2026 American Academy of Neurology Abstract Website

Objective:

To describe a case of severe sensorimotor polyneuropathy secondary to thiamine deficiency induced by semaglutide-associated malnutrition, emphasizing the importance of early recognition and intervention.

Background:

Dry beriberi, a neurologic manifestation of thiamine deficiency, presents as a symmetric, length-dependent polyneuropathy that may mimic acute neuromuscular syndromes such as Guillain-Barré and Miller Fisher syndromes. While rare in developed countries, thiamine deficiency may occur in patients with effective malnutrition from causes such as persistent vomiting. Glucagon-like peptide-1 (GLP-1) receptor agonists, including semaglutide, can cause significant gastrointestinal side effects leading to malnutrition and, in rare cases, micronutrient deficiencies.

Design/Methods:

We report a 65-year-old woman with type 2 diabetes, obesity, and multiple comorbidities who developed profound weakness, dysphagia, and cranial nerve deficits following several months of semaglutide use associated with intractable nausea, vomiting, and >90-pound weight loss. Neurologic evaluation, cerebrospinal fluid analysis, and electromyography (EMG) were performed. High-dose thiamine was administered empirically while further diagnostic studies were pending.

Results:

EMG demonstrated absent sensory responses with mild motor slowing, consistent with severe sensory neuropathy and possible motor involvement. Following initiation of intravenous thiamine (500 mg three times daily), the patient experienced improvement in cognition, bulbar strength, lower limb power, and tolerance for oral intake over one week. This significant recovery, though not completely back to the patient's baseline, reinforced the critical role of early empiric therapy in potentially reversible nutritional neuropathies.

Conclusions:

This case illustrates a severe but reversible neurologic complication of semaglutide-induced malnutrition. Persistent gastrointestinal symptoms in patients receiving GLP-1 receptor agonists should prompt evaluation for nutritional deficiencies, including thiamine. Early empiric thiamine supplementation is critical, as prompt recognition and treatment can prevent irreversible neurologic injury. Clinicians should maintain a high index of suspicion and maintain a broad differential including malnutrition for patients with neuropathies on GLP-1 agonists, as rapid intervention can restore neurologic function and avert long-term disability.