Sella and Central Skull Base

Anatomy

True story: in order to understand imaging of the skull base you are going to have to appreciate the normal anatomy first. We define the skull base as the region from the upper surface of the ethmoid bone and orbital plate of the frontal bone to the occipital bone. Central to the skull base is the sphenoid bone—the main attraction, so to speak. The bone itself has the appearance of a bat with its wings extended ( Fig. 10-1 ). The feet of the bat are the medial and lateral pterygoid processes, the head being the body of the sphenoid bone, and wings being the greater and lesser wings of the sphenoid. The body of the sphenoid bone is just behind the cribriform plate of the ethmoid bone.

The roof of the sphenoid sinus, the planum sphenoidale, is anterior to the sella turcica and connects the two lesser wings of the sphenoid. The posterior aspect of the planum sphenoidale is termed the limbus of the planum sphenoidale. Just posterior to the limbus is the chiasmatic groove; then a bony prominence, the tuberculum sellae; and then the sella turcica ( Fig. 10-2 ). The pituitary gland sits in the sella turcica, which is bounded anteriorly by the chiasmatic groove (the optic chiasm is not located here; however, the lateral portions of the sulcus lead to the optic canals), the tuberculum sellae, and the anterior clinoid processes (part of the lesser wing of the sphenoid), onto which the tentorium cerebelli attaches. The posterior boundary of the sella is the dorsum sellae, from which arises the posterior clinoid processes, onto which the tentorium and petroclinoid ligaments (from the petrous apex) also insert.

Inferior to the dorsum sellae is the clivus, which extends inferiorly to the foramen magnum. Anteriorly, the clivus merges with the sphenoid sinus. Its lateral margins are the petrooccipital fissures. Beneath the sella is the sphenoid sinus, which is usually separated asymmetrically by a vertical bony septum. The high-riding ethmoid sinus variant, Onodi cell, can occasionally be seen above the sphenoid sinus and be intimately associated with the anterior clinoid and optic canal.

The sphenoid sinus displays a wide range of normal variations including asymmetric expansion of its lateral recess into the pterygoid plate or the greater wing of the sphenoid bone. The sinus wall adjacent to the groove for the carotid artery can be quite thin normally.

The lateral surface of the sphenoid body joins with the greater wings of the sphenoid and the medial pterygoid plates. The superior margin of the junction of the sphenoid body with the greater wings of the sphenoid is the carotid sulcus, over which the carotid artery runs. The inner surface of the greater wings of the sphenoid forms part of the floor of the middle cranial fossa and the posterior part of the lateral wall of the orbit.

The pterygopalatine fossa (PPF) is an important conduit for the spread of tumor and infection in and around the skull base. This region can be easily recognized on axial computed tomography (CT; Fig. 10-3 ). The PPF is bounded anteriorly by the maxillary bone, anteromedially by the perpendicular plate of the palatine bone, and posteriorly by the base of the pterygoid process. The numerous communications of the PPF with other skull base foramina allow for spread of disease into the orbit, nasal cavity, infratemporal fossa, and hard palate, as well as intracranially. Specifically, the PPF communicates with the orbit via the inferior orbital fissure. The PPF communicates medially with the sphenopalatine foramen (entering the posterosuperior nasal fossa); laterally with the pterygomaxillary fissure (leading to the masticator space); superoposteriorly with the foramen rotundum (and therefore the Meckel cave and the cavernous sinus); inferoposteriorly with the vidian canal (which communicates with the region of the foramen lacerum); and inferiorly with the greater and lesser palatine canals and foramina (to the hard palate).

Table 10-1 lists important foramina at the base of the skull and their contents. You should know these inside and out, upside down and right-side up, in your sleep and when you wake...you get the picture. Let us start from below and work our way up.

The hypoglossal canal courses obliquely within the occipital bone ( Fig. 10-4 ). Through it runs the hypoglossal nerve and, occasionally, the persistent hypoglossal artery (a primitive connection between the proximal cervical internal carotid artery at approximately C1-C2 level and the proximal basilar artery). The meningeal branch of the ascending pharyngeal artery as well as a small emissary vein (anterior condyloid) arising from the inferior petrosal sinus may inconstantly also run through this foramen. The jugular tubercles separate the hypoglossal canal from the jugular foramen with the two regions being about 8 mm apart on the inner surface of the skull. Intracanalicular enhancement on magnetic resonance (MR) is always present representing multiple emissary venous radicles, and linear filling defects in the enhancing regions are the hypoglossal nerve rootlets. In addition, dural enhancement can be seen along the margins of the entrance of the canal and anteriorly into the carotid space. Box 10-1 lists the lesions involving the hypoglossal canal.

