Introduction
Background
The pituitary gland is the master gland of the body because it controls most of the body's endocrine functions by means of the hypothalamic-pituitary axis. The anterior lobe of the pituitary gland secretes 6 hormones: thyroid-stimulating hormone (TSH), previously adrenocorticotropic hormone (ACTH), follicle-stimulating hormone (FSH), leuteinizing hormone (LH), growth hormone (GH), and prolactin (PRL). The posterior pituitary gland secretes vasopressin and oxytocin.
Lateral skull radiograph in a patient with pituitary adenoma shows an enlarged sella and focal calcification in the adenoma (arrow)
T1-weighted sagittal MRI through the pituitary fossa shows a normal, isointense anterior pituitary and a hyperintense posterior pituitary gland.
Pituitary adenomas are almost always benign with no malignant potential. In general, pituitary lesions can be subdivided into nonsecretory and secretory tumors of the pituitary gland, other intrasellar tumors, and parasellar tumors. The last group occurs in the vicinity of the sellar turcica and can mimic the pituitary tumors in terms of the symptoms they cause. Nonsecretory pituitary tumors are called null-cell tumors. Small null-cell tumors measuring a few millimeters are common and found in up to 25% of autopsied pituitary glands. These may grow slowly, destroying normal pituitary function (hypopituitarism), or they may compress nearby structures and cause neurologic problems.
Functioning pituitary adenomas can be clinically classified by means of the hormone they elaborate. These tumors become symptomatic because they secrete hormones, and they are less likely than like null-cell tumors to become large enough to compress adjacent structures. As pituitary tumors grow, destruction of normal pituitary tissue results in various hormonal deficiencies. In rare cases, these tumors may spontaneously hemorrhage or become infarcted. The pressure they exert on nearby structures can produce double vision and facial numbness. The optic chiasm is directly above the pituitary gland, and upward growth of pituitary tumors frequently causes progressive visual loss. This visual loss typically begins from each side of the field of vision and leads to tunnel vision and then blindness.1,2
Pathophysiology
Pituitary adenomas are slow growing, encapsulated tumors of epithelial origin that penetrate adjacent structures. The tumors can contain necrotic, cystic, or hemorrhagic regions. In rare cases, the tumors become calcified. The incidence of malignant degeneration among pituitary adenoma is exceedingly small.
On microscopy, pituitary adenomas consist of sheets and cords of cells with a delicate stroma. Functioning adenomas generally contain granulated cells indicative of endocrine activity.
Vascular compromise at the diaphragmatic sellae causes tumor ischemia, which leads to necrosis and hemorrhage. These events may cause a rapidly expanding sellar mass with consequent compression of the optic nerve, headache, and occasional meningeal irritation. Most adenomas arise from the anterior lobe of the pituitary gland and can produce both systemic and visual signs. The pituitary gland lies approximately 8-13 mm below the optic chiasm. Pituitary adenomas may compromise the nasal retinal fibers that represent the temporal visual fields in each eye.
Cephalic growth of pituitary tumors may impinge on the anterior notch of the chiasm at its lowest aspect. This effect produces bitemporal hemianopsia, with increasing density at the superior aspect. Because tumoral growth is usually asymmetrical, the field loss between the eyes is also typically asymmetrical.
Pituitary adenomas can be differentiated by measuring the size of the tumor. Microadenomas are defined as intrasellar adenomas as large as 1 cm in diameter without sellar enlargement and have little effect on the visual system or on the function of the gland. Macroadenomas cause symptoms of mass effect (eg, headache) and measure larger than 1 cm with generalized sellar enlargement. Macroadenomas include nonsecreting adenomas, PRL-secreting (chromophobe) adenomas, GH-secreting (acidophil) adenomas, ACTH-secreting (basophil) adenomas, and FSH- or TSH-secreting adenomas.
Frequency
United States
Pituitary tumors represent 10-15% of all intracranial tumors, with an annual incidence of 0.2-2.8 cases per 100,000 persons. Incidental pituitary tumors are found in approximately 10% of autopsies. About 25-30% pituitary adenomas are nonfunctioning, 25% produce PRL, 20% produce GH, and 10% produce ACTH.
International
No data suggest that the international incidence of pituitary tumors internationally is different from that in the United States.
Mortality/Morbidity
The mortality rate related to pituitary tumors is low. Advances in both medical and surgical therapies and the availability of hormone replacement have contributed to successful management.
- Morbidity related to macroadenomas is associated with expansion of the tumor into the optic tracts and the cranial nerves adjacent to the cavernous sinus and may include permanent visual loss, ophthalmoplegia, and other neurologic complications. Some tumors recur after radiation therapy and surgery. Pituitary apoplexy is rare complication of pituitary tumors caused by sudden bleeding into the tumor or infarction of the pituitary gland. Headache of sudden and severe onset is the main symptom, associated with visual disturbances or ocular palsy. Signs of meningeal irritation or altered consciousness may be present. Secondary adrenal failure due to ACTH deficiency may be life threatening.
- In rare cases, a pituitary adenoma may invade the orbit, and devastating consequences to the integrity of the globe and ocular structures may result. Therefore, early recognition of this complication is of the utmost importance to begin appropriate treatment to minimize ocular and orbital damage.
