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Pituitary Tumours

🧠 Pituitary Tumours

Anatomy, classification, functional syndromes, mass effects, pituitary apoplexy, trans-sphenoidal surgery, and the MEN1 connection.

Anatomy & Embryology of the Pituitary Gland

Understanding pituitary tumour presentations requires knowing the gland’s geography intimately. The clinical signs of a growing pituitary mass are entirely dictated by which surrounding structure gets compressed first. The local anatomy is the examination curriculum.

Location

The pituitary gland sits in the hypophyseal fossa — a saddle-shaped bony recess in the body of the sphenoid bone called the sella turcica (Latin: “Turkish saddle”). The roof is formed by a dural fold, the diaphragma sellae, through which the pituitary stalk (infundibulum) passes to connect the gland to the hypothalamus above.

The Two Lobes — Different Embryological Origins

The pituitary is not one organ — it is two embryologically distinct structures fused together, which explains why tumours arising from each behave completely differently:

LobeProportionEmbryological OriginKey Tumours
Anterior lobe
(Adenohypophysis)
75% of gland Ectodermal outpouching of the primitive oral cavity — Rathke’s pouch. Migrates superiorly to fuse with the downgrowth from the brain. All pituitary adenomas (prolactinoma, GH-oma, ACTH-oma, TSH-oma). Craniopharyngioma from Rathke’s pouch remnants.
Posterior lobe
(Neurohypophysis)
25% of gland Downward diverticulum of the floor of the diencephalon — neural tissue, not glandular. It stores and releases hormones made in the hypothalamus. Does not form adenomas. Damage causes Diabetes Insipidus (loss of ADH storage/release).

Rathke’s Pouch — Why It Matters

Rathke’s pouch is the ectodermal outpouching that migrates upward from the roof of the primitive mouth to form the anterior pituitary. Remnants of this tract can persist along its migratory path — particularly at the pituitary stalk and floor of the third ventricle.

These remnants can proliferate into a Craniopharyngioma — a histologically benign but behaviourally aggressive tumour arising from squamous epithelial remnants. It typically affects children and young adults, grows in the suprasellar region, and characteristically contains calcification, cysts, and cholesterol (“motor oil”) fluid on imaging. Despite its benign histology, it causes devastating compression of the optic chiasm, hypothalamus, and pituitary stalk.

Critical Anatomical Relations — The Danger Zones
⬆ Superiorly
Optic chiasm and the hypothalamus
Upward tumour growth → bitemporal hemianopia (chiasm compression). Hypothalamic compression → hormonal dysregulation, temperature instability, hyperphagia.
⬇ Inferiorly
Sphenoid sinus (air-filled cavity in sphenoid bone)
This is the surgical route — the trans-sphenoidal approach accesses the pituitary directly through the nose and sphenoid sinus. Inferior tumour invasion is unusual.
↔ Laterally (Bilateral)
Cavernous sinuses — venous spaces containing ICA + CN III, IV, V1, V2, VI
Lateral tumour invasion → cranial nerve palsies (especially CN VI — most vulnerable, most medially placed), ICA encasement, proptosis. Cavernous sinus invasion = inoperability marker.
↗ Anterior/Superior
Third ventricle (if tumour grows superiorly enough)
Large suprasellar extension can obstruct the foramen of Monro → obstructive hydrocephalus and raised ICP. Rare but catastrophic complication of giant macroadenomas.

The Cavernous Sinus — Know Your Contents

The cavernous sinuses sit on either side of the sella. Their contents are the most important anatomical memory in this topic — lateral invasion by a pituitary tumour will damage these structures in order of vulnerability:

ICA — Internal Carotid Artery
CN III — Oculomotor
CN IV — Trochlear
CN V1 — Ophthalmic
CN V2 — Maxillary
CN VI — Abducens (most medial → most vulnerable)

CN VI — Why It Is Hit First by Lateral Pituitary Invasion

The abducens nerve (CN VI) runs through the cavernous sinus in the most medial position — closest to the pituitary. When a pituitary tumour invades the cavernous sinus laterally, CN VI is the first nerve encountered and the first to be damaged. The result is a lateral rectus palsy — the eye cannot abduct, causing a convergent squint (esotropia) and diplopia on lateral gaze.

The other nerves (CN III, IV, V1, V2) run in the lateral wall of the cavernous sinus and require more extensive invasion before being affected.

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