Brachial Plexopathy: Patterns and Pathogenesis
Abstract & Commentary
By Michael Rubin, MD, Professor of Clinical Neurology, NewYork-Presbyterian Hospital, Cornell Campus. Dr. Rubin is on the speaker's bureau for Athena Diagnostics, and does research for Pfizer and Merck.
Synopsis: The most common etiology of brachial plexopathy is Parsonage-Turner syndrome.
Source: Moghekar AR, Karli N, et al. Brachial plexopathies: etiology, frequency, and electrodiagnostic localization. J Clin Neuromuscl Dis 2007;9:243-247.
Between february 1999 and october 2003, 203 patients evaluated at the Electromyography (EMG) Laboratory of Johns Hopkins Hospital were diagnosed with brachial plexopathy, based on a history of acute or subacute onset of weakness or numbness in one or more regions of the brachial plexus that was confirmed electrodiagnostically. Nerve conduction studies encompassed study of the median and ulnar motor nerves, and the median, ulnar, radial, and medial and lateral antebrachial cutaneous sensory nerves. Needle EMG encompassed examination of all muscles necessary for localization, and electrodiagnostic criteria for plexus localization included a combination of sensory and motor nerve amplitude loss with evidence of denervation in appropriate muscles. Etiology was determined through records obtained from the referring physicians.
Men outnumbered women 125 to 78. Plexopathy was unilateral in 181, without side predominance, and bilateral in 22, of which 19 were idiopathic (Parsonage-Turner syndrome), and 3 were radiation induced. Overall, Parsonage-Turner syndrome was the most common etiology, diagnosed in 81 patients (40%). Birth trauma, usually affecting the upper trunk; or direct trauma, most often involving all 3 trunks, accounted for 22% and 20%, respectively (n=45 and 40). Post-surgical plexopathy due to faulty positioning (n=16, 8%), post-radiation (n=11, 5%), neoplastic (n=7, 3.5%), and cervical rib (n=3, 1.5%) accounted for the remaining cases. Supraclavicular localization involving the trunks (n=189, 93%) was more frequent than infraclavicular involvement affecting the cords and branches (n=14, 7%). Purely upper trunk plexopathy (n=54, 27%) was more prevalent than involvement of all 3 trunks (n=51, 25%) or only the lower trunk (n=23, 11%). Exclusive middle trunk plexopathy was not seen. Nerve conduction studies revealed motor abnormalities more often than sensory, always axonal, and never primarily demyelinating in nature.
Of note, 47% of Parsonage-Turner syndrome patients experienced no pain prior to onset, and 57% had no identifiable antecedent precipitant. Focal involvement of a single trunk or nerve branch (bilateral phrenic nerve [n=4], suprascapular [n=3], long thoracic [n=7], was more likely in Parsonage-Turner syndrome than in other causes of brachial plexopathy. Post-radiation plexopathy most often involved all 3 trunks (8/11); however, post-surgical cases were more diverse in localization, with almost any combination equally likely. Pain was a feature in only 3 of 11 post radiation patients and 1 of 7 neoplastic cases.
Depressed sensory nerve action potential (SNAP) amplitude or absent sensory response on nerve conduction studies identifies a lesion as distal to the dorsal root ganglion. When documented in the appropriate clinical setting, such findings confidently localize the lesion to the brachial plexus. In the absence of sensory nerve abnormalities, a radicular localization remains possible. In a retrospective study of 56 brachial plexopathy patients (in the interest of full disclosure, published by this reviewer), the yield of sensory nerve abnormalities was increased (up to 82.5%) when sensory nerves sharing the distribution of motor nerve abnormalities were specifically studied.1 For example, the lateral cutaneous nerve of the forearm should be included in any study of suspected upper trunk lesions, and the medial cutaneous nerve of the forearm in suspected lower trunk/medial cord plexopathy. Targeting sensory nerves for study in this manner enhances the accuracy of brachial plexopathy diagnosis.
1. Rubin M, Lange DJ. Eur Neurol 1992;32:245-247.