Background: Although diabetes is considered a major risk factor for carpal tunnel syndrome (CTS), the characteristics of diabetic CTS have not been fully understood. Objective: This study is aimed at evaluation of the clinical, electrophysiological, and ultrasonographic findings of non-diabetic and diabetic CTS. Methods: This retrospective, cross-sectional study included patients diagnosed with CTS. Patient age, sex, involved side, body mass index, clinical and electrophysiological findings, and median nerve cross-sectional area (CSA) were identified. Diabetes was identified through patient or guardian interviews, medical records, and medication history. Linear and binary logistic regression models were established to confirm the associations between the electrophysiological findings, median nerve CSA, and clinical outcomes. Covariates, such as age, sex, body mass index, diabetes, symptom duration, and thenar muscle weakness were adjusted. Results: Out of the 920 hands, 126 and 794 belonged to the diabetic and non-diabetic CTS groups, respectively. The patients were significantly older in the diabetic CTS group (P < 0.001). The rate of thenar weakness in the diabetic CTS group was also significantly higher than that in the non-diabetic CTS group (P = 0.009). The diabetic CTS group had a more severe electrodiagnostic grade (P = 0.001). The prolonged onset latency of the compound motor nerve action potential (CMAP) and median nerve CSA were well associated with the degree of clinical symptoms. Increased median nerve CSA was significantly associated with prolonged CMAP onset latency (β = 0.64; P = 0.012), prolonged transcarpal latency (β = 0.95; P = 0.044), and decreased CMAP amplitude (β = -0.17; P = 0.002) in the non-diabetic CTS group. Conclusion: Diabetic CTS had more profound electrophysiological abnormalities. Distal motor latency and median nerve CSA were not only associated with each other, but also with clinical symptoms. Further studies are needed to investigate the pathophysiological mechanisms underlying diabetic CTS.
Keywords: Carpal tunnel syndrome; Diabetic complications; Electrodiagnosis; Neurologic manifestations; Ultrasonography
Supplementary Information The online version contains supplementary material available at https://doi.org/10.1186/s12891-023-06881-1.
Carpal tunnel syndrome (CTS) is a common entrapment neuropathy [[
Diabetes is a risk factor and the incidence of CTS is higher in patients with diabetes than in the general population [[
In this study, we hypothesized that diabetic and non-diabetic CTS had different clinical, electrophysiological, and sonographic features. Therefore, we aimed to elucidate these features in both diabetic and non-diabetic CTS groups. We compared these findings in CTS patients with and without diabetes. Additionally, a stratified subgroup was analyzed based on severity to identify whether the differences between the two groups were valid. Finally, we investigated whether the electrophysiological findings and median nerve CSA were associated with the severity of clinical symptoms in the diabetic and non-diabetic CTS groups.
This was a retrospective cross-sectional study of patients diagnosed with CTS at a single hospital between May 2017 and December 2022. We defined the diagnosis of CTS as follows: (
Graph: Fig. 1Flowchart of patient inclusion
The Institutional Review Board of Pohang Stroke and Spine Hospital reviewed and approved this study (approval number: PSSH0475-202303-HR-004-01). Owing to the retrospective study design, the Institutional Review Board approved the omission of informed consent. This study was conducted in compliance with the principles of the Declaration of Helsinki.
We identified the patients' age, sex, affected side, and body mass index at the time of CTS diagnosis. Diabetes was identified through patient or guardian interviews, medical records, and medication history. Cases of diabetic polyneuropathy were excluded. Through patient interviews, we confirmed the timing and duration of symptom onset. The degree of subjective symptoms of the patients was confirmed using a numeric rating scale (NRS) for pain. Provocative night pain and thenar weakness were evaluated.
Experienced physiatrists performed all electrodiagnostic evaluations using Sierra®wave (Cadwell, Kennewick, WA, USA). All tests were performed with the patients lying down. The examination room temperature was set at 23 − 25 °C.
Based on previous electrodiagnostic classifications [[
We identified median nerve CSA as a sonographic parameter. All sonographic evaluations were performed by experienced physiatrists at the time of index electrodiagnosis. The CSA of the median nerve was measured using a transverse view at the pisiform and scaphoid levels (just proximal to the carpal tunnel level) [[
All statistical analyses were performed using R software version 4.2.2 (R Core Team, The R Foundation for Statistical Computing, Vienna, Austria). Statistical significance was defined as P-value < 0.05.
