Pituitary Adenomas

What are pituitary tumors, and what are the main types?

Most lesions are adenomas of the anterior pituitary—benign in pathology, but clinically important due to hormone effects and/or compression.

The pituitary is a “central regulator” of multiple endocrine axes. Pituitary tumors are most often adenomas arising from anterior pituitary cells. In practical clinical terms, adenomas are categorized as:

• Functioning (hormone-secreting): cause a clinical syndrome due to hormone hypersecretion.
• Nonfunctioning: do not produce a classic hypersecretion syndrome and often present with mass effect and/or pituitary hormone deficiency.

By size:

• Microadenoma: < 10 mm (very common).
• Macroadenoma: ≥ 10 mm (more likely to produce mass effect/visual symptoms).

How common are they, and at what ages do they occur?

Pituitary tumors are among the most common primary intracranial tumors and are most frequently diagnosed in adulthood.

Pituitary tumors account for approximately 10–15% of primary intracranial neoplasms and represent the third most common primary intracranial tumor group. They are most often diagnosed between the third and sixth decades of life.

Autopsy and imaging-based series do not show a consistent sex predilection; however, surgical series often report a higher proportion in women— likely because menstrual and reproductive manifestations prompt earlier evaluation.

Functioning adenomas: which hormonal syndromes do they cause?

Roughly 60–70% of adenomas are hormone-secreting. Clinical features depend on the specific hormone produced.

The most common functioning adenomas include:

• Prolactinomas (PRL): menstrual irregularity/amenorrhea and galactorrhea in women; reduced libido and erectile dysfunction in men.
• Somatotroph adenomas (GH → IGF-1): acromegaly in adults (and rarely gigantism in children).
• Corticotroph adenomas (ACTH): Cushing disease.
• Thyrotroph adenomas (TSH): clinical hyperthyroidism.

Gonadotroph adenomas also occur; however, many are clinically nonfunctioning and often present as macroadenomas due to mass effect.

Nonfunctioning adenomas: what does “mass effect” mean in the sellar region?

Larger lesions may compress visual and neural structures, with extension superiorly and laterally beyond the sella.

Nonfunctioning adenomas are frequently discovered after they have enlarged. The pituitary sits within the confined space of the sella turcica and is adjacent to critical structures:

• Optic chiasm (superiorly) → visual field deficits.
• Cavernous sinus (laterally) → cranial nerves III, IV, V1, V2, VI.
• Hypothalamus and the third ventricle (in very large lesions) → rarely CSF pathway effects/hydrocephalus.

Headache is common in macroadenomas, although it is not specific and should be interpreted in clinical context.

Pituitary hormone deficiency: which symptoms suggest hormonal insufficiency?

Chronic compression of normal pituitary tissue can result in gradual decline of hormonal output.

When a tumor compresses the normal pituitary gland, it may lead to hypopituitarism or even panhypopituitarism. Symptoms depend on the affected axis:

• Gonadotropins: reduced libido, menstrual irregularity, infertility.
• Thyroid axis: fatigue, weight gain, cold intolerance, constipation.
• GH/IGF-1 (adults): reduced energy and changes in body composition (often nonspecific).
• ACTH/cortisol: weakness, hypotension, nausea—this axis is clinically critical.

Gonadotropin function is often affected early in chronic compression; however, every patient requires a tailored endocrine assessment.

What happens to vision? (optic chiasm & bitemporal hemianopsia)

The classic “alarm” finding in macroadenoma is a visual field defect—sometimes present even when day-to-day vision seems intact.

Superior extension of a pituitary tumor can compress the optic chiasm. The most characteristic deficit is bitemporal hemianopsia (loss of the temporal halves of the visual fields). In many patients, the superior temporal fields are affected first, reflecting the fiber arrangement within the chiasm.

How is the endocrine evaluation performed? (PRL, ACTH, IGF-1, etc.)

Endocrine testing must be comprehensive—assessing for hypersecretion while also screening for hormonal deficiency.