- Surgery by means of the transsphenoidal approach is considered the technique of choice when pituitary surgery is indicated. Surgery has the advantage of rapidly lowering hormone levels. For microadenomas, the cure rate is greater than 50%. Tumors larger than 1 cm can recur and may require additional treatment. Infection, cerebrospinal leakage, vascular injury, double vision, visual loss, and pituitary deficiency are rare postoperative complications. A false aneurysm of the cavernous carotid artery and a carotid cavernous fistula have been reported as complications after transsphenoidal surgery.3
Sex
In general, autopsy series show equal distributions of pituitary tumors between men and women.
- Corticotrophin-secreting tumors are an exception. These tumors occur mainly in women, with a female-to-male ratio of 4:1.
- In general, pituitary adenomas are diagnosed more frequently in women of childbearing age than in men probably because of the association of these tumors with menstrual irregularities. Amenorrhea is common in women with macroadenomas; this finding suggests a pituitary lesion.
Age
Tumors affect individuals of all ages, but the incidence increases with age, peaking between the third and sixth decades.
Pituitary gigantism is very rare in the pediatrics age group; however, it is extremely rare in a child that is less than 3 years of age.4
Anatomy
The hypothalamic-pituitary axis is responsible for most of the endocrine function of the body. The hypothalamus is in the midline at the base of the brain and encapsulates the ventral portion of the third ventricle.
The shape of the pituitary gland has been likened to that of a garbanzo bean; it lies immediately beneath the hypothalamus, resting in the sella turcica. The gland is divided as follows: (1) anterior pituitary (adenohypophysis), which is predominantly composed of cells that secrete protein hormones, and (2) the posterior pituitary (neurohypophysis), which is not a separate organ but an extension of the hypothalamus. The posterior pituitary is largely composed of the axons of hypothalamic neurons (pituitary stalk), which extend downward as a large bundle behind the anterior pituitary.
The hormones of the anterior pituitary are under the control of the hypothalamus. Messenger hypothalamic hormones reach the anterior pituitary by means of vascular links between the hypothalamus and the pituitary gland. A branch of the hypophyseal artery ramifies into a capillary bed in the low hypothalamus, and hypothalamic hormones destined for the anterior pituitary are secreted into that capillary blood. Blood from this capillary is then transported by means of the hypothalamic-hypophyseal portal veins. The hypothalamic-hypophyseal portal veins branch again into another series of capillaries in the anterior pituitary. Capillaries in the anterior pituitary, which carry hormones secreted by the gland, coalesce into veins that drain into the systemic venous blood. These veins also collect capillary blood from the posterior pituitary gland.
Presentation
Clinical features
Features based on secretory ability
The clinical features of pituitary adenoma vary depending on the location and size of the tumor and its secretory capability. Pituitary adenomas typically appear during early adulthood, and no sex predilection is known. Secretory pituitary adenomas are usually small and generally do not cause neurologic symptoms or hypopituitarism, though they can. The symptoms of functioning tumors are related to the specific hormone the tumor produces.5,6
Neurologic symptoms of pituitary adenomas include headaches; double vision; and loss of peripheral vision leading to blindness, facial pain, or numbness. Hypopituitarism manifests itself by lack of energy, weight loss, nausea, vomiting, constipation, amenorrhea and infertility, dry skin, increase pigmentation of the skin, cold intolerance, and mental status changes (eg, sleepiness, psychosis, collapse).
A prolactinoma is the most common pituitary tumor and may cause amenorrhea, irregular periods, galactorrhea, infertility in women and osteoporosis. It may cause hypogonadism, loss of libido, and impotence in men.
Tumors that secrete excess GH cause gigantism in children and acromegaly in adults. Acromegaly is associated with enlargement of facial features, hands and feet, heart disease, hypertension, arthritis, carpel tunnel syndrome, amenorrhea, and impotence.
ACTH-secreting adenomas produce Cushing disease, which itself results in a widened face with acne and flushing, fatty deposits over the back of the neck, stretch marks, easy bruising, hair growth, diabetes mellitus, muscle loss, fatigue, depression, and psychosis.
Tumors that elaborate TSH produce signs and symptoms of thyrotoxicosis, such as heat intolerance, sweating, tachycardia, fine tremor, and weight loss. Some tumors may secrete more than one hormone, such as GH and PRL.
Rare tumors secrete LH or FSH (gonadotrophins). When pituitary tumors compromise the secretory cells, the first evidence of cellular failure usually affects the gonadotrophins. Therefore, the disappearance of menstrual periods may be the first sign of a pituitary tumor in female patients. In male patients, the most common symptom of deficiency is impotence. Isolated deficiencies of both LH and FSH do occur, but only rarely. In a male individual, LH deficiency alone leads to the appearance of a fertile eunuch. In this condition, sufficient FSH is present to permit the maturation of spermatozoa; however, because of the LH deficiency, the patient has many of the characteristics of a castrated individual. Tumors also can produce an excess of LH or FSH, and pituitary tumors that secrete only the nonspecific, hormonally inactive alpha unit of glycoprotein hormones are not rare.
