Abstract Thyrotoxic periodic paralysis manifests with painless muscle weakness, mostly in the proximal lower extremities. It is often precipitated byexercise, high carbohydrate meals, and occasionally fasting. Though most cases are hereditary, and affect Asian men disproportionately, some cases may occur sporadically. This thyrotoxicosis is most often attributable to Graves disease and patients typically have symptoms of thyrotoxicosis for months leading up to the episodes of paralysis. This is an 18-year-old Asian man with a history of Autism Spectrum Disorder who presents for evaluation of lower extremity weakness. He was seen two weeks prior for similar complaints. At that time, he had hypokalemia, hypomagnesemia, hypophosphatemia and was repleted and discharged home. The day prior to admission, he had pain in his bilateral posterior legs. On the morning of presentation, he could no longer ambulate which led him to present to the emergency room. Per his collateral, he had lost forty-five pounds in the last 6 months. He has not been tolerating oral food well with early satiety. He denies any diarrhea or constipation, fever/chills, or recent illness. He denies any family history of muscle disorders, thyroid disease, or any other autoimmune disease. He does not smoke tobacco, drink alcohol, or use any illicit substances. On physical exam, he is notably tachycardic to 120 bpm. He has thyromegaly but no palpable nodules. He has no exophthalmos on eye exam. On his neurologic exam, patient has 2/5 strength in his bilateral lower extremities. On laboratory evaluation, patient has fully suppressed TSH <0. 0015 mcunit/mL, free thyroxine of 3.43 ng/dL, total T3 of 463 ng/dL, TSI >40 IU/L, and TSH Receptor Antibody 31 IU/L. His potassium is low at 2.8 with a magnesium of 1.7. His thyroid ultrasound is without evidence of any nodules, has a homogenous parenchymal pattern, with increased vascularity diffusely. Patient is started on methimazole 20mg daily which is then increased to 20mg twice daily as well as propranolol 120mg daily, with plans for definitive therapy in the future. Though mechanism by which thyrotoxicosis can produce electrolyte abnormalities including hypokalemia leading to periodic paralysis is poorly understood, it is thought that thyroid hormone may increase tissue responsiveness to B-adrenergic stimulation like exercise or stress. This may lead to hyperpolarization of the muscle membrane and relative excitability. A variety of other factors play a role in the pathogenesis of thyrotoxic paralysis including insulin and testosterone through activation of the sodium potassium ATPase. Treatment for TPP includes aggressive electrolyte repletion, correction of the underlying cause with methimazole and propranolol-taking advantage of its beta adrenergic blocking ability, and often times planning for definitive therapy. Presentation: No date and time listed