ANATOMY

Appreciation of the normal anatomy is the key to the radiologic evaluation of the sella and central skull base. Small lesions can have profound endocrinologic and neurologic manifestations. 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 bone itself has the appearance of a bat with its wings extended (Fig. 11-1). The feet of the bat are the medial and lateral pterygoid processes, the head being the body of the sphenoid bone, and the 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 medial anterior surface of the body of the sphenoid bone is flat and is termed the planum (jugum) sphenoidale. The planum sphenoidale is anterior to the sella turcica and connects the two lesser wings of the sphenoid, thus forming a central portion of the anterior cranial fossa. 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. 11-2). The pituitary gland sits in the sella turcica, which (to reiterate) 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 arise the posterior clinoid processes, onto which the tentorium and petroclinoid ligaments (from the petrous apex) also insert. Behind the dorsum sellae is the clivus, which extends inferiorly to the foramen magnum. Anteriorly, the clivus merges with the sphenoid sinus and the inferior third of the nasopharynx. Its lateral margins are the petro-occipital fissure. Beneath the sella is the sphenoid sinus, which is usually separated asymmetrically by a vertical bony septum. The surgeons figured this out and designed the transsphenoidal hypophysectomy.

Figure 11-1 Diagram of the sphenoid bone. A, Superior view. B, Anterior view. C, Posterior view. Anterior clinoid (a), tuberculum sellae (t), optic canal (large arrows), foramen spinosum (curved arrows), foramen ovale (o), foramen rotundum (small open arrows), dorsum sellae (d), lesser wing of sphenoid (L), greater wing of sphenoid (G), vidian canal (small closed arrows), medial pterygoid plates (mp), lateral pterygoid plates (lp), superior orbital fissure (f).

Figure 11-2 Lateral radiograph of the sella. You can appreciate the floor of the anterior cranial fossa (black arrows), the planum sphenoidale (open black arrows), the anterior clinoid process (white arrow), the sella turcica (curved arrow), the dorsum sellae (open white arrow), and the clivus (arrowheads).

The sphenoid sinus displays a wide range of normal variations, including asymmetric expansion of the 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 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. 11-3). The pterygopalatine fossa is defined anteriorly by the maxillary bone, anteromedially by the perpendicular plate of the palatine bone, and posteriorly by the base of the pterygoid process. The pterygopalatine fossa is shaped like a deflated balloon, narrower inferior and larger superior. Anteriorly, the pterygopalatine fossa communicates with the orbital apex via the inferior orbital fissure and sphenopalatine foramen (entering the posterosuperior nasal fossa), laterally with the pterygomaxillary fissure (leading to the masticator space), superoposteriorly with the foramen rotundum (and therefore Meckel’s 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 palate). An inconstant palatovaginal canal may lead medially to the nasopharynx.

Figure 11-3 Anatomy of pterygopalatine fossa. Axial computed tomography scan through the ptyergopalatine process shows the margins of the pterygopalatine fossa (consisting of the max-illary bone, angled upper part of the perpendicular plate of the palatine bone, and base of the pterygoid process, with the latter two forming the small fossa). Also evident and by conventional usage is the lateral opening of the pterygo-palatine fossa, the pterygomaxillary fissure (dotted line).

(From Daniels DL, Mark LP, Ulmer JL, et al: Osseous anatomy of the pterygopalatine fossa, AJNR Am J Neuroradiol 19(8):1423–1432, 1998. Copyright © D. Daniels, 1998.)

Table 11-1 lists important foramina at the base of the skull and their contents. These need to be learned or relearned.

Table 11-1 Major (and Some Minor) Foramina at the Base of the Skull and their Contents

Let us start from below and work our way up.

The hypoglossal canal (anterior condyloid foramen) courses obliquely within the occipital bone (Fig. 11-4). Through it runs the hypoglossal nerve and, when present, the hypoglossal artery (a primitive connection between the 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 MR is always present, representing multiple emissary venous radicles. Linear filling defects within the enhancement 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 11-1 lists the lesions involving the hypoglossal canal.

