Sella & pituitary f

Sella & Pituitary

Imaging Anatomy & Pathology

Pituitary Anatomy

Sella

• Sella (concave midline depression in basisphenoid)

• Anterior borders:

• Tuberculum sellae, anterior clinoid processes of lesser sphenoid wing

• Posterior borders:

• Dorsum sellae, posterior clinoid processes

• Dural reflections

• Diaphragma sellae covers sella

• Variable-sized central opening transmits infundibulum

• Dura lines floor of hypophyseal fossa

Hypophysis (pituitary)

• Adenohypophysis (anterior lobe)

• 80% of gland; wraps anterolaterally around NH

• Includes pars anterior (pars distalis or glandularis), pars

intermedia, pars tuberalis

• Function: Cells secrete somato-, lactogenic, other hormones

• Vascular supply: Venous (portal venous via hypothalamus)

• Neurohypophysis (posterior lobe)

• 20% of pituitary

• Includes pars posterior (nervosa), infundibular stem, median

eminence of tuber cinereum

• Contains pituicytes, hypothalamohypophysial tract

• Function: Stores vasopressin, oxytocin from hypothalamus

• Vascular supply: Arterial (superior and inferior hypophyseal

arteries)

Hypophysis (pituitary)

• Pars intermedia

• < 5% of pituitary, located between AH/NH

• Contains axons from hypothalamus, infundibulum

• Function: Carries releasing hormones to adenohypophysis &

neurohypophysis

Cavernous Sinuses

• Paired septated, dural-lined venous sinuses that lack valves

• Venous drainage

• Inferiorly to pterygoid venous plexi via emissary veins, to IJV via

inferior petrosal sinuses

• Venous tributaries

• Superior/inferior ophthalmic veins & sphenoparietal sinus

• Contents

• CN3 within superior lateral dural wall

• CN4 just below CN3

• V1 (ophthalmic division of CN5) in lateral wall below CN4

• V2 (maxillary division of CN5) is most inferior CN in lateral wall

• V3 (mandibular division of CN5) does NOT enter sinus (passes from Meckel

cave inferiorly into foramen ovale)

• CN6 lies within sinus itself, next to ICA

• Cavernous ICA segments

Imaging Techniques

• CT

• Calcifications & bony changes

• MRI

• Multiplanar resolution

• Soft tissue characterization

• Sagittal T1 sequence

• Every routine MRI of he brain!

• Pituitary protocols:

• Thin section (2-3 mm)

• Small FOV

• Coronal T2

• Unenhanced coronal/sagittal T1

• Post contrast coronal/sagittal T1

• +/- Dynamic imaging for microadenomas (serial coronal post contrast images over

time)

Normal Imaging Appearance

• T1:

• Adenohypophysis isointense

• Neurohypophysis hyperintense (2/2 neurophysin, carrier protein for

oxytocin and vasopressin, NOT fat)

• Posterior bright spot can be absent in up to 15% of endocrinologically normal

individuals

• Kiddos:

• In the fetus and neonate, the anterior lobe is very hyperintense.

• Beginning at about 2 months of age, the high signal intensity of the

anterior lobe diminishes, and by 4 months (it is approximately

isointense to brain.

• Normal size varies with age, gender

• ≤ 6 mm children

• 8 mm males, post-menopausal females;

• Physiologic hypertrophy with 10 mm upper limit in young females (can

bulge upwards)

• 12 mm pregnant/lactating females

Pathology

• Intrasellar lesions• Pituitary adenoma (micro/macro)

• Rathke’s cleft cyst

• Craniopharyngioma

• Meningioma

• Lymphocytic adenophyphysitis

• Metastases

• Aneurysm

• Suprasellar lesions• Pituitary adenoma (macro)

• Aneurysm

• Infundibular lesions


• Dermoid/epidermoid

• Tuber cinereum hamartoma

• Pituitary apoplexy

• Arachnoid cyst

• Chordoma

• Choristoma

• Granulomatous diseases

• Infection

• Meningioma

• Arachnoid cyst

• Chiamatic or hypothalamic glioma


• Germinoma

• Intrasellar lesions• Pituitary adenoma (micro/macro)