Other features
Visual symptoms are generally related to compression of visual pathways and include bitemporal visual-field loss, which is denser from the superior to inferior than in other orientations, color desaturation, diplopia, and ophthalmoplegia. The funduscopic sign of long-standing chiasmal compression is primary optic atrophy. Severe optic atrophy indicates a poor prognosis for visual recovery after surgical decompression. In pregnant women, bitemporal visual-field loss and headache may indicate pituitary apoplexy.
Pituitary apoplexy is a potentially life-threatening condition. Women with pituitary adenomas and MRI evidence of subarachnoid bleeding should deliver by cesarean section to prevent apoplexy during delivery. Postpartum hemorrhage can cause infarction of the pituitary gland, leading to hypopituitarism (Sheehan syndrome).
Other problems to consider
Clinical masquerades
Clinical masquerades of pituitary adenoma include chronic retrobulbar optic neuritis, nutritional amblyopia, uncorrected refractive error, normal-tension glaucoma, and age-related maculopathy. Bilateral tilted-disc syndrome can result in a superior bitemporal field defect similar to that observed in pituitary adenoma. However, the field defect in tilted-disc syndrome is unchanging and does not respect the vertical midline, whereas the field defects in chiasm-compressive lesions are progressive and do respect the vertical midline.
Craniopharyngioma
Craniopharyngiomas are benign, slow-growing tumors that originate from epithelial remnants of the Rathke pouch at the junction of the infundibulum and the pituitary gland. These lesions are composed of both solid epithelial tissue and cystic components. The cystic components contain variable amounts of cholesterol, keratin, necrotic debris, proteinaceous fluid, and hemorrhage. Calcification is present in 75-85%.
MRI appearances vary depending on the amount of solid and cystic components and on the nature of cystic contents. Heterogeneous signal intensity on images obtained with all sequences is the most typical finding. Solid components are hypointense on T1-weighted images and hyperintense on T2-weighted images. The cysts also have a long T2; however, if they have a high cholesterol content or methemoglobin, shortening of T1 results in high signal intensity on T1-weighted images. Calcification in the tumor is better detected with CT than with MRI because MRI may not reliably depict calcification. Craniopharyngioma may also cause truncation of the dorsum sellae and upward growth into the third ventricle, which is readily identified on MRI.
Aneurysm
Aneurysms in the parasellar region may originate from the circle of Willis or intracavernous carotid arteries. MRI features include a mass of heterogeneous signal intensity due to flow effects and thrombus formation. Low signal intensity is caused by high flow and chronic thrombus; high signal intensity may represent slow flow or subacute thrombus. Flow in the patent lumen may also cause a band of artifact in the phase-encoding direction on spin-echo images. Magnetic resonance angiography (MRA) is useful in confirming an aneurysm. A potential pitfall in diagnosis is a pneumatized anterior clinoid or calcification, which can simulate the flow void of an aneurysm.
Empty sella
An empty sella occurs as a result of herniation of the arachnoid through an incompetent diaphragma sellae. Over time, cerebrospinal fluid (CSF) pulsations may enlarge the sella and compress the gland against the floor of the sella. An empty sella is usually asymptomatic and an incidental finding, but can be a manifestation of increased intracranial pressure. However, they are occasionally severe. Compression of the pituitary gland may affect function, or traction on the optic chiasm and nerves may cause visual symptoms.
Chiasmatic and hypothalamic gliomas
Gliomas of the optic chiasm and the hypothalamic pathways are primarily tumors of children and young adults. The tumors tend to be low grade, but they infiltrate along the visual pathways. Neurofibromatosis is strongly associated with optic and chiasmatic gliomas. Hypothalamic gliomas are generally aggressive and produce symptoms early, resulting in 1 of many hypothalamic syndromes: diabetes insipidus; inappropriate secretion of antidiuretic hormone (ADH); Fröhlich syndrome; or disturbances of temperature, appetite, or metabolism.
Chiasmatic gliomas are usually isointense or slightly hypointense on T1-weighted images and hyperintense on T2-weighted images. MRI is useful in determining degree of infiltration of the optic chiasm or optic nerves and for assessing posterior extension into the lateral geniculate body and the occasional exophytic growth into the suprasellar and interpeduncular cisterns. Both hypothalamic and chiasmatic gliomas are enhancing after the intravenous administration of gadolinium-based contrast agent. The multiplanar capability of MRI enables it to depict extension into surrounding structures well.
Pituicytomas
Pituicytomas are also called choristomas, granular cell tumors, or myoblastomas and are rare largely noninfiltrating sellar or parasellar tumors in adults. They arise along the distribution of the neurohypophysis, including both the stalk and the posterior lobe. They occur in the suprasellar space, in the sella, or both. Most symptomatic pituicytomas appear as suprasellar masses. They may originate from the posterior pituitary and remain confined within the sella turcica. Pituicytoma is generally a surprise finding in that it is seldom considered in the preoperative differential diagnosis of a suprasellar lesion. The MRI signal-intensity characteristics vary depending on the cystic components. The solid parts of the tumor are enhancing.
