Amiodarone remains an important class III antiarrhythmic drug used in the medical treatment of malignant arrhythmias. However, it is associated with various adverse effects including thyroid dysfunction. We present a case of a 52 year old man who presented with a 2 month history of weight loss, increased lethargy and dyspnoea more than 3 years after commencing amiodarone for recurrent ventricular tachycardia. His medical history was significant for idiopathic cardiomyopathy with ICD and previous stroke. Biochemical testing showed thyrotoxicosis with fT4 99, fT3 23 and TSH <0.05. Antibodies including anti-thyroid peroxidase, anti-thyroglobulin and TSH-receptor antibodies were negative. The patient was diagnosed with likely type II amiodarone-induced thyrotoxicosis and placed on oral corticosteroid therapy. Clinical and biochemical improvement was noted after 3 weeks. However, the patient represented 2 weeks later with acute confusion. Repeat testing revealed slightly worsened thyroid function. Extensive investigations for delirium did not reveal a clear infective cause although 14-3-3 protein was weakly positive on CSF examination. Creutzfeldt- Jakob disease was thought unlikely in the absence of other suggestive clinical features. Autoimmune screening and anti-neuronal antibodies were negative. CT head showed encephalomalacia and gliosis of the bilateral anterolateral superior temporal gyri with no acute pathology. His ICD unfortunately precluded further MR examination. The patient subsequently underwent total thyroidectomy with histopathology showing involuted follicular architecture with atrophy and fibrosis, consistent with type II amiodarone-induced thyrotoxicosis. The question of steroid responsive encephalopathy associated with thyrotoxicosis (SREAT) was raised by another team. This is an uncommon syndrome previously described in patients with Hashimoto’s thyroiditis and remains a controversial entity without specific diagnostic markers. Multifactorial delirium in a susceptible brain was considered the most likely cause of the patient’s unusual presentation in the setting of high dose corticosteroid therapy. Significant cognitive improvement was noted with gradual reduction in corticosteroid dose.