The jugular foramen is demarcated by the petrous portion of the temporal bone anterolaterally and by the occipital bone posteromedially ( Fig. 10-5 ). It is divided into two parts, the pars nervosa (anteromedial) and the pars vascularis (posterolateral), by a bony or fibrous septum (jugular spur). Cranial nerve IX runs lateral to the inferior petrosal sinus within the pars nervosa portion of the jugular foramen. The inferior petrosal sinus runs posterolaterally along the petrooccipital fissure to the pars nervosa and then into the jugular vein (within the pars vascularis). The pars vascularis is the larger of the two compartments and contains cranial nerves X and XI in a common sheath medial to the jugular bulb, which is also in the pars vascularis (yes, it is ironic that two nerves run through the pars vascularis versus the pars nervosa). The jugular bulb is the confluence between the sigmoid sinus and the jugular vein. It is usually larger on the right side. The petrous portion of the carotid artery is anterolateral to the pars nervosa.

The internal auditory canal is just superior to the jugular foramen. It contains cranial nerves VII and VIII. These nerves are discussed in detail in Chapter 11 (Temporal Bone). Other skull base foramina in the temporal bone including vestibular and cochlear aqueducts are also described in this same chapter.

The inferior petrosal sinus can be visualized on contrast-enhanced CT or MR ( Fig. 10-6 ). The basilar venous plexus connects the superior portions of the inferior petrosal sinuses. Dorello canal is located just below the petrous apex and is a conduit for cranial nerve VI to reach the cavernous sinus. The canal is located within the inferior petrosal sinus and can be observed on contrast-enhanced axial MR as an unenhanced line crossing the enhancing sinus obliquely. There may be asymmetry and differences in size in this structure.

The abducens nerve (cranial nerve VI) exits the pontomedullary sulcus, courses through the subarachnoid space, enters the Dorello canal, and passes into the cavernous sinus running just lateral to the intracavernous internal carotid artery. Exiting the cavernous sinus, it then enters the orbit through the superior orbital fissure and terminates on the lateral rectus muscle.

The dorsal meningeal artery (from the meningohypophyseal trunk), or a branch of it, may also run through the Dorello canal. It is located between two dural layers and demarcates an interdural venous confluence. The cranial nerve VI courses in this venous confluence and is separated from blood by a dural and/or arachnoidal sheath. The posterior portion of the cavernous sinus, the lateral basilar sinus along the clivus, and the superior petrosal sinus drain this region, which then forms the inferior petrosal sinus draining into the jugular bulb.

There are conditions that produce abducens palsy precisely because of fixation of the nerve in the Dorello canal. These include nerve injury caused by brain stem shifts from trauma or mass lesions, and Gradenigo syndrome (cranial nerve VI palsy associated with inflammatory lesions of the petrous apex and facial pain caused by involvement of cranial nerve V as it crosses the petrous apex). Increased venous pressure in the PVC from carotid-cavernous fistula and dural malformations may compress and injure the nerve.

The foramen lacerum is not a true foramen and the carotid artery does not run through it. Rather, the carotid artery runs over the fibrocartilage (making up the endocranial floor of the foramen lacerum) on its way to the cavernous sinus.

The greater superficial petrosal nerve (GSPN) is a branch of the facial nerve that innervates the lacrimal glands and mucous membranes of the nasal cavity and palate. It is a mixed nerve containing sensory and parasympathetic fibers. The parasympathetic fibers exit the brain stem as the nervus intermedius of cranial nerve VII. The GSPN courses anteromedially from the geniculate ganglion and exits the facial hiatus in the petrous bone. It passes under the gasserian ganglion in the Meckel cave and goes forward to the region of the foramen lacerum. Here it merges with the deep petrosal nerve, arising from the sympathetic carotid plexus, and forms the vidian nerve. This nerve runs anteriorly in the vidian canal with the parasympathetic fibers synapsing in the pterygopalatine ganglia and the sensory fibers passing through the ganglion to the nasal cavity and palate. The vidian canal connects the pterygopalatine fossa anteriorly to the foramen lacerum posteriorly and transmits the vidian artery (see Fig. 10-3 ). The vidian artery, a branch of the maxillary artery, joins the carotid artery in its petrous segment.