Initial laboratory evaluation for a suspected sellar lesion typically includes (tailored to the clinical context):

• PRL (prolactin)
• GH / IGF-1 (growth hormone axis)
• ACTH and cortisol
• TSH and free T4
• LH / FSH and sex hormones (testosterone / estradiol, as appropriate)

Prolactin: two classic “pitfalls”

• Hook effect: at extremely high PRL levels, some assays may yield a falsely low result. If a prolactinoma is strongly suspected, request serial dilution with repeat testing.
• Stalk effect: mild PRL elevation may result from disruption of dopaminergic inhibition due to pituitary stalk/hypothalamic compression—this does not necessarily indicate a true prolactinoma.

In suspected Cushing disease, additional specialized testing is often required to confirm endogenous hypercortisolism and define ACTH dependence and source.

Pituitary MRI: why is a “dynamic” protocol needed for microadenomas?

MRI with contrast is the study of choice, but microadenomas often require a dedicated protocol to maximize sensitivity.

Pituitary MRI with gadolinium is the cornerstone of imaging. In microadenomas, contrast against normal gland tissue can be subtle: normal pituitary typically enhances briskly (reflecting its vascularity), whereas a microadenoma may enhance more slowly or less intensely. For this reason, a dynamic MRI protocol with timed post-contrast sequences is preferred.

MRI is also essential for defining:

• relationship to the optic chiasm
• lateral extension and/or invasion into the cavernous sinus
• relationship to the carotid arteries
• degree of suprasellar extension

Very small hormone-secreting adenomas (for example, in Cushing disease) may not be clearly visualized on MRI; in such cases, localization may require additional specialized methods, depending on the clinical scenario.

When is observation appropriate, and when is treatment necessary?

Decisions are driven by symptoms, endocrine function, and evidence of compression or growth.

Not every pituitary tumor requires immediate intervention. In patients with asymptomatic microadenomas, many lesions remain stable over time. In such cases, the standard approach is often:

• surveillance with pituitary MRI at appropriate intervals,
• periodic hormonal reassessment,
• visual field testing when there is proximity to the optic chiasm.

More urgent treatment is considered when there is:

• visual impairment and/or clear optic chiasm compression,
• a clinically significant hypersecretion syndrome,
• progressive growth on serial imaging,
• worsening hypopituitarism,
• features consistent with pituitary apoplexy.

Medical therapy (especially prolactinomas): what should I expect?

Prolactinomas are the key exception in which first-line therapy is typically medical rather than surgical.

Prolactinomas represent a substantial proportion of pituitary adenomas. Unlike most other adenoma subtypes, medical therapy is usually the initial approach—provided neurologic status is stable and close follow-up is feasible.

Primary medications: dopamine agonists such as cabergoline or bromocriptine.

• Goals: reduce PRL levels, achieve tumor shrinkage, and improve symptoms.
• Cabergoline is often favored due to better tolerability and strong effectiveness in many patients.

For other functioning adenomas (GH/ACTH/TSH), medications may have a role in selected contexts, but are not typically first-line when a clear surgical indication exists.

Pituitary surgery (transsphenoidal approach): indications, technique, safety

The transsphenoidal approach is the established surgical corridor for the vast majority of pituitary tumors.

Surgery is often indicated—particularly when there is optic chiasm compression, significant mass effect, or a functioning adenoma in which resection provides the most direct and durable disease control.

Key indications for surgery include:

• Macroadenoma with visual compromise and/or optic chiasm compression.
• Functioning adenomas such as ACTH-secreting, TSH-secreting, and GH-secreting tumors (typically first-line when feasible).
• Nonfunctioning adenomas with progressive growth, hypopituitarism, or mass effect.
• Prolactinomas with medication resistance or intolerance plus clinically meaningful symptoms.

The transsphenoidal route can be performed using a microscopic or endoscopic technique. In experienced hands—such as the Neuroknife team—both approaches can deliver excellent safety and efficacy; the optimal choice is individualized based on anatomy and technical considerations.

Potential complications include CSF leak and transient—or less commonly permanent—diabetes insipidus. Major complications such as injury to large vessels or damage to the visual apparatus are uncommon in experienced centers, but are always discussed preoperatively.