# Recurrent bilateral brachial plexus neuritis following rapid semaglutide-induced weight loss: a case report

## TL;DR

A man experienced recurrent brachial plexus neuritis after rapid weight loss with semaglutide, suggesting a possible link between the drug and this condition.

## Contribution

This case report is the first to suggest a possible association between semaglutide use and brachial plexus neuritis.

## Key findings

- A 39-year-old man developed bilateral brachial plexus neuritis following significant semaglutide-induced weight loss.
- Corticosteroids provided pain relief, but motor and sensory deficits persisted despite physiotherapy.
- The case suggests a temporal link between rapid weight loss via semaglutide and recurrent brachial plexus neuritis.

## Abstract

Brachial plexus neuritis, or Parsonage–Turner syndrome, is an uncommon neuropathy marked by acute pain followed by weakness, often triggered by infection, vaccination, trauma, or metabolic stress but the exact cause of this disease remained unknown. Semaglutide is widely used for the treatment of type 2 diabetes and obesity. With its increasing use, there have been reports suggesting a possible association with neuropathies. Currently, there is no information suggesting a possible association between the use of semaglutide and brachial plexus neuritis.

A 39-year-old man with a prior episode of unilateral brachial neuritis developed recurrent bilateral upper limb weakness after an eight-month, 70-pound semaglutide-associated weight loss. He presented with bilateral radial sensory loss, finger extensor paralysis, right triceps weakness and decreased grip strength on the left side. Corticosteroids provided pain relief, but motor and sensory deficits persisted despite physiotherapy.

This case highlights a temporal association between rapid pharmacologic weight loss and recurrent idiopathic brachial plexus neuritis, emphasizing the importance of gradual, nutritionally supported weight reduction and vigilance for neuromuscular complications during GLP-1 receptor agonist therapy.