The foramen of Vesalius (just saying it out loud makes you feel fancy, doesn’t it?) is an inconstant emissary foramen that can be seen anterior and medial to foramen ovale. Besides the emissary vein, the ascending intracranial branch of the accessory meningeal artery can enter the middle cranial fossa through the foramen of Vesalius or the foramen ovale (see Fig. 10-3 ).

On either side of the sella is the cavernous sinus, a trabeculated venous plexus containing cranial nerves III, IV, VI, and the first and second divisions of V ( Figs. 10-7, 10-8 ). These are located in the lateral portion of the sinus. Cranial nerves III, IV, and the first and second divisions of V are in the lateral wall of the cavernous sinus and maintain that order from superior to inferior in the coronal plane. Cranial nerve VI is medial in the cavernous sinus but lateral to the cavernous carotid artery.

Now pay attention because this is important! Cranial nerve V exits the ventral pons as separate motor and sensory roots at the “root entry zone,” an area often compressed from above by the superior cerebellar arteries, and less commonly by other basilar branches, which may cause symptoms of trigeminal neuralgia. The roots run forward together through the prepontine cistern and exit through the porus trigeminus of the petrous apex. These roots enter the trigeminal cistern (the space containing cerebrospinal fluid [CSF]), which is in the Meckel cave, a dural invagination at the posterior aspect of the cavernous sinus. The dural layers of the Meckel cave demonstrate thin peripheral enhancement. In addition, a discrete semilunar enhancing structure within the inferolateral aspect of the Meckel cave representing the gasserian (aka trigeminal) ganglion has been observed to enhance suggesting the lack of a blood-nerve barrier. The gasserian ganglion is a meshwork of sensory neural fibers permeated by CSF from the trigeminal cistern. On CT or magnetic resonance imaging (MRI) the CSF in the trigeminal cistern is clearly visualized, and with high resolution MR the nerve fibers can be seen. The three sensory divisions of the trigeminal nerve leave the gasserian ganglion, with the first and the second divisions running in the lateral wall of the cavernous sinus to exit the superior orbital fissure (along with cranial nerves III, IV, and VI and the superior ophthalmic vein) and foramen rotundum, respectively. The motor root passes under the gasserian ganglion and, after it exits foramen ovale, combines with its sensory root counterpart to form the mandibular nerve.

The superior and inferior ophthalmic veins drain into the cavernous sinus via the superior and inferior orbital fissures, respectively; however, there are many variations of this venous drainage pattern. The cavernous sinus is formed by two layers of dura mater. The periosteal layer forms the floor and most of the medial wall, and the meningeal layer (dura propria) forms its roof, lateral wall, and the upper part of its medial wall. The lateral wall may have two layers of dura: a deep layer, which ensheathes cranial nerves III and IV and first and second divisions of cranial nerve V, and a superficial dural layer. In addition, like most other venous structures in the body, the cavernous sinus has many variations and much controversy about its exact internal venous anatomy. It has been reported that the true cavernous sinus (a large venous channel surrounding the internal carotid artery) exists in only 1% of patients. In the other instances the cavernous sinus is formed by numerous small veins including (1) the veins of the lateral wall, (2) the veins of the inferolateral group, (3) the medial vein, and (4) the vein of the carotid sulcus. In point of fact, enhancement within the cavernous sinus can be asymmetric because of these anatomic variations, and this asymmetry alone should not prompt a diagnosis of cavernous sinus thrombosis without other supportive imaging findings. Fat in the cavernous sinus is a frequent occurrence.

The cavernous sinus enhances dramatically within 30 seconds after contrast injection for CT or MR. The cavernous sinus drains into the superior and inferior petrosal sinuses. Many venous connections exist between the cavernous sinuses around the sella. The basilar venous plexus, the largest intercavernous connection, lies within the dura behind the clivus connecting the two cavernous sinuses and the superior and inferior petrosal sinuses. The coronary sinus is located along the roof of the sphenoid sinus and joins the two cavernous sinuses. There are also venous communications between the cavernous sinus and the pterygoid plexus of veins via emissary veins in the foramen ovale and foramen rotundum, and through the inconstant foramen of Vesalius (oh so fancy!). These basilar foramina can be a path (and can demonstrate enlargement) for nasopharyngeal tumors coursing into the cavernous sinus.

