Abstract
Hashimoto encephalopathy (HE) is a heterogenous neurological syndrome that can manifest with encephalopathy, seizures, headaches, and variable neuropsychiatric disturbances. The underlying mechanism remains unclear; however, autoimmune pathogenesis is suspected due to its association with autoimmune thyroid disease, high titers of anti-thyroid antibodies, and quick response to steroid therapy. We report a 59-year-old female patient with a remote history of hypothyroidism who presented with status epilepticus and complaints of chronic headaches and cognitive impairment. The presence of sharp frontal waves was identified on her EEG. The patient was initially started on anti-epileptics only; however, her headaches and memory loss escalated, further diagnostic workup was pursued, which revealed high anti-thyroid peroxidase antibodies with normal thyroid function tests. The only cerebrospinal fluid (CSF) abnormality noticed was an elevated protein concentration. MRI showed non-specific right frontal lobe pial enhancement. Remaining infectious, rheumatologic, and neurologic testing was unremarkable. The patient was started on a steroid regimen with successful resolution of symptoms and return of cognitive baseline. Hashimoto’s encephalopathy is a diagnosis of exclusion; however, it should be considered in patients with high titers of anti-thyroid antibodies and neurological symptoms that cannot be explained by thorough infectious, metabolic, and autoimmune testing. It is essential to recognize this neurological entity as fast clinical improvement may be achieved with steroids and other immunotherapies.
Highlights
Hashimoto encephalopathy (HE), known as steroid-responsive encephalopathy with autoimmune thyroiditis (SREAT), is a clinically heterogeneous neurological syndrome that is commonly associated with Hashimoto thyroiditis [1]
Hashimoto encephalopathy has been associated with Hashimoto thyroiditis; some pundits argue this relationship may be confounded by elevated titers of anti-thyroid antibodies occurring in up to 20% of healthy individuals [5, 6]
Hashimoto encephalopathy should be suspected in patients with unexplained neurological syndromes and a history of thyroid disorder or elevated anti-TPO antibodies
Summary
Hashimoto encephalopathy (HE), known as steroid-responsive encephalopathy with autoimmune thyroiditis (SREAT), is a clinically heterogeneous neurological syndrome that is commonly associated with Hashimoto thyroiditis [1]. She described a one-month history of mild, dull, constant headache in the bilateral temporal area radiating to the jaw, not associated with nausea, vomiting, or photophobia. CSF - cerebrospinal fluid; RPR - rapid plasma reagin; VDRL - venereal disease research laboratory; HBV - hepatitis B virus; HCV - hepatitis C virus; ANA - antinuclear antibody; ANCA - antineutrophil cytoplasmic antibody; PCR - polymerase chain reaction; CMV - cytomegalovirus; HSV - herpes simplex virus; HHV - human herpes virus; HPV - human papillomavirus; VZV - varicella zoster virus; AGNA - anti-glial nuclear antibody; ANNA - antineuronal nuclear antibody; CRMP - collapsin response-mediator protein; IgG - immunoglobulin G; PCA - Purkinje cell antibody; AMPAR-Ab - Alpha-Amino-3-Hydroxyl-5-Methyl-4-Isoxazolepropionic acid receptor Ab; CASPR2 - contactin-associated protein-2; DDPX - dipeptidylpeptidase–like protein 6; GAD65 - glutamic acid decarboxylase 65; GFAP IFA - glial fibrillary acidic protein immunofluorescence assay; LGI1 - leucine‐rich glioma‐inactivated 1; mGluR1 - metabotropic glutamate receptor 1; NMDA-R - anti-N-methyl D-aspartate receptor; LCM - lymphocytic choriomeningitis. Upon reassessment in an outpatient setting, the patient showed significant improvement in the cognitive evaluation and denied any further headaches or breakthrough seizures for more than 10 months
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