"Isolated Long Thoracic Nerve Palsy": More Than Meets The Eye
Andrés A. Maldonado, MD, PhD1,2; Scott Zuckerman, MD3; B. Matthew Howe, MD4; Michelle Mauermann, MD2; Robert J. Spinner, MD5
1BG Unfallklinik, Frankfurt, Germany, 2Mayo Clinic, Rochester, MN, 3Vanderbilt University Medical Center, Nashville, TN, 4Radiology, Mayo Clinic, Rochester, MN, 5Neurosurgery, Mayo Clinic, Rochester, MN
Introduction: Two main hypotheses have been proposed for the pathophysiology of long thoracic nerve (LTN) palsy: nerve compression and nerve inflammation. We hypothesized that critical reinterpretation of electrodiagnostic (EDX) studies and MRIs of patients with a diagnosis of non-traumatic isolated LTN palsy could provide insight into the pathophysiology and, potentially, the treatment.
Material and methods: A retrospective review was performed of all patients with a diagnosis of non-traumatic isolated LTN palsy and an EDX and brachial plexus or shoulder MRI studies performed at our institution. The original EDX studies and MR examinations were reinterpreted by a neuromuscular neurologist and musculoskeletal radiologist, respectively, both blinded to our hypothesis.
Results: Seven patients met the inclusion criteria as having a non-traumatic isolated LTN palsy. Upon reinterpretation, all of them were found to have findings not consistent with an isolated LTN. On physical examination, three of them (43%) presented with weakness in muscles not innervated by the LTN. Four of them (57%) had additional EDX abnormalities beyond the distri- bution of the LTN. Five of them (71%) had MRI evidence of enlargement of nerves or denervation atrophy of muscles outside the innervation of the LNT, without evidence of compression of the LTN in the middle scalene muscle.
Conclusion: In our series, all 7 patients presented with at least one finding incompatible with isolated compression of the LTN. These data would favor an underlying inflammatory pathophysiology.
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