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 Table of Contents  
Year : 2021  |  Volume : 38  |  Issue : 4  |  Page : 234-244

Asymptomatic median neuropathy in patients with diabetic polyneuropathy

Department of Neurology, Faculty of Medicine, Sakarya University, Sakarya, Turkey

Date of Submission27-Mar-2021
Date of Decision10-Sep-2021
Date of Acceptance07-Oct-2021
Date of Web Publication29-Dec-2021

Correspondence Address:
Murat Alemdar
Sakarya University, Faculy of Medicine, Department of Neurology, Second Floor, Adnan Menderes c., Sağlık s., No: 195, Adapazari 54100, Sakarya
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/nsn.nsn_54_21

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Aim: This study aims to investigate whether asymptomatic median neuropathy (AMN) in patients with diabetic peripheral polyneuropathy (DPNP) is a result of polyneuropathic involvement of median nerve (MN) or its true entrapment. Subjects and Methods: We determined the grades of the Michigan severity scale and the rates of peripheral nerve conduction abnormalities in study subgroups, including patients with carpal tunnel syndrome (CTS), AMN, and normal MN conductions to highlight if the severity of polyneuropathic involvement was different between them. In addition, the results of conventional and comparative nerve conduction studies (NCSs) were compared between these study subgroups. Results: Distributions of Michigan grades and rates of abnormalities in peroneal and sural NCSs were similar between the subgroups (P > 0.05 for all analyses). Abnormality rates of ulnar NCSs were higher in the AMN group than in the other groups, whereas those of comparative transcarpal NCSs were higher in the CTS group. The mean distal sensory latency (DSL) and motor latency (DML) of MN were longer, sensory conduction velocity (SCV) was slower in the CTS group than AMN group, whereas MN motor conduction velocity (MCV) was slower, UN DSL was longer, SCV was slower, SNAP amplitude was smaller, DML was longer, and MCV were slower in the AMN group (P < 0.05 for all analyses). Discussion: Our findings reveal that grade of polyneuropathic involvement is more prominent in AMN, whereas transcarpal MN conduction delay is greater in CTS. The results of the study suggest that the prominence of polyneuropathic impairment in addition to a lesser degree of MN sheet compression obscures the clinical signs in patients with diabetes with AMN.

Keywords: Carpal tunnel syndrome, diabetic polyneuropathy, nerve compression

How to cite this article:
Alemdar M. Asymptomatic median neuropathy in patients with diabetic polyneuropathy. Neurol Sci Neurophysiol 2021;38:234-44

How to cite this URL:
Alemdar M. Asymptomatic median neuropathy in patients with diabetic polyneuropathy. Neurol Sci Neurophysiol [serial online] 2021 [cited 2022 Jun 28];38:234-44. Available from: http://www.nsnjournal.org/text.asp?2021/38/4/234/334054

  Introduction Top

Diabetes mellitus (DM) is the most common etiology of polyneuropathy, comprising more than one-half of all cases in developed countries.[1],[2] Diabetic peripheral polyneuropathy (DPNP), mononeuropathy, autonomic neuropathy, and lumboscral plexopathy are common clinical phenotypes of neuropathic involvement in diabetics.[3],[4] Carpal tunnel syndrome (CTS) is the most common mononeuropathy in patients with DM. Its prevalence is 2%–3% among the general population,[5],[6] whereas it is 7%–33% in diabetics.[7],[8],[9],[10] Although there are a few controversial reports,[11],[12],[13] many previous studies revealed DM as a major risk factor for CTS.[11],[14],[15],[16],[17] However, it is not easy to document the presence of CTS in patients with DPNP because both disorders may present with similar symptoms. Electrophysiologic studies are expected to help in differential diagnosis and to navigate the management of these patients. However, the electrodiagnosis of CTS also has particular difficulties in patients with DPNP and CTS. Transcarpal conduction abnormalities of the median nerve (MN) in the presence of normal ipsilateral ulnar nerve (UN) conduction are accepted as the main indicator of CTS.[18],[19],[20] However, documenting the presence of CTS in patients with DPNP is not easy because both disorders may cause similar conduction abnormalities in the MN, and many patients with diabetes also have disturbances of UN conduction in the context of polyneuropathic involvement.[20],[21],[22],[23],[24]

Abnormal MN conduction values without corresponding clinical symptoms and signs, named as either asymptomatic median neuropathy (AMN) or asymptomatic CTS, occur quite frequently in patients with DPNP.[8],[9],[10],[11],[12],[13],[14],[15],[16],[17] However, the underlying mechanisms for the absence of neuropathic symptoms in patients with diabetes with AMN have not been highlighted to date. In the present study, we aimed to investigate whether the AMN in patients with DPNP was a result of polyneuropathic involvement of MN or its true entrapment in the carpal tunnel. For this aim, we analyzed the probable differences in nerve conduction functions between patients with clinically confirmed CTS, AMN and patients with completely normal MN conduction values using an extensive number of nerve conduction parameters. The grades of neuropathic severity and the rates of conduction abnormalities in each measured individual peripheral nerve were also compared between them.