Ectopic pituitary
An ectopic pituitary gland results in high signal intensity adjacent to the median eminence of the hypothalamus with an absence of the normal posterior pituitary bright spot on T1-weighted MRIs. An ectopic pituitary may be associated with perinatal asphyxia and disruption of the normal hypothalamic-pituitary axis. Traumatic transection of the stalk is exceptionally rare, but it can result in abnormal accumulation of posterior-lobe hormones proximal to the disruption.
Metastasis
Most metastases to the pituitary gland are small, clinically silent, and rare in the clinical setting, though they are frequently reported in autopsy series. Large metastasis may cause diabetes insipidus. Leukemia, lymphoma, and cancers of the lung or breast are the most common primary origins. The demonstration of rapid growth distinguishes metastases from slow-growing pituitary adenomas.
Rathke cleft cyst
Rathke cleft cysts arise from remnants of the Rathke cleft, a fetal link between the hypothalamus and nasopharynx that obliterates in normal individuals. Rathke cleft cysts are benign cysts lined by a single layer of ciliated columnar or cuboidal epithelium, and they often contain goblet cells. When small, Rathke cleft cysts are intrasellar. However, as they grow, they extend into the suprasellar region. Rathke cleft cysts are smoothly marginated and well-defined lesions. Their MRI signal-intensity characteristics vary depending on the contents of the cyst. After gadolinium enhancement, only the capsule is enhancing; the nodular component is not enhancing. This feature helps distinguish these lesions from craniopharyngiomas.
Hamartoma of the tuber cinereum
Hamartomas of the tuber cinereum of the hypothalamus are benign, slow-growing tumors that consist of hyperplastic hypothalamic glial and neural tissue. The usual presentation is precocious puberty. The tumors may be sessile or pedunculated, occurring between the infundibulum and mamillary bodies. They are usually isointense to the brain on T1-weighted images and mildly hyperintense on T2-weighted images. They do not show contrast enhancement, a feature that distinguishes them from hypothalamic gliomas and germinomas.
Lymphoma
Favored sites for primary malignant non-Hodgkin lymphomas are the hypothalamus, the cavernous sinuses, and the perisellar regions. These rapidly growing tumors mostly affect patients who are immunocompromised because of chemotherapy, HIV infection, or organ transplantation. Lymphomas typically appear as homogeneous, slightly hyperintense masses on T2-weighted images. In general, lymphomas are uniformly and intensely enhancing. Cystic, hemorrhagic, and necrotic areas in these tumors are unusual.
Germinoma
Germinomas occur in the pineal and suprasellar region and affect children and young adults. Because of their propensity to invade the hypothalamus and to grow into the third ventricle, they may cause endocrine dysfunction. They are known to disseminate through CSF pathways. The tumors are usually well defined and isointense with the brain on T1- and T2-weighted images. They generally do not show necrosis, cystic change, or hemorrhage. Contrast enhancement is moderate and essential in the assessment of CSF spread of the tumor. Calcification in germinomas may make them difficult to visualize on MRIs.
Arachnoid cyst
Arachnoid cysts are CSF-containing spaces that are generally not confused with pituitary or parasellar tumors. These cysts have CSF signal intensity, they are well defined, they do not calcify, and they are not enhancing after the administration of contrast material.
Epidermoid cyst
Epidermoid cysts are benign, slow-growing tumors that arise from epithelial cell rests in the basal cisterns. They have a propensity to grow along the subarachnoid spaces and into the various crevices at the base of the brain. Intradural epidermoids are usually large, with lobulated outer margins and an insinuating pattern of growth. Epidermoid cysts are classically confused with arachnoid cysts on CT and MRI because they are similar to CSF in attenuation and intensity, respectively, and because they have similar T1 and T2 signal intensities. Diffusion-weighted images, proton density–weighted images, and fluid-attenuated inversion recovery (FLAIR) images are useful in making the distinction. Epidermoid cysts do not show contrast enhancement.
Dermoid cyst
Dermoid cysts occur in the pineal and suprasellar regions, as well as other midline locations. On histology, they have both mesodermal and ectodermal derivatives, which account for their varied appearance on MRI. The MRI appearances are those of a heterogeneous tumor. Fatty tissues in the tumor produce high signal intensity on T1-weighted images, and a fat-fluid level may be seen. These cysts may rupture, causing the cystic contents to leak into a ventricle or subarachnoid space and then produce an ependymitis or meningitis, respectively.
Meningioma
Parasellar meningiomas commonly involve the cavernous sinus and produce ophthalmoplegia. Meningiomas are hypervascular tumors that derive their blood supply from the dural vessels. They also induce an osteoblastic reaction in the adjacent bone, resulting in a characteristic focal hyperostosis, which is well depicted on plain radiographs and CT. MRI signal is isointense relative to the brain on T1- and T2-weighted images. MRI is particularly good for assessing encasement of the cavernous sinus and carotid artery. The tumor is intensely enhancing on contrast-enhanced images.
