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charges. The CSF was proteinaceous (2.42 g/l) but acellular and sterile. On suspicion of viral encephalitis, the patient received treatment with both systemic acyclovir (dose/day) and methylprednisolone (dose/ day), resulting in rapid improvement of mental status. After 10 days acyclovir was stopped and methylprednisolone was tapered off over 5 days. Four weeks later (January 2005) the patient was referred to our neurological ward due to persistent confusion and two generalized tonic-clonic seizures. A new CSF examination disclosed raised protein levels (0.92 g/l) without cells. EEG was diffusely slow. Neuroimaging studies were unremarkable. Serum titers of anti-thyroid antibodies were elevated (anti-thyroperoxidase Ab: 591 U/ml, anti-thyroglobulin Ab: 905 U/ml), whereas thyroid-stimulating hormone, free triiodothyronine and free thyroxine were in the normal range. A presumptive diagnosis of NAIM associated with thyroid autoimmunity was made. Systemic methylprednisolone and valproic acid were administered. The clinical picture promptly improved and she was discharged after 10 days on oral valproic acid 1,000 mg/day. The patient was admitted again 3 weeks later (February 2005) due to drowsDear Sir, Nonvasculitic autoimmune inflammatory meningoencephalitis (NAIM) is a rare cause of usually steroid-responsive encephalopathy characterized by multiple and nonspecific autoimmune serologic associations [1] . Hashimoto encephalopathy may represent an acute or subacute form of NAIM associated with high titers of antithyroid antibodies independent of thyroid function [2] . The clinical picture is variable and usually involves delirium, hallucinations, myoclonus, seizures and strokelike episodes [3] . In steroid-resistant patients other treatments such as plasma exchange and intravenous immunoglobulin (IVIG) have been employed [4, 5] . MRI studies may provide evidence of focal or diffuse, nonenhancing altered signal areas [2, 3] . Normalization of NAIM-associated white matter MRI alterations has been reported following steroid therapy but not following IVIG and plasma exchange [3, 6, 7] .

Regression of White Matter MRI Abnormalities in Nonvasculitic Autoimmune Inflammatory Meningoencephalitis following Intravenous Immunoglobulin