The cavernous sinus can be subdivided into an intracavernous and interdural compartments. Cavernous sinus tumors that arise interdurally (within the lateral wall) such as schwannomas of the cranial nerves, epidermoid tumors, melanomas, and cavernous angiomas have smooth contours, oval shape, and displace the intracavernous portion of the internal carotid without encasement or narrowing. Intracavernous lesions include pituitary macroadenomas, meningiomas, hemangiopericytomas, and ganglioneuroblastomas. These lesions tend to encase and the meningiomas may narrow the internal carotid artery. The cavernous sinus may be compressed but not obliterated by interdural lesions whereas it may be obliterated by intracavernous tumors.

The pituitary gland is surrounded by a dural bag with the medial wall of the cavernous sinus being the lateral extent of the dural bag. The gland is divided into anterior and posterior lobes. The anterior lobe of the pituitary (adenohypophysis) is divided into the pars tuberalis, pars intermedia, and the pars distalis. The pars tuberalis consists of thin anterior pituitary tissue along the median eminence and anterior infundibulum. Rarely, suprasellar adenomas and other suprasellar pituitary tumors may originate from this tissue, and it may function after hypophysectomy. The pars intermedia lies between the pars distalis and the posterior lobe of the pituitary. It is noted to contain small cysts (pars intermedia cysts, colloid cysts) and may be the origin of Rathke cleft cysts.

The adenohypophysis secretes prolactin (from lactotrophs), growth hormone (from somatotrophs), thyroid-stimulating hormone (from thyrotrophs), follicle-stimulating hormone and luteinizing hormone (from gonadotrophs), and corticotropin (ACTH) precursor and melanocyte-stimulating hormone (from corticotrophs).

The neurohypophysis is composed of the neural (posterior) lobe, the infundibular stem, and the median eminence. Besides storing antidiuretic hormone and oxytocin, the neural lobe also contains nonsecreting cells termed pituicytes. Their exact role is uncertain. The posterior lobe of the pituitary has a direct blood supply from the inferior hypophyseal artery, a branch of the meningohypophyseal trunk arising from the cavernous carotid. The superior hypophyseal arteries, arising from the supraclinoid internal carotid arteries and posterior communicating arteries (usually not visualized on angiography) supply a plexus around the base of the hypophyseal stalk and median eminence and then supply the anterior lobe of the pituitary indirectly through the pituitary portal system. The implications of this quaint blood supply are that, on dynamic imaging, the posterior pituitary and infundibulum enhance immediately because of their direct blood supply, whereas the anterior pituitary is slightly delayed because of the portal system. The indirect blood supply to the anterior lobe of the pituitary makes it susceptible to ischemia, which can be seen in cases of autoinfarction of pituitary tumors and in postpartum pituitary necrosis (Sheehan syndrome). The venous drainage of the pituitary is into the cavernous sinuses.

The diaphragma sellae is the sheet of dura forming a roof over the sella turcica overlying the pituitary gland. The diaphragm has a central hiatus of variable size through which the infundibulum passes. The portion of the hypophysis located just below the diaphragm is concave superiorly like the region just around the stem of an apple and creates the hypophyseal cistern. This cistern is an expansion of the chiasmatic cistern and is separated from the interpeduncular and prepontine cisterns by the membrane of Liliequist. This membrane is just below the floor of the third ventricle and is entered to approach a basilar tip aneurysm.

The infundibulum arises from the tuber cinereum (a prominence of the inferior portion of the hypothalamus) and courses in an anterior inferior direction towards the pituitary gland. It is an important landmark in pituitary anatomy, marking the anterior portion of the posterior pituitary gland.

The suprasellar cistern is superior to the diaphragma sellae. This cistern contains the circle of Willis with anterior cerebral arteries, anterior and posterior communicating arteries, and the tip of the basilar artery. Anteriorly, the cistern is bounded by the inferior frontal lobes and the interhemispheric fissure, laterally by the medial portions of the temporal lobes, and posteriorly by the prepontine and interpeduncular cisterns. Lying central in the suprasellar cistern is the optic chiasm, which is anterior to the infundibular stalk. The normal chiasm is about 3 to 4 mm posterosuperior to the tuberculum sellae. In some circumstances the chiasm can overlie either the tuberculum sellae (prefixed optic chiasm, seen in 9% of cases) or the dorsum sellae (postfixed optic chiasm, seen in 11% of cases). Such anatomic anomalies are important with respect to visual symptoms and surgical approach to suprasellar lesions.