Schwannomas
Schwannomas are nerve-sheath tumors that may involve cranial nerves III-XII or peripheral nerves. Schwannomas in the parasellar region arise from the trigeminal nerve and, in rare cases, from the third, fourth, or sixth cranial nerves. These tumors are benign, well encapsulated, and globular; all of these features that distinguish them from broad-based meningiomas. The tumors are isointense on T1-weighted MRIs and mildly hyperintense on T2-weighted MRIs. Cystic degeneration is frequent; hemorrhage and calcification are rare. The solid portions of these tumors are strongly enhancing with the use of intravenous contrast material.
Primary and secondary tumors of the skull base
A wide variety of primary and metastatic tumors of the skull base can involve the parasellar region. Nasopharyngeal carcinomas and malignant tumors of the paranasal sinuses may invade the parasellar region, and metastases from distant primary tumors may also involve the sphenoid bone and the parasellar region. The primary tumors include chordoma, chondroma, chondrosarcoma, and plasmacytoma.
Chordomas have uniform high signal intensity on T2-weighted MRIs. Chondrosarcomas are heterogeneous on images obtained with all sequences because of their variable calcification and chondral elements, but they usually have areas of high T2 signal intensity. Chordomas characteristically arise in the midline, whereas chondrosarcomas arise off midline at the synchondroses. Alteration of the normal hyperintense clival fat is a sensitive indicator of these tumors; therefore, nonenhanced non–fat-saturated T1-weighted imaging is particularly useful. Contrast enhancement is helpful in assessing the intracranial components of these tumors.
Carotid-cavernous fistula
The fistulous communication between the carotid artery and cavernous sinus may result from a dural arteriovenous malformation, trauma, or transsphenoidal surgery. Arterial pressures cause expansion of the cavernous sinus and dilation of parasellar and orbital veins. Proptosis, chemosis, and visual loss may complicate such fistulas. Flow effects and flow artifacts on MRI may confirm the diagnosis.
Granulomatous hypophysitis
Granulomatous hypophysitis is a rare entity that mimics a pituitary adenoma both clinically and radiologically. The reported causes of granulomatous hypophysitis include tuberculosis, syphilis, sarcoidosis, mycotic granuloma, and foreign body granuloma due to a ruptured Rathke cleft cyst. Lymphocytic hypophysitis represent inflammation of the pituitary gland and may complicate pregnancy or the postpartum period. MRI findings include diffuse enlargement of the anterior lobe and pituitary stalk. The gland is strongly enhanced with gadolinium-based contrast agents, and the enhancement commonly extends along the diaphragma sellae.
McCune-Albright syndrome
McCune-Albright syndrome (MAS) may clinically mimic acromegaly or gigantism. The syndrome is characterized by polyostotic fibrous dysplasia, café au lait pigmentation of the skin, and autonomous endocrine hyperfunction. The most common form of autonomous endocrine hyperfunction in this syndrome is gonadotropin-independent precocious puberty; however, affected individuals also may have hyperthyroidism, hypercortisolism, pituitary gigantism, or acromegaly. Nonendocrine abnormalities in this disorder include hypophosphatemia, chronic liver disease, tachycardia, and sudden death (which is rare and possibly due to cardiac arrhythmias).
Preferred Examination
The clinical diagnosis of pituitary adenomas depends on the combination of symptoms and signs resulting from the size of the tumor and/or the type of hormone produced. CT and MRI have largely replaced plain radiography because conventional radiography is poor for delineating soft tissues.7
Angiography is seldom performed; if indicated, CT angiography (CTA) and MRA have largely replaced conventional angiography. Angiography has a role when intervention is indicated in the cavernous sinus or in the cavernous part of the carotid artery.
Conventional single-section CT has a limited role in pituitary imaging, with a sensitivity of 17-22% in detecting microadenomas. Multidetector-row CT with 64 channels may have a role, especially in patients unable to undergo MRI. CT is best for visualizing bony detail and calcification in tumors such as germinomas, craniopharyngiomas, and meningiomas. CTA is excellent for showing the morphology of parasellar aneurysms and for presurgical planning. CT scans are valuable when MRI is contraindicated, as in patients with pacemakers or metallic implants in the brain or eyes.
MRI is generally preferred over CT for the diagnosis of pituitary adenomas because of its superior definition of small lesions in the pituitary sella and its improved anatomic definition before surgery. MRI is also preferred for postsurgical surveillance.
Somatostatin-receptor scintigraphy may be used to distinguish recurrent or residual tumor from scar or necrotic tissue after surgery.
Limitations of Techniques
Conventional radiographs are poor for delineating soft tissues. MRI is more expensive than CT, but it is the preferred imaging study for the pituitary because it improves visualization of the soft tissues and vascular structures. Other limitations of CT include suboptimal imaging of the soft tissues compared with MRI, the need for intravenous contrast medium to enhance images, and the exposure to radiation.
A potential pitfall of MRI diagnosis is a pneumatized anterior clinoid or calcification, which can simulate the flow void of an aneurysm. In addition, MRI is contraindicated in patients with pacemakers or ferromagnetic implants in the brain or eyes. With CT or MRI, pituitary adenoma remnants can be hard to differentiate from radiotherapy-induced fibrosis, especially in patients with clinically nonfunctioning pituitary adenomas, who lack circulating markers that aid in monitoring the progression or cure of the disease.