Continuous variables were tested for normality through the Anderson-Darling test and expressed as median (interquartile range). The Wilcoxon rank-sum test was then applied to compare the groups. Categorical variables are expressed as frequency and proportion and the chi-squared test was applied for comparison between groups. Propensity score matching (PSM) was conducted using the "MatchIt" R software package for sensitivity analyses [[
Of the 920 hands, 126 were in the diabetic CTS group and 794 in the non-diabetic CTS group. The patients in the diabetic CTS group were significantly older (61.5 [56.0–68.0] vs. 57.0 [51.0–64.0] years old; P < 0.001). The rate of thenar weakness in the diabetic CTS group was 22.2%, which was significantly higher than 13.0% in the non-diabetic CTS group (P = 0.009). The diabetic CTS group showed higher proportion of moderate-to-severe electrodiagnostic grades (P = 0.001) with significant differences from the non-diabetic CTS group in all nerve conduction study parameters. However, the CSA of the median nerve was not significantly different between the two groups. After PSM, there was no significant difference between the non-diabetic and diabetic CTS groups regarding age and symptom duration (Table 1).
Table 1 Baseline characteristics in all included patients
Variables CTS with DM (n = 126) Before PSM After PSM CTS without DM (n = 794) P-value CTS without DM (n = 252) P-value Age, years 61.5 (56.0–68.0) 57.0 (51.0–64.0) < 0.001 61.0 (56.0–68.0) 0.723 Male, n (%) 51 (40.5) 308 (38.8) 0.793 100 (39.7) 0.970 Right hand, n (%) 68 (54.0) 396 (49.9) 0.448 122 (48.4) 0.363 Body mass index, kg/m2 24.9 (22.7–26.7) 24.1 (22.3–26.7) 0.130 24.1 (22.8–26.7) 0.330 Symptom duration, months 5.0 (2.0–12.0) 4.0 (2.0–10.0) 0.125 4.0 (1.0–12.0) 0.144 NRS of pain 4.0 (3.0–6.0) 4.0 (3.0–5.0) 0.480 4.0 (3.0–5.0) 0.620 Night pain, n (%) 60 (47.6) 304 (38.3) 0.058 91 (36.1) 0.410 Thenar weakness, n (%) 28 (22.2) 103 (13.0) 0.009 32 (12.7) 0.025 Electrophysiological findings CMAP latency, ms 4.0 (3.7–4.6) 3.8 (3.4–4.3) < 0.001 3.9 (3.5–4.4) 0.011 CMAP amplitude, mV 7.4 (5.7–8.7) 7.9 (6.5–9.7) 0.002 7.6 (6.1–9.4) 0.082 SNAP latency, ms 3.5 (3.2–3.9) 3.2 (3.0–3.6) < 0.001 3.3 (3.0–3.6) < 0.001 SNAP amplitude, uV 15.9 (11.7–21.6) 21.4 (15.5–27.1) < 0.001 20.4 (15.1–24.6) < 0.001 Transcarpal latency, ms 2.2 (1.9–2.6) 2.0 (1.8–2.3) < 0.001 1.9 (1.8–2.3) < 0.001 Severity grades, n (%) 0.001 0.018 Milda 49 (38.9) 440 (55.4) 132 (52.4) Moderate to Severeb 77 (61.1) 354 (44.6) 120 (47.6) Ultrasonographic finding Cross sectional area, mm2 15.0 (12.0–17.0) 14.0 (12.0–17.0) 0.241 14.0 (12.0–17.0) 0.391
For the subgroup analysis, we stratified the patients according to electrodiagnostic severity. The mild group contained 49 and 440 hands with diabetic and non-diabetic CTS, respectively. The mild group showed significant differences in sensory nerve action potential (SNAP) parameters between the two groups; the onset latency was significantly longer (P = 0.004) and the amplitude was significantly lower (P = 0.033) in the diabetic CTS group. Furthermore, the transcarpal latency was prolonged in the diabetic CTS group (P = 0.014). There was no significant difference in the onset latency and amplitude of the compound motor nerve action potential (CMAP) between the two groups, and there was no difference in the median CSA between the two groups (Table 2). Meanwhile, 77 and 354 hands with diabetic and non-diabetic CTS were included in the moderate-to-severe group, respectively. There was a significant difference between the two groups in the onset latency of SNAP (P = 0.047) but not in CMAP. Further, significantly lower amplitudes of SNAP and CMAP were found in the diabetic CTS group (P = 0.027 and P = 0.001, respectively). The transcarpal latency and median nerve CSA were not significantly different between the two groups (Table 3).
