Atypical Neuropsychiatric Presentation of Addison's Disease: A Case Report.

Sir: Addison's disease is a potentially life-threatening endocrine condition with known neuropsychiatric presentations. Anglin and colleagues’ review1 of the existing literature reported disturbances of mood, motivation, and behavior as the common presentations. Psychosis was associated with severe conditions and Addisonian crisis. Rare presentations included self-mutilation and catatonia.1 We report a case of Addison's disease with episodic neuropsychiatric presentations. Case report. Mr. A, a 43-year-old man, presented to us in April 2007 with forgetfulness, motor restlessness, rearranging household articles repeatedly, and talking excessively for 1 day. He had experienced an episode in January 2007 of perceptual abnormalities of seeing his body transform into a tube containing multiple revolving discs and visual and command auditory hallucinations, which resolved spontaneously in 1 day. His family and personal history and a systemic examination revealed no abnormalities. Results of serum electrolytes, liver and renal function, and blood glucose tests; hemogram; brain magnetic resonance imaging; and electroencephalogram were within normal limits. A subsequent episode in early July 2007 was characterized by crying spells, depressive ruminations, and insomnia lasting 3 days, and an episode in late July 2007 was characterized by increased speech, decreased need for sleep, and elated affect lasting 7 days. All episodes were abrupt in onset, preceded by headache and vomiting of 2 days' duration, and resolved spontaneously without medications. Mr. A was asymptomatic between episodes. A thyroid function test revealed low triiodothyronine and thyroxine levels and normal thyroid-stimulating hormone levels. A complete metabolic investigation revealed low serum cortisol (baseline 2.54 mg/dL). The short Synacthen test indicated possible adrenal failure, as serum cortisol level (13.09 mg/dL) did not increase to expected values (18 mg/dL) at 60 minutes post-Synacthen challenge. The patient was started on replacement treatment with thyroxine 50 mg/day and prednisolone 10 mg/day and has remained asymptomatic to date. Although neuropsychiatric manifestations are common in Addison's disease, our understanding of its pathophysiology remains unclear. Hyponatremia,2 hypoglycemia,3 Hashimoto's thyroiditis,1 and increased endorphin production4 have been hypothesized to underlie these presentations. In our patient, decreased glucocorticoid production may possibly explain the presentations. Henkin and Daly5 have proposed that decreased glucocorticoid production results in increased neural excitability and increased conduction velocity along peripheral axons while prolonging conduction across synapses. This probably delays the arrival of signals from the periphery to the central nervous system, resulting in a deficit between perception and integration of sensory signals, and is a possible mechanism for hallucinations and psychosis. The reasons behind the atypical presentations, however, remain unclear. Vidya Narayan, M.B.B.S. Janardhanan C. Narayanaswamy, M.B.B.S. Manepalli Krishnakanth, M.D. Kesavan Muralidharan, M.D. National Institute of Mental Health and Neurosciences, Bangalore, India