• Meningioma

• Lymphocytic adenophyphysitis

• Metastases

• Aneurysm

• Suprasellar lesions• Pituitary adenoma (macro)

• Aneurysm

• Infundibular lesions


• Dermoid/epidermoid

• Tuber cinereum hamartoma


• Arachnoid cyst

• Chordoma

• Choristoma

• Granulomatous diseases

• Infection

• Meningioma

• Arachnoid cyst

• Chiamatic or hypothalamic glioma


• Germinoma

Pituitary PathologyCongenital

Congenital Abnormalities

• Two main forms

• Posterior pituitary ectopia

• Duplication of the pituitary stalk

• Posterior pituitary ectopia

• Absent or truncated pituitary stalk

• Ectopic posterior pituitary on midline sagittal T1 MR images

• Duplication of the pituitary stalk

• 2 pituitary stalks on coronal view, thick tuber cinereum on midline

sagittal view

• Tubo-mamillary fusion: Tuber cinereum/mamillary bodies fused into single mass

• Associated anomalies:

• Posterior pituitary ectopia midline abnormalities such as septo-

optic dysplasia

Tuber Cinereum Hamartoma

• Congenital, non-neoplastic heterotopia

• Classic patient presentation:

• Precocious puberty

• Hamartoma may secrete excess luteinizing hormone

• Gelastic seizures (spasmodic laughter)

• ? 2/2 aberrant connections with the limbic system

• Imaging:

• Lesion center on the tuber cinereum

• T1: Iso/hypointense to grey matter

• T2/FLAIR: Iso or possibly hyperintense (? fibrillary gliosis)

• T1+C: Non enhancing

Rathke’s Cleft Cyst

• Embryology

• Arise from remnants of embryonic Rathke’s cleft/pouch, of

ectodermal origin

• Primitive oral cavity (stomatodeum) invaginates, extends dorsally,

and forms ectodermal-lined craniopharyngeal duct

• Meets infundibulum (outgrowth of 3rd ventricle) by 11th fetal week,

gives rise to hypophysis

• Anterior wall of pouch forms anterior lobe, pars tuberalis

• Posterior wall forms pars intermedia

• Lumen forms narrow cleft normally regresses by 12th week of

gestation

• Persistence, expansion gives rise to RCC


• Arise from remnants of embryonic Rathke’s cleft/pouch

• 70% intra/suprasellar >25% intrasellar > 5% suprasellar

• Benign lesions lined with cuboidal /columnar epithelium,

may contain goblet cells and mucus

• Diff b/w craniopharyngioma is in the wall cell type

• In craniopharyngiomathick walls of squamous or basal cells

• Rathke cleft cysts may cause visual disturbances, pituitary

insufficiency, and diabetes insipidus


• CT• Well-delineated, round/lobulated, intra/suprasellar mass

• Hypo- (75%), mixed iso-/hypodense (20%)

• Hyperdense (5-10%)

• Uncommonly Ca++ (10-15%), curvilinear, in cyst

• MR

• T1

• Varies with cyst content (serous vs.

mucoid)

• Hyper- (50%), hypointense (50%)

• Hyperintense intracystic nodule (75%)

• Mixed (5-10%), may have fluid-fluid

level

• T1+C

• No internal enhancement

• "Claw" sign = enhancing rim of

compressed pituitary surrounding

nonenhancing cyst

• Small nonenhancing intracystic nodule

(75%)

• T2

• Varies with cyst content

• Hyper- (70%), iso-/hypointense (30%)

• Hypointense intracystic nodule (75%)

• FLAIR hyperintense

Arachnoid Cyst

• ~15% of arachnoid cysts arise in suprasellar region

• Possible 2/2 a lack of perforation of the membrane of

Liliequist.

• If the membrane is imperforate, normal CSF flow anterior to the

pons can produce a wind sock which can subsequently close

off and become a cyst.

• Can cause mass effect on adjacent structures,

• Hypothalamus, chiasm, midbrain.

