MRI Pituitary

MRI of the pituitary is a dedicated, thin section study of the sella turcica, pituitary gland, stalk, optic chiasm, cavernous sinuses and adjacent skull base. It is the imaging test of choice for pituitary and hypothalamic disease.

The study uses a 1.5 or 3 tesla scanner with a head coil. Slices are 2 to 3 mm thick, with a small field of view, in coronal and sagittal planes. Axial sequences are added as needed.

The core sequences are T1-weighted before and after gadolinium, and T2-weighted. Dynamic contrast imaging (sequential coronal T1 images over the first 1 to 2 minutes) is used when a small microadenoma is suspected but not seen on routine images. Thin section 3D sequences, and MR angiography when an aneurysm is in question, can be added.

The examination takes 20 to 30 minutes. Gadolinium (0.1 mmol each kg of a macrocyclic agent) is used in nearly all studies. There is no ionising radiation.

Pituitary adenomas are found in about 10 to 20% of unselected imaging and autopsy series, and most are small and silent. Clinically important pituitary tumours affect about 1 in 1000 people.

Prolactinoma is the commonest functioning adenoma, followed by non-functioning adenomas, growth hormone secreting and corticotroph adenomas. MRI detects macroadenomas (over 10 mm) in over 95% of cases. For microadenomas the sensitivity is about 70 to 90%, and it is lowest for corticotroph adenomas under 5 mm.

Indications.

• Biochemical pituitary hormone excess: raised prolactin, suspected acromegaly (raised IGF-1), Cushing disease, TSH-secreting tumours.
• Hypopituitarism or unexplained low pituitary hormones.
• Visual field defect, especially bitemporal hemianopia, or optic nerve compression.
• Persistent headache with endocrine features.
• Diabetes insipidus.
• Sellar and parasellar masses seen on other imaging.
• Delayed puberty or growth failure in children (ectopic posterior pituitary, hypoplasia).
• Suspected pituitary apoplexy (sudden severe headache, visual loss, ophthalmoplegia).
• Post-operative and post-radiotherapy follow up.
• Hyperprolactinaemia on drugs only after the cause has been checked.

Not indicated for mild isolated hyperprolactinaemia explained by drugs, pregnancy, hypothyroidism or macroprolactin. Not for routine screening of well people.

Contraindications and precautions.

• The usual MRI safety screen applies: pacemakers (unless conditional), non-conditional aneurysm clips, cochlear implants, metallic foreign bodies in the eye.
• Gadolinium: avoid in severe renal impairment (estimated glomerular filtration rate under 30 mL each minute) with linear agents. Use a macrocyclic agent at the lowest dose if essential.
• Pregnancy: non-contrast MRI is acceptable if needed, and gadolinium is avoided. Pituitary enlargement is physiological in late pregnancy.
• Claustrophobia: preparation, a wide bore scanner or sedation.

Preparation and technique.

No fasting is needed. The patient lies supine with the head in the coil, and earplugs are used.

Coronal and sagittal T1 and T2 images without contrast are taken first. Post-contrast T1 images are taken in coronal and sagittal planes, with an axial series added when the lesion extends.

For a suspected microadenoma, a dynamic series starts as the contrast is injected, because a microadenoma enhances later than the normal gland. Delayed images (5 to 20 minutes) can show a lesion that was not seen earlier.

Thin cuts through the cavernous sinuses and optic chiasm are included. Pre- and post-operative comparison uses the same plane and slice thickness.

Normal appearances.

The anterior pituitary is isointense to grey matter on T1 and T2. It enhances avidly and uniformly after gadolinium, because it has no blood brain barrier.

The posterior pituitary shows a bright spot on non-contrast T1 in 80 to 90% of people. This represents stored vasopressin and is often absent in diabetes insipidus.

Height varies with age and sex. The upper limit is 6 mm in infants and children, 8 mm in adult men and post-menopausal women, 10 mm in young women, and up to 12 mm in pregnancy and the early postpartum period.

The upper surface is flat or mildly concave, and a convex upper surface is normal in young women and during pregnancy. The stalk is midline, tapers from 3 mm at the chiasm to 2 mm at the gland, and enhances.

The optic chiasm lies over the diaphragma sellae, and the cavernous sinuses lie lateral to the gland. The internal carotid arteries are seen as flow voids.

Interpretation.