Differential Diagnoses
Arachnoid Cyst
Carotid-Cavernous Fistula
Craniopharyngioma
Rathke Cleft Cyst
Other Problems to Be Considered
Clinical masquerades
McCune-Albright syndrome
Pituicytomas
Granulomatous hypophysitis
Empty sella
Ectopic pituitary
Metastasis
Chiasmatic and hypothalamic gliomas
Hamartoma of the tuber cinereum
Lymphoma
Germinoma
Epidermoid cyst
Dermoid cyst
Meningioma
Schwannomas
Primary and secondary tumors of the skull base
Aneurysm
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References
Serhal D, Weil RJ, Hamrahian AH. Evaluation and management of pituitary incidentalomas. Cleve Clin J Med. Nov 2008;75(11):793-801. [Medline].
Vance ML. Pituitary adenoma: a clinician's perspective. Endocr Pract. Sep 2008;14(6):757-63. [Medline].
Kachhara R, Menon G, Bhattacharya RN, et al. False aneurysm of cavernous carotid artery and carotid cavernous fistula: complications following transsphenoidal surgery. Neurol India. Mar 2003;51(1):81-3. [Medline]. [Full Text].
Narayanaswamy V, Rettig KR, Bhowmick SK. Excessive Growth. Clin Pediatr (Phila). Jul 14 2008;[Medline].
Wolffenbuttel BH, van den Berg G, Hoving EW, van der Klauw MM. [The natural course of non-functioning pituitary adenomas]. Ned Tijdschr Geneeskd. Nov 22 2008;152(47):2537-43. [Medline].
Kim JP, Park BJ, Kim SB, Lim YJ. Pituitary Apoplexy due to Pituitary Adenoma Infarction. J Korean Neurosurg Soc. May 2008;43(5):246-9. [Medline].
Bonneville JF, Cattin F, Bonneville F. [Imaging of pituitary adenomas]. Presse Med. Jan 2009;38(1):84-91. [Medline].
Hagiwara A, Inoue Y, Wakasa K, et al. Comparison of growth hormone-producing and non-growth hormone-producing pituitary adenomas: imaging characteristics and pathologic correlation. Radiology. Aug 2003;228(2):533-8. [Medline]. [Full Text].
Suzuki M, Takashima T, Kadoya M, et al. Height of normal pituitary gland on MR imaging: age and sex differentiation. J Comput Assist Tomogr. Jan-Feb 1990;14(1):36-9. [Medline].
Colao A, Ferone D, Lombardi G, Lastoria S. (99m)Technetium pentavalent dimercaptosuccinic acid scintigraphy in the follow-up of clinically nonfunctioning pituitary adenomas after radiotherapy. Clin Endocrinol (Oxf). Jun 2002;56(6):713-21. [Medline].
Alexiadou-Rudolf C, Hildebrandt G, Schröder R, Ernestus RI. Lymphocytic adenohypophysitis mimicking a pituitary macroadenoma. Neurosurg Rev. Jun 2000;23(2):112-6. [Medline].
Amersham Health. Neuroradiology and head and neck imaging. In: The Encyclopedia of Medical Imaging. Vol 7. Available at: www.amershamhealth.com. [Full Text].
Argyropoulou M, Perignon F, Brunelle F, et al. Height of normal pituitary gland as a function of age evaluated by magneticresonance imaging in children. Pediatr Radiol. 1991;21(4):247-9. [Medline].
Arunkumar MJ, Rajshekhar V. Intrasellar tuberculoma presenting as pituitary apoplexy. Neurol India. Dec 2001;49(4):407-10. [Medline].
Asa SL. The pathology of pituitary tumors. Endocrinol Metab Clin North Am. Mar 1999;28(1):13-43, v-vi. [Medline].
Bhansali A, Sharma BS, Sreenivasulu P, et al. Acromegaly with fibrous dysplasia: McCune-Albright syndrome. Clinical studies in 3 cases and brief review of literature. Endocr J. Dec 2003;50(6):793-9. [Medline].
Cappabianca P, Cirillo S, Alfieri A, et al. Pituitary macroadenoma and diaphragma sellae meningioma: differential diagnosis on MRI. Neuroradiology. Jan 1999;41(1):22-6. [Medline].
Cattin F, Bonneville F, Andrea I, et al. Dural enhancement in pituitary macroadenomas. Neuroradiology. Jul 2000;42(7):505-8.
Chanson P, Lepeintre JF, Ducreux D. Management of pituitary apoplexy. Expert Opin Pharmacother. Jun 2004;5(6):1287-98.
Cottier JP, Destrieux C, Brunereau L, et al. Cavernous sinus invasion by pituitary adenoma: MR imaging. Radiology. May 2000;215(2):463-9. [Medline].
Cox TD, Elster AD. Normal pituitary gland: changes in shape, size, and signal intensity duringthe 1st year of life at MR imaging. Radiology. Jun 1991;179(3):721-4. [Medline].
De Boucaud L, Dousset V, Caillaud P, et al. Metastases from a pituitary adenoma: MRI. Neuroradiology. Oct 1999;41(10):785-7. [Medline].