  Subjects and Methods Top


The population of the present study comprised subjects who were referred to the electroneuromyography (ENMG) laboratory of Sakarya University Education and Research Hospital for searching polyneuropathy within the past 3 years. Patients with type 2 DM (T2DM) according to the criteria of the American Diabetes Association and those with typical DPNP according to the definition of the Toronto Expert Panel on Diabetic Neuropathy were enrolled.[25],[26] The study protocol complied with the Declaration of Helsinki and was approved by the Local Medical Ethics Committee of Sakarya University.

The history of the patients and the results of nerve conduction studies (NCSs) examined by the author were derived from recordings of our ENMG laboratory. Medical history and clinical findings including the presence of polyneuropathic signs and symptoms, recurring night-time or activity-related numbness on two of the first three fingers, the presence of positive Tinel/Phalen's test, and any sensory or motor deficits were all noted. We included patients with T2DM in whom NCS confirmed the presence of DPNP. Patients with a history of carpal tunnel release surgery, signs of entrapment neuropathy of the UN, plexopathy, cervical radiculopathy, or any abnormality in ENMG presuming neuromuscular junction or muscle diseases were excluded. The NCS recordings of the nondominant upper extremities of the patients with DPNP with or without co-existing CTS findings were included to prevent bias resulting from the possibility of subclinical CTS in dominant hands.


In our ENMG laboratory, electrophysiologic studies are conducted according to the American Association of Electrodiagnostic Medicine practice guidelines.[19] All participants were studied using the same 4-channel ENMG device (Nihon Kohden, Neuropack, Tokyo, Japan) by the same practitioner, the author of the present study. NCSs were performed using conventional procedures with supramaximal percutaneous stimulation with a constant current stimulator and recording surface electrodes by the same physician. As in the defined standards of instrumentation of EMG, the gain was adjusted as 10 μV/division for sensory conduction studies, 2 mV/division for motor conduction studies, and 10 μV/division for F wave studies. Sweep speed was 1 ms/division for sensory conduction studies, 2 ms/division for motor conduction studies, and 5–10 ms/division for F wave studies.[27],[28]

Motor NCSs of the MN, UN, tibial nerve (TN), and peroneal nerve (PN) were performed. The compound muscle action potential (CMAP) was recorded with surface electrodes from the abductor pollicis brevis (APB) muscle for the MN, the abductor digiti minimi muscle for the UN, the abductor hallucis muscle for the TN, and extensor digitorum brevis muscle for PN. Distal motor latency (DML), CMAP amplitude, and motor nerve conduction velocity (MCV) were recorded. For sensory NCSs, the median, ulnar, and sural nerves were measured. Sensory NCSs were recorded using ring electrodes from the second digit for MN antidromically and from the fifth digit for the UN. Surface electrodes placed on the midpoint of the calf posterior to lateral malleolus were used for sural nerve measurement. Minimum F wave latency (mFWL) was measured for UN and TN. Elicitation of 6-F wave responses at least upon 16 repetitive simulations (firing ratio over 1/3) was warranted for the mFWL recording. In addition to these conventional recordings, we compared the sensory responses of the MN and UN over the ring finger with equal distances from the stimulation points on the wrist to search for the presence of CTS.

Electrodiagnosis of DPNP was tested in our ENMG laboratory normative values. We also routinely record MN and UN sensory responses over the ring finger in our laboratory, and our normative value is <0.45 msec for antidromic MN to UN distal sensory onset latency difference (DSOLD), and is <1 msec for the DML difference (DMLD) of the MN to the APB muscle and the UN to the ADM muscle.

Patients with abnormal electrodiagnostic results other than findings of compressive neuropathy in one or more nerves in the upper limbs in addition to one or more nerves in the lower limbs were considered to have DPNP. The electrophysiologic testing was extended if a suspicious condition (such as ulnar compressive neuropathy, radiculopathy, or plexopathy) was present. Extremities with any other neuropathic findings such as UN entrapment neuropathy at the elbow, Guyon channel neuropathy, plexopathy, or radiculopathy were excluded.

The study population was divided into three groups according to clinical symptoms and the results of the MN conduction studies. The AMN group was composed of patients with abnormalities on conventional transcarpal MN conduction parameters (DSOL, DML, SNAP, and/or CMAP amplitude) without symptoms of CTS. The CTS group comprised all subjects with clinical symptoms and/or signs of CTS. The symptoms were defined as the presence of recurring nighttime or activity-related numbness or tingling involving the palmar aspects of at least two of the first four fingers in the history. Among the clinical findings, one of the following was needed to support the diagnosis: The presence of a positive Tinel or Phalen's test, isolated sensory deficits over the skin of MN-innervated fingers, or motor deficit upon thumb abduction. The normal group was constituted by patients with DPNP with completely normal MN conduction values without any signs or symptoms of CTS.

