Motor nerve conduction (amplitude reduction) becomes impaired in 7 to 10 days, as described earlier. The lesions are presumably of axonal type, and electrophysiologic features of denervation follow. There are highly restricted forms that affect only one or two nerves of the brachial plexus, as mentioned earlier. The most common of these is probably an isolated palsy of the serratus anterior (long thoracic nerve). The suprascapular, axillary, posterior interosseus, and phrenic nerves are other occasional sites of solitary neuritis. In the case of a unilateral phrenic nerve paralysis, there is mild dyspnea on exertion and one hemidiaphragm is found to be elevated on the chest radiographs. When the process is not progressive and no mediastinal lesion can be detected with extensive imaging, a phrenic palsy can be assumed to fall into this idiopathic category. We have seen a Horner syndrome in association with brachial neuritis but this finding is always of greater concern as a sign an infiltrating neoplasm or granulomatous process.
We have had experience with patients who had this syndrome following parvovirus B19 infection, as has been cited in the literature. Most cases had been preceded within days by an erythematous rash spreading from the limbs to the trunk and face, somewhat similar to the eruption of fifths disease caused by this virus in children. One of our patients had no premonitory features, but her child had just recovered from fifth disease (parvovirus) by the pediatrician. Some reported patients have had preceding influenza-like symptoms and adenopathy as well. A summary of cases that have appeared in the literature can be found in the paper by Maas and coworkers. Duchowny and colleagues described a patient in whom a typical brachial neuritis occurred as part of a febrile illness that proved to be caused by a CMV infection and the same has been observed (albeit rarely) in patients with HIV. A few outbreaks of brachial neuritis have been recorded and prompted the suggestion that the Coxsackievirus was the cause. Whether Lyme infection can cause brachial neuritis is unsettled, but we have seen at least one instance that was more of a cervical radiculopathy—there was a pleocytosis in the CSF. The therapeutic use of interleukin-2 and interferon has apparently precipitated a few cases. In the past, when animal antisera were in common use, this entity was frequent; in the modern era it has been seen rarely after injection of tetanus toxoid, typhoid-paratyphoid vaccine, and triple vaccine (pertussis, diphtheria, and tetanus).
Plexitis also occurs as an uncommon idiopathic complication of the postpartum state (Lederman and Wilbourn, 1996). Some of these are repetitive or bilateral and some are familial, but otherwise the plexopathy has no distinguishing features from the idiopathic type. The heredofamilial variety is described later.
One must differentiate idiopathic brachial plexitis from the following conditions: (1) spondylosis or ruptured disc with root compression, particularly the C5 and C6 roots, in which paralysis is rarely as severe as it is in plexitis; (2) brachialgia from bursitis, labral tear, or rotator cuff syndrome; (3) polymyalgia rheumatica; (4) entrapment neuropathies, particularly of the subscapular or dorsal scapular nerve; (5) carcinomatous plexopathy; (6) radiation plexopathy; and (7) sarcoid and other granulomatous infiltrations. Dissection of the vertebral artery may rarely simulate the pain and weakness of brachial neuritis (Berroir et al).