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The distribution of neuralgic amyotrophy lesions is overwhelmingly extraplexal

Neuralgic amyotrophy is a disorder of the peripheral nervous system (PNS) that is associated with a wide range of clinical phenotypes. For this reason, roughly 2 dozen terms have been applied to it, some reflecting the muscle involved (serratus magnus palsy) and others reflecting the presumed lesion site (idiopathic brachial plexitis, idiopathic brachial neuritis). In 1948, Parsonage and Turner recognized that all of these entities represented the same disorder and introduced the term neuralgic amyotrophy to highlight its 2 quintessential features, severe pain and pronounced muscle wasting. In addition to these 2 features, an antecedent event (trigger) is often identified. In the presence of this unifying triad (antecedent event, severe pain, and pronounced muscle wasting), neuralgic amyotrophy is easily recognized. Regarding its localization, although most investigators initially considered neuralgic amyotrophy to be a brachial plexus disorder, many authors have since speculated that at least some of the time it behaves more like an extraplexal disorder. Others, on the basis of both clinical and electrodiagnostic (EDX) findings, have suggested that it rarely involves the brachial plexus and, instead, represents an extraplexal disorder of the forequarter region of the body that presents as either a mononeuropathy or a multiple mononeuropathy, depending on the number of individual nerves involved. We recently evaluated the lesion distribution among 281 patients with sporadic neuralgic amyotrophy. In that study, 699 of 703 lesions were extraplexal nerve lesions; only 4 involved the brachial plexus. The extraplexal lesions had a mononeuropathy (46%) or a multiple mononeuropathy (54%) distribution. Consistent with the belief that neuralgic amyotrophy has a predilection for motor axons, the incidence of nerve involvement in that study reflected the percentage of motor axons composing the nerve as follows: pure motor nerves (e.g., suprascapular, long thoracic, distal motor branch, anterior interosseous)>predominantly motor nerves (e.g., axillary, musculocutaneous)>>mixed nerves (e.g., median, ulnar, radial)>> cutaneous sensory nerves (e.g., lateral antebrachial cutaneous). As a result of this motor axon predilection, nerves innervating the shoulder girdle muscles are frequently involved. Whenever 2 or more such nerves are involved, an upper plexus localization is suggested. However, unlike upper plexopathies, in which nerve conduction study abnormalities are simultaneously present in both the lateral antebrachial cutaneous nerve and the median sensory nerve recording from the thumb 96% of the time, this pattern is unexpected with neuralgic amyotrophy; in our study of 281 patients, it was never observed. In addition to EDX studies, imaging studies are also frequently employed in the evaluation of neuralgic amyotrophy patients, not only to assess the brachial plexus but also to exclude mimicking entities. In this issue of Muscle & Nerve, Sneag et al., having used high-resolution MRI, report the MRI manifestations of neuralgic amyotrophy in 27 patients. Through a retrospective search of the imaging database of their institution, they identified 27 patients with clinically and electrodiagnostically confirmed neuralgic amyotrophy. The clinical and EDX findings in these patients indicated 38 extraplexal (nerve) lesions. None of the clinical or EDX assessments suggested brachial plexus involvement. Among these 38 nerve lesions, 37 were based on both clinical and EDX assessments and 1 was based on clinical assessment alone (this patient had presented with a suprascapular mononeuropathy, the classic triad of neuralgic amyotrophy, and did not undergo EDX assessment). Two radiologists independently assessed the brachial plexus MRI studies, which included the preterminal (e.g., suprascapular) and terminal (e.g., musculocutaneous) nerves of the brachial plexus whenever they were present within the field of view of the study. Correspondence to: M. A. Ferrante; e-mail: mafmd1@gmail.com