39 An Unusual Cause of Memory Loss

Abstract

Clinical Context and History: This 65-year-old white male patient presented to the VA Medical Center in 2013 with a chief complaint of memory loss. Past medical history included hypothyroidism and depression, and diagnoses of Alzheimer disease (AD) and posterior cortical atrophy were made at ages 55 and 62 years, respectively. The patient continued to work as an HVAC technician after the diagnosis of AD but was compelled to retire secondary to progressive cognitive decline. History was negative for cerebrovascular accident, seizures, lightheadedness, balance difficulties, hallucinations, and substance abuse. The patient's mother had been diagnosed with AD. Neuropsychological evaluation revealed deterioration of short-term memory and constructional apraxia with clinical progression over the ensuing three years. MRI studies done in 2012, 2014, and 2016 were interpreted as stable and within normal limits. Sleep studies were unremarkable. Cerebrospinal fluid (CSF) glucose, IgG/albumin index, oligoclonal bands, VDRL, anti Yo and anti-Hu antibodies and taw, 14-3-3 and prion proteins were all non-contributory. CSF total protein was borderline elevated (45 mg/dL). Non-contributory serum/plasma assays included FT-4, TT-3, TSH, myeloperoxidase and anti-proteinase antibodies, homocysteine, vitamin B-12, ANA, C and p-ANCA, atypical p-ANCA, and HIV and RPR serologies. Thyroid microsomal, anti-thyroglobulin, and anti-TPO antibodies were, however, all strongly positive. Results/Discussion: Review of the lab and imaging data suggested to neurology that the likely diagnosis was Hashimoto encephalopathy (HE) rather than AD. This rare entity is hypothesized to be of autoimmune etiology, has a strong female predominance, and is not related to thyroid function. Age of onset is generally 45–55 years old with pleiotropic presenting complaints frequently including cognitive decline. The patient was placed on high-dose prednisone with improvement of cognition. Conclusion: Although rare the diagnosis of HE is consequential as, in contrast to AD, HE irresponsive to immunosuppressive therapy. [ABSTRACT FROM AUTHOR]