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In 1973, after assessing a large group of patients with cervical root lesions (CRLs) and upper extremity peripheral entrapment neuropathies-either carpal tunnel syndrome (CTS), ulnar neuropathy at the elbow (UN-E), or both-Upton and McComas1 proposed that focal compression often occurs at more than one level along the course of a single nerve fiber. They proposed that under these circumstances a disturbance of axonal transport caused by compression at the proximal site (e.g., the cervical root) might impair the capacity of the nerve segment distal to it to resist further focal compressive injury. In this manner, an otherwise subclinical focal entrapment neuropathy (e.g., CTS) could be converted into a clinically evident one (figure 1). They assumed that this may occur even though the proximal lesion, while symptomatic, was not clinically severe. Thus, a cervical radiculopathy manifesting as little more than neck pain and stiffness could still precipitate a distal focal entrapment neuropathy. For this mechanism of nerve injury-serial compromise of axonal transport along the same nerve fiber, causing a subclinical lesion at the distal site to become symptomatic-they proposed the term double-crush syndrome (DCS). They acknowledged that this term was too restrictive because (1) the proximal focal disturbance could result from traction, rather than compression; (2) there could be more than two sites of injury along an axon; and (3) a generalized subclinical polyneuropathy, by reducing the amount of "trophic material manufactured by the perikaryon" in all peripheral nerve fibers, could serve as the proximal compression site.1
Figure 1. Diagram of the double-crush hypothesis of Upton and McComas. Shown is the perikaryon and axon, with the antegrade axoplasmic flow represented by an arrow (thickness of the arrow indicates amount of transported material). (A) Normal. (B) Severe distal injury causing axon death with degeneration. (C) Mild proximal compression causing only …
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