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 Table of Contents  
Year : 2020  |  Volume : 11  |  Issue : 1  |  Page : 3-16

Imaging of sella: Pituitary adenoma and beyond

1 Department of Radiology, Seth GS Medical College, KEM Hospital, Mumbai, Maharashtra, India
2 Department of Radiology, Nanavati Superspeciality Hospital, Mumbai, Maharashtra, India

Date of Submission11-Dec-2019
Date of Acceptance13-Dec-2019
Date of Web Publication04-Jun-2020

Correspondence Address:
Dr. Rutwik Ketkar
Department of Radiology, Seth GS Medical College, KEM Hospital, Mumbai, Maharashtra
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jrcr.jrcr_23_19

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Sella is a small structure in the skull base housing the pituitary gland. Our aim is to show common and not so common lesions in the sellar-suprasellar region and to highlight unique imaging features which can clinch the diagnosis. A study of pituitary should always include the pituitary–hypothalamic axis. Pituitary masses can be divided into various categories, and the focus of this article will be mainly on primary pituitary tumors. Pituitary adenoma is the most common tumor. Based on the size, it is divided into microadenoma (<1 cm) and macroadenoma (≥1 cm). While radiography and computed tomography were used initially for suspected pituitary tumors, magnetic resonance imaging with its multiplanar imaging and an excellent soft-tissue contrast is the investigation of choice. Dynamic imaging is helpful in diagnosing and localizing microadenomas enabling effective surgical management when medical treatment fails. The sellar region is one of the most anatomically complex central nervous system locations. The key to diagnosis lies in understanding the gross and imaging anatomy by dedicated protocols. Structured reporting of pituitary masses ensures a comprehensive analysis of the lesion, based on several imaging characteristics as described in this article, which is finally aimed at dispensing the information required by the treating physician or surgeon. Imaging can now help in predicting surgical outcome, response to medical treatment, and to avoid complications.

Keywords: Adenoma, imaging strategy and reporting, magnetic resonance imaging, pituitary, sella

How to cite this article:
Sankhe S, Ambadipudi L, Ketkar R, Susheel Kumar S K. Imaging of sella: Pituitary adenoma and beyond. J Radiat Cancer Res 2020;11:3-16

How to cite this URL:
Sankhe S, Ambadipudi L, Ketkar R, Susheel Kumar S K. Imaging of sella: Pituitary adenoma and beyond. J Radiat Cancer Res [serial online] 2020 [cited 2022 Dec 6];11:3-16. Available from:

  Introduction Top

The pituitary gland is divided into larger anterior adenohypophysis and smaller posterior neurohypophysis, which are embryologically, anatomically, and physiologically distinct. Adenohypophysis develops from Rathke's pouch, an ectodermal derivative of the primitive buccal cavity. Neurohypophysis develops from the neuroectoderm of the diencephalon as an extension of the hypothalamus connected by a stalk.[1],[2]

A study of pituitary should always include the pituitary–hypothalamic axis. This complex comprises the hypothalamus, stalk, and pituitary gland proper with the hypothalamic neurons and pituitary cells performing a complex regulation of hormonal secretion, connected by the infundibulum.

Adenohypophysis is divided anatomically into the pars tuberalis, the pars intermedia, and the main cellular and functional mass called pars distalis. The anterior pituitary does not have a direct arterial supply and receives blood supply through the hypophyseal portal system. Venous drainage of each half of the gland is into the ipsilateral cavernous sinus and subsequently to the petrosal sinuses.[1],[3],[4]

The pituitary in the sella turcica, within the central portion of the sphenoid bone, is bounded superiorly by the diaphragma sellae, suprasellar cistern, optic chiasma, and hypothalamus. Cavernous sinuses, ICAs, and cranial nerves III, IV, VI, and V1 and V2 form the lateral relations [Figure 1]. Anteriorly, it is bounded by the tuberculum sellae, anteroinferiorly by the sphenoid sinus, and posteriorly by dorsum sella, clivus and brain stem.[4],[5]
Figure 1: Anatomy. (a) T2-weighted coronal image shows the normal sellar and parasellar anatomical structures. Optic chiasma (1), pituitary stalk (2), pituitary gland (3), ICA (4). (b) Corresponding diagrammatic depiction of sellar and parasellar anatomical structures. Optic chiasma (1), pituitary stalk (2), pituitary gland (3), ICA (4), cavernous sinus (5), sphenoid sinus (6), oculomotor N-Nerve. (7), trochlear N. (8), ophthalmic N. (9), abducens N. (10), maxillary N. (11), third ventricle (12). (c) T1-weighted imaging in sagittal plane showing the normal sellar anatomy. Optic chiasma (1), pituitary stalk (2), posterior pituitary (3), and anterior pituitary (4)

