SAT-384 - Progressive Weakness in Thyrotoxic Periodic Paralysis: A Case of Overlapping Inflammatory Neuropathy

Background
Thyrotoxic periodic paralysis (TPP) is a rare complication of thyrotoxicosis characterized by hypokalemia and acute muscle weakness. While the severity of neuromuscular symptoms in TPP does not always correlate with the degree of thyrotoxicosis, progression of neuromuscular symptoms despite thyroid-directed therapy should prompt evaluation for alternative or overlapping etiologies.
Case Description
A 54-year-old woman presented with several weeks of progressive lower-extremity weakness with recurrent falls, ultimately becoming bedbound. On presentation, she was hemodynamically stable with mild tachycardia. Neurologic exam showed severe symmetric lower-extremity weakness with preserved upper-extremity strength, intact sensation, normal tone, preserved upper-extremity and patellar reflexes, and absent ankle reflexes. Initial labs revealed severe hypokalemia (2.6 mmol/L), hypomagnesemia, normal phosphate and CK, and elevated inflammatory markers (ESR and CRP). Thyroid studies demonstrated biochemical thyrotoxicosis (TSH < 0.01 μIU/mL; fT4 2.14 ng/dL), which appeared mild relative to the severity of weakness. The etiology of thyrotoxicosis was unclear, with negative TRAb testing and no clinical features of Graves disease. A 24-hour urine potassium collection showed low urinary potassium excretion, consistent with intracellular potassium shift and supportive of TPP. Additional endocrine evaluation showed normal ACTH and DHEAS levels, and dexamethasone suppression testing excluded Cushing syndrome. Thoracic spine MRI demonstrated multilevel degenerative changes without cord compression or structural findings to explain the weakness.
She was treated with methimazole and electrolyte repletion, with only slight symptomatic improvement and no return to baseline function. Despite partial biochemical improvement, weakness persisted for several days, raising concern for an overlapping neuromuscular process. Chronic Inflammatory Demyelinating Polyradiculoneuropathy (CIDP) was considered. CSF analysis showed mildly elevated protein without pleocytosis, and empiric IVIG resulted in rapid improvement in lower-extremity strength within 24–48 hours, with only mild residual asymmetric distal weakness, supporting a coexisting inflammatory neuropathy.
Conclusion
Severe neuromuscular weakness may occur in the setting of mild thyrotoxicosis and may be multifactorial. Although initial findings supported TPP, incomplete recovery, inadequate response to thionamides, and a robust response to IVIG were consistent with a concurrent inflammatory neuropathy. Maintaining a broad differential when weakness is disproportionate to thyroid hormone abnormalities is essential, as early recognition of overlapping etiologies can change management and outcomes.

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