Endocrine Abstracts

Cushing’s syndrome is a multisystem disorder with hallmark metabolic features, but its neuropsychiatric manifestations—particularly catatonia—are under-recognised. We present a 38-year-old woman with no prior endocrinopathy admitted with acute confusion, persecutory delusions, and catatonia. Labs showed hypercortisolaemia (serum cortisol 1544 nmol/l), elevated ACTH (64 ng/l), raised urinary cortisol (>3300 nmol/l) and hypokalaemia (2.9 mmol/l). Adrenal androgens were raised (testosterone 2.9 nmol/l, androstenedione 22.6 nmol/l), while other anterior pituitary hormones were normal, suggesting preserved pituitary function aside from corticotrophin hyperactivity. A pituitary MRI revealed a 4 mm microadenoma and ^68 Ga-DOTATATE PET excluded ectopic sources. Despite partial cortisol suppression on high-dose dexamethasone, ACTH levels stayed elevated, supporting pituitary-origin ACTH-dependent Cushing’s syndrome. She was started on metyrapone (1 g TDS), benzodiazepines, and treated with insulin and electrolytes. Antipsychotics were avoided due to risk of worsening catatonia. Apixaban was initiated for thrombotic risk. Psychiatric input was sought early and integrated into multidisciplinary care to guide benzodiazepine use and provide psychological support. She underwent trans-sphenoidal resection; histology confirmed an ACTH-positive corticotroph adenoma with Ki-67 <3%. Given her substantial cortisol burden, peri-operative care included stress-dose hydrocortisone. Although biochemical remission was achieved post-operatively, she developed steroid withdrawal symptoms—fatigue, myalgia, mood lability—indicating higher supplementation than standard dosing was required. Glucagon stimulation confirmed secondary adrenal insufficiency and GH deficiency, prompting tailored hydrocortisone replacement with gradual weaning. Anticipatory counselling before surgery helped mitigate psychological distress during withdrawal. The literature suggests a mechanistic link between hypercortisolaemia and catatonia via GABAergic and dopaminergic dysregulation. Gunther et al. report 80% zolpidem response [1]. Catatonic episodes show elevated ACTH and DHEAS [2], exacerbated by cortisol surges [3]. The Endocrine Society recommends surgical resection as first-line, with medical therapy for pre-operative control or inoperable cases [5]. Cognitive deficits may persist post-remission [4]. Only one prior case of catatonia in Cushing’s syndrome is reported (Yamaguchi et al., 2019); ours is the second [6]. This case highlights recognition of catatonia as manifestation of endocrine disease. Interpreting pituitary function, anticipating steroid withdrawal, and individualised hydrocortisone dosing—essential to manage high-burden cortisol states. Early endocrine input and multidisciplinary care are vital to optimise outcomes.

References: 1. Gunther M et al. Zolpidem in catatonia. J Acad Consult Liaison Psychiatry. 2025;66(1):49–56. 2. Muneoka K et al. Neurosteroids in periodic catatonia. JCEM Case Rep. 2023;1(1):luad009. 3. Zwiebel S et al. Catatonia with hypercortisolaemia. Case Rep Psychiatry. 2018;2018:4264763. 4. Katragadda A et al. Cognitive decline in Cushing’s. J Neuroendocrinol. 2025;37(1):e13466. 5. Nieman LK et al. Cushing’s treatment guideline. J Clin Endocrinol Metab. 2015;100(8):2807–13. 6. Yamaguchi H et al. Subclinical Cushing’s catatonia. Psychogeriatrics. 2019;19(4):402–3. doi:10.1111/psyg.12394.