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The pituitary gland is usually 5–7 mm in vertical dimension. Normally, the height of the pituitary is more in females than males.[6] The height of the normal pituitary gland for different age groups is given in [Table 1]. The gland undergoes changes in size and shape throughout life with a physiological increase in size in both sexes during puberty, pregnancy, and perimenopausal period along with a gradual age-related decline in pituitary height proving that the changes in the endocrine milieu correlated with pituitary morphology.[7] The pituitary stalk has a thickness of about 2 mm and it should not exceed 4 mm or the width of the basilar artery.
Table 1: Height of normal pituitary gland

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Pituitary masses can be divided into various categories, as mentioned in [Table 2], and the focus of this article will be mainly on primary pituitary tumors.
Table 2: Classification of pituitary masses

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Pituitary incidentalomas have increased in incidence owing to improved resolution of modern MRI techniques. Pituitary hyperplasia, besides the physiological enlargement, may also be encountered in end-organ failure (e.g., hypothyroidism), hypothalamic tumors, central precocious puberty, drugs, and tumors secreting hypothalamic-releasing hormones ectopically.[1],[8]

Pituitary adenomas constitute 10%–15% of all intracranial tumors.[1],[5],[9] Pituitary adenomas are classified based on their largest dimension into microadenomas [Figure 2], those that are less than 1 cm, and macroadenomas [Figure 3] which are greater than a cm. Macroadenomas that are greater than 4 cm are referred to as giant adenomas. Giant pituitary tumors are further classified into four grades by Goel et al.[10] Grade 1 giant pituitary tumors are limited superiorly by the lifted diaphragma sellae without cavernous sinus invasion. Grade 2 tumors invade cavernous sinus and Grade 3 tumors elevate the roof of the cavernous sinus. Grade 4 tumors breach the diaphragma sellae extending into the subarachnoid space. This grading helps in surgical planning and also portends incomplete resection, thereby suggesting the need for adjuvant treatment. They can also be classified into functioning and nonfunctioning groups. Functioning adenomas can be further divided into various types based on the hormone(s) secreted.
Figure 2: Microadenoma. (a and b) T2 and T1 coronal images show the right half of pituitary gland to be slightly bulky with superior and inferior convexity bulging into sphenoid, but no definite lesion is seen. (c) Postcontrast volume-interpolated Gradient recalled echo image shows hypoenhancing microadenoma in the right half of pituitary gland. (d-i) Postcontrast dynamic spin echo images show a well-defined hypoenhancing microadenoma as compared to the normal pituitary gland

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Figure 3: Typical macroadenoma. (a-c) T2 and T1 isointense figure of eight-shaped sellar suprasellar lesion with homogeneous postcontrast enhancement is seen

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Microadenomas come into light because they are functioning tumors. Prolactinomas are the most common adenomas accounting for about 30% of all pituitary adenomas.[11] Adrenocorticotropic hormone (ACTH) and prolactin-secreting adenomas are usually small in size at the time of presentation, whereas GH-secreting tumors are larger at presentation, although this is not definite.[12] About 25%–30% of pituitary adenomas are nonfunctioning.[11]

Pituitary adenomas are generally soft solid masses, and as they grow bigger, hemorrhage in up to 10%–15%[11] and necrosis in 5%–18%[13] of adenomas are seen within the tumor. They cause sellar enlargement initially and then grow out of the sella turcica extending superiorly, with a constriction at its waist caused by the indentation of diaphragma sellae, into the suprasellar cerebrospinal fluid (CSF) space causing mass effect on the optic chiasm and on the third ventricle. Parasellar extension generally leads to cavernous sinus invasion and carotid encasement. These invasive adenomas are then considered to have an aggressive behavior foreshadowing a poor prognosis due to increased morbidity and difficult surgery, despite the benignity on cytological examination. Adenomas can also erode the floor of sella with infrasellar extension into the sphenoid sinus.