Table 2 Baseline characteristics of carpal tunnel syndrome in the mild group
Variables CTS with DM (n = 49) CTS without DM (n = 440) P-value Age, years 60.0 (54.0–66.0) 57.0 (51.0–63.0) 0.069 Male, n (%) 19 (38.8) 173 (39.3) > 0.999 Right hand, n (%) 26 (53.1) 234 (53.2) > 0.999 Body mass index, kg/m2 24.8 (23.0–26.7) 23.6 (21.8–26.0) 0.011 Symptom duration, months 2.0 (1.0–3.0) 3.0 (1.0–5.0) 0.026 NRS of pain 3.0 (2.0–4.0) 3.0 (2.0–4.0) 0.182 Night pain, n (%) 11 (22.4) 84 (19.1) 0.709 Thenar weakness, n (%) 0 (0.00) 0 (0.00) NA Electrophysiological findings CMAP latency, ms 3.6 (3.4–3.8) 3.5 (3.3–3.8) 0.400 CMAP amplitude, mV 8.0 (7.0–9.7) 8.6 (7.0–10.1) 0.617 SNAP latency, ms 3.2 (3.0–3.3) 3.0 (2.9–3.2) 0.004 SNAP amplitude, uV 21.5 (15.7–25.9) 23.8 (19.2–29.2) 0.033 Transcarpal latency, ms 1.9 (1.8–2.0) 1.8 (1.7–2.0) 0.014 Ultrasonographic finding Cross sectional area, mm2 13.0 (11.0–15.0) 13.0 (11.0–15.0) 0.846
Abbreviations: CMAP, compound motor nerve action potential; DM, diabetes mellitus; NA, not applicable; NRS, numeric rating scale; SNAP, sensory nerve action potential
Table 3 Baseline characteristics of carpal tunnel syndrome in the moderate-to-severe group
Variables CTS with DM (n = 77) CTS without DM (n = 354) P-value Age, years 63.0 (56.0–69.0) 57.0 (51.0–64.0) < 0.001 Male, n (%) 32 (41.6) 135 (38.1) 0.667 Right hand, n (%) 42 (54.6) 162 (45.8) 0.203 Body mass index, kg/m2 24.9 (22.6–26.6) 24.9 (23.1–27.3) 0.469 Symptom duration, months 9.0 (4.0–23.0) 7.0 (3.0–12.0) 0.098 NRS of pain 5.0 (4.0–6.0) 5.0 (4.0–7.0) 0.419 Night pain, n (%) 49 (63.64) 220 (62.15) 0.909 Thenar weakness, n (%) 28 (36.4) 103 (29.1) 0.263 Electrophysiological findings CMAP latency, ms 4.5 (4.2–5.0) 4.4 (4.1–4.8) 0.302 CMAP amplitude, mV 6.9 (4.9–7.8) 7.2 (5.8–8.8) 0.027 SNAP latency, ms 3.8 (3.5–4.1) 3.6 (3.3–4.1) 0.047 SNAP amplitude, uV 13.7 (9.8–17.8) 17.6 (11.4–23.9) 0.001 Transcarpal latency, ms 2.4 (2.2–2.8) 2.3 (2.0–2.8) 0.116 Ultrasonographic finding Cross sectional area, mm2 16.0 (14.0–18.0) 16.0 (14.0–18.0) 0.597
Abbreviations: CMAP, compound motor nerve action potential; DM, diabetes mellitus; NRS, numeric rating scale; SNAP, sensory nerve action potential
The linear and logistic regression models for all CTS cases are presented in Supplementary Material 1: Tables S1 and S2. Symptom duration showed a significant association with prolonged CMAP onset latency (β = 1.94; P < 0.007) and increased median nerve CSA (β = 0.26; P = 0.001). NRS of pain was significant association with prolonged CMAP onset latency (β = 0.37; P < 0.003), transcarpal latency (β = 0.49; P = 0.018), and increased median nerve CSA (β = 0.11; P < 0.001). Prolonged CMAP onset latency (adjusted odds ratio [aOR], 1.91; 95% confidence interval [CI], 1.35–2.70; P < 0.001) and increased median nerve CSA (aOR, 1.13; 95% CI, 1.08–1.18; P < 0.001) were significantly associated with provocative night pain. Further, prolonged CMAP onset latency (aOR, 1.76; 95% CI, 1.18–2.63; P = 0.006), prolonged transcarpal latency (aOR, 2.13; 95% CI, 1.04–4.34; P = 0.038), and increased median nerve CSA (aOR, 1.21; 95% CI, 1.14–1.29; P < 0.001) were significantly associated with the risk of thenar weakness.