Electrophysiologic staging of DPNP was performed according to the Michigan severity scale.[29] The scale is based on the electrophysiologic studies of MN and PN motor conduction and MN, UN, and SN sensory conduction on the nondominant side. Staging of DPNP according to the Michigan severity scale is as follows: Patients with two abnormalities of nerve conductions are considered as Class 1 (mild), patients with three or four abnormalities are Class 2 (moderate), and patients with five abnormalities are Class 3 (severe). Conduction abnormality is defined as either absence of the response or having slowed conduction velocity and/or decreased amplitude in motor or sensory conduction studies.

  Statistics Top

All data were analyzed using the Statistics Open For All package (released with open source AGPL3 license 2009–2014; Paton-Simpson and Associates Ltd, New Zealand). A P < 0.05 was considered statistically significant. After tests for normality, the statistical significance of the differences between the means of the groups and groups was tested using an independent sample t-test for normally distributed data and the Mann–Whitney U-test for nonnormally distributed data. Analysis of variance was used to test the possible differences between the averages of the obtained values in comparisons between multiple groups in normally distributed data and the Kruskal–Wallis H-test for nonnormally distributed data. The distributions of the Michigan severity stages and conduction abnormalities in each individual peripheral nerve were analyzed between the study groups. The Chi-square (χ2) test or Fisher's exact probability test was used to consider the distribution of these categorized variables.

  Results Top

NCS recordings of 105 patients (60 females and 45 males) with the diagnosis T2DM and DPNP were included. There were 17 females and 16 males in the AMN group, 38 females and 20 males in the CTS group, and five females and nine males in the normal MN group. The distribution of sexes was not different between the study groups (P = 0.095). The mean age was 63.2 ± 9.8 (range, 39–85) years; the median age was 64 years. The mean disease age of DM onset was 12.8 ± 9.1 (range, 1–38) years; the median age of disease onset was 10 years. All patients were right-handed. There were no significant differences between the study groups in terms of mean ages and mean disease-onset ages (P > 0.05 for both analyses) [Table 1].
Table 1: Distribution of ages and disease ages between the study groups

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All patients had at least two conduction abnormalities in the MN and PN motor conduction, and MN, UN, and SN sensory conduction studies on the nondominant side, confirming the diagnosis of DPNP. There were 91 patients (86.7%) with MN conduction abnormalities in our study population. The clinical diagnosis of CTS was made in 58 patients (CTS group). Thirty-three patients had MN conduction abnormalities without any signs or symptoms of CTS (AMN group); the remaining 14 asymptomatic patients had completely normal MN conduction values (normal MN group).

Among the entire study population, we detected conduction abnormalities in 85 (80.9%) patients in MN sensory NCS, 71 (67.6%) patients in MN motor NCS, 53 (50.5%) patients in MN F wave studies, 78 (74.3%) patients in UN sensory NCS, 40 (38.1%) patients in UN motor NCS, 50 (47.6%) patients in UN F wave studies, 81 (77.1%) patients in PN motor NCS, 83 (79.0%) TN motor NCS, 80 (76.2%) patients in TN F wave studies, and 95 (90.5) patients in SN sensory NCS.

When we analyzed the upper NCS results of the entire study population, there were six patients with unelicitable MN sensory responses in the second finger, 12 with unelicitable MN responses in the ring finger, one patient with unelicitable UN response in the fifth finger, and six with unelicitable UN sensory responses in the ring finger. Among patients with responses, 63 (60.0%) patients had slowed MN SCV, 55 (52.4%) had decreased MN SNAP amplitude, 62 (59.0%) had slowed UN SCV, and 50 (47.6%) patients had decreased UN SNAP amplitude. Eighty-four (80.0%) patients had abnormal MN to UN sensory conduction comparisons in the ring finger, including 76 patients with elongated MN to UN DSOLD and eight with unelicitable MN responses with elicitable UN responses in the ring finger. Considering the motor conduction parameters, 47 (44.8%) patients had elongated MN DML, 12 (11.4%) had decreased MN CMAP amplitude, 49 (46.7%) had slowed forearm MN MCV, 25 (23.8%) had elongated UN DML, four (3.8%) had decreased UN CMAP amplitude, 29 (27.6%) had slowed forearm UN MCV, 10 (9.5%) had slowed across-elbow UN MCV, and 76 (72.4%) patients had elongated MN to UN DMLD.

The CTS and AMN groups had a similar distribution in terms of severity stages on the Michigan scale (P = 0.387) [Table 2]. The normal MN group was not included in that statistical comparison because Stage 3 is not possible in that group owing to the nature of the Michigan scale. When the rates of abnormal results in the measured peripheral nerves were analyzed between the three study groups, the rates of having abnormal MN sensory or motor conduction abnormalities of both the AMN group and the CTS group were higher than in the normal MN group (P < 0.001 for all comparisons). However, the rate of having MN sensory or motor conduction abnormalities was not different between the AMN group and the CTS group (P = 0.877 and P = 0.894, respectively). The rate of abnormal results in studies of the MN to UN DSOLDs in the ring finger in the CTS group was higher than in the AMN group and the normal MN group (P < 0.001 and P < 0.001, respectively). The abnormality rate in the MN to UN DMLD in the CTS group was higher than the AMN and normal MN group (P < 0.001 and P = 0.001, respectively). The rate of having abnormal ulnar sensory responses in the AMN group was higher than in the CTS group and the normal MN group (P = 0.031 and P = 0.009, respectively). The CTS and AMN groups had higher rates of abnormal TN motor responses than the normal MN group (P = 0.003 and P < 0.001, respectively). The abnormal result rates in peroneal motor NCSs and sural sensory NCSs were similar between the three study groups (P > 0.05 for all comparisons). The distributions of abnormality rates in conduction abnormalities on each studied individual peripheral nerve are shown in [Table 2].
Table 2: Distribution of diabetic neuropathy severity and involvement of the investigated peripheral nerves between the study groups