Di Sarno A, Rota F, Auriemma R, et al. An evaluation of patients with hyperprolactinemia: have dynamic tests had their day?. J Endocrinol Invest. 2003;26(7 Suppl):39-47. [Medline].
Edal AL, Skjodt K, Nepper-Rasmussen HJ. SIPAP--a new MR classification for pituitary adenomas. Suprasellar, infrasellar, parasellar, anterior and posterior. Acta Radiol. Jan 1997;38(1):30-6. [Medline].
Elster AD. Modern imaging of the pituitary. Radiology. Apr 1993;187(1):1-14. [Medline].
Elster AD, Chen MY, Williams DW III, Key LL. Pituitary gland: MR imaging of physiologic hypertrophy in adolescence. Radiology. Mar 1990;174(3 Pt 1):681-5. [Medline].
Evanson J. The hypothalamic-pituitary axis. Summer School; July 9-13, 2001; York, UK. Revised September 4, 2003. Bristol, UK: Society for Endocrinology. Available at: www.endocrinology.org. [Full Text].
FitzPatrick M, Tartaglino LM, Hollander MD, et al. Imaging of sellar and parasellar pathology. Radiol Clin North Am. Jan 1999;37(1):101-21, x. [Medline].
Freda PU, Post KD. Differential diagnosis of sellar masses. Endocrinol Metab Clin North Am. Mar 1999;28(1):81-117, vi. [Medline].
Freda PU, Wardlaw SL. Clinical review 110: diagnosis and treatment of pituitary tumors. J Clin Endocrinol Metab. Nov 1999;84(11):3859-66. [Medline].
Gazioglu N, Kadioglu P, Ocal E, et al. An unusual presentation of Nelson''s syndrome with apoplexy and subarachnoid hemorrhage. Pituitary. 2002;5(4):267-74. [Medline].
Gsponer J, De Tribolet N, Déruaz JP, et al. Diagnosis, treatment, and outcome of pituitary tumors and other abnormal intrasellar masses. Retrospective analysis of 353 patients. Medicine (Baltimore). Jul 1999;78(4):236-69. [Medline].
Hall WA, Luciano MG, Doppman JL, et al. Pituitary magnetic resonance imaging in normal human volunteers: occult adenomas in the general population. Ann Intern Med. May 15 1994;120(10):817-20. [Medline]. [Full Text].
Jalali R, Brada M. Radiosurgery for pituitary adenoma. Crit Rev Neurosurg. May 25 1999;9(3):167-173.
Karcioglu ZA, Aden LB, Cruz AA, et al. Orbital invasion with prolactinoma: a clinical review of four patients. Ophthal Plast Reconstr Surg. Jan 2002;18(1):64-71. [Medline].
Kiortsis DN, Argyropoulou MI, Bitsis S, et al. Magnetization transfer technique: a new diagnostic tool for the postoperative assessment of pituitary adenomas. Clin Endocrinol (Oxf). Sep 2000;53(3):399-400. [Medline].
Kricheff II. The radiologic diagnosis of pituitary adenoma: an overview. Radiology. Apr 1979;131(1):263-5. [Medline].
Kunwar S, Wilson CB. Pediatric pituitary adenomas. J Clin Endocrinol Metab. Dec 1999;84(12):4385-9. [Medline]. [Full Text].
Kurihara N, Takahashi S, Higano S, et al. Hemorrhage in pituitary adenoma: correlation of MR imaging with operative findings. Eur Radiol. 1998;8(6):971-6. [Medline].
Majos C, Coll S, Aguilera C, et al. Imaging of giant pituitary adenomas. Neuroradiology. Oct 1998;40(10):651-5. [Medline].
Marcou Y, Plowman PN. Stereotactic radiosurgery for pituitary adenomas. Trends Endocrinol Metab. May-Jun 2000;11(4):132-7. [Medline].
Marro B, Zouaoui A, Sahel M, et al. MRI of pituitary adenomas in acromegaly. Neuroradiology. Jun 1997;39(6):394-9. [Medline].
Matsuki M, Kaji Y, Matsuo M, Kobashi Y. MR findings of subarachnoid dissemination of a pituitary adenoma. Br J Radiol. Jul 2000;73(871):783-5. [Medline]. [Full Text].
Mindermann T, Wilson CB. Age-related and gender-related occurrence of pituitary adenomas. Clin Endocrinol (Oxf). Sep 1994;41(3):359-64. [Medline].
Molitch ME, Russell EJ. The pituitary "incidentaloma". Ann Intern Med. Jun 15 1990;112(12):925-31. [Medline].
Naidich MJ, Russell EJ. Current approaches to imaging of the sellar region and pituitary. Endocrinol Metab Clin North Am. Mar 1999;28(1):45-79, vi. [Medline].
Oruckaptan HH, Senmevsim O, Ozcan OE, Ozgen T. Pituitary adenomas: results of 684 surgically treated patients and review of the literature. Surg Neurol. Mar 2000;53(3):211-9. [Medline].
Pany A, Sobri M, Valarmathi S, et al. Giant aneurysm or pituitary macroadenoma: a diagnostical misconstrue. Med J Malaysia. Mar 2004;59(1):123-5. [Medline].