The hypothalamus forms the ventral and rostral part of the wall of the third ventricle. The chiasmatic and infundibular recesses of the third ventricle project inferiorly into these respective structures (chiasm and infundibulum). Posterior to the infundibular stalk are the anteroinferior third ventricle and mammillary bodies. The tuber cinereum is the lamina of gray substance from the floor of the third ventricle (hypothalamus) between the mammillary bodies and the optic chiasm.

Imaging of the Normal Pituitary Gland and the Parasellar Region

MR has several advantages over CT in imaging the sellar region; however, CT does have some use. MR can demonstrate the relationship of pituitary lesions to the optic chiasm and cavernous sinuses. It has the capability of distinguishing solid, cystic, and hemorrhagic components of lesions. Preservation or absence of the expected flow voids within major cerebral vasculature in the sellar region can be observed on MRI. Calcification, although usually imaged as low intensity on T1-weighted imaging (T1WI) and T2-weighted imaging (T2WI), is better seen on CT. Bony septa in the sphenoid sinus are also better visualized on CT. This may be important if a transsphenoidal surgical approach is being considered.

In general, sagittal and coronal T1WI before and following gadolinium administration with thin sections (<3 mm) is all that is necessary to image the pituitary gland. Dynamic postcontrast scanning with serial imaging as the gadolinium infuses the pituitary gland has been shown to identify an additional 20% of microadenomas over static imaging. T2WI can occasionally add additional information for the differential diagnosis by providing the intensity characteristics of a particular lesion. This is not necessarily essential in typical cases of “rule out microadenoma.”

In women, the maximal height of the pituitary has been reported as 9 mm whereas in men it is 8 mm. In children younger than 12 years of age, the gland should be 6 mm or less, with its upper surface flat or slightly concave. The gland changes shape and size during puberty and pregnancy and lactation up to 12 mm because of physiologic hypertrophy. After the first postpartum week, the gland rapidly returns to normal. In teenaged girls, it may measure up to 10 mm in height, and convex upper margins may be identified. This can be noted in teenaged boys but appears to be less striking. Convexity has been observed in children with precocious puberty. Similar to some other “organs,” the gland gradually decreases in size after the age of 50 years.

Intensity is important in MR diagnosis. The anterior lobe of the pituitary gland is isointense to brain on T1WI and T2WI ( Fig. 10-9 ). However, in children younger than 2 months of age the pituitary is rounder, larger, and of high intensity on T1WI. This is most likely related to its high level of metabolic and hormonal function during early infancy, although it has been suggested that the high-intensity results from an increase in the bound fraction of water molecules caused by hormone secretion. Hyperintensity on T1WI during pregnancy has also been noted. Reversible hyperintensity has been reported in patients receiving parenteral nutrition (as seen with the basal ganglia secondary to manganese deposition). Iron can accumulate in the anterior lobe of the pituitary gland in patients with hemochromatosis and produce low intensity on T2WI and gradient echo T2∗ weighted images ( Fig. 10-10 ).

The posterior pituitary gland is high intensity on the T1WI and of lower intensity on the T2WI (see Fig. 10-9 ). It is much more conspicuous in younger people and becomes less conspicuous with increase in age. The precise cause of the high signal in the posterior of the pituitary is probably related to the carrier protein (neurophysin) stored in the neurosecretory granules of the posterior pituitary, intracellular lipid in glial cell pituicytes, water interactions with paramagnetic substances, or low molecular weight molecules such as vasopressin or oxytocin. Posterior to the posterior pituitary is a rim of hypointensity, representing cortical bone of the dorsum. Posterior to this hypointense margin is the hyperintensity of fatty marrow in the clivus. High signal intensity has also been observed in the infundibular stalk on fluid-attenuated inversion recovery (FLAIR) images presumably related to the fluid rich component (prolonged T2) in the pituitary stalk. The high intensity of the posterior pituitary gland has been noted to be absent in patients with diabetes insipidus.

After intravenous contrast injection, enhancement is promptly noted on T1WI in the infundibulum and the cavernous sinuses with more delayed enhancement at the anterior pituitary. Remember that the posterior pituitary is already high intensity, so that any enhancement would be difficult to ascertain. The initial enhancement gradually fades in 20 to 30 minutes or more. The pituitary and cavernous sinuses generally enhance to a similar extent.

Intrasellar Lesions

See list of intrasellar lesions in Box 10-2 .