Figure 11-4 A, The hypoglossal foramen is outlined by arrows. B, Coronal view. The hypoglossal foramen is indicated by arrows. It is separated from the jugular foramen (JF) by the jugular tubercles.

The jugular foramen is demarcated by the petrous portion of the temporal bone anterolaterally and by the occipital bone posteromedially (Fig. 11-5). 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 petro-occipital 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, the pars vascularis has more nerves than 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.

Figure 11-5 Jugular foramen. Note the pars nervosa anteromedially (black arrow), and the pars vascularis posterolaterally (open arrow). Between them is the jugular spur (white arrow).

The internal auditory canal is just superior to the jugular foramen. It contains cranial nerves VII and VIII, which are discussed in Chapter 12.

The inferior petrosal sinus can be visualized on contrast CT or magnetic resonance (MR) imaging (Fig. 11-6). The basilar venous plexus connects the superior portions of the inferior petrosal sinuses. Dorello’s canal (petroclival venous confluence) is located just below the petrous apex and is a conduit for cranial nerve VI to reach the cavernous sinus (Fig. 11-7). The canal is located within the inferior petrosal sinus and can be observed on contrast-enhanced axial MR as an unenhanced line crossing the enhanced sinus obliquely. There may be asymmetry and differences in size in this structure. The abducens nerve exits the pontomedullary sulcus, courses through the subarachnoid space, and enters Dorello’s canal and into the cavernous sinus, running just lateral to the intracavernous internal carotid artery. Exiting the cavernous sinus, it 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 Dorello’s canal (see Fig. 11-7). It is located between two dural layers and demarcates an interdural venous confluens. Cranial nerve VI courses in this venous confluens and is separated from blood by a dural or arachnoidal sheath. The posterior portion of the cavernous sinus, the lateral basilar sinus along the clivus, and the superior petrosal sinus fill this region, which then forms the inferior petrosal sinus draining into the jugular bulb.

Figure 11-6 Inferior petrosal sinus. On contrast-enhanced magnetic resonance, the inferior petrosal sinus is behind the clivus and enhances. The sixth cranial nerves can be seen coursing as an outline (arrows) in the enhancing inferior petrosal sinus.

Figure 11-7 A, Superior view of a right petroclival venous confluence (PVC). The posterolateral part of the roof of the cavernous sinus (Rcs) and the posterior part of the anterior petroclinoid fold (Apf) were removed. Posteriorly, the PVC was limited by the inner layer of the dura mater covering the clivus (Cl) and petrous bone (Pb). The abducens nerve (cranial nerve VI) pierced the dura mater and entered the PVC. The posterior petroclinoid fold (Ppf) was the superior limit of the PVC. The oculomotor and trochlear nerves (cranial nerves III and IV) pierced the lateral part of the roof of the cavernous sinus and ran into the lateral wall of the cavernous sinus (Lwcs). The trigeminal nerve (cranial nerve V) was also partially embedded in this lateral wall. B, Posterior view of a right PVC. The dura covering the PVC, the basal sinus of the clivus (Bs), and the inferior petrosal sinus (Ips) was removed, except for a square around the abducens nerve. The PVC was limited inferiorly (dots) by the axial plane located below the dural foramen of the abducens nerve and medially by the sagittal plane extending upward from the medial limit of the inferior petrosal sinus. The PVC and inferior petrosal sinus were contained in a bone groove limited laterally by the medial aspect of the petrous bone apex and anteroinferiorly by the lateral border of the clivus. C, Transverse section of a right PVC after the roof of the cavernous sinus was removed. The PVC was quadrangular. Its four sides consisted of the inner layer (il) of dura mater posteriorly, the axial plane (dots) below the dural foramen of the abducent nerve inferiorly, the outer layer (Ol) of dura mater anteroinferiorly, and the vertical plane (open dots) containing the posterior petroclinoid fold anteriorly. The abducens nerve perforated the dura, coursed in the PVC below the petrosphenoidal ligament of Grüber (G), and reached the lateral wall of the intracavernous internal carotid artery (Ca). The PVC was continuous with the cavernous sinus (Cs) and the inferior petrosal sinus.