Pergolizzi RS, Nabavi A, Schwartz RB, et al. Intra-operative MR guidance during trans-sphenoidal pituitary resection: preliminary results. J Magn Reson Imaging. Jan 2001;13(1):136-41. [Medline].
Rand T, Kink E, Sator M, et al. MRI of microadenomas in patients with hyperprolactinaemia. Neuroradiology. Nov 1996;38(8):744-6. [Medline].
Reza-Albarran AA, Gomez-Perez FJ, Lopez JC, et al. Myelolipoma: A New Adrenal Finding in Carney''s Complex?. Endocr Pathol. 1999;10(3):251-257.
Rodriguez O, Mateos B, de la Pedraja R, et al. Postoperative follow-up of pituitary adenomas after trans-sphenoidal resection: MRI and clinical correlation. Neuroradiology. Nov 1996;38(8):747-54. [Medline].
Sade B, Mohr G, Tampieri D, Rizzo A. Intrasellar aneurysm and a growth hormone-secreting pituitary macroadenoma. Case report. J Neurosurg. Mar 2004;100(3):557-9. [Medline].
Saeki N, Iuchi T, Isono S, et al. MRI of growth hormone-secreting pituitary adenomas: factors determining pretreatment hormone levels. Neuroradiology. Oct 1999;41(10):765-71. [Medline].
Shimamura N, Ogane K, Takahashi T, et al. Pituitary abscess showing high uptake of thallium-201 on single photon emission computed tomography--case report. Neurol Med Chir (Tokyo). Feb 2003;43(2):100-3. [Medline].
Smallridge RC, Czervionke LF, Fellows DW, Bernet VJ. Corticotropin- and thyrotropin-secreting pituitary microadenomas: detection by dynamic magnetic resonance imaging. Mayo Clin Proc. May 2000;75(5):521-8. [Medline].
Suhardja AS, Kovacs KT, Rutka JT. Molecular pathogenesis of pituitary adenomas: a review. Acta Neurochir (Wien). 1999;141(7):729-36. [Medline].
Sumida M, Arita K, Migita K, et al. Demonstration of the optic pathway in sellar/juxtasellar tumours with visual disturbance on MR imaging. Acta Neurochir (Wien). 1998;140(6):541-8. [Medline].
Syvertsen A, Haughton VM, Williams AL, Cusick JF. The computed tomographic appearance of the normal pituitary gland and pituitary microadenomas. Radiology. Nov 1979;133(2):385-91. [Medline].
Uesaka T, Miyazono M, Nishio S, Iwaki T. Astrocytoma of the pituitary gland (pituicytoma): case report. Neuroradiology. Feb 2002;44(2):123-5. [Medline].
Valente M, Marroni M, Stagni G, et al. Acute sterile meningitis as a primary manifestation of pituitary apoplexy. J Endocrinol Invest. Aug 2003;26(8):754-7. [Medline].
Whee SM, Lee JI, Kim JH. Intrasellar schwannoma mimicking pituitary adenoma: a case report. J Korean Med Sci. Feb 2002;17(1):147-50. [Medline]. [Full Text].
Yamashita S, Matsumoto Y, Kunishio K, Nagao S. Craniopharyngiomas with intratumoral hemorrhage--two case reports. Neurol Med Chir (Tokyo). Jan 2004;44(1):43-6. [Medline].
Yoshioka H, Kurisu K, Arita K, Tominaga A. A case of non-functioning pituitary adenoma accompanied by a large cyst. Acta Neurochir (Wien). 1998;140(3):293-4. [Medline].
Zahariadis G, Kontogeorgos G, Liberopoulos K, et al. Ossifying pituitary gonadotroph adenoma: A case report. Acta Neurochir (Wien). 1999;141(9):1001-3; discussion 1004. [Medline].
Zee CS, Go JL, Kim PE, et al. Imaging of the pituitary and parasellar region. Neurosurg Clin N Am. Jan 2003;14(1):55-80, vi. [Medline].
Further Reading
Related eMedicine topics
Pituitary Macroadenomas
Pituitary Microadenomas
Pituitary Tumors
Pituitary Disease and Pregnancy
Hormone Therapy
Clinical guidelines
Stereotactic Radiosurgery for Patients with Pituitary Adenomas
ACR Appropriateness Criteria Neuroendocrine Imaging
Clinical studies
Study Assessing the Efficacy and Safety of Octreotide Acetate in Patients With Acromegaly, With Micro or Macroadenomas
Keywords
pituitary adenoma, macroadenoma, microadenoma, eosinophil adenoma, nonsecretory tumors, secretory tumors of the pituitary gland, other intrasellar tumors, parasellar tumors, prolactinomas, thyroid-stimulating hormone, TSH, adrenocorticotropic hormone, ACTH, follicle-stimulating hormone, FSH, leuteinizing hormone, LH, growth hormone, GH, ACTH-secreting adenomas, corticotrophin-secreting adenomas, GH-secreting adenomas, FSH-secreting adenomas, prolactin-secreting adenomas, TSH-secreting adenomas, macroadenomas