Congenital Lesions of the Pituitary

Classically, it is taught that the anterior lobe develops from a Rathke pouch, a diverticulum of the primitive buccal (oral) cavity. The posterior lobe originates from neuroectoderm and migrates inferiorly from the hypothalamus. A Rathke pouch starts growing toward the brain during the fourth week of gestation. By the eighth week, the connection with the oral cavity disappears and the pouch is in close contact with the infundibulum and posterior lobe of the pituitary. A Rathke cyst is most often located as an intrasellar cyst between anterior and posterior lobes and may grow to the suprasellar location. The remnants of embryological tract can persist in the form of the craniopharyngeal canal (which can be visualized on axial CT with bone windows as a small foramen in the sphenoid in up to 9% of children younger than 3 months and up to 0.5% of adults) or as ectopic pituitary tissue in the nasopharynx or sphenoid sinus. The craniopharyngeal canal extends from the floor of the sella through the sphenoidal septum into the vomer. Ectopic craniopharyngioma can therefore arise anywhere along this pathway, but the classic location is in the suprasellar cistern.

Congenital abnormalities of the pituitary include aplasia, hypoplasia, ectopia or duplication ( Fig. 10-11 ). These have been observed to occur alone or with a variety of different developmental syndromes, including septooptic dysplasia; holoprosencephaly; anencephaly, sphenoidal encephalocele; Kallmann syndrome; Pallister-Hall syndrome; CHARGE syndrome (coloboma, heart defects, atresia of the choana, retarded growth and development, and ear anomalies); and 17q, 18p, or 20p chromosomal deletions. For this reason, when congenital abnormalities of the pituitary are observed, it is important to evaluate the brain parenchyma and face for additional congenital malformations and/or anomalies.

Intracranial ectopic pituitary adenoma occurs most frequently in the suprasellar cistern most often contiguous with the pituitary stalk. These lesions result from cells of the pars tuberalis located above the diaphragma sellae or from aberrant pituitary cells. Rarely, a connection with the stalk is not demonstrated and all that is observed is a T1 hyperintense mass in the suprasellar cistern.

Pituitary dwarfism, produced by diminished levels of growth hormone, presents as delayed skeletal maturation, slow growth, short stature, and delayed dentition. More males than females have growth hormone deficiency, and isolated growth hormone deficiency can progress to multiple pituitary hormonal deficiencies. In most cases with only isolated growth hormone deficiency, the infundibulum may be thin or truncated (most common), normal or absent, and the adenohypophysis is either normal or small. Isolated growth hormone deficiency may in some cases just be associated with abnormalities intrinsic to the pituitary cells producing growth hormone or perhaps to partial transections of the infundibulum. Ectopic posterior pituitary glands with isolated growth hormone deficiency are uncommonly seen.

Patients with multiple pituitary hormonal deficiencies, however, do tend to have a small or absent anterior pituitary and/or stalk, with the neurohypophysis being either ectopic or absent. This occurs more commonly after a breech delivery, neonatal hypoglycemia, and PROP1 AG deletions. The absent infundibulum and ectopic location of the normal posterior pituitary bright spot are identified on T1WI near the median eminence (ectopic posterior pituitary bright spot) (see Fig. 10-11 ). Thus the presence of a thin stalk is very indicative of isolated growth hormone deficiency, whereas its absence strongly suggests multiple pituitary hormonal abnormalities. To evaluate the pituitary stalk, contrast enhancement is essential.

Disruption of the infundibulum, which is distal to the ectopic neurohypophysis, interferes with the hypothalamohypophyseal portal system and anterior pituitary function. In the setting of ectopic posterior pituitary, the neurohypophysis functions normally. This is because communication still exists between the neurohypophysis and the hypothalamus, so that diabetes insipidus is not present. Transections lead to bright signal above the cut, because of accumulations of neurosecretory granules.

Pituitary Adenoma

Autopsy series indicate that the pituitary gland can be a reservoir for the “incidentaloma,” including asymptomatic microadenomas (14% to 27% of cases), pars intermedia (Rathke) cysts (13% to 22%), and occult metastatic lesions (about 5% of patients with malignancy). This means that clinical input is critical in assessing small lesions of the pituitary because many “normal” patients may have small, insignificant nonsecretory abnormalities visualized on CT or MR. On the other hand, serum prolactin levels of more than 200 ng/mL are highly specific for prolactin-secreting adenomas. Intermediate levels of prolactin (30-70 ng/mL) may be on the basis of glandular compression from nonprolactinoma lesions.