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The mean MN DSOL in the second finger was longer, SCV was slower, and SNAP was smaller in the AMN and CTS groups compared with the normal group (P < 0.001 for all comparisons) [Table 3]. The median MN mFWL in the AMN (29.8 ms) and CTS (29.3 ms) groups were similar (P = 0.748), but both were longer than in the normal group (26.75 ms) (P = 0.018 and P = 0.014, respectively). The statistical comparisons of the conduction values between the CTS and AMN groups revealed that the mean DSOL of the MN was longer and the mean SCV was slower in the CTS group than in the AMN group, whereas the mean SNAP amplitudes were similar (P = 0.008, P = 0.019, and P = 0.594, respectively). The mean MN DML of the AMN group was longer than in the CTS group, whereas the mean MN CMAP amplitudes and mFWLs were similar (P = 0.003, P = 0.883, and P = 0.862, respectively). The mean forearm MN MCV of the AMN group was slower than in the CTS group (P = 0.005). The mean DSOL of the UN in the fifth finger was longer, SCV was slower, and SNAP was smaller in the AMN group than in the CTS group (P = 0.014, P = 0.001, and P = 0.005, respectively). The mean UN DML was longer, forearm, and across-elbow MCV was slower, and mFWL was longer in the AMN group than in the CTS group (P = 0.016, P < 0.001, P = 0.026, and P < 0.001, respectively). Although the mean UN CMAP amplitude of the AMN group was smaller than in the CTS group, the difference was not statistically significant (P = 0.071).
Table 3: Comparison of nerve conduction values of median nerve and ulnar nerve between the study groups and normal values of our laboratory

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The distribution of the conduction study results in lower extremities between the study groups is shown in [Table 4]. The means conduction study results obtained in peripheral nerves of the lower extremities were similar between the three study groups (P > 0.05 for all comparisons). The only exception was the slowness of the mean TN MCV of the AMN group compared with the normal MN group (P = 0.034).
Table 4: Comparison of nerve conduction values of lower extremities between the study groups and normal values of our laboratory

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Compared with our laboratory normative values, the rates of abnormalities in the measured conduction parameters of the MN and UN between the AMN and CTS groups are shown in [Table 5]. The rate of elongated MN DML and increased MN to UN ring finger latency difference was higher in the CTS group than in the AMN group. On the other hand, the AMN group had more frequent slowed forearm MN MCV, slowed UN SCV, decreased UN SNAP amplitudes, decreased UN CMAP amplitudes, slowed forearm UN MCV, slowed UN MCV, and elongated UN mFWL compared with the CTS group.
Table 5: Distribution of abnormalities on upper extremity conduction parameters between the asymptomatic median neuropathy and carpal tunnel syndrome groups

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  Discussion Top

NCSs are useful in documenting the disturbances of sensory and motor nerve fibers and predicting other morbidities in patients with DPNP, even if the neuronal dysfunction is subclinical.[29],[30],[31],[32] Conduction impairments of MN could exist even in the early stages of DPNP, and a substantial rate of these hands do not have clinical symptoms or signs of CTS.[33],[34],[35],[36],[37],[38],[39],[40] It remains a subject of debate whether these patients should be considered as having true CTS or defined as having AMN in the context of DPNP. In the present study, we investigated whether the occurrence of AMN resulted from the polyneuropathic involvement of MN and/or from its entrapment in the carpal tunnel.

Our study groups had homogeneous distribution in terms of sex, mean age, and mean disease-onset ages, which could affect the severity of neuropathic involvement. Among the 91 patients with MN conduction abnormalities in our population, the rate of asymptomatic patients was 36.2%. In a previous study, Celiker et al. investigated patients with diabetes to obtain electrophysiologic data of possible neurologic abnormalities, even in the absence of neuropathy symptoms in 55 patients with diabetes and 20 healthy controls.[34] They detected that 49.1% of their patients had peripheral nerve conduction slowing and 33.7% had CTS. Among the patients with CTS, 38.8% were asymptomatic. Rota et al. performed conventional NCSs in 39 patients with newly diagnosed diabetes and found conduction abnormalities in 32 (82%); 62.2% of the patients had multiple (two to five) abnormal parameters.[36] They reported that 42% of the patients had NCS alterations suggestive of a distal median mononeuropathy, and 36% were asymptomatic. El-Salem et al. reported that 26 (52%) of 50 neurologically asymptomatic patients with DM had subclinical DPNP, and 25 (50%) of these 50 patients had abnormal MN responses with more common increased F wave and distal latencies.[39] The rate of asymptomatic patients among the MN conduction abnormalities in our study was similar to previous.[33],[34],[35],[36],[39]

