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SYNOPSIS: This careful analysis of MRI imaging of the brachial plexus in patients with well-defined Parsonage-Turner Syndrome showed that the lesions are in peripheral branches of the brachial plexus and not in the roots or cords.
SOURCE: Sneag DB, Schneider KR, Wolfe SW, et al. Brachial plexitis or neuritis? MRI features of lesion distribution in Parsonage-Turner syndrome. Muscle Nerve 2018 Feb. 20; doi: 10.1002/mus.26108. [Epub ahead of print].
Considered an inflammatory disorder of the brachial plexus affecting children and adults, Parsonage-Turner syndrome (PTS) also is referred to as neuralgic amyotrophy, brachial neuritis, idiopathic brachial plexopathy, brachial plexus neuropathy, and acute brachial radiculitis. As biopsy or autopsy in these cases is rare, pathology and etiology remain speculative, although an immune-mediated process is hypothesized, with up to 50% of patients reporting an antecedent event including strenuous exercise, infection, pregnancy, vaccination, or surgery. Although some patients may have involvement of single or multiple nerves in the limb, resembling mononeuritis or mononeuritis multiplex, the distribution sometimes suggests focal involvement of a part, or parts, of the brachial plexus. Is this anatomically accurate?
To address this question, Sneag et al conducted a retrospective search of the imaging database at the Hospital for Special Surgery in New York, for MRI scans of the brachial plexus in patients with suspected PTS. Only those performed with a 3.0 T magnet and those with fat-suppressed, T2-weighted sequences orthogonal to the longitudinal course of the nerve were collected. All patients who met imaging criteria were reviewed to confirm the diagnosis of PTS based on clinical history, physical examination, and electrodiagnostic findings, the latter encompassing a complete or near complete pattern of denervation, with absent or reduced interference pattern on needle electromyography, and nerve conduction studies showing no evidence of multifocal motor neuropathy or other generalized neuropathy that might mimic PTS. Patients were excluded if comorbidities or alternative diagnoses could not be excluded. Investigators reviewed brachial plexus MRI scans were reviewed at every level of the plexus for fascicular morphology, signal intensity, and size, as well as for edema or fatty infiltration of regional muscles. Side and terminal branches of the plexus and more peripheral nerves also were evaluated for the presence of hourglass constrictions, defined as a short segment of decreased nerve caliber.
Among 87 MRI studies, 35 met MRI inclusion criteria, of which eight were excluded because of alternative diagnoses, including cervical radiculopathy (n = 4), diabetic neuropathy (n = 1), hereditary neuropathy with liability to pressure palsies (n = 1), or insufficient electromyography (EMG) data (n = 2). Of the 27 subjects who met all inclusion criteria, 19 were men and eight were women, with a mean age of 42 years. EMG revealed abnormalities in 37 nerves, half of which comprised an isolated mononeuropathy, usually the suprascapular nerve, and no abnormality localized to the brachial plexus proper, roots or cords, on electrodiagnostic studies. MRI of the brachial plexus was normal in 24 of 27 patients. Two of the remaining three cases comprised isolated suprascapular nerve involvement clinically, with MRI in one patient demonstrating signal hyperintensity in the suprascapular nerve extending proximally to the extra-foraminal C5 nerve root, 3.5 cm lateral to the neural foramen, and, in the other, signal hyperintensity of the nerve extending into the superior trunk, proximal to the suprascapular nerve take-off. In the third patient, signal hyperintensity was seen in the axillary nerve extending proximally into the posterior cord. Intrinsic constrictions were seen in 32 of 38 nerves, with hyperintensity and enlargement of imaged nerves and muscle denervation edema present in all patients. PTS appears to affect either branches of the brachial plexus or more peripheral nerves rather than the brachial plexus proper.
No specific treatment exists for PTS. Physical therapy can maintain range of motion but does not hasten recovery. Often, analgesics are required to control pain, but steroids are of no demonstrable benefit. Approximately 60% of patients are left with residual pain or fatigue, even three years post-PTS, and recurrence may be seen in 25%, occurring in a median of just over two years following the initial event.
Financial Disclosure: Neurology Alert’s Editor in Chief Matthew Fink, MD; Peer Reviewer M. Flint Beal, MD; Executive Editor Leslie Coplin; Editor Jonathan Springston; and Editorial Group Manager Terrey L. Hatcher report no financial relationships relevant to this field of study.
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