In the non-diabetic CTS group, symptom duration showed a significant relationship with prolonged CMAP onset latency (β = 1.59; P = 0.007) and increased median nerve CSA (β = 0.27; P < 0.001). NRS of pain showed a significant association with prolonged CMAP onset latency (β = 0.36; P = 0.003) and transcarpal latency (β = 0.49; P = 0.026). Increased median nerve CSA (β = 0.11; P < 0.001) was also significantly associated with NRS of pain (Table 4). Similarly, prolonged CMAP onset latency (adjusted aOR, 1.93; 95% CI, 1.31–2.84; P < 0.001) and increased median nerve CSA (aOR, 1.13; 95% CI, 1.08–1.31; P < 0.001) were found to increase the risk of provocative night pain significantly. Further, prolonged CMAP onset latency (aOR, 1.98; 95% CI, 1.25–3.13; P = 0.004) and increased median nerve CSA (aOR, 1.23; 95% CI, 1.15–1.32; P < 0.001) were associated with the risk of thenar weakness (Table 5).
Table 4 Multivariable linear regression models for symptom duration and subjective pain scale in both diabetic and non-diabetic carpal tunnel syndrome
Groups Outcomes Variables SE Non-diabetic Symptom duration (months) CMAP onset latency, ms 1.59 0.58 0.007 CMAP amplitude, mV -0.2 0.13 0.132 SNAP onset latency, ms 2.18 0.92 0.018 SNAP amplitude, µV -0.02 0.02 0.270 Transcarpal latency, ms 0.53 1.08 0.624 Cross-sectional area, mm2 0.27 0.08 < 0.001 Final model = -10.26 + 3.23CMAP onset latency + 0.31Cross-sectional area NRS of pain CMAP onset latency, ms 0.36 0.12 0.003 CMAP amplitude, mV -0.004 0.03 0.876 SNAP onset latency, ms 0.25 0.19 0.186 SNAP amplitude, µV -0.004 0.004 0.311 Transcarpal latency, ms 0.49 0.22 0.026 Cross-sectional area, mm2 0.11 0.02 < 0.001 Final model = -0.54 + 0.44CMAP onset latency + 0.67transcarpal latency + 0.11Cross-sectional area Diabetic Symptom duration (months) CMAP onset latency, ms 4.63 1.80 0.012 CMAP amplitude, mV 0.19 0.44 0.670 SNAP onset latency, ms -6.45 3.96 0.106 SNAP amplitude, µV -0.07 0.12 0.595 Transcarpal latency, ms 10.33 4.33 0.019 Cross-sectional area, mm2 0.23 0.27 0.394 Final model = -20.39 + 4.08CMAP onset latency + 5.55transcarpal latency NRS of pain CMAP onset latency, ms 0.45 0.29 0.129 CMAP amplitude, mV -0.06 0.07 0.375 SNAP onset latency, ms -0.06 0.64 0.900 SNAP amplitude, µV -0.02 0.02 0.252 Transcarpal latency, ms 0.47 0.70 0.506 Cross-sectional area, mm2 0.13 0.04 0.006 Final model = 1.31 + 0.20Cross-sectional area
Table 5 Multivariable logistic regression models for night pain and thenar weakness in both diabetic and non-diabetic carpal tunnel syndrome
Groups Outcomes Variables ORa 95% CI Non-diabetic Night pain CMAP onset latency, ms 1.93 1.31–2.84 < 0.001 CMAP amplitude, mV 0.97 0.90–1.05 0.446 SNAP onset latency, ms 0.75 0.42–1.36 0.343 SNAP amplitude, µV 0.99 0.97–1.01 0.410 Transcarpal latency, ms 1.91 0.93–3.94 0.078 Cross-sectional area, mm2 1.13 1.08–1.31 < 0.001 Thenar weakness CMAP onset latency, ms 1.98 1.25–3.13 0.004 CMAP amplitude, mV 0.99 0.88–1.11 0.884 SNAP onset latency, ms 1.04 0.53–2.04 0.908 SNAP amplitude, µV 1.00 0.99–1.02 