Carpal Tunnel Syndrome in Diabetes Mellitus

Abstract

: The aim of the present brief review was to discuss carpal tunnel syndrome (CTS) in diabetes mellitus (DM). Generally, CTS is more common in DM, especially in subjects with coexisting diabetic polyneuropathy (DPN) and/or long DM duration. There is no agreement if it is more frequent in type 1 or type 2 DM. The precise underlying mechanisms are not entirely clear but appear to involve hyperglycaemia-induced median nerve oedema, increased sensitivity to exogenous trauma and nerve myelin ischaemia and axonal degeneration. More recently, increased vascular endothelial growth factor (VEGF) and advanced glycation endproducts (AGEs) appear to also play an important role. Median nerve conduction study remains the cornerstone of CTS diagnosis in DM, being more sensitive than clinical examination. Treatment of CTS is medical or surgical. The latter appears now to be equally effective in subjects with vs. without DM in terms of recurrence rates and quality of life.

Prevalence of carpal tunnel syndrome in patients with long-term type 2 diabetes mellitus

“…Furthermore, DM patients with DPN exhibit an accelerated risk of developing CTS compared to their non-DPN counterparts [ 3 ]. Generally, CTS is more common in chronic T2DM patients with co-existing DPN pathology [ 1 ]. According to a statistical report, the rate of prevalence of CTS is only 2% among the general population, while that rises to 14% in T2DM patients without DPN and 30% in case of T2DM combined with DPN [ 4 ].…”

“…The examiner was blinded to the CTS diagnoses in the cohort of T2DM patients. The CTS diagnosis largely relies on the NCV scores of the median nerve across the carpal tunnel (CT) to date, indicating a normal flow of electrical signals in the other parts of the hands remains [ 1 ]. Extensive clinical investigations led by three major US scientific societies have recommended the diagnostic importance of electromyographical tests for CTS diagnosis [ 11 ].…”

“…Carpal tunnel syndrome (CTS), characterized by the compression neuropathy of the median nerve of the palm, is the commonest among compression neuropathies in the upper extremity [ 1 ]. Anatomically, the carpal groove is a narrow U-shaped palmar concavity on the anterior part of the carpus attached to the transverse carpal ligament and surrounded by carpal bones that provides a narrow passageway for the median nerve, which makes the nerve highly susceptible to compression-related impairments, leading to the numbness, burning sensations and/or pain in affected fingers and hand.…”

“…Anatomically, the carpal groove is a narrow U-shaped palmar concavity on the anterior part of the carpus attached to the transverse carpal ligament and surrounded by carpal bones that provides a narrow passageway for the median nerve, which makes the nerve highly susceptible to compression-related impairments, leading to the numbness, burning sensations and/or pain in affected fingers and hand. Above the limit of physical activities of the hand, tendon damage and inflammation, edema, and hormonal disturbances are among the commonest etiological factors contributing to nerve compression syndromes [ 1 ]. The CTS first manifests as intermittent dysesthesia and paresthesia symptoms in hand and fingers at night, which may last through the morning with associated muscle stiffness [ 2 ].…”

The impacts of poor glycemic control and disease duration on peripheral nerves in children and adolescents with type 1 diabetes mellitus

“…However, hyperglycemiainduced edema of the MN, increased sensitivity to exogenous trauma, nerve myelin ischemia, and axonal injury appear to be the probable causes. 41 In a cohort study by Arnold et al, a pattern of change that was consistent with axonal depolarization, which may occur in the context of dysfunction of the energy-dependent axonal Na + /K + a-ATPase, or microvascular perfusion abnormality was found in patients with T1DM. 42 Additionally, previous studies demonstrated that Na + /K + -ATPase dysfunction led to the intra-axonal accumulation of Na + , axonal swelling, structural change, and subsequently, apoptotic processes and axonal loss occurred by the reversal of Na + /Ca +exchanger.…”