(From Destrieux C, Velut S, Kakou MK, et al: A new concept in Dorello’s canal microanatomy: the petroclival venous confluence, J Neurosurg 87:68–70, 1997.)

There are conditions that produce abducens palsy precisely because of fixation of the nerve in Dorello’s 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 Dorello’s canal 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. The GSPN courses anteromedially from the geniculate ganglion and exits the facial hiatus in the petrous bone. It passes under the gasserian ganglion in Meckel’s cave and goes forward to the region of the foramen lacerum. Here it merges with the deep petrosal nerve from the sympathetic carotid plexus to form 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. The vidian artery, a branch of the maxillary artery, joins the carotid artery in its petrous segment.

The foramen of Vesalius is an inconstant emissary foramen that can be seen anterior and medial to the 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 (Fig. 11-8).

Figure 11-8 Foramen ovale. A, Axial computed tomography (CT) scan of skull base with bone windows. Arrows point to foramen ovale. B, Coronal CT scan with arrows pointing to foramen ovale. Note the medial to lateral slant in the foramen. C, Arrows point to foramen of Vesalius.

On either side of the sella is the cavernous sinus (discussed later in this section), a trabeculated venous plexus containing cranial nerves III, IV, VI, and the first and second divisions of cranial nerve V. These are located in the lateral portion of the sinus. Cranial nerves III, IV, and the first and second divisions of cranial nerve V are in the lateral wall of the cavernous sinus and maintain that order from superior to inferior in the coronal plane (Fig. 11-9). Cranial nerve VI is medial in the cavernous sinus but lateral to the cavernous carotid artery. Cranial nerve V exits the ventral pons as separate motor and sensory roots at the “root entry zone,” an area often compressed by vascular structures with trigeminal neuralgia. The roots run forward together through the prepontine cistern and exit through the porus trigeminus of the petrous apex. These roots pass over the petrous apex, with the motor root exiting the foramen ovale without merging with the sensory root or gasserian ganglion (semilunar ganglion). The sensory root enters the trigeminal cistern (the space containing cerebrospinal fluid [CSF]), which is in Meckel’s cave, a dural invagination at the posterior aspect of the cavernous sinus. The dural layers of Meckel’s cave demonstrate thin peripheral enhancement. In addition, a discrete semilunar enhancing structure within the inferolateral aspect of Meckel’s cave representing the gasserian 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 MR the CSF in the trigeminal cistern is obviously 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.

Figure 11-9 A, Diagram of cranial nerves in the cavernous sinus. B, Cranial nerves in cavernous sinus. Enhanced computed tomography showing cranial nerves in cavernous sinus. Cranial nerve III (black arrow) is directly under the anterior clinoid process (large arrowhead). Also identified on the patient’s right side are cranial nerves IV (arrowhead) and the first division of cranial nerve V (squiggly arrow). On the right side, the second division of cranial nerve V is marked (open arrow). C, Magnetic resonance imaging with contrast outlines the cranial nerves in the cavernous sinus (short skinny arrow on CN III, fat closed arrow on CN IV, open fat arrow on CN V-1, arrowhead on CN V-2, and black arrowhead on CN VI). Note that cranial nerve VI is medial to cranial nerves IV and V-1 and is the closest to the carotid artery. In this case, those cranial nerves blur together.

(A, From Latchaw RE: MR and CT imaging of the head, neck, and spine, ed 2, vol 2, St. Louis, Mosby-Year Book, 1991.)

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 the 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 (Fig. 11-10).

