Ultrasound-guided botulinum neurotoxin injections for thoracic outlet syndrome

Abstract

Introduction Thoracic outlet syndrome (TOS) is a rare, often perplexing disorder caused by compression of neurovascular structures, leading to cervicogenic–brachial pain and other symptoms in neck and upper limb. Thoracic outlet syndrome is a group of disorders, not a single disorder, and patients may present with a wide variety of signs and symptoms. The wide range of symptoms and signs in TOS may confound clinicians unfamiliar with this condition (Sanders et al ., 2008; Ferrante, 2012; Foley et al ., 2012). Again, because TOS is a group of disorders, there is no “gold standard” to establish the diagnosis. This may lead to misdiagnosis or overdiagnosis of TOS in patients who present with symptoms suggesting TOS but who have other causes for their symptoms. It is, therefore, imperative that physicians be familiar with the range of symptoms and signs of TOS and testing that either supports or refutes this diagnosis. It is also critical that the diagnosis be correctly established before proceeding to invasive interventions for a presumed diagnosis of TOS, including botulinum neurotoxin (BoNT) injections. One of the many emerging applications for BoNT therapy is for the treatment of musculoskeletal pain disorders, including TOS. While the efficacy of BoNT on decreasing pain associated with cervical dystonia and chronic migraine is established, the antinocioceptive mechanism of action of BoNT is not fully understood (Mense, 2004; Aoki, 2005). Reports of reduced pain with BoNT have been reported in various musculoskeletal pain disorders, including joint pain, myofascial pain and cerebral palsy (Barwood et al ., 2000; Gobel et al ., 2006; Singh et al ., 2009). Although there are numerous reports in the literature citing the efficacy of BoNT for pain and other symptoms associated with TOS, additional research is needed to establish the role of BoNT in TOS and other pain disorders (Jordan et al ., 2007; Danielson and Odderson, 2008; Torriani et al ., 2010; Foley et al ., 2012). The proposed mechanism of action includes reduced muscle spasm leading to decreased compression of neurovascular structures (Jordan et al ., 2007; Tsao, 2007; Danielson and Odderson, 2008). Injection of BoNT into muscles also leads to denervation atrophy, which may reduce compression and neurogenic or vasogenic symptoms. It has also been reported that BoNT reduces the release of nocioceptive neurotransmitters, which could also be a contributing factor in reduced pain in TOS.