ArticleCureus2026
Endocrinologically Silent Crooke Cell Adenoma With Apoplexy Causing Oculomotor Palsy: An Uncommon and Underrecognised Entity.
Article in Cureus, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Crooke cell adenomas (CCAs) are among the most aggressive pituitary neuroendocrine tumours (PitNET). The convergence with pituitary apoplexy and endocrinological silence is very rare, as these factors add to the diagnostic complexity and delayed recognition of this entity. A 41-year-old male patient with a known untreated non-functional pituitary macroadenoma, presented with acute right oculomotor palsy and headache. Magnetic resonance imaging (MRI) demonstrated haemorrhagic infarction with bilateral internal carotid artery (ICA) encasement and cavernous sinus extension. He underwent urgent endoscopic endonasal transsphenoidal resection. Subtotal resection was performed given bilateral cavernous ICA encasement. Post-operatively, there was complete resolution of the oculomotor palsy and he remained endocrinologically silent throughout. Given its aggressive histological profile, adjuvant volumetric modulated arc therapy (VMAT, 54 Gy in 30 fractions) was administered three months postoperatively, with stable residual disease on serial MRI. This case is the tenth documented case of CCA presenting with pituitary apoplexy. Its paucity in the literature reflects not only the rarity of CCA with apoplexy but also underdiagnosis driven by its silent clinical presentation, absence of standardised histological protocols for apoplectic specimens, and immunohistochemical constraints in necrosis-heavy specimens. This case is the first to document subtotal resection with adjuvant fractionated radiotherapy as a safe and effective strategy in CCA apoplexy complicated by ICA encasement. CCA must be actively excluded in corticotroph pituitary neuroendocrine tumours (PitNETs) presenting with apoplexy, with viable tissue undergoing a minimum staining panel. Endocrinological silence can be falsely reassuring, as tumour aggressiveness is predicted by morphology and molecular profile rather than cortisol levels. Post-treatment surveillance via neuroimaging is crucial in biochemically silent CCA. Multicentre collaboration and prospective registry data are essential to establish evidence-based protocols for this rare but clinically consequential entity.
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