0.620 Transcarpal latency, ms 1.79 0.85–3.76 0.124 Cross-sectional area, mm2 1.23 1.15–1.32 < 0.001 Diabetic Night pain CMAP onset latency, ms 1.88 0.80–4.43 0.147 CMAP amplitude, mV 0.99 0.82–1.12 0.956 SNAP onset latency, ms 1.47 0.22–9.84 0.694 SNAP amplitude, µV 0.98 0.92–1.04 0.428 Transcarpal latency, ms 1.19 0.16–9.16 0.866 Cross-sectional area, mm2 1.13 0.99–1.29 0.063 Thenar weakness CMAP onset latency, ms 1.27 1.18–2.63 0.602 CMAP amplitude, mV 1.03 0.89–1.09 0.792 SNAP onset latency, ms 0.55 0.56–2.01 0.578 SNAP amplitude, µV 0.93 0.98–1.02 0.167 Transcarpal latency, ms 6.71 0.60–75.34 0.123 Cross-sectional area, mm2 1.13 0.97–1.32 0.108
In the matched non-diabetic CTS group, symptom duration showed a significant association with prolonged CMAP onset latency (β = 2.51; P = 0.035), while NRS of pain showed a significant association with both prolonged CMAP onset latency (β = 0.52; P = 0.015) and median nerve CSA (β = 0.06; P = 0.025) (Supplementary Material 1: Table S3). Meanwhile, increased median nerve CSA (aOR, 1.14; 95% CI, 1.05–1.25; P = 0.002) significantly increased the risk of provocative night pain. Prolonged CMAP onset latency (aOR, 5.56; 95% CI, 2.09–15.24; P < 0.004) and increased median nerve CSA (aOR, 1.16; 95% CI, 1.02–1.33; P = 0.028) were also associated with the risk of thenar weakness (Supplementary Material 1: Table S4).
In the diabetic CTS group, symptom duration was strongly associated with prolonged CMAP onset latency (β = 4.63; P = 0.012) and transcarpal latency (β = 10.33; P = 0.019). Meanwhile, NRS of pain significantly correlated with the increase in median CSA (β = 0.13; P = 0.006) (Table 4). Provocative night pain and thenar weakness did not significantly correlate with any electrodiagnostic or sonographic parameters in the diabetic CTS group (Table 5).
In the non-diabetic CTS group, increased median nerve CSA was significantly associated with prolonged CMAP onset latency (β = 0.64; P = 0.012) and transcarpal latency (β = 0.95; P = 0.044). Further, decreased CMAP amplitude (β = -0.17; P = 0.002) was also significantly associated with increased median nerve CSA (Table 6). In the matched non-diabetic CTS group, increased median nerve CSA was significantly associated with prolonged transcarpal latency (β = 1.56; P = 0.032) (Supplementary Material 1: Table S5).
Table 6 Associations between electrodiagnostic findings and median nerve cross-sectional area
Groups Outcome Variables SE Non-diabetic Median nerve CSA CMAP onset latency, ms 0.64 0.26 0.012 CMAP amplitude, mV -0.17 0.06 0.002 SNAP onset latency, ms 0.002 0.40 0.996 SNAP amplitude, uV -0.01 0.008 0.055 Transcarpal latency, ms 0.95 0.47 0.044 Diabetic Median nerve CSA CMAP onset latency, ms 0.89 0.62 0.156 CMAP amplitude, mV -0.11 0.15 0.455 SNAP onset latency, ms 0.16 1.35 0.907 SNAP amplitude, uV -0.02 0.04 0.613 Transcarpal latency, ms 0.89 1.49 0.555
However, no significant association was observed between the electrophysiological findings and median nerve CSA in the diabetic CTS group (Table 6).