Figure 11-10 Cavernous sinus diagram. A, Coronal of cavernous sinus. Cranial nerves (III, IV, V-1, V-2, VI). ACA, anterior cerebral artery; ICA, internal carotid artery; MCA, middle cerebral artery. B, Base view. 1, greater wing of sphenoid; 2, anterior clinoid process; 3, superior orbital fissure; 4, foramen rotundum; 5, foramen ovale; 6, region of Meckel’s cave 7, foramen spinosum; 8, foramen magnum.

The cavernous sinus can be subdivided into 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 and oval shape, and displace the intracavernous portion of the internal carotid without encasement or narrowing. Intracavernous lesions include meningiomas, hemangiopericytomas, and ganglioneuroblastomas. These lesions tend to encase and 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 cavernous sinus enhances dramatically within 30 seconds after contrast injection for CT or MR. Dynamic coronal MR (rapid imaging of the same region repeated for a short time: six to eight thin sections every 30 seconds, for 3 to 5 minutes) has been advocated in pituitary adenomas to distinguish invasion of the medial wall of the cavernous sinus from tumor bulging along the medial wall. On a dynamic scan the venous spaces enhance before the tumor does, potentially demarcating the exact extent of the lesion. Dynamic imaging has also been advocated for the diagnosis of microadenomas by demonstrating greater conspicuity between the normally enhancing pituitary and the more slowly enhancing microadenoma (see discussion in this chapter under Intrasellar Lesions). Some people think that cavernous sinus invasion of pituitary tumors is best visualized on unenhanced coronal 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. 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. These basilar foramina can be a path (and can demonstrate enlargement) for nasopharyngeal tumors coursing into the cavernous sinus.

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 coronary sinus is located between the dural bag and the roof of the sphenoid sinus and joins the two cavernous sinuses.

The anterior lobe of the pituitary 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 pars distalis is the large intrasellar portion of the anterior pituitary. The adenohypophysis secretes prolactin (from lactottrophs), growth hormone (from somatotrophs), thyroid-stimulating hormone (from thyrotrophs), follicle-stimulating hormone and luteinizing hormone (from gonadotrophs), and corticotropin 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, but they may take up polypeptides and phospholipids released at the secretory terminals.

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 diaphragma has a central hiatus of variable size through which the infundibulum passes. The portion of the hypophysis located just below the diaphragma 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.

The infundibulum arises from the tuber cinereum (a prominence of the inferior portion of the hypothalamus) and courses in an anteroinferior direction. It is an important landmark in pituitary anatomy, marking the anterior portion of the posterior pituitary gland. The anterior lobe of the pituitary is derived from Rathke’s pouch, as are the pars intermedia and pars tuberalis. The posterior lobe develops as a downward projection of the neuroectoderm from the base of the brain.

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 is the anteroinferior third ventricle and mamillary bodies. The tuber cinereum is the lamina of gray substance from the floor of the third ventricle (hypothalamus) between the mamillary bodies and the optic chiasm. The infundibulum projects downward from the tuber cinereum.

IMAGING OF THE NORMAL PITUITARY GLAND AND THE PERISELLAR 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. Calcification, although usually imaged as low intensity on T1-weighted images (T1WI) and T2-weighted images (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. Rapidly flowing blood on spin-echo MR appears as absence of signal intensity from the vessel’s lumen (flow void). This flow void can be observed in the cavernous and supraclinoid carotid arteries. Suprasellar aneurysms may be diagnosed without angiography, and old clotted blood in the wall of these aneurysms usually appears as high intensity.

In general, the coronal T1WI with thin sections (<3 mm) is all that is necessary to image the pituitary gland. The T2WI can occasionally add additional information for the differential diagnosis by providing the intensity characteristics of a particular lesion. This is not usually the problem in cases of “rule out microadenoma.” The normal pituitary gland has been measured on T1WI in several different studies. In women, the maximal height was 9 mm, whereas in men it was 8 mm. In children younger than age 12 years, the gland should be 6 mm or less, with its upper surface flat or slightly concave. The gland may be increased in size and may change shape during puberty, pregnancy, and lactation up to 12 mm because of physiologic hypertrophy. After the first postpartum week, the gland rapidly returns to normal. In teenage girls it may measure up to 10 mm in height, and convex upper margins may be identified. This can be noted in teenage boys but appears to be less striking. Convexity has been observed in children with precocious puberty. Like some other organs, the gland gradually decreases in size after age 50 years. The authors think that size criteria are overrated. If the pituitary looks large, it probably is.

