In clinical practice, it is difficult to distinguish CTS from other neuropathic syndromes in diabetic patients, even when electrodiagnostic tests are also applied for such purposes
]. An enlargement of median nerve CSA measured in CTS hands is a well established US finding
], and with multiple-level CSA measurements, the complementary role of US in the diagnosis of CTS becomes more valuable
]. The same US findings were also noted in the present study which showed enlarged CSAs in patients with idiopathic CTS as well as in those with diabetic CTS and DPN CTS. There are reports
] of US studies of peripheral nerves in diabetic patients, however using US to measure the CSAs at 8 points such as in the “inching test” to assess CTS in diabetic patients has not been reported before.
The study results showed that the measured CSAs in both the diabetic and DPN groups were larger than those measured in the idiopathic and control groups. The BMIs of patients of the CTS groups were significantly larger than those of patients in the control group. It has been proposed that a higher BMI may increase the incidence of symptomatic CTS
], however a significant correlation with median nerve CSA measured at the wrist level was not found in the study of Werner et al.
]. It may deserve further investigations to demonstrate if a correlation exists between BMI and CSA in diabetic patients with CTS. BH was another statistically significant factor between the different groups. It has been proposed that a difference in BH may influence the result of nerve conduction velocity
], however it is not a known factor to influence the median nerve CSA
In US studies, different CSA cut-off values (9
) at the entry level (inlet) of the carpal tunnel have been reported for CTS confirmation in idiopathic CTS patients
]. In the present study, we revealed the cut-off values of CSAs measured at different levels of the patients with idiopathic, diabetic and DPN CTS. Although larger CSAs measured in the carpal tunnel 5
cm proximal to the wrist and elbow joint of the median nerve in diabetic and diabetic polyneuropathy patients were reported by Watanabe et al.
], comparative results of measured CSAs at the inlet level of diabetic patients have not been reported before. In the present study, we measured the CSAs within the carpal tunnel in the hands of the diabetic patients with CTS, and the results also showed larger CSAs when compared with the CSAs measured in both the control and idiopathic groups. Several factors are known to be contributing factors to CTS, including mechanical and ischemic factors, external epineurial and perineurial thickening and fibrosis
], and all of these factors may in-part explain the local enlargement of median nerve CSAs. However, as shown in this study, there may be additional factors contributing to the focal enlargement of median nerve CSAs in diabetic patients, and especially at the level of the inlet. In DM, the polyol pathway, glycation and proinflammatory reactions are known to contribute to the presence of diabetic peripheral nerve injuries
], and a reduction in myelinated nerve fibers and capillary density may predispose DM patients to the development of CTS
]. In addition, more ischemic and biochemical changes may further result in the enlargement of median nerve CSAs.
One peculiar finding of the present study is that the measured median nerve CSAs of the patients in the DPN group, especially at i
1 and w
levels, were smaller than those measured in the diabetic group. This finding has not been reported previously, but may be partially related to the loss of nerve regeneration capacity in advanced diabetic neuropathy
]. This finding may also partially explain why the response to CTS treatment in diabetic patients varies greatly, especially when different intervention methods are used, when compared with the therapeutic results of idiopathic CTS
There are limitations to this study. First, some of the patients may have been included twice if they had bilateral CTS symptoms. Second, the number of cases is limited; therefore, US findings in the different subgroups of CTS patients could not be fully analyzed. Further large-scale studies of US findings in CTS among diabetic patients are needed for a better delineation.