We read with great interest the article by Lo et al. [1], who compared median nerve conduction among patients with only symptoms, patients with sole cases of carpal tunnel syndrome (CTS), and patients with double crush syndrome (DCS). As no significant difference was observed between the latter two, the authors believe that there is no substantive evidence supporting double crush hypothesis. However, we ask for clarification of some issues. First, the distal nerve lesion in patients with DCS should not necessarily be more severe than those with isolated CTS. According to Upton and McComas [2], the proximal compression of a nerve may impair axonal flow and lessen the ability of the nerve to withstand a more distal compression. This theory emphasizes the higher vulnerability of the distal nerve caused by the proximal lesion rather than accumulate it. If so, even less compression of the median nerve at carpal tunnel may be required to produce a symptomatic CTS. Therefore, the similar median nerve conduction in patients with DCS or isolated CTS, as described in this study, may not be regarded as evidence against double crush hypothesis. In a prospective study of DCS, Osterman [3] also observed that the motor distal latency at the carpal tunnel area was similar in both DCS and isolated CTS patients, the slowing of distal sensory latency was even more pronounced in the latter. Second, when diagnosing a DCS, the proximal and distal lesions should have damaged the same axons [4]. The fibers of median nerve, including those traversing carpal tunnel, originate from four roots (C6, C7, C8, and T1) of brachial plexus. Due to its extensive proximal origin, two focal nerve lesions along the median nerve pathway do not automatically fulfill this anatomic criterion of DCS, unless the same axons are compromised at both sites. When the proximal and distal lesions would not have damaged the same axons, e.g., a C5 cervical radiculopathy (CR) and a CTS, DCS could not be diagnosed. Likewise, a C6 CR and a CTS, in which nerve conduction slowing affect only motor distal nerve, were also not a DCS. In this article, the detail information about the segment of CR was not provided, so was the diagnostic criteria of DCS. The coexistence of CR and CTS, according to our opinion, may be too nonspecific to validate the diagnosis of DCS. Third, nerve conduction slowing is a pathophysiological change caused by demyelination rather than by axon loss. As DCS is a pattern of axon loss, the uniformly reduction of amplitudes of compound muscle action potential may have more diagnostic significance [5]. In this study, however, only the nerve conduction was investigated, and there is insufficient evidence to support DCS existing as a clinical entity. Overall, it is an interesting study, and we thoroughly enjoy reading this article.