{"title":"Serratus anterior palsy secondary to long thoracic nerve dysfunction","authors":"Pablo Sanchez-Urgelles MD , Blanca Diez Sánchez MD , Joaquin Sanchez-Sotelo MD, PhD","doi":"10.1016/j.xrrt.2025.01.011","DOIUrl":null,"url":null,"abstract":"<div><h3>Background</h3><div>Paralysis of the serratus anterior (SA) is most frequently caused by dysfunction of the long thoracic nerve (LTN). Although this condition presents with classic physical examination findings, it is occasionally missed. The purpose of this study is to review the etiology, diagnosis, and treatment options for SA palsy.</div></div><div><h3>Methods</h3><div>This study summarizes the anatomy of the SA and LTN, most common causes of SA palsy, physical examination findings, utility of diagnostic tests, the natural history of this condition, and all treatment options that can be contemplated.</div></div><div><h3>Results</h3><div>SA palsy should be suspected in patients with weak forward flexion and abnormal prominence of the medial edge of the scapula with weakness in shoulder protraction. The diagnosis can be confirmed with electromyography and nerve conduction studies. Magnetic resonance may show neurogenic fatty infiltration or atrophy. Although most patients benefit from conservative treatment (mostly physical therapy) for the first 12 months, many patients experience persistent weakness with various degrees of severity. For patients with disabling symptoms, nerve release or transfers have been reported to lead to SA reinnervation with functional improvements. However, long-standing palsy is best managed with a split pectoralis major transfer of the sternal head to the inferior pole of the scapula. Scapulothoracic arthrodesis is an uncommon procedure for patients in whom a previous tendon transfer has failed.</div></div><div><h3>Conclusion</h3><div>LTN dysfunction leading to SA palsy can be typically diagnosed with certain physical examination findings and confirmed using electromyogram with nerve conduction studies. Although spontaneous recovery can occur, patients with persistent serratus weakness may be considered for neurolysis, nerve transfer, or tendon transfer. Currently, direct transfer of the sternal head of the pectoralis major to the inferior pole of the scapula is our management of choice for patients with disabling symptoms and no improvement despite a good program of physical therapy.</div></div>","PeriodicalId":74030,"journal":{"name":"JSES reviews, reports, and techniques","volume":"5 2","pages":"Pages 170-181"},"PeriodicalIF":0.0000,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"JSES reviews, reports, and techniques","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S2666639125000343","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"Medicine","Score":null,"Total":0}
引用次数: 0
Abstract
Background
Paralysis of the serratus anterior (SA) is most frequently caused by dysfunction of the long thoracic nerve (LTN). Although this condition presents with classic physical examination findings, it is occasionally missed. The purpose of this study is to review the etiology, diagnosis, and treatment options for SA palsy.
Methods
This study summarizes the anatomy of the SA and LTN, most common causes of SA palsy, physical examination findings, utility of diagnostic tests, the natural history of this condition, and all treatment options that can be contemplated.
Results
SA palsy should be suspected in patients with weak forward flexion and abnormal prominence of the medial edge of the scapula with weakness in shoulder protraction. The diagnosis can be confirmed with electromyography and nerve conduction studies. Magnetic resonance may show neurogenic fatty infiltration or atrophy. Although most patients benefit from conservative treatment (mostly physical therapy) for the first 12 months, many patients experience persistent weakness with various degrees of severity. For patients with disabling symptoms, nerve release or transfers have been reported to lead to SA reinnervation with functional improvements. However, long-standing palsy is best managed with a split pectoralis major transfer of the sternal head to the inferior pole of the scapula. Scapulothoracic arthrodesis is an uncommon procedure for patients in whom a previous tendon transfer has failed.
Conclusion
LTN dysfunction leading to SA palsy can be typically diagnosed with certain physical examination findings and confirmed using electromyogram with nerve conduction studies. Although spontaneous recovery can occur, patients with persistent serratus weakness may be considered for neurolysis, nerve transfer, or tendon transfer. Currently, direct transfer of the sternal head of the pectoralis major to the inferior pole of the scapula is our management of choice for patients with disabling symptoms and no improvement despite a good program of physical therapy.