This study analyzed the differences in the clinical, electrodiagnostic, and sonographic findings between patients with and without diabetic CTS. We investigated whether the electrophysiological findings and CSA of the median nerve were associated with symptom severity in each group.
Our results confirmed that the diabetic group had a more advanced CTS. Moreover, stratified analyses revealed that SNAP abnormalities were more prominent in diabetic CTS in the mild group. In contrast, both CMAP and SNAP amplitudes, rather than latency, were identified as characteristics that differentiated diabetic CTS from non-diabetic CTS in the moderate-to-severe group. We inferred that this reflected the progression of neuropathy. In the early stages of neuropathy, sensory nerves are more vulnerable, with dominating demyelinating features. As the disease progresses, motor neurons get involved, and axonopathic features appear [[
Previous studies have found inconsistent results regarding whether the comorbidity of diabetes in CTS causes significant differences in electrophysiological findings. Tony et al. [[
Broadly, median CSA is associated with CTS severity [[
Additionally, our results suggested that median nerve CSA and electrophysiological findings showed a significant association in the non-diabetic group, but not in the diabetic group. In previous studies analyzing the diagnostic accuracy of CTS in patients with diabetic neuropathy, it was generally reported that abnormal results of nerve conduction studies and CSA enlargement were associated [[
This study has several strengths compared with previous studies. First, it analyzed a relatively large sample size compared with previous related studies. Moreover, we utilized data based on the clinical pathway in which clinical, electrodiagnostic, and ultrasound examinations were performed almost simultaneously when a patient visited the hospital. Consequently, we could analyze various clinical outcomes as dependent variables. Therefore, the characteristics of diabetic and non-diabetic CTS can comprehensively be described as multifaceted. We further validated our findings by performing sensitivity analyses by matching some of the non-diabetic CTS. Finally, considering the broad spectrum of CTS itself, our study was significant in that we presented focused results that were adjusted for the severity and presence of diabetes through stratified subgroup analyses.
The limitations of this study were as follows. First, this study was a single hospital-based retrospective study. Since we excluded cases of diabetic polyneuropathy and unobtainable nerve conduction study results, it is difficult to state whether the overall characteristics of diabetic CTS were appropriately reflected in this study. Glycemic control is a factor that explains the degree of diabetic neuropathy [[
This study analyzed the differences in the clinical, electrophysiological, and sonographic findings between patients with and without diabetic CTS. In addition, we identified associations between each result and the severity of the clinical symptoms. Diabetic CTS has more profound electrophysiological abnormalities, showing sensory-prominent demyelinating features in the early stages of the disease that progress to sensory and motor axonopathy features as the disease progresses. In addition, distal motor latency and median nerve CSA not only correlated with each other but also correlated well with clinical symptoms. The relationship between clinical, electrophysiological, and sonographic findings was more prominent in the non-diabetic CTS group than in the diabetic CTS group. Future studies to determine the cause of this phenomenon and better understanding the underlying pathophysiological mechanism of diabetic CTS are warranted.
The authors would like to thank the medical laboratory technologists of our institute for their technical support and faithful discussions.
Study concept and design, drafting of manuscript: Dougho Park. Acquisition of data, or analysis of data: Sang-Eok Lee, Jae Man Cho, Joong Won Yang, Mansu Kim, and Heum Dai Kwon. Revision of manuscript for important intellectual content: Dougho Park. All authors have read and approved of the final version of the manuscript.
None.
The dataset supporting the conclusions of this article is provided in additional files.
This study was approved by the Institutional Review Board of Pohang Stroke and Spine Hospital (PSSH0475-202303-HR-004-01); informed consent was waived owing to its retrospective design. The research complied with the guidelines of the Declaration of Helsinki.
Not Applicable.
The authors declare that they have no competing interests.
• aOR
- Adjusted odds ratio
• CI
- Confidence interval
• CMAP
- Compound motor nerve action potential
• CSA
- Cross-sectional area
• CTS
- Carpal tunnel syndrome
• NRS
- Numeric rating scale
• PSM
- Propensity score matching
• SNAP
- Sensory nerve action potential
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Graph: Supplementary Material 1
Graph: Supplementary Material 2
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By Dougho Park; Sang-Eok Lee; Jae Man Cho; Joong Won Yang; ManSu Kim and Heum Dai Kwon
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