Pituitary microadenomas (<10 mm) are generally hypointense compared with the normal gland on T1WI and display a variable intensity on T2WI. On CT, the microadenoma is of low density compared with the normal gland with or without enhancement. In about 75% of cases, microadenomas present because of symptoms from the hormones they secrete. Nonhormonally active lesions become symptomatic because of their size (macroadenomas), producing headache, visual disturbances (classically bitemporal visual defects), cranial nerve palsy, and CSF rhinorrhea. The diagnosis of pituitary microadenoma can be made without contrast ( Fig. 10-12 ), but microadenomas are more conspicuous with administration of intravenous contrast. In most cases with contrast-enhanced MRI, on T1WI the microadenoma appears hypointense relative to the normally enhancing pituitary gland ( Fig. 10-13 ), especially using dynamic MR after contrast (rapid imaging of the same region repeated for a short time: six to eight thin sections every 30 seconds, for 3 to 5 minutes, typically in the coronal plane). The dynamic images obtained within the first minute appear to provide the greatest contrast between enhancing normal gland and pituitary adenoma that does not initially enhance. If a delayed scan (20 minutes after the injection of contrast) is performed, the tumor may appear hyperintense relative to the normal glandular tissue.

Macroadenomas (>1 cm) are obvious abnormalities on unenhanced T1WI. Coronal MR beautifully shows the relationship of the macroadenoma to the optic chiasm, third ventricle, and cavernous sinuses ( Fig. 10-14 ). Macroadenomas have roughly the same signal characteristics as microadenomas; however, they have a propensity for hemorrhage and infarction because of their marginal blood supply. Thus, these tumors can possess a variable intensity pattern. Treatment with bromocriptine increases the likelihood of intratumoral hemorrhages which may be asymptomatic or may be associated with the syndrome of pituitary apoplexy ( Fig. 10-15 ). Cystic regions in macroadenomas produce low intensity on T1WI and high intensity on T2WI. Pituitary adenomas associated with hemorrhage may be confused with craniopharyngiomas or Rathke cysts on MR.

Detection of cavernous sinus invasion may be made with either unenhanced or dynamic enhanced sequences. If the pituitary tumor remains medial to a line drawn through the mid diameter of the cavernous carotid artery, cavernous sinus invasion is not present. If the tumor extends lateral to a line drawn along the lateral edge of the cavernous carotid artery wall, cavernous sinus invasion is present (see Fig. 10-14 ). When the tumor is between those lines, all bets are off, but markedly elevated hormonal levels usually mean the cavernous sinus is violated. If the tumor infiltrates the venous compartment inferomedial to the basal turn of the cavernous carotid artery or greater than 50% of the intracavernous artery is encased, it means that cavernous sinus invasion has occurred. Noninvasion can be assured if (1) there is intervening normal pituitary tissue between the adenoma and cavernous sinus, or (2) less than 25% of the intracavernous carotid artery is encased.

Pituitary macroadenomas can become very large, to the point that it may be difficult to discern whether the tumor is in fact of pituitary or extrapituitary origin. Such adenomas can result in significant mass effect on the chiasm and adjacent brain parenchyma, resulting in obstructive hydrocephalus and herniation syndromes ( Fig. 10-16 ).

Adenomas have rarely been reported at extrasellar sites not in continuity with the sella, including the sphenoid sinus, nasal cavity, petrous bone, and third ventricle.

Pituitary Apoplexy

Pituitary apoplexy is a syndrome that appears suddenly with combinations of ophthalmoplegia, headache, visual loss, and/or vomiting. This syndrome occurs as a consequence of pituitary hemorrhage and/or ischemia most commonly in the setting of a preexisting pituitary tumor. Sheehan syndrome presents as hypopituitarism as a consequence of pituitary ischemia in the peripartum period. Pituitary hemorrhages follow the pattern of intraparenchymal hemorrhages, with acute hemorrhage revealing hypointensity on T2WI and subacute hemorrhages exhibiting high intensity on T1WI ( Fig. 10-17 ). As opposed to most simple intracranial hemorrhages, in which hemosiderin is deposited in the walls of the cavity, pituitary hemorrhage is not associated with hemosiderin deposition.