  Imaging Top

Radiography and tomography were the initial imaging techniques available to evaluate pituitary tumors. Computed tomography (CT) was the investigation of choice in the 70s and 80s for imaging the pituitary.[12],[14] Magnetic resonance imaging (MRI) has now become the gold standard in imaging sellar and juxtasellar regions.

Pituitary adenomas are usually hypodense compared to the normal gland on CT.[1] CT is useful in identifying soft-tissue calcification and bony erosion caused by the invasive adenomas, evaluation of sphenoid sinus anatomy before transsphenoidal surgery, and in those patients where MRI is contraindicated. However, its use is limited due to a lesser soft-tissue contrast as compared to MRI and due to radiation exposure.

MRI with its multiplanar imaging and an excellent soft-tissue contrast is the investigation of choice. The aim of the pituitary imaging protocol is to obtain images with a high spatial resolution with a reasonably good signal-to-noise ratio. The standard MRI sequences and their parameters used as part of the pituitary imaging protocol are given in [Table 3].
Table 3: Magnetic resonance imaging pituitary protocol

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Normal anterior pituitary appears isointense on T1 and T2 to the white matter. The MRI signal characteristics of macroadenomas are quite variable.

Plain MRI is adequate to detect most adenomas, and dynamic contrast-enhanced magnetic resonance is particularly useful in imaging microadenomas where the pituitary gland appears normal on plain sequences. Ancillary signs such as lateral deviation of the infundibulum and focal upward convexity of the gland are less reliable and are usually not employed in the diagnosis of microadenomas as there are standard techniques in place to spot the adenoma directly. Most microadenomas are hypointense on T1-weighted precontrast imaging, and bleeding within the adenoma makes it appear hyperintense.

On a dynamic study, the stalk enhancesfirst at 20 s and the anterior lobe attains peak enhancement by 30–60 s. Microadenomas, on the other hand, have a delayed peak enhancement between 60 and 200 s. Microadenomas enhance later than the normal gland and hence appear hypointense on the early phases of a dynamic scan, and the enhancement persists long after washout of contrast from the normal gland. On the delayed scans, 30–60 min after contrast injection, microadenomas appear bright as compared to the rest of the gland.[15] Yuh et al. reported early enhancing microadenomas much before the anterior lobe which was attributed to having a direct arterial blood supply.[16]

Prolactin-secreting pituitary adenomas

Hyperprolactinemia leads to secondary amenorrhea, galactorrhea, and infertility in women. Men usually present at a later stage, with symptoms related to compression rather than with clinical manifestations of elevated prolactin levels which include loss of libido and impotence.[11] Giant prolactinomas can have bizarre and irregular shape, often invading the skull base presenting as nasopharyngeal or sinusoidal mass or with exophthalmos. Most prolactinomas respond to medical treatment with dopamine agonists. This leads to hemorrhage in over half of the cases which are often clinically silent. Cystic degeneration is also common [Figure 4], [Figure 5], [Figure 6]. In our experience, prolactinomas have a high tendency to invade the skull base and undergo shrinkage upon treatment causing CSF leaks.
Figure 4: Giant prolactinoma. (a-c) T2-weighted images (a and b) show a heterogeneous intensity lesion in the sella with supra- and infrasellar extension and invading the right cavernous sinus, causing encasement of right ICA and its branches. The lesion is isointense on T1-weighted imaging (c) and shows homogeneous postcontrast enhancement. (d-f) Follow-up scan after 6 months of cabergoline therapy shows a significant reduction in size and extent of the lesion which is now predominantly T2 hyperintense and shows peripheral enhancement suggestive of cystic degeneration due to cabergoline treatment

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Figure 5: Cystic prolactinoma. (a and b) T2-weighted imaging shows hyperintense well-defined lesion in the right half of pituitary gland. (c) Postcontrast T1-weighted GRE image shows the corresponding lesion to be nonenhancing

