Characteristics of diabetic and non-diabetic carpal tunnel syndrome in terms of clinical, electrophysiological, and Sonographic features: a cross-sectional study

Abstract

BackgroundAlthough diabetes is considered a major risk factor for carpal tunnel syndrome (CTS), the characteristics of diabetic CTS have not been fully understood.ObjectiveThis study is aimed at evaluation of the clinical, electrophysiological, and ultrasonographic findings of non-diabetic and diabetic CTS.MethodsThis 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.ResultsOut 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.ConclusionDiabetic 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.