MON-465 Acute Neuropsychiatric Illness and Catatonia in the Setting of Adrenal Crisis

Abstract Disclosure: R. Dankar: None. E. Abidor: None. S. Barakat: None. S. Quyyumi: None. Background: Psychotic disorders are rare manifestations of endocrinologic abnormalities. Reports linking neuropsychiatric symptoms with hypopituitarism and adrenal insufficiency are limited. We present an atypical case of catatonia in a patient with panhypopituitarism admitted with adrenal crisis secondary to insufficient glucocorticoid replacement. Our case likely represents the fourth documented case of catatonia with adrenal insufficiency. Case Presentation: A 29-year-old male with a medical history of panhypopituitarism of unknown etiology presented with nausea, vomiting, abdominal pain, and poor appetite. He had a recent intensive care unit hospitalization for recurrent viral myopericarditis complicated by cardiac tamponade and had been discharged home with steroid tapering. On presentation, he was alert and oriented but showed some signs of agitation compared to his baseline. Vitals signs were stable, and the patient had normal laboratory findings and a negative infectious workup. During hospitalization, the patient’s mental status quickly deteriorated to a state of non-responsiveness and non-verbal behavior whereby the patient would only track with his eyes, raising concerns for catatonia. Extensive imaging and video electroencephalography excluded any structural or seizure-related causes, raising suspicion for idiopathic catatonia. Empirical treatment with lorazepam was initiated, with minimal response. The patient soon became hypotensive and labs revealed distinct electrolyte imbalances, including hyponatremia and hypoglycemia, with undetectable ACTH (<1.5 pg/mL), serum cortisol (<1 µg/dL), and free cortisol (<0.02 µg/dL). The patient was started on stress dose steroids for adrenal crisis. Notably, the patient’s cognition drastically improved following resolution of the adrenal crisis with glucocorticoid therapy, averting the need for any medications. Discussion: Although several reports have established neuropsychiatric manifestations of adrenal insufficiency and panhypopituitarism, the underlying pathophysiology remains unclear. Hyponatremia, hypoglycemia, and increased endorphin production have been hypothesized as potential contributors. Reduced glucocorticoid levels might lead to increased neural excitability and conduction velocity. This delay in signal transmission may result in a deficit between the perception and integration of sensory inputs, potentially underlying hallucinations and psychosis. However, the causes for atypical presentations remain unclear. Conclusion: This case highlights the potential for adrenal insufficiency to manifest with psychiatric symptoms, including catatonia, in the setting of steroid tapering. Prompt recognition and treatment can lead to cognitive recovery without the need for medications. Presentation: Monday, July 14, 2025