• William E Clifton, Jonathan J Stone, Neeraj Kumar, Tomas Marek, and Robert J Spinner.
• Department of Neurological Surgery, Mayo Clinic, Jacksonville, Florida, USA.
• World Neurosurg. 2019 Feb 1; 122: e1562-e1569.

BackgroundCervical and upper thoracic nerve root avulsions are preganglionic lesions that occur after extreme traction of the brachial plexus. The tearing of the roots from the spinal cord pia leads, not only to immediate and permanent deficits, but also to delayed neurologic complications. Symptomatic myelopathy can present in a late fashion owing to chronic sequelae from the inciting traumatic event. No unifying theory has yet been provided that can explain the causes of delayed spinal cord dysfunction after preganglionic brachial plexus injury. We have proposed a collective mechanism for the development of delayed spinal cord injury.MethodsAn institutional database search and a literature review were performed to find patients who had presented with delayed myelopathy after brachial plexus injury.ResultsWe found 454 adult patients with traumatic brachial plexus injury and spinal cord injury from 1997 to 2018 in the institutional search. Of these patients, 74 had a delayed presentation of new myelopathic findings on physical examination that had developed ≥6 months after the initial presentation. In these 74 patients with delayed myelopathic symptoms, radiologic findings of spinal cord herniation, syringomyelia, superficial siderosis, or pathologic intradural or extradural cerebrospinal fluid collections from traumatic dural tears were present. Each of these pathologic entities was present in isolation or combination in our patient population.ConclusionsFour overlapping etiologies appeared to compose the primary foundation for delayed spinal cord dysfunction after brachial plexus injury. We have highlighted this continuum by providing institutional case examples and a review of the reported data.Copyright © 2018 Elsevier Inc. All rights reserved.

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