In many previous reports, lower extremity nerves, mostly the SN and PN, were reported to be affected earlier and more commonly than other nerves in DPNP, followed by the MN.[32],[41],[42] In our study, the most commonly observed abnormality was in SN sensory conduction in the lower extremities and MN sensory conduction in the upper extremities, in accordance with the characteristic involvement pattern of DPNP affecting the sensory nerve fibers primarily.[43],[44] Conduction abnormalities of the SN or PN were reported not to be correlated with the frequency of AMN.[33] Similarly, the rates of conduction abnormalities in the SN and PN were not different between our AMN, CTS, and normal MN groups.

In our study population, the Michigan severity stages were not different between the CTS and AMN groups. Moreover, the abnormality rates of peroneal and sural NCSs were similar between the study groups, and the abnormality rates in tibial NCSs were similar between the AMN and CTS groups, both having higher rates than the normal MN group. These results could be considered as indicators of similarity in terms of neuropathy severity between the AMN and CTS groups. However, the rates of having abnormal UN conduction parameters including long segment studies and forearm MN MCV, another long segment study parameter, were higher in the AMN group than in the CTS group, suggesting the severity of polyneuropathic involvement of upper extremities was greater in the AMN group. The mean SNAP and CMAP amplitudes of the MN were not different between the AMN and CTS groups, revealing that the axonal impairment in the MN was similar in these groups. The MN forearm MCV, a parameter of long segment study of the MN, in the AMN group was slower than in the CTS group. In addition, the mean value UN conduction parameters in the AMN group, referring to both the axonal (SNAP and CMAP amplitudes) and myelination status of the nerve (distal latencies, SCV, MCV, and mFWLs), were worse than in the CTS and normal MN groups. The rate of having abnormal UN sensory responses in the AMN group was also higher than in the CTS group and the normal MN group. The long segment conduction impairments, the disturbances in sensory conductions, and the decreases in amplitudes indicating the axonal dysfunctions are major conduction abnormalities seen in DPNP. The results of our study reveal that the patients with AMN had a more progressed polyneuropathy in the upper limbs than the other groups.

Although conventional distal conduction parameters (DSOL, DML, and SCVs) are commonly used in the electrodiagnosis of CTS, the addition of comparative conduction techniques could be necessary for patients with early grades or in the presence of other coexisting peripheral disorders, including PNP. Remembering the length-dependent involvement pattern of DPNP,[43],[44],[45] the use of comparative techniques could confirm the diagnosis of CTS in these patients if they reveal more prominent distal conduction abnormalities on MN compared with the ulnar or radial nerve.[40],[41],[44],[45],[46],[47],[48],[49],[50],[51],[52],[53],[54] The results of comparative parameters have the advantage of less susceptibility to individual factors than conventional parameters because the peripheral nerves of the same extremity of an individual are affected by the same subjective characteristics (e.g., age, temperature, and anthropometric factors).[32] We also used the MN to UN DSOLD in the ring finger and the DMLD of the MN on the APB muscle and UN in the ADM muscle in our study to better evaluate the transcarpal MN conduction, besides the conventional parameters. The mean DSOL and DML of the MN were longer, and the mean SCV was slower in the CTS group compared with the AMN group, although the rate of having abnormal MN sensory conduction or motor conduction abnormalities was similar between our study groups. However, the rates of having abnormal MN to UN DSOLD in the ring finger and abnormal DMLD were higher in the CTS group than in the AMN and normal MN groups. Moreover, the mean values of DSOLDs and DMLDs in the CTS group were higher compared with the AMN and normal MN groups, revealing that the transcarpal conduction slowing due to myelin sheet compression in the CTS group was more prominent than in the AMN group. Taken together with the more progressed neuropathic involvement in the upper limbs of the AMN group, this less prominent transcarpal conduction delay suggests that the DPNP probably obscures the classic clinical signs of MN entrapment in patients with AMN, already having a lesser degree of compression than patients with signs of CTS.

Although AMN occurs in approximately one-third of patients with DM, the association between AMN and DPNP has not yet been clarified. There are a limited number of studies in the current literature investigating whether the conduction abnormalities in AMN are a result of polyneuropathic involvement or due to true entrapment of nerve fibers in the carpal tunnel.[34],[35],[36],[39] Some of these previous reports suggested that the presence of AMN in NCSs was a sign of true compressive neuropathy in the carpal tunnel with obscured clinical symptoms, whereas others claimed that it was a result of polyneuropathic involvement of MN without any direct compression to the nerve sheet. The latter reports suggested that a true diagnosis of CTS in patients with DPNP required the occurrence of typical signs and symptoms of CTS. Celiker et al. suggested that the presence of lesions in the proximal nerve or a change in the threshold of the sensory nerve fibers could make patients with DPNP less likely to develop clinically evident CTS than otherwise healthy individuals.[34] Rota et al. and Stamboulis et al. suggested that asymptomatic CTS was a direct manifestation of distal neuropathic involvement of DPNP in patients with DM.[36],[37] They also presumed that the increased sensory threshold in diabetics was the major factor obscuring the classic symptoms of CTS. However, Kim et al. thought that asymptomatic CTS was a manifestation of increased vulnerability to entrapment of the nerve.[33] Similarly, Han et al. reported that symptoms of CTS in patients with diabetes were related to swelling of the MN rather than to the duration of DM, glycemic control, coexistence of DPNP, and nerve conduction values.[55]