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Figure 6: Cystic prolactinoma causing expansion of the sella, (a) T2-weighted imaging showing a sellar suprasellar hyperintense lesion with cystic areas within, (b and c) T1-weighted imaging pre- and postcontrast show the lesion to be isointense with heterogeneous postcontrast enhancement, (d and e) plain computed tomography images show a hypodense sellar suprasellar lesion causing expansion of sella and erosion and thinning of the floor of sella

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Adrenocorticotropic hormone-secreting pituitary adenomas

ACTH-secreting adenomas cause Cushing's disease leading to elevated glucocorticoid levels. Adenomas in Cushing's disease are notoriously small and can escape detection even on a contrast-enhanced dynamic spin-echo sequence. Surgical removal is the treatment of choice. A recent study by Rajeev and Shilpa et al. compared the efficiency of dynamic contrast spin echo and volume-interpolated three-dimensional (3D)-spoiled gradient echo sequences in diagnosis of ACTH-dependent Cushing's syndrome, and it was demonstrated that addition of contrast-enhanced volume-interpolated 3D-spoiled gradient echo sequence increases the yield of MRI in detection of corticotropin-secreting microadenomas and overall accuracy. It could avoid complicated diagnostic interventions such as bilateral inferior petrosal sinus sampling and improve surgical outcome. In addition, it was shown that both the sequences can clearly rule out pituitary disease in cases of ectopic Cushing's syndrome, i.e., 100% specificity.[17]

Growth hormone-secreting pituitary adenomas

Growth hormone (GH)-secreting adenomas cause acromegaly in adults and gigantism before puberty. They tend to be more invasive in men than in women, and in our experience, infrasellar extension is more common than suprasellar growth. These adenomas are generally hypointense on T2-weighted imaging (WI) with low ADC values as compared to the rest of secretory adenomas [Figure 7] and [Figure 8].
Figure 7: Growth hormone-secreting macroadenoma. (a-c) T2 and T1 isointense sellar lesion without any suprasellar extension with predominantly infrasellar extension. It is invading the left cavernous sinus and shows homogeneous postcontrast enhancement

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Figure 8: Growth hormone-secreting macroadenoma showing diffusion restriction. (a) T2-weighted axial image shows a sellar, parasellar lesion which is slightly bright in comparison to cortex invading the right cavernous sinus and encasing the cavernous segment of right ICA. (b) T1-weighted postcontrast Fat saturated image shows the lesion to be hypoenhancing. (c and d) Diffusion-weighted imaging and ADC show the corresponding lesion with restricted diffusion

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Hagiwara et al. showed that densely granulated GH-secreting adenomas, containing prominent active Golgi apparatus and numerous secretory granules, are T2 hypointense.[18] Heck et al. showed that these have a better responsiveness to somatostatin analogs as compared to hyperintense GH-secreting adenomas which tend to be larger and sparsely granulated with a blunted response to somatostatin analogs and may, therefore, become candidates for direct surgery.[19] Puig-Domingo et al. reported that T2 hypointense signal of the residual pituitary GH-secreting adenomas predicts a better response to postoperative somatostatin analogs than those with a hyperintense signal.[20]

Nonfunctioning pituitary adenomas

Nonfunctioning pituitary adenomas are usually macroadenomas or giant adenomas presenting with symptoms related to the mass effect. Imaging features are similar to secretory adenomas. Areas of hemorrhage, necrosis, and cystic change are often noted in these large tumors. Large nonsecretory pituitary adenomas can sometimes cause secondary hyperprolactinemia due to pituitary stalk compression syndrome or stalk-section effect, and the reason for this is unclear.[21],[22],[23],[24]

  Preoperative Pituitary Imaging Top

Preoperative MR assessment of adenomas has assumed a new role of predicting surgical outcome and response to medical treatment.