Intensity is important in MR diagnosis. The anterior lobe of the pituitary gland is isointense to brain on T1WI and T2WI. However, in children younger than age 2 months the pituitary is rounder, larger, and of higher intensity on T1WI than during the rest of infancy. 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 in liver disease). 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. 11-11).

Figure 11-11 Hemochromatosis affecting the pituitary. A, Sagittal T1-weighted image (T1WI) of the pituitary. Note the bright posterior pituitary but the isointense anterior aspect. B, T2WI revealing marked anterior pituitary hypointensity representing iron deposition in the anterior pituitary. C, Gradient-echo image emphasizing T2* shows increased susceptibility. Bone marrow abnormality also reflects iron deposition.

(Courtesy of Y. Miki, MD.)

The posterior pituitary gland is high intensity on T1WI and of lower intensity on the T2WI (Fig. 11-12). The precise cause of the high signal in the posterior of the pituitary is unknown but 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.

Figure 11-12 Normal sellar anatomy. Sagittal T1-weighted image with the posterior pituitary bright spot (asterisk), fat in the dorsum (white arrow), infundibular recess (+), infundibulum (open white arrow), chiasm (white arrowhead), mamillary body (m), basilar artery (b), clivus (c), floor of sella (black arrows), sphenoid sinus (s), anterior commissure (curved arrow), and massa intermedia (squiggly arrow).

The high intensity of the posterior pituitary gland has been noted to be absent in patients with diabetes insipidus but is identified in only about two thirds of healthy infants. In pituitary dwarfism, a high-intensity nodule on T1WI has been observed at the infundibular apex, possibly from incomplete descent (see below) (Fig. 11-13).

Figure 11-13 Ectopic posterior pituitary. A, Noncontrast coronal T1- weighted image (T1WI) showing high intensity in an ectopic posterior pituitary (arrow). The normal pituitary bright spot was missing. B, Sagittal T1WI shows the ectopic posterior pituitary gland’s relationship to the adenohypophysis.

After injection, enhancement is promptly noted on T1WI in the anterior pituitary gland, the infundibulum, and the cavernous sinuses. 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 (BOX 11-2)

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 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 abnormalities visualized on CT or MR. Serum prolactin levels of more than 200 ng/mL are highly specific for prolactin-secreting adenomas, whereas markedly elevated prolactin levels (>1000 ng/mL) imply cavernous sinus invasion.

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, adenomas in general have associated hormonal abnormality, whereas nonhormonally active lesions become symptomatic because of their size, producing headache, visual disturbances (classically bitemporal hemianopsia), cranial nerve palsy, and CSF rhinorrhea. Usually the diagnosis of pituitary microadenoma may be made without contrast (Fig. 11-14). In most cases, on T1WI the microadenoma appears initially hypointense relative to the normally enhancing pituitary gland (Fig. 11-15). Dynamic MR after contrast has been advocated not only for the detection of microadenomas, but also for imaging what is left of the normal gland in cases of large tumor. 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 gland. However, if extrinsic causes of hyperprolactinemia have been excluded and the patient is considered likely to possess a microadenoma, then an unenhanced MR may be all that is necessary, particularly if the philosophy of the institution is to treat the tumor with drug therapy (bromocriptine). If, however, surgery is contemplated, then contrast is useful to direct the surgical approach to a particular side of the sella.

Figure 11-14 Microadenoma. Unenhanced coronal magnetic resonance shows lower intensity lesion (arrow) compared with normal pituitary.

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