There are some limitations to our study. The major limitation is the low number of patients with normal MN conductions because the study was conducted in an ENMG laboratory of a tertiary level reference hospital. Furthermore, because no neuropathic symptom scale was applied to the participants, we could not evaluate the potential association between their neuropathic symptoms and electrophysiologic findings.

In summary, our findings suggested that a more severe polyneuropathic involvement was present in the upper limbs of patients with diabetes with AMN compared with the others. In addition, transcarpal MN conduction slowing due to myelin sheet compression was more prominent in the CTS group than in the other groups. Therefore, we suggest that the prominence of neuropathic impairment in addition to a lesser degree of nerve sheet compression than in the CTS group obscured the clinical signs of MN entrapment in the AMN group.


The author has full access to data and has the right to publish such data. He designed the study, interpreted the data, and wrote manuscript. There is no commercial or financial involvements that might present an appearance of a conflict of interest in connection with the submitted article.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

Dyck PJ, Kratz KM, Karnes JL, Litchy WJ, Klein R, Pach JM, et al. The prevalence by staged severity of various types of diabetic neuropathy, retinopathy, and nephropathy in a population-based cohort: The Rochester Diabetic Neuropathy Study. Neurology 1993;43:817-24.  Back to cited text no. 1
Hanewinckel R, Drenthen J, van Oijen M, Hofman A, van Doorn PA, Ikram MA. Prevalence of polyneuropathy in the general middle-aged and elderly population. Neurology 2016;87:1892-8.  Back to cited text no. 2
Boulton AJ. Diabetic neuropathy: Classification, measurement and treatment. Curr Opin Endocrinol Diabetes Obes 2007;14:141-5.  Back to cited text no. 3
Vinik AI, Maser RE, Mitchell BD, Freeman R. Diabetic autonomic neuropathy. Diabetes Care 2003;26:1553-79.  Back to cited text no. 4
Atroshi I, Gummesson C, Johnsson R, Ornstein E, Ranstam J, Rosén I. Prevalence of carpal tunnel syndrome in a general population. JAMA 1999;282:153-8.  Back to cited text no. 5
Buchberger W, Schön G, Strasser K, Jungwirth W. High-resolution ultrasonography of the carpal tunnel. J Ultrasound Med 1991;10:531-7.  Back to cited text no. 6
Phalen GS. The carpal-tunnel syndrome. Seventeen years' experience in diagnosis and treatment of six hundred fifty-four hands. J Bone Joint Surg Am 1966;48:211-28.  Back to cited text no. 7
Chammas M, Bousquet P, Renard E, Poirier JL, Jaffiol C, Allieu Y. Dupuytren's disease, carpal tunnel syndrome, trigger finger, and diabetes mellitus. J Hand Surg Am 1995;20:109-14.  Back to cited text no. 8
Perkins BA, Olaleye D, Bril V. Carpal tunnel syndrome in patients with diabetic polyneuropathy. Diabetes Care 2002;25:565-9.  Back to cited text no. 9
Onde ME, Ozge A, Senol MG, Togrol E, Ozdag F, Saracoglu M, et al. The sensitivity of clinical diagnostic methods in the diagnosis of diabetic neuropathy. J Int Med Res 2008;36:63-70.  Back to cited text no. 10
Becker J, Nora DB, Gomes I, Stringari FF, Seitensus R, Panosso JS, et al. An evaluation of gender, obesity, age and diabetes mellitus as risk factors for carpal tunnel syndrome. Clin Neurophysiol 2002;113:1429-34.  Back to cited text no. 11
Hendriks SH, van Dijk PR, Groenier KH, Houpt P, Bilo HJ, Kleefstra N. Type 2 diabetes seems not to be a risk factor for the carpal tunnel syndrome: A case control study. BMC Musculoskelet Disord 2014;15:346.  Back to cited text no. 12
Kim YH, Yang KS, Kim H, Seok HY, Lee JH, Son MH, et al. Does diabetes mellitus influence carpal tunnel syndrome? J Clin Neurol 2017;13:243-9.  Back to cited text no. 13
Akulwar AS, Ghugare BW, Singh R, Kanchankar N, Joshi N, Ramavat M. Clinical and electrophysiological evaluation of carpal tunnel syndrome in diabetes mellitus to assess association of age, gender and duration of diabetes on median neuropathy at wrist. Health Agenda 2013;1:71-6.  Back to cited text no. 14
Oge A, Demir S, Gemalmaz A, Ak F. Relationship between carpal tunnel syndrome and polyneuropathy in diabetics: Is the polyneuropathy a risk factor or not? Turk J Endocrinol Metab 2004;1:43-7.  Back to cited text no. 15