T2-weighted imaging

It has been reported that T2 signal intensity correlates with tumor consistency. Adenomas showing iso- or hypointense T2 signal contained more collagen and are firm in consistency.[25],[26],[27],[28],[29] Hyperintense tumors are soft and are easily resectable. Nonfunctioning adenomas are usually hyperintense on T2-weighted MRI. On the contrary, Pierallini reported that soft tumors had lower signal intensity than intermediate and hard tumors.[30]

Bahuleyan et al. concluded that tumor consistency cannot be accurately predicted based on MRI T2 signal intensities.[31] Similar observations have been made by several authors that T2 signal does not necessarily correlate with firmness or fibrous tissue in the tumor.[18],[31],[32]

Diffusion-weighted imaging

The role of diffusion-weighted imaging (DWI) in predicting tumor consistency has gained importance in recent times, but it remains controversial. While according to some studies, DWI and ADC maps correlated well with tumor consistency, other studies reported that there was no significant difference between tumor consistency and ADC values of soft and intermediate groups using line-scan DWI.[30],[33],[34],[35],[36]

Cavernous sinus invasion

Medial dural reflection of the cavernous sinus, separating it from the pituitary, is not visible on MRI, thus making it difficult to detect early invasion.[5],[9],[37] Encasement of intracavernous Internal Carotid Artery (ICA) is the most reliable sign of cavernous sinus invasion [Figure 9]. The presence of abnormal tissue between intracavernous ICA and lateral wall of the cavernous sinus and cavernous sinus expansion are also features of adenoma invading the cavernous sinus. Invasion is less likely when there is intervening normal pituitary gland between tumor and cavernous sinus or if a venous compartment is visible between the tumor and intracavernous ICA.[37],[38]
Figure 9: Macroadenoma with cavernous sinus invasion. (a) T2-weighted imaging shows an isointense lesion in the sella invading the left cavernous sinus and encasing the cavernous segment of left ICA. (b) Postcontrast T1 fat sat images show homogeneous enhancement of the lesion

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Knosp et al. classified parasellar growth into five grades (0–4) with ICA as the landmark, and it was reported that cavernous sinus invasion is more likely when the tumor extends beyond the intercarotid line, a line passing through the cross-sectional centers of supra- and intracavernous ICA.[39] Similarly, Cottier et al. published helpful criteria for cavernous sinus invasion in terms of percentage of encasement of carotid, tumor extension across the various venous compartments of the cavernous sinus, and the intercarotid lines.[38]

Pituitary apoplexy

Pituitary apoplexy is a clinical syndrome characterized by headache, vomiting, visual deficits, ophthalmoplegia, or altered mental status.[40],[41],[42] It may present over weeks or may be fulminant leading to coma and death. It is due to infarction or hemorrhage of the pituitary gland and occurs commonly in a preexisting pituitary adenoma. Owing to a relatively tenuous blood supply, pituitary tumors are susceptible to infarction, necrosis, and hemorrhage. Frequently, this will be subclinical and subacute to chronic on MRI or detected at the time of surgery, without culminating in an apoplectic event. Several risk factors for apoplexy have been identified which include trauma, raised intracranial pressure, bromocriptine therapy, pregnancy, diabetic ketoacidosis, anticoagulation, and cardiac surgery.[43]

T1- and T2-weighted MRI is sufficient to diagnose pituitary hemorrhage; however, T2* gradient echo MRI is the most sensitive technique for the detection of intratumoral hemorrhage [Figure 10] and [Figure 11]. Albeit the high sensitivity, T2* GE imaging is not without a caveat. Hypointense signal of hemorrhage can also be seen in the presence of calcification, melanin, or iron deposits.[44] Pituitary hemorrhage undergoes resorption as a long-term effect.
Figure 10: Macroadenoma with apoplexy. (a and b) T2-weighted images in a patient presenting with acute onset headache and diplopia show a heterogeneously hyperintense sellar suprasellar lesion with a fluid level within. (c and d) T1-weighted imaging shows lesion to be iso- to hypointense with postcontrast enhancement of the isointense solid component

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Figure 11: Macroadenoma with hemosiderosis. (a) T2-weighted image shows a large hypo- to isointense sellar lesion with supra- and infrasellar extension with hemosiderin staining around. (b) The lesion shows blooming on gradient-weighted image. (c) T1 postcontrast fat sat image shows heterogeneous enhancement of the lesion

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Rogg et al.first reported that in cases of acutely presenting pituitary apoplexy, early detection by diffusion restriction and lack of enhancement on contrast indicating the presence of infarction in the adenoma can lead to early surgical intervention and excellent outcome.[45]

  Postoperative Pituitary Imaging Top

Postoperative imaging of pituitary adenomas requires a baseline preoperative imaging and details of the surgical procedure. Preoperative imaging gives us information regarding the tumor extension into areas which are difficult to access during surgery such as the cavernous sinus, the posterior clivus, and the suprasellar cistern. A search for residual tumor in these areas will improve detection rates.

