A 58-year old female with long standing type 1 diabetes and treated hypothyroidism presented to casualty with a 1-day history of vomiting and breathlessness. Clinically she was dehydrated with a depressed conscious level (GCS=12). Initial investigations confirmed diabetic ketoacidosis (pH=6.8, bicarbonate=4.7 mmol/l, urinary ketones=4+, blood glucose=54.6 mmol/l) and acute renal failure, likely to be secondary to pneumonia as there was consolidation on her CXR and a raised WCC. Despite correcting her acidosis and electrolyte disturbances and treating her sepsis she remained drowsy and was subsequently ventilated. Abnormal bodily movements were observed. Brain MRI was normal and EEG showed generalised slow waves with diffuse cortical dysfunction without any epiletiform features. Lumber puncture showed raised CSF protein with negative viral PCR studies. Abnormal admission TFTs were noted: FT4=8.0 pmol/l (NR: 9.019.0), TSH=0.72 mIU/l (NR: 0.354.94). Thyroid microsomal antibodies were raised: 113 IU/ml (NR<50). Four months prior to admission TFTs were normal (FT4=15.3 pmol/l, TSH=0.48 mIU/l) on 100 μg of thyroxine. TFTs may be in keeping with the sick euthyroid syndrome but hashimotos encephalopathy was considered especially as other causes for coma were excluded. Subsequently she was commenced on intravenous Methylprednisolone and gradually ventilatory support was weaned off. A full recovery was made. Hashimotos encephalopathy is a rare condition characterized by non-specific neurological and/or psychiatric symptoms often associated with high serum and/or CSF levels of anti-thyroid antibodies, increased CSF protein concentration, non-specific diffuse EEG abnormalities, and responsiveness to treatment with steroids. Many cases go undiagnosed. Hashimotos encephalopathy should be considered in investigation negative encephalopathies as it is responsive to steroid therapy and is readily reversible. Normal or slightly abnormal TFTs do not exclude the diagnosis. The association with type 1 diabetes is not well reported.