Metastatic Disease

Metastatic lesions can occur in the pituitary with a frequency reported from 1.8% to 12% of all pituitary lesions; in clinical practice, however, these are rarely identified. The most common primary tumor is breast followed by gastrointestinal carcinoma ( Fig. 10-18 ). Lymphoma can also enlarge the stalk. Usually, one cannot distinguish metastatic lesions from adenomatous disease. Obviously, clinical history of known primary tumor and lesion multiplicity helps suggest the diagnosis of metastatic disease.

Lymphocytic Hypophysitis

This is an uncommon inflammatory disease of the pituitary gland that can also involve the infundibulum. It is seen in young women during late pregnancy or in the postpartum period. However, it can also occur in nonpregnant women and men of all ages. The condition has also been termed lymphocytic infundibuloneurohypophysitis (if the neurohypophysis and infundibulum are involved). There is enlargement and enhancement of the pituitary gland and thickening of the stalk ( Fig. 10-19 ). Endocrinologic abnormalities can include all anterior pituitary hormonal functions, and when the infundibulum and neurohypophysis are affected, diabetes insipidus can ensue. The inflammation has been reported to occasionally extend into the cavernous sinus. Dynamic enhanced MR studies indicate that the blood supply to the posterior pituitary is compromised by the inflammatory process. The enlargement may regress spontaneously or with steroids.

Posterior Pituitary Tumors

Although unusual, tumors of the posterior pituitary gland occur and can often be diagnosed on MR ( Fig. 10-20 ). Pituicytomas and granular cell tumors (choristoma/myoblastoma of the posterior pituitary) may produce visual or endocrinologic disturbances. They are of variable intensity on T1WI, proton density–weighted images (PDWI) and T2WI, and they enhance. However, some reports indicate a characteristic low intensity on T2WI. The key to the diagnosis is the sagittal MR, which localizes the lesion to the posterior pituitary. These tumors have also been reported in the suprasellar region and third ventricle.

Intrasellar Meningioma

An intrasellar meningioma can simulate the appearance of a pituitary tumor; however, careful attention can show that these masses are not arising from the pituitary gland proper. Intrasellar meningiomas can arise from the diaphragma sellae. The diagnosis can be suggested if the diaphragma sellae is visualized. In lesions originating in the suprasellar cistern the diaphragm should be depressed, whereas with intrasellar lesions the diaphragm is elevated. Careful observation also reveals slightly different intensity on MR between the meningioma and the inferior pituitary tissue. A dural tail and homogeneous enhancement may be visualized with meningioma, distinguishing it from pituitary adenoma. Meningiomas can also arise from the planum sphenoidale and infiltrate the sella (and optic canals) from anterosuperiorly ( Fig. 10-21 ). When these tumors involve the cavernous sinuses, narrowing of the internal carotid artery (ICA) flow void may be seen. Just as with macroadenomas, these tumors can compress the optic chiasm with suprasellar extension.

Aneurysm

Internal carotid artery aneurysms arising from the cavernous ICAs or ectatic cavernous portions of the carotid arteries may produce sellar enlargement and mass effect ( Fig. 10-22 ). Pulsation artifact related to cavernous ICA aneurysms can raise suspicion for vascular etiology of the apparent sellar/parasellar mass and should prompt further evaluation by computed tomographic angiography (CTA) or magnetic resonance angiography (MRA). About 50% of cases of persistent trigeminal artery (which arises from the carotid and courses posteriorly, penetrating the sella, before joining the basilar artery) have an intrasellar course, potentiating iatrogenic injury. Surgeons need to be informed by us and cognizant of these anatomic variations or else, after the transsphenoidal hypophysectomy, the radiologist may be on the receiving end of an epistatic event.

Empty Sella Syndrome

CSF is easily noted in the empty or partially empty sella because of a patulous diaphragma sella and extension of the suprasellar arachnoid space inferiorly ( Fig. 10-23 ). The sellar floor is often expanded and downwardly displaced. This may be seen with aging and in patients with pseudotumor cerebri (idiopathic intracranial hypertension). Other findings associated with pseudotumor include an enlarged tortuous optic nerve sheath, bulging of the optic nerve head (papilledema), and meningoceles in other locations. Cases have been reported in which the appearance of the empty sella was observed to be reversible following treatment of the intracranial hypertension.

Occasionally, the suprasellar visual system is noted to herniate into the sella. In fact, this results from traction from previous adhesions and from arachnoiditis after surgery for macroadenomas. These patients seldom have symptoms. On coronal and sagittal images the herniated chiasm and floor of the third ventricle are noted in the sella.