Hormonal assays in functioning adenomas and follow-up MRI are used to detect residual tumor in a postoperative sella. Hemorrhage and fat are the most common constituents of a postoperative pituitary mass. Postoperative changes stabilized by 4 months and follow-up MRI for residual tumor are recommended after 4 months in a clinically stable patient.[46],[47] Early postoperative MRI within 48 h and another after 4 months is, therefore, recommended as part of the protocol.

Radiotherapy is an adjunctive treatment given for residual tumors, tumor recurrence, or after failure of medical management. The aim is to control tumor growth and hormonal normalization in secretory tumors. Delayed hypopituitarism is the most common complication.

Postradiotherapy imaging shows the arrest of tumor progression with no significant change in its size.

Imaging strategy and reporting

An optimal imaging strategy has to be devised in conjunction with the referring endocrinologist and the surgeon as treatment protocols vary between different centers. For example, benign, asymptomatic pituitary incidentalomas and functioning adenomas such as prolactinomas may not require surgery and medical treatment may be the initial choice of treatment in case of a functioning adenoma obviating the need for surgery. On the other hand, surgery is thefirst-line therapy for patients with Cushing's disease.

Structured reporting becomes paramount in this age of advanced and varied imaging techniques and protocols. [Table 4] shows a reporting format/model that can be used to provide all the information needed for a complete diagnosis with nature, accurate extent, prognostication, and surgical planning of a pituitary tumor.
Table 4: Structured reporting for pituitary macroadenoma

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  Differential Diagnoses Top


Lymphocytic hypophysitis

It is an autoimmune disorder that is seen primarily in women, and it presents in the peri- or postpartum period in 60%–70% of cases.[48] Headache, visual impairment, and diabetes insipidus (DI) are the most common symptoms. The typical MRI findings include a symmetric enlargement of a homogeneously enhancing pituitary gland, a thickened stalk with a diameter >3.5 mm at the level of the median eminence and loss of the normal smooth tapering, loss of posterior pituitary bright spot, and a usually intact sellar floor [Figure 12]. Parasellar T2 dark sign is a characteristic finding in lymphocytic hypophysitis (LYH) helpful in differentiating it from an adenoma.[49] DI corresponds well to pituitary stalk thickening on MRI. It is worth noting that hypopituitarism, which ensues as a result of inflammatory destruction of pituitary parenchyma, often appears disproportionate to the extent of changes on pituitary MRI.
Figure 12: Lymphocytic hypophysitis. (a) T2-weighted coronal image shows isointense sellar-suprasellar lesion with peripheral T2 dark sign. (b and c) T1-weighted postcontrast image shows intense homogeneous enhancement with stalk thickening. (d) Follow-up scan after corticosteroid therapy shows normal pituitary gland

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Langerhans cell histiocytosis

Langerhans cell histiocytosis has an affinity for the pituitary–hypothalamic axis and affects children. DI is seen in half of these patients, and posterior pituitary bright spot is lost in all the patients affected with DI. Imaging findings are similar to that of LYH. A thickened stalk and hypothalamic lesion in addition to a suprasellar mass are common findings. They appear hyperintense on T2 and hypointense or isointense on T1 and enhance brightly with contrast.[50],[51]


Sarcoidosis is a systemic inflammatory noncaseating granulomatous disease which may involve the central nervous system (CNS) (neurosarcoidosis) and has a predilection for the leptomeninges, pituitary–hypothalamic axis, and optic chiasm. Radiological findings are indistinguishable from other forms of hypophysitis caused by inflammatory infiltrative processes. Parenchymal and sellar lesions, thickening of the basilar leptomeninges, and dural and bone lesions are seen which are contrast enhancing. The pituitary stalk maybe thickened.[50],[52]


