MON-416 Unmasking the Mystery: Hashimoto's Encephalopathy Hidden Beneath Metabolic Encephalopathy

Abstract Disclosure: A. Marwat: None. H. Bangash: None. Introduction: Hashimoto’s encephalopathy (HE) is a rare and reversable form of autoimmune encephalitis that predominantly affects females, responds to steroids, and is associated with thyroid autoimmunity. HE typically presents with neuropsychiatric symptoms, including altered mental status (AMS), visual hallucinations, and seizures, along with elevated anti-TPO antibodies. Diagnosing HE can be challenging due to the need to exclude other causes of encephalopathy. This case emphasizes the importance of considering HE in patients with persistent AMS when symptoms fail to resolve after addressing common causes like metabolic encephalopathy Case: A 69-year-old woman with a history of hypothyroidism on levothyroxine presented to the emergency department with subacute onset of (AMS), vivid audiovisual hallucinations, body-wide tremulousness, night terrors, sleep disturbances, and memory deficits. Initial evaluation revealed acute kidney injury (AKI) with a creatinine level of 1.5 mg/dL (baseline: 0.8 mg/dL; normal: 0.6-1.10 mg/dL) and a urinary tract infection (UTI) with WBC >50/HPF (normal: 0-5/HPF) on urinalysis. A provisional diagnosis of metabolic encephalopathy secondary to AKI and UTI was made. However, despite correcting AKI with intravenous fluids and treating the UTI with antibiotics, her mental status failed to improve. Neurology was consulted, and further investigations were performed. Brain MRI showed diffuse cerebral and cerebellar atrophy with T2 hyperintensity in the subcortical region. EEG was limited by artifacts but otherwise normal. Cerebrospinal fluid (CSF) analysis revealed mildly elevated protein at 55.4 mg/dL (normal: 20-40 mg/dL) with no pleocytosis. The CSF autoimmune encephalopathy and multiple sclerosis (MS) panels were negative, and blood cultures were negative. Further testing showed markedly elevated thyroid peroxidase antibodies (anti-TPO) at 7,720 IU/mL (normal: 0-60 IU/mL). TSH was normal at 0.47 µIU/mL (normal: 0.35-4.94 µIU/mL), while free T4 was elevated at 1.83 ng/dL (normal: 0.89-1.76 ng/dL). The exclusion of other causes of encephalopathy, combined with elevated anti-TPO antibodies, neuropsychiatric symptoms, nonspecific T2 subcortical hyperintensity, and CSF protein elevation, led to the diagnosis of Hashimoto’s encephalopathy. The patient was treated with high-dose intravenous Solu-Medrol, 1 g daily for three days, with excellent response and complete neurological recovery. She was discharged on a tapering dose of oral steroids with outpatient neurology follow-up. Conclusion: This case highlights the importance of early recognition and management of the diagnostically challenging HE. Prompt treatment with corticosteroids can result in rapid and significant neurological improvement. Increased clinician awareness is essential. Presentation: Monday, July 14, 2025