Subacute cognitive deterioration with high serum anti‐thyroid peroxidase antibodies: two cases and a plea for pragmatism

Autoimmune encephalopathy is a rare but potentially reversible cause of cognitive deterioration and neuropsychiatric disturbances. We describe two older female patients with subacute cognitive decline and marked neuropsychiatric disturbances in the presence of high serum anti‐thyroid peroxidase anti...

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Bibliographic Details
Published in:Psychogeriatrics 2013-09, Vol.13 (3), p.175-179
Main Authors: Segers, Kurt, Braconnier, Philippe, Corazza, Francis, Divano, Luisa, Mabrouk, Asmaa, Robberecht, Jean, Surquin, Murielle
Format: Article
Language:English
Subjects:
Aged
Anti-Inflammatory Agents - therapeutic use
Antibodies
anti‐thyroid peroxidase antibodies
Autoantibodies - blood
Autoimmune diseases
autoimmune encephalopathy
Biomarkers
Biomarkers - blood
Brain diseases
Brain Diseases - blood
Brain Diseases - complications
Brain Diseases - drug therapy
Cognition & reasoning
Cognition Disorders - blood
Cognition Disorders - complications
Cognition Disorders - drug therapy
dementia
Diagnosis, Differential
Drug therapy
Encephalitis
Female
Hashimoto Disease - blood
Hashimoto Disease - complications
Hashimoto Disease - drug therapy
Hashimoto's encephalopathy
Humans
Iodide Peroxidase - blood
Methylprednisolone - therapeutic use
Older people
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Summary:Autoimmune encephalopathy is a rare but potentially reversible cause of cognitive deterioration and neuropsychiatric disturbances. We describe two older female patients with subacute cognitive decline and marked neuropsychiatric disturbances in the presence of high serum anti‐thyroid peroxidase antibodies and with normal dosage of free thyroxine 4. One patient recovered almost completely after oral corticotherapy. Differential diagnosis and the role of biomarkers, in particular, are discussed. We support a pragmatic approach involving a short empirical therapeutic trial with intravenous or oral corticoids; this should be considered in all patients with subacute encephalopathy and with laboratory arguments for an underlying autoimmune aetiology.
ISSN:1346-3500
1479-8301
DOI:10.1111/psyg.12018