Basal cisterns are usually involved in tuberculosis and can show leptomeningeal enhancement in the suprasellar cistern. Sellar and suprasellar granulomas may be seen with thickening and enhancement of the pituitary stalk [Figure 13]. Some of them may be calcified [Figure 14]. The presence of other lesions in rest of the brain and pulmonary tuberculosis is helpful in diagnosis.[53]
Figure 13: Central nervous system tuberculosis with sellar involvement. (a) T2-weighted imaging shows hypointense sellar suprasellar lesions. (b-e) T1-weighted image shows isointense sellar and suprasellar lesions, and postcontrast fat sat images show multiple ring enhancing lesions in the sellar suprasellar region abutting the infundibulum and pituitary. Similar lesions are seen in the left temporal lobe and basal cistern

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Figure 14: Calcified sellar tuberculoma. (a) T2-weighted imaging shows a hypointense suprasellar lesion. (b and c) T1-weighted pre- and postcontrast images show a nonenhancing isointense lesion without any enhancement abutting the pituitary gland superiorly and just anterior to the infundibulum. (d) On plain computed tomography image, the corresponding lesion appears calcified

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Pituitary abscess

Although rare, pituitary abscess is a potentially life-threatening disease. It usually develops by hematogenous seeding or direct spread of adjacent infection. It shows typical MR features of a round sellar mass, being hyper- to isointense on T2 and hypo- to isointense on T1 with postcontrast rim enhancement and a central nonenhancing portion.[11]



Meningioma is the second most common tumor after pituitary adenomas in this region originating from the tuberculum sella, diaphragma sellae, anterior clinoid processes, planum sphenoidale, dural covering of cavernous sinuses, and upper clivus. On CT, meningiomas are hyperdense lesions with intense homogeneous enhancement and show osseous changes in the form of hyperostosis or erosion.

On MRI, they are isointense to slightly hypointense as compared to cortex on T1WI. They are isointense to slightly hyperintense on T2WI and show intense homogeneous enhancement with an enhancing dural tail. CSF cleft with vessels seen as flow voids on T2WI is seen around them [Figure 15]. Meningiomas show calcification in up to 25% of the cases. The sella turcica is normal in size or is mildly enlarged as compared to macroadenomas, and the pituitary gland is visualized separately in many cases.
Figure 15: Meningioma. (a and b) T2 and T1 isointense sellar suprasellar lesion arising from tuberculum sellae compressing the pituitary gland which is seen in the left half. (c and d) It shows intense homogeneous postcontrast enhancement with dural tail. However, note the differential enhancement of meningioma with respect to the pituitary gland

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Tuberculum sellae meningioma with intrasellar extension causes compression of pituitary parenchyma which may not be seen separately. However, “dural tail” sign is an important diagnostic clue.

When meningiomas invade the cavernous sinus, they tend to constrict the lumen of the carotid artery which is not usually seen in case of adenomas.[11],[53]


Craniopharyngiomas are uncommon tumors arising from the squamous cell rests in the remnant of Rathke's pouch along the craniopharyngeal duct, anywhere from the nasopharynx to the third ventricle. They show bimodal age distribution with thefirst peak in children and a second smaller peak in older adults.

Adamantinomatous and squamous papillary are the two main histological subtypes. The adamantinomatous type is the most common, mainly affecting children and adolescents. It is a predominantly suprasellar solid-cystic lesion with necrotic debris, fibrous tissue, and lobulated calcification. The solid component is almost always calcified and is usually inferior to the cystic component. The cystic components show variable T1 intensity depending on the amount of protein content [Figure 16]. The squamous papillary subtype presents more frequently in adults and is predominantly solid and rounded. Calcifications are rare.[54],[55],[56]
Figure 16: Craniopharyngioma. (a-d) T2 and T1 heterogeneous intensity sellar suprasellar solid cystic lesion is seen compressing the pituitary gland but separates from it and showing heterogeneous postcontrast enhancement

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Often, craniopharyngiomas cause a compression of the pituitary gland; however, a compressed, displaced gland can be identified separately.


Metastases to this region are rare. Breast and lung cancers are the most common primary tumors causing metastases to this region in females and males, respectively. Metastasis involves the posterior pituitary or the stalk initially and spreads to the anterior pituitary later. CSF seeding of primary brain tumors to suprasellar and infundibular locations can also occur.

