1WI (arrow, F) combined with abnormal T2WI/FLAIR signal hyperintensity on axial image of the cerebellum is consistent with Langerhan’s Cell Histiocytosis. (H) Lymphocytic hypophysitis, as depicted by symmetric enlargement of the pituitary gland/stalk with homogenous enhancement on sagittal post-contrast T1WI.

Figure 3.

Central skull base lesions. (A,B) Large hyperintense soft tissue mass centered in the clivus on coronal T2WI (A) with invasion of the right cavernous sinus, and heterogenous enhancement on sagittal post-contrast T1WI (B), consistent with clival chordoma. (C,D) Paramedian lytic soft tissue mass centered at the petroclival synchondrosis on axial CT (C), which is hyperintense on T2WI (D), and consistent with chondrosarcoma. (E,F) Large expansile parasellar soft tissue mass is hyperintense on pre-contrast coronal T1WI, splays the carotid arteries (E), and demonstrates heterogenous enhancement on axial post-contrast T1WI (F), consistent with plasmacytoma.

Figure 4.

Lateral parasellar lesions. (A,B) Cavernous sinus meningioma with complete encasement of the right internal carotid artery cavernous segment on coronal T2WI (arrow, A), and sellar/parasellar extension on post-contrast coronal T1WI (B). (C) Schwannoma as depicted by a right parasellar expansile avidly enhancing mass centered in the trigeminal nerve V2 division of the cavernous sinus segment causing smooth/benign bony expansion of the foramen rotundum on coronal post-contrast T1WI; medialization of the ipsilateral internal carotid artery and cavernous sinus, without invasion. (D,E) Langerhan’s Cell Histiocytosis as demonstrated by extra-axial infiltrative enhancing soft tissue mass centered in the left sphenoid wing on axial T1WI (arrows, D); it erodes the left sphenoid lateral margin, extends into the left cavernous sinus, and compresses the left internal carotid artery on axial post-contrast T1WI (E). (F,G) Giant aneurysm, as depicted by a large homogeneously enhancing parasellar lesion centered in the right cavernous sinus on axial CT angiography (F); it demonstrates flow voids and incomplete rim hypointensity related to calcification/thrombus on axial T2WI (G), consistent with the complex imaging features of giant aneurysm. (H,I) Coronal T2WI demonstrates homogenous hyperintense mass (H) with peripheral discontinuous enhancement on coronal post-contrast T1WI (I), consistent with cavernous sinus hemangioma. (J) Axial contrast-enhanced fat-sat T1WI shows left lateral rectus enlargement/enhancement which extends to the orbital apex, cavernous sinus, consistent with Tolosa-Hunt Syndrome in a patient presenting with proptosis and diminished vision.