Tirzepatide-Induced Rapid Weight Loss Linked to Brachial Plexopathy in a 60-Year-Old Man

Rapid weight loss is a known risk factor for compressive peripheral neuropathies, including brachial plexopathy, due to reduced protective adipose tissue and altered biomechanics. Tirzepatide, a dual GLP-1R and GIPR agonist, is highly effective for weight reduction and type 2 diabetes mellitus management, leading to significant and often rapid weight loss. While its metabolic benefits are well-established, the potential for exacerbating or precipitating neuropathic conditions in the context of rapid weight loss warrants investigation. This case highlights a possible rare adverse event, emphasizing the need to consider neurological symptoms during intensive weight management.

This case report describes a 60-year-old right-handed man with a history of hypertension and hypercholesterolemia who developed neuromuscular symptoms after initiating tirzepatide treatment. The patient received tirzepatide for a 6-month course. During this period, his clinical course was monitored for weight changes and any emerging symptoms. Diagnostic evaluations included electromyography (EMG) and nerve conduction studies (NCS) to assess nerve function, and imaging studies to rule out structural causes of neuropathy. Conservative interventions were attempted before discontinuation of the medication.

During 6 months of tirzepatide treatment, the patient experienced a significant weight loss of 60 pounds. Concurrently, he developed right-sided brachial plexopathy symptoms, including scapular pain, paresthesia, and progressive triceps weakness. Imaging studies of the affected area were unremarkable, ruling out structural compression. Despite initial conservative interventions, symptoms persisted. However, after the tirzepatide regimen was ended, the patient's condition gradually improved. At 2 months post-cessation, his pain score decreased significantly from 5/10 to 1-2/10, and his strength also improved. Follow-up EMG/NCV demonstrated the resolution of the denervation-caused changes, supporting the association with tirzepatide discontinuation.

Electromyography and nerve conduction studies confirmed denervation potentials at the right C5-C7 roots, consistent with brachial plexopathy.