In March 2005, 4 weeks after 131I radiotherapy, the patient started to develop progressive dementia-like disorientation, tremor, and psychomotor deficits. A cerebral head magnetic resonance image (MRI) in October 2005 revealed only slight and putatively unspecific frontal and temporal white matter lesions (Figure). Neuropsychological symptoms further progressed with depression, decreased alertness, and cognitive function, including severe amnestic deficits and semantic paraphasia. In November 2005, neurological examination revealed an intention tremor, myoclonus, spasticity, and truncal ataxia. Thyroid function measures were as follow: TSH level, 17.71 μU/mL (reference, 0.35-4.5 μU/mL); FT4 level, 6.3 pg/mL (reference, 8.0-18 pg/mL); and FT3 level, 0.96 mmol/L (reference, 0.7-2.9 mmol/L). Tests for TSH-receptor antibodies and TG-Ab were negative. Levels of TPO antibodies (>1000 U/mL, reference, <35 U/mL) were elevated. Routine hematological and biochemical analyses had normal findings. Antineuronal antibodies (Yo, Hu, RI) were undetectable. Cerebrospinal fluid (CSF) analysis revealed an elevated protein level of 1630 mg/L (reference, <500 mg/L), 150 lymphocytes per microliter, an albumin quotient of 30.3 (reference, <8.9), normal glucose levels, weakly positive oligoclonal bands, and the presence of 14-3-3 protein. No intrathecal antibody synthesis or elevated viral titers were detected for human immunodeficiency virus 1/2, herpes simplex virus, varicella-zoster virus, Epstein-Barr virus, rubeola, rubella, or coxsackie. Tests for Borrelia burgdorferi antibody titers were negative, and sterile CSF cultures ruled out a bacterial or fungal etiology. The amyloid β protein level was 637 pg/mL (reference, >797 pg/mL) and tau protein level was 321 pg/mL (reference, <318 pg/mL). The electroencephalogram showed a generalized diffuse slowing (6-7 per second). Interestingly, the cerebral head MRI now revealed symmetric, widespread, periventricular, and subcortical hyperintense signals on fluid-attenuated inversion recovery (FLAIR) and T2-weighted images (Figure). Corticosteroid therapy was started with initially 100-mg prednisolone per day. During the following weeks, the patient improved dramatically concerning neurological examination findings, alertness, psychomotor behavior, memory, speech, and mood. In accordance with this, an MRI scan in January 2007 documented an almost complete resolution of the frontal and temporal lesions (Figure).