• Imaging:

• Isodense & isointense to CSF on CT and MRI

• No diffusion restriction (vs. epidermoid)

• No enhancement

Epidermoids & Dermoids

• Though to result from inclusions of epithelium during the

time of neural tube closure during the 3rd-5th week of

embryogenesis

• Epidermoids:

• More commonly off midline

• Basilar and CP angle cisterns > parasellar region

• Cyst wall with stratified sq. epithelium with cyst containing keratin

• T1/T2 can look similar to CSF

• FLAIR incomplete suppression (hyperintense)

• DWI: Restriction

• Dermoids

• More commonly midline

• 4th ventricle and vermian regions >> subfrontal or juxtasellar

• Cyst wall contains stratified sq. epithelium and dermal

appendages (hair follicles, sebaceous /sweat glands)

• Imaging Heterogeneous

• Fat, fluid, calcifications.

Pituitary PathologyNeoplasms

Pituitary Adenomas

• Incidentaloma is common

• 15-25% of autopsies have cysts or non-functioning

microadenomas

• Micro versus Macro

• Microadenoma < 10 mm; macroadenoma >10 mm

• Imaging Features

• CT: Low density relative to remainder of the gland

• MR: Hypointense to normal gland on T1, variable on T2

• Clinical history

• Macroadenona—patients present with mass effect related

symptoms

• Visual changes 2/2 optic chiasm involvement or diplopia from cranial

neuropathy

• Microadenoma—those that present for imaging are usually

“functional” and present with hormone level abnormalities

Pituitary Adenomas

Microadenomas• Dynamic post contrast imaging

• Microadenoma enhances slower and less avidly than pituitary

parenchyma

• Look for region of hypoenhancement

• Delayed imaging (> 20 min) may appear brighter than normal gland however

• Location in gland:

• Prolactin and growth hormone secreting → lateral and posterior

• ACTH, thyroid-stimulating hormone, and LH/FSH → centrally

• Corticotropin secreting → may originate in the infundibulum

Pituitary Adenoma

Macroadenomas• Relatively obvious on imaging (both unenhanced or enhanced)

• Clinically:

• Mass effect symptoms (optic compression, cranial neuropathies)

• Apoplexy secondary to hemorrhage

• Sellar mass without separate identifiable pituitary gland

• Mass is gland

• “Figure 8” or “snowman” appearance.

• Indentation caused by constriction from the diaphragma sellae

Pituitary Adenoma

Macroadenomas

• MRI:

• Hypointense on T1 and iso/hyper on T2

• Can appear heterogeneous → foci of hemorrhage and infarction 2/2 poor vascular supply

• Cavernous sinus invasion -Rule of thumb:

• If tumor remains medial to line drawn through mid portion of the cavernous ICA

cavernous invasion likely NOT present.

• If tumor extends lateral to line drawn through the lateral wall of the cavernous ICA

cavernous sinus invasion IS LIKELY.

• T1+C:

• Enhance strongly, often heterogeneously

• MRA:

• May encase the cavernous ICA segments, but rarely occlude them

Pituitary Apoplexy

• Syndrome

• Acute onset with combination of sx of ophthalmoplegia,

headache, visual loss, or vomiting

• Secondary to pituitary infarction (usually hemorrhagic )

• Hemorrhagic infarction:

• MR signal changes ~ intraparenchymal hemorrhages

• Acute: Iso T1 and ↓ T2

• Subacute (late & early): ↑ on T1

• If paucity of hemorrhage, may see ↑ T2 due to edema

Craniopharyngioma

• Origin

• Arise from metaplasia of squamous epithelial remnants(Rathke’s

pouch) of the adenohypophysis and anterior infundibulum or from

ectopic embryonic cell rests of enamel organs

• 2 Types:

• Adamantinomatous:

• More cystic, seen in childhood

• Papillary

• More solid, seen more frequently in adults.

• Location:

• Epicenter → Suprasellar cistern

• Suprasellar (20%) < suprasellar/sellar (70%) > sellar (10%).

• Can extend in multiple cranial fossae anterior>middle>posterior fossae

• Rare: Intraventricular (3rd ventricle)

• Surgical division: Sellar, prechiasmatic, retrochiasmatic

Craniopharyngioma

Imaging Findings• CT

• Classic adamantinomatous type:

• Cystic (90%), Ca++ (90%), enhance (90%)

• Classic papillary:

• Solid, isodense, rarely calcified

• MR: Signal varies with cyst contents

• Cysts variably hyperintense on T1, T2

• Classic adamantinomatous

• Hyperintense cyst and heterogeneous nodule on T1

• Variability of T1 signal secondary to methemoglobin and high protein.

