Abstract
GLP-1 agonists have been a welcome addition to the armamentarium in the treatment of diabetes and obesity. While this class of medications is generally considered safe and effective, potentially severe neurological complications may be associated with rapid weight loss and nutritional deficiencies following GLP-1 agonist use. We present a 37-year-old woman who was prescribed semaglutide for diabetes and weight loss who subsequently experienced significant weight reduction and rapid glycemic control over three months. Thereafter, she developed progressive right leg numbness and weakness, followed by similar symptoms in the left leg, and blurred vision. Initially diagnosed with B12 deficiency, her symptoms worsened despite supplementation, leading to acute encephalopathy and transfer to a tertiary center. Neurological examination revealed disorientation, ocular abnormalities, weakness, sensory deficits, and preserved ankle jerks. Diagnostic workup was notable for thiamine deficiency, NCS/EMG showing a severe, axonal polyneuropathy, and nerve biopsy redemonstrating severe axonal neuropathy. After extensive diagnostic workup, the most likely etiology of her clinical presentation was favored to be non-alcoholic Wernicke's encephalopathy (NAWE) and treatment-induced neuropathy of diabetes (TIND). This case suggests that vulnerable individuals may experience significant adverse neurological complications from the metabolic effects of GLP-1 agonist use. As a class effect, the benefits of these medications outweigh the risks, but their use warrants consideration of their potential sequelae.