Singh R, Gamble G, Cundy T. Lifetime risk of symptomatic carpal tunnel syndrome in type 1 diabetes. Diabet Med 2005;22:625-30.  Back to cited text no. 16
Ramchurn N, Mashamba C, Leitch E, Arutchelvam V, Narayanan K, Weaver J, et al. Upper limb musculoskeletal abnormalities and poor metabolic control in diabetes. Eur J Intern Med 2009;20:718-21.  Back to cited text no. 17
Stevens JC. AAEM minimonograph #26: The electrodiagnosis of carpal tunnel syndrome. American Association of Electrodiagnostic Medicine. Muscle Nerve 1997;20:1477-86.  Back to cited text no. 18
Jablecki CK, Andary MT, Floeter MK, Miller RG, Quartly CA, Vennix MJ, et al. Practice parameter: Electrodiagnostic studies in carpal tunnel syndrome. Report of the American Association of Electrodiagnostic Medicine, American Academy of Neurology, and the American Academy of Physical Medicine and Rehabilitation. Neurology 2002;58:1589-92.  Back to cited text no. 19
Werner RA, Andary M. Electrodiagnostic evaluation of carpal tunnel syndrome. Muscle Nerve 2011;44:597-607.  Back to cited text no. 20
Walter-Sack I, Zöllner N. Unrecognised carpal tunnel syndrome in diabetic polyneuropathy (author's transl). Dtsch Med Wochenschr 1980;105:19-21.  Back to cited text no. 21
Hamilton ML, Santos-Anzorandia C, Viera C, Coutin G, Cordies L. Motor and sensory nerve conduction in patients with carpal tunnel syndrome and diabetic polyneuropathy. Rev Neurol 1999;28:1147-52.  Back to cited text no. 22
Gazioglu S, Boz C, Cakmak VA. Electrodiagnosis of carpal tunnel syndrome in patients with diabetic polyneuropathy. Clin Neurophysiol 2011;122:1463-9.  Back to cited text no. 23
Padua L. Distinguishing in a puddle the water from two rains: A crucial methodological issue. Clin Neurophysiol 2011;122:1277.  Back to cited text no. 24
American Diabetes Association. Standards of medical care in diabetes-2010. Diabetes Care 2010;33 Suppl 1:S11-61.  Back to cited text no. 25
Dyck PJ, Albers JW, Andersen H, Arezzo JC, Biessels GJ, Bril V, et al. Diabetic polyneuropathies: Update on research definition, diagnostic criteria and estimation of severity. Diabetes Metab Res Rev 2011;27:620-8.  Back to cited text no. 26
Bischoff C, Fuglsang-Fredriksen A, Vendelbo L, Sumner A. Standards of instrumentation of EMG. The International Federation of Clinical Neurophysiology. Electroencephalogr Clin Neurophysiol Suppl 1999;52:199-211.  Back to cited text no. 27
Tankisi H, Burke D, Cui L, de Carvalho M, Kuwabara S, Nandedkar SD, et al. Standards of instrumentation of EMG. Clin Neurophysiol 2020;131:243-58.  Back to cited text no. 28
Feldman EL, Stevens MJ, Thomas PK, Brown MB, Canal N, Greene DA. A practical two-step quantitative clinical and electrophysiological assessment for the diagnosis and staging of diabetic neuropathy. Diabetes Care 1994;17:1281-9.  Back to cited text no. 29
Tesfaye S, Boulton AJ, Dyck PJ, Freeman R, Horowitz M, Kempler P, et al. Diabetic neuropathies: Update on definitions, diagnostic criteria, estimation of severity, and treatments. Diabetes Care 2010;33:2285-93.  Back to cited text no. 30
Carrington AL, Shaw JE, Van Schie CH, Abbott CA, Vileikyte L, Boulton AJ. Can motor nerve conduction velocity predict foot problems in diabetic subjects over a 6-year outcome period? Diabetes Care 2002;25:2010-5.  Back to cited text no. 31
Albers JW, Brown MB, Sima AA, Greene DA. Nerve conduction measures in mild diabetic neuropathy in the Early Diabetes Intervention Trial: The effects of age, sex, type of diabetes, disease duration, and anthropometric factors. Tolrestat Study Group for the Early Diabetes Intervention Trial. Neurology 1996;46:85-91.  Back to cited text no. 32
Kim WK, Kwon SH, Lee SH, Sunwoo IN. Asymptomatic electrophysiologic carpal tunnel syndrome in diabetics: Entrapment or polyneuropathy. Yonsei Med J 2000;41:123-7.  Back to cited text no. 33
Celiker R, Basgöze O, Bayraktar M. Early detection of neurological involvement in diabetes mellitus. Electromyogr Clin Neurophysiol 1996;36:29-35.  Back to cited text no. 34
Al-Sulaiman AA, Ismail HM, Al-Sultan AI. Electrophysiological findings in newly diagnosed non-insulin-dependent diabetics: A prospective study. Ann Saudi Med 1997;17:399-401.  Back to cited text no. 35
