Graves' disease presenting with catatonia: a probable case of encephalopathy associated with autoimmune thyroid disease
Article first published online: 4 APR 2012
© 2012 John Wiley & Sons A/S
Volume 24, Issue 6, pages 374–379, December 2012
How to Cite
Bharadwaj, B., Sugaparaneetharan, A. and Rajkumar, R. P. (2012), Graves' disease presenting with catatonia: a probable case of encephalopathy associated with autoimmune thyroid disease. Acta Neuropsychiatrica, 24: 374–379. doi: 10.1111/j.1601-5215.2012.00654.x
- Issue published online: 7 NOV 2012
- Article first published online: 4 APR 2012
- Accepted manuscript online: 13 FEB 2012 01:20PM EST
- Accepted for publication February 8, 2012
Bharadwaj B, Sugaparaneetharan A, Rajkumar RP. Graves' disease presenting with catatonia: a probable case of encephalopathy associated with autoimmune thyroid disease.
Introduction: Encephalopathy associated with autoimmune thyroid disease (EAATD) is diagnosed when neuropsychiatric symptoms of acute or sub-acute onset occur along with clinical or subclinical autoimmune thyroid dysfunction. Supporting evidence includes the presence of anti-thyroid antibodies in the serum and/or cerebrospinal fluid. The thyroid hormone alteration is not sufficient to explain the neuropsychiatric manifestations. The most commonly described electroencephalographic abnormality in this condition is a generalised background slowing. Clinical descriptions of EAATD have focused mainly on neurological symptoms including seizures, loss of consciousness, myoclonus and cognitive symptoms.
Case: We present the case of a 48-year-old lady who presented with catatonia. Her clinical and laboratory features were suggestive of Graves' disease which was hitherto undiagnosed. Anti-thyroid antibodies were positive. Electroencephalogram showed a brief period of temporal delta activity. The findings are suggestive of EAATD. Differential diagnoses of metabolic derangements like electrolyte imbalance, hepatic and renal failure, neuroinfections and psychiatric conditions like acute psychosis were ruled out.
Discussion: Treatment involves a course of corticosteroids. Response to corticosteroids, however, is not essential for the diagnosis of EAATD as the patient may respond to symptomatic treatment alone as in our case. Outcomes reported in case series have been generally good as in our patient.
Conclusion: This report illustrates the need to keep a high index of suspicion for an organic aetiology in cases presenting with catatonia. A thorough neuropsychiatric evaluation is useful in such cases. In patients with severe neuropsychiatric manifestations associated with thyroid disease, an autoimmune thyroid disease should be considered as a possibility.