• Ultra high protein (maybe hypointense)

• Solid portions enhance heterogeneously; cyst walls enhance strongly

• Classic papillary

• Isointense solid component which enhances

• Cysts often hypointense on T1

Pituicytoma

• Rare tumor arising from pituicytes

• Specialized glial cells in infundibulum and neurohypophysis

• WHO I

• Imaging:

• Enhancing, well-demarcated, round or oval, sellar /suprasellar

mass arising from neurohypophysis or infundibulum

• Isointense to hypointense on unenhanced T1 images

• Posterior pituitary "bright spot" often absent

• T1+C:

• Variable enhancement, typically strong & uniform

Meningioma—Intrasellar & Parasellar

• Can simulate pituitary tumors

• More often originate off of the diaphragma sellae or

adjacent parasellar regions

• Imaging:

• Look for mass which is distinct from pituitary parenchyma

• Contiguity with diaphragma sellae or dural tail extending from

adjacent parasellar structures

• Anterior clinoid processes, planum sphenoidale, clivus

• If cavernous sinus involved → often narrow cavernous ICA

• Adenomas, in contrast, do not typically narrow the ICA .

• CT can reveal hyperostosis of the adjacent bone

Metastatic Disease

• Not so infrequent

• 2-12% of autopsies of pts with metastatic cancer

• Breast > gastrointestinal carcinoma

• Lymphoma: may diffusely infiltrate and enlarge the stalk

• Imaging:

• Difficult to differentiate from primary pituitary tumors

• More likely to incite edema in adjacent parenchyma

• Multiple lesions elsewhere in the brain

• Increased degree of enhancement c/w adenomas

Pituitary PathologyMiscellaneous

Granulomatous Diseases

• Pituitary can be infiltrated by granulomatous processes

• E.g. Langerhans, sarcoidosis

• Imaging:

• Langerhans:

• Most common cause of infundibular thickening in children

• Hand-Schüller-Christian syndrome:

• Triad of diabetes insipidus, exophthalmos, and lytic bone lesions

• Sarcoid:

• Can have intrasellar or suprasellar involvement

• Difficult to differentiate between adenoma or meningioma

• CNS sarcoid; variable and protean MR findings

• Multiple small lesions ↔ large solitary masses,

• Thickening or distortion of the cranial nerves

• Pachymeningeal ↔ leptomeningeal thickening & enhancement

Lymphocytic Hypophysitis

• Inflammatory disease involving infundibulum +/- pituitary

• Two subtypes

• Infundibuloadenohypophysitis:

• Peripartum females with headache and multiple endocrinopathies

• Infundibuloneurohypophysitis:

• Middle age men presenting with diabetes insipidus

• Imaging:

• Thickened infundibulum, > 2mm

• Pituitary enlargement (if involved)

• T1: 75% loss of pituitary bright spot

• T1 + C: Intense uniform enhancement

Pituitary Hyperplasia

• Can be physiologic or non-physiologic

• Physiologic

• Pregnant or lactating females (up to 12 mm CC)

• Young menstruating females (up to 10 mm CC)

• Non physiologic

• Addison’s disease

• Hypothyroidism

• Other end organ failure

• Imaging

• Diffuse, fairly homogenous enlargement of the gland

• Upwardly convex superior contour

• Enhancement is similar to normal pituitary, but with overall

enlargement of the gland

Empty Sella

• Arachnoid-lined, CSF-filled intrusion from suprasellar cistern

through wide diaphragma sellae into sella turcica

• Sella turcica is partially filled with CSF

• Thin, flattened rim of residual pituitary tissue, generally along sellar floor

• Primary empty sella

• Idiopathic

• Normal variant

• No history of trauma, surgery, radiation

• Patients typically endocrinologically normal

• Imaging:

• CSF/fluid attenuation and signal filling the sella, with pituitary flattened to the

floor

• Secondary empty sella

• Surgery

• Radiation

• Bromocriptine therapy

• Trauma

• Sheehan syndrome


• Pituitary abscess

Thank You

Sella & pituitary f

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