A hyper- or isodense mass, with homogeneous or heterogeneous enhancement, is seen on CT. On MRI, they are usually hyperintense on T2 and appear iso- or hypointense on T1 with enhancement on contrast. The metastatic deposit is usually a small enhancing pituitary lesion with lack of sellar enlargement. Bony erosion may occur [Figure 17]. Loss of posterior pituitary bright spot and stalk thickening are other nonspecific findings.[57],[58]
Figure 17: Metastasis to sella. (a-c) T2 and T1 isointense sellar lesion with supra- and infrasellar extension and infiltration of stalk. It shows cavernous sinus invasion encasing both ICAs with narrowing of left ICA. The lesion shows heterogeneous postcontrast enhancement. (d and e) Contrastenhanced computed tomography images show a large heterogeneously enhancing lesion in the sella with supra and infrasellar extension and eroding the surrounding bones

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Rathke's cleft cyst

Rathke's cleft cysts (RCCs) are nonneoplastic epithelial cysts, lined by a single layer of columnar or cuboidal cells, arising from remnants of Rathke's pouch along the craniopharyngeal duct. They are usually intrasellar in location, between anterior and posterior pituitary lobes, in the region of pars intermedia. They can have a suprasellar extension or originate anterior to the infundibulum. CT attenuation and MRI signal intensities of the cyst vary greatly depending on the protein content. RCCs contain serous or mucinous fluid along with cellular debris, and lack of calcification differentiates them from craniopharyngiomas. The cyst fluid never enhances on contrast; however, a thin peripheral rim of enhancement of the cyst wall may be seen in few cases.[59] The presence of a nonenhancing intracystic nodule, which is hypointense on T2 and hyperintense on T1, composed of protein and cellular debris is virtually pathognomonic for the RCC.[60]

Arachnoid cyst

Arachnoid cysts can occur in the suprasellar or sellar compartment and are thought to arise from the herniation of an arachnoid diverticulum through an incomplete diaphragma sellae. These are smoothly marginated lesions which follow CSF imaging characteristics on CT and MRI without any enhancement [Figure 18]. Although they may appear similar to RCCs [Figure 19], the anterior lobe and the infundibulum are typically displaced posteriorly.[11]
Figure 18: Arachnoid cyst. (a and b) T2 hyperintense T1 hypointense well-defined sellar suprasellar lesion following cerebrospinal fluid signal intensity is seen. (c) T1-weighted postcontrast image shows the lesion to be nonenhancing with enhancement of the laterally compressed pituitary parenchyma

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Figure 19: Rathke's cleft cyst. (a) T2-weighted imaging shows a hyperintense sellar lesion with isointense nodule within. (b) T1-weighted imaging shows the lesion to be isointense with hyperintense nodule within. (c) T1 postcontrast image shows peripheral enhancement around the lesion

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Intracranial germinomas or extra-gonadal seminomas are a type of germ cell tumour which are predominantly seen in pediatric populations. They usually occur in midline, either in pineal region (majority) or along the floor of third ventricle/suprasellar region. They commonly present with diabetes insipidus due to pituitary stalk involvement. On CT, they appear hyperdense due to high cellularity. Calcifications are common. On MRI, they appear as soft tissue masses, ovoid or lobulated in contour with homogenous post contrast enhancement [Figure 20].[53]
Figure 20: Germinoma. (a) T2-weighted imaging shows a lobulated sellar lesion with supra- and infrasellar extension which is T2 isointense with few hyperintense foci within suggestive of microcysts. (b and c) The lesion is isointense on T1 and shows homogeneous postcontrast enhancement. (d) On susceptibility-weighted imaging, the lesion shows foci of calcification and hemorrhage within

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  Conclusion Top

The sellar region is one of the most anatomically complex CNS locations. The key to diagnosis lies in understanding the gross and imaging anatomy by dedicated protocols. Structured reporting of pituitary masses ensures a comprehensive analysis of the lesion, based on several imaging characteristics as described in this article, which is finally aimed at dispensing the information required by the treating physician or surgeon. Imaging can now help in predicting surgical outcome, response to medical treatment, and to avoid complications.

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  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8], [Figure 9], [Figure 10], [Figure 11], [Figure 12], [Figure 13], [Figure 14], [Figure 15], [Figure 16], [Figure 17], [Figure 18], [Figure 19], [Figure 20]

  [Table 1], [Table 2], [Table 3], [Table 4]


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