• Microadenoma: a focus under 10 mm that is hypointense to the gland on T1 and enhances less than the normal gland. The stalk may deviate away from the lesion, and the gland may bulge on one side. T2 appearance is variable.
• Macroadenoma: a mass over 10 mm, often with suprasellar extension giving a "snowman" or "figure of eight" shape at the diaphragma sellae. It may compress the optic chiasm, invade the cavernous sinus (encasement of the carotid artery over 67% of its circumference, or tumour medial to the carotid), or extend into the sphenoid sinus.
• Functional types: prolactinomas often show a cystic or haemorrhagic component and respond to dopamine agonists. Growth hormone adenomas are typically hypointense on T2. Corticotroph adenomas are usually small, with subtle hypoenhancement.
• Pituitary apoplexy: acute haemorrhage or infarction in an adenoma, with a heterogeneous mass, fluid fluid levels, T1 hyperintensity (methaemoglobin) and restricted diffusion. The chiasm is compressed.
• Rathke cleft cyst: a well defined midline cyst between the anterior and posterior lobes, with variable signal on T1 and T2. It usually does not enhance, though the rim may.
• Craniopharyngioma: a suprasellar cystic and solid mass with calcification, a high signal cyst content on T1 (protein) and heterogeneous enhancement. It occurs in children and in older adults.
• Meningioma: a suprasellar or parasellar extra-axial mass with homogeneous avid enhancement and a dural tail, often with hyperostosis.
• Germinoma and other germ cell tumours: midline masses in the pineal and suprasellar region in young people, with loss of the posterior pituitary bright spot and diabetes insipidus.
• Hypophysitis: diffuse enlargement of the gland with a thickened stalk and avid enhancement, in autoimmune disease, pregnancy or with checkpoint inhibitor treatment.
• Empty sella: CSF fills the sella with a flattened gland on the floor. It is often incidental, or associated with raised intracranial pressure.
• Hypothalamic hamartoma, optic nerve and chiasm glioma and Langerhans cell histiocytosis: stalk or hypothalamic masses and thickening in children.
• Pituitary hypoplasia and ectopic posterior pituitary: a small gland, a thin or absent stalk and a bright spot at the median eminence, in children with growth hormone deficiency.
• Metastasis and lymphoma: a rapidly enlarging mass, often with diabetes insipidus and cranial nerve palsy. Look for a known primary.
• Vascular: a carotid aneurysm projecting into the sella has a flow void and pulsation artefact. Always check before surgery.
• Post-operative changes: fat or muscle packing, blood products, and CSF leak. Residual tumour is a nodular enhancing soft tissue that grows on follow up.
• Incidental lesions (pituitary incidentaloma): a small adenoma or cyst, found in over 10% of scans. Most need only a hormone screen and later imaging.

Critical values and findings needing immediate action.

• Pituitary apoplexy with visual loss, ophthalmoplegia or altered consciousness: urgent neurosurgical and endocrine review, intravenous hydrocortisone, and decompression if deficits are severe or progressive.
• Chiasm compression with visual field loss: urgent endocrine and neurosurgical referral. Dopamine agonist for a prolactinoma may restore vision quickly.
• Large mass with hypopituitarism: replace cortisol first (hydrocortisone) before thyroid hormone.
• Aneurysm in the sella: neurovascular referral before any surgery.
• Suspected malignant sellar mass (metastasis, lymphoma, germinoma): urgent biopsy and oncology.
• CSF leak or meningitis after surgery: antibiotics and neurosurgical review.

Limitations and artefacts.

• Small microadenomas (under 4 mm) may be missed, and a normal MRI does not exclude them. Dynamic imaging, 3 tesla, and thin sections improve detection.
• Incidental non-functioning lesions are common, so findings must match the biochemistry. Treating a lesion that is unrelated to the hormone excess is a risk.
• Corticotroph microadenomas are often invisible. Inferior petrosal sinus sampling may be needed to confirm the source of ACTH.
• Dental metal, sphenoid sinus air and bone cause susceptibility artefact at the sellar floor. Motion blurs the thin slices.
• The normal gland can look enlarged or convex in young women and in pregnancy, mimicking hyperplasia. Hypothyroidism and puberty also cause physiological hyperplasia.
• Gadolinium can cause a false impression of lesion size by enhancing the gland around it. Delayed images can reverse the contrast.
• Cavernous sinus invasion is hard to prove. Only encasement of the carotid or medial wall breach is reliable.
• Post-operative change and packing mimic residual tumour in the first 3 to 6 months. Baseline imaging at 3 months is helpful.
• Optic chiasm position and visual fields should be correlated. MRI cannot show function.

Special groups.

• Children: pituitary hypoplasia, ectopic posterior pituitary and craniopharyngioma. Use sedation if needed. A normal anterior pituitary height is smaller.
• Pregnancy: avoid gadolinium. Prolactinomas may enlarge, and monitoring is by visual fields and clinical symptoms, with MRI if compression is suspected.
• Older adults: non-functioning macroadenomas often present with visual loss or hypopituitarism.
• Patients with multiple endocrine neoplasia type 1 or familial isolated pituitary adenoma: earlier and repeated screening.
• Patients on checkpoint inhibitors: hypophysitis causes hypopituitarism and headache.
• Regions: late presentation with large macroadenomas, blindness and apoplexy is common. Where MRI is not available, CT with contrast shows macroadenomas, and hormone assays and visual fields direct treatment. Dopamine agonists are the cheap first line therapy for prolactinomas.

Follow up tests.

• Hormone tests: prolactin (with serial dilution to exclude the hook effect), IGF-1 and oral glucose tolerance test with growth hormone, 24-hour urinary free cortisol, late night salivary cortisol and dexamethasone suppression, morning cortisol and ACTH stimulation, TSH and free T4, LH, FSH, testosterone or oestradiol, and water deprivation test for diabetes insipidus.
• Formal visual field testing and optical coherence tomography of the retinal nerve fibre layer.
• Inferior petrosal sinus sampling for Cushing disease when MRI is negative.
• Repeat MRI at 3 to 6 months after surgery, then yearly.
• CT of the sella for bone detail before surgery.
• Referral to endocrinology, pituitary neurosurgery, ophthalmology or radiotherapy.