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Marcel Dihné, MD; Franz J. Schuier, MD; Maximilian Schuier, MD; Joachim Cordes, MD; Hans-Peter Hartung, MD; Andreas Knehans, MD; Stefan Mueller, PhD

Arch Neurol. 2008;65(2):282-283.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

Hashimoto encephalopathy (HE) is defined by spontaneous subacute encephalopathy with raised thyroid autoantibodies and a remarkable responsiveness to steroids.^1-2 Pathophysiologically, an association with Hashimoto thyroiditis is characterized by observations of elevated thyroid peroxidase antibody (TPO-Ab) levels or thyroglobulin antibody (TG-Ab) levels.^3-4 We describe a patient who developed HE following iodine 131 (¹³¹I) radiotherapy of Graves disease.

Report of a Case

In February 2005, a 61-year-old man with a 6-year history of Graves disease was admitted to hospital for ¹³¹I radiotherapy. Thyroid function measures were as follow: thyroid-stimulating hormone (TSH) level, 0.29 µU/mL (reference, 0.35-4.5 µU/mL); free thyroxine (FT₄) level, 17.1 pg/mL (reference, 8.0-18 pg/mL); free triiodothyronine (FT₃) level, 3.6 ng/L (reference, 1.8-4.6 ng/L); and TSH-receptor antibody level, 1.6 mU/L (reference, <1 mU/L). Tests for TG-Ab were negative, and TPO-Ab . . . [Full Text of this Article]

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