2 were all normal. Autoimmune screen and haematinics including vitamin B12 levels were likewise normal. Thyroid function showed T4 10.3 and TSH 9.97 with markedly elevated anti-thyroid peroxidase antibodies at 25600 and normal antithyroglobulin antibodies. A diag- nosis of Hashimoto’s encephalopathy was made and high- dose steroids initiated. Within days, there was marked clinical improvement with full resolution of confusion and myoclonus. He was discharged well several days later on high-dose oral prednisolone. This was gradually reduced over six months, without relapse. One year after this hospital admission, routine thyroid function tests revealed overt hypothyroidism with T4 of 7.4 and TSH of 51. At this point, thyroxine replacement was introduced. 3. Discussion Hashimoto’s encephalopathy remains a controversial entity since its ﬁrst description in 1966 [1]. The exact aetiology has yet to be elucidated although is assumed to be autoimmune. Current opinion is divided on the exact nature of this autoimmune response. Primary demyelination, vasculitis, immune complex deposition, and direct antibody-mediated neuronal injury have all been proposed as mechanisms of disease. It is characterised by confusion with or without myoclonus, seizures, hyperreﬂexia, and psychosis. Presenta- tion may be an insidious development of cognitive impair- ment or recurrent acute episodes of focal neurological deﬁcit with confusion [2]. Laboratory ﬁndings are largely nonspeciﬁc. There is typically a raised CSF protein level with normal glucose with or without a lymphocytic pleocytosis. Nonspeciﬁc EEG abnormalities usually comprising slowing of background activity are seen in the majority of patients, whilst focal spikes or sharp waves are less common [3]. There are reports of EEG abnormalities recovering rapidly with steroid therapy while other cases illustrate a lag between EEG improvement and clinical improvement [4]. Magnetic resonance imaging (MRI) may be normal or demonstrate nonspeciﬁc T2 signal abnormalities in the subcortical white matter that do not enhance with gadolinium. In rare cases, diﬀuse white matter changes or meningeal enhancement have been described [2]. Imaging using higher ﬁeld magnets such as 3T MR scanners may detect subtle abnormalities not seen on the 1.5T machine used in our case. Thyroid dysfunction may be present. The most striking abnormality is raised antithyroid antibodies. Antithyroid peroxidase antibodies are markedly elevated with or without elevated antithyroglobulin antibod- ies [4]. Initial treatment is with high-dose steroids titrated according to clinical response [5]. Thyroid dysfunction should also be appropriately treated if present. Response to steroid therapy is usually excellent and is followed by slow steroid tapering and eventual discontinuation. Steroid intol- erant patients may respond to cyclosporine or azathioprine. There are also several case reports describing good clinical outcomes following plasma exchange [6] and intravenous immunoglobulin [7]. It is unclear whether this condition is directly related to thyroid disease or whether the relationship Case Reports in Medicine is due to diﬀerential expression of an autoimmune phe- notype. The term steroid-responsive encephalopathy asso- ciated with autoimmune thyroiditis (SREAT) is, therefore, preferred by some authorities. The long-term neurological prognosis in Hashimoto’s encephalopathy is good. Persistent cognitive deﬁcits develop in a minority and are more likely if treatment is considerably delayed [8]. There remains much to be discovered regarding the pathogenesis of Hashimoto’s encephalopathy. It should be considered in the diﬀerential diagnosis of any metabolic encephalopathy as prompt treatment can lead to excellent recovery. References [1] L. Brain, E. H. Jellinek, and K. Ball, “Hashimoto’s disease and encephalopathy,” Lancet, vol. 2, no. 7462, pp. 512–514, 1966. [2] P. Castillo, B. Woodruﬀ, R. Caselli et al., “Steroid-responsive encephalopathy associated with autoimmune thyroiditis,” Archives of Neurology, vol. 63, no. 2, pp. 197–202, 2006. [3] A. J. Rodriguez, G. A. Jicha, T. D. L. Steeves, E. E. Benarroch, and B. F. Westmoreland, “EEG changes in a patient with steroid-responsive encephalopathy associated with antibodies to thyroperoxidase (SREAT, Hashimoto’s encephalopathy),” Journal of Clinical Neurophysiology, vol. 23, no. 4, pp. 371–373, 2006. [4] A. Chaudhuri and P. O. Behan, “The clinical spectrum, diagno- sis, pathogenesis and treatment of Hashimoto’s encephalopathy (recurrent acute disseminated encephalomyelitis),” Current Medicinal Chemistry, vol. 10, no. 19, pp. 1945–1953, 2003. [5] I. Kothbauer-Margreiter, M. Sturzenegger, J. Komor, R. Baum- gartner, and C. W. Hess, “Encephalopathy associated with Hashimoto thyroiditis: diagnosis and treatment,” Journal of Neurology, vol. 243, no. 8, pp. 585–593, 1996. [6] L. Nieuwenhuis, P. Santens, P. Vanwalleghem, and P. Boon, “Subacute Hashimoto’s encephalopathy, treated with plasma- pheresis,” Acta Neurologica Belgica, vol. 104, no. 2, pp. 80–83, 2004. [7] S. Jacob and Y. A. Rajabally, “Hashimoto’s encephalopathy: Steroid resistance and response to intravenous immunoglobu- lins,” Journal of Neurology, Neurosurgery and Psychiatry, vol. 76, no. 3, pp. 455–456, 2005. [8] N. A. Gayatri and W. P. Whitehouse, “Pilot survey of Hashimoto’s encephalopathy in children,” Developmental Medicine and Child Neurology, vol. 47, no. 8, pp. 556–558, 2005.