Rota E, Quadri R, Fanti E, Isoardo G, Poglio F, Tavella A, et al. Electrophysiological findings of peripheral neuropathy in newly diagnosed type II diabetes mellitus. J Peripher Nerv Syst 2005;10:348-53.  Back to cited text no. 36
Stamboulis E, Voumvourakis K, Andrikopoulou A, Koutsis G, Tentolouris N, Kodounis A, et al. Association between asymptomatic median mononeuropathy and diabetic polyneuropathy severity in patients with diabetes mellitus. J Neurol Sci 2009;278:41-3.  Back to cited text no. 37
Ali Z, Hakim M, Islam M, Bhowmik NB, Nahar S, Ullah AA, et al. Role of electrodiagnostic tests in early detection of diabetic neuropathy. Bangladesh J Neurosci 2008;24:34-44.  Back to cited text no. 38
El-Salem K, Ammari F, Khader Y, Dhaimat O. Elevated glycosylated hemoglobin is associated with subclinical neuropathy in neurologically asymptomatic diabetic patients: A prospective study. J Clin Neurophysiol 2009;26:50-3.  Back to cited text no. 39
Garg R, Kumar A, Dhar U. A study of median nerve conduction velocity in diabetes mellitus type 2 in neurologically asymptomatic patients. Int J Health Sci Res 2013;3:1-6.  Back to cited text no. 40
Dyck PJ, Karnes JL, Daube J, O'Brien P, Service FJ. Clinical and neuropathological criteria for the diagnosis and staging of diabetic polyneuropathy. Brain 1985;108:861-80.  Back to cited text no. 41
Karsidag S, Morali S, Sargin M, Salman S, Karsidag K, Us O. The electrophysiological findings of subclinical neuropathy in patients with recently diagnosed type 1 diabetes mellitus. Diabetes Res Clin Pract 2005;67:211-9.  Back to cited text no. 42
Lozeron P, Nahum L, Lacroix C, Ropert A, Guglielmi JM, Said G. Symptomatic diabetic and non-diabetic neuropathies in a series of 100 diabetic patients. J Neurol 2002;249:569-75.  Back to cited text no. 43
Said G. Diabetic neuropathy. Handb Clin Neurol 2013;115:579-89.  Back to cited text no. 44
Allen MD, Kimpinski K, Doherty TJ, Rice CL. Length dependent loss of motor axons and altered motor unit properties in human diabetic polyneuropathy. Clin Neurophysiol 2014;125:836-43.  Back to cited text no. 45
Johnson EW, Kukla RD, Wongsam PE, Piedmont A. Sensory latencies to the ring finger: Normal values and relation to carpal tunnel syndrome. Arch Phys Med Rehabil 1981;62:206-8.  Back to cited text no. 46
Uncini A, Lange DJ, Solomon M, Soliven B, Meer J, Lovelace RE. Ring finger testing in carpal tunnel syndrome: A comparative study of diagnostic utility. Muscle Nerve 1989;12:735-41.  Back to cited text no. 47
Jackson DA, Clifford JC. Electrodiagnosis of mild carpal tunnel syndrome. Arch Phys Med Rehabil 1989;70:199-204.  Back to cited text no. 48
Uncini A, Di Muzio A, Awad J, Manente G, Tafuro M, Gambi D. Sensitivity of three median-to-ulnar comparative tests in diagnosis of mild carpal tunnel syndrome. Muscle Nerve 1993;16:1366-73.  Back to cited text no. 49
Sander HW, Quinto C, Saadeh PB, Chokroverty S. Sensitive median-ulnar motor comparative techniques in carpal tunnel syndrome. Muscle Nerve 1999;22:88-98.  Back to cited text no. 50
Sheu JJ, Yuan RY, Chiou HY, Hu CJ, Chen WT. Segmental study of the median nerve versus comparative tests in the diagnosis of mild carpal tunnel syndrome. Clin Neurophysiol 2006;117:1249-55.  Back to cited text no. 51
Imada M, Misawa S, Sawai S, Tamura N, Kanai K, Sakurai K, et al. Median-radial sensory nerve comparative studies in the detection of median neuropathy at the wrist in diabetic patients. Clin Neurophysiol 2007;118:1405-9.  Back to cited text no. 52
Alemdar M. Median to ulnar nerve comparative conduction studies on diagnosis of carpal tunnel syndrome in early grades. Turk Klin J Neur 2016;11:1-10.  Back to cited text no. 53
Alemdar M. Ring finger sensorial conduction studies in grading carpal tunnel syndrome. J Back Musculoskelet Rehabil 2016;29:309-15.  Back to cited text no. 54
Han HY, Kim HM, Park SY, Kim MW, Kim JM, Jang DH. Clinical findings of asymptomatic carpal tunnel syndrome in patients with diabetes mellitus. Ann Rehabil Med 2016;40:489-95.  Back to cited text no. 55


  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5]


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