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Year : 2018  |  Volume : 45  |  Issue : 1  |  Page : 30-33

Nerve conduction abnormalities in patients with newly diagnosed diabetes mellitus

1 Department of Neurology, Jawaharlal Nehru Medical College and KLE's Dr. Prabhakar Kore Hospital and MRC, Belagavi, Karnataka, India
2 Department of Endocrinology, Jawaharlal Nehru Medical College and KLE's Dr. Prabhakar Kore Hospital and MRC, Belagavi, Karnataka, India

Date of Web Publication27-Jul-2018

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DOI: 10.4103/jss.JSS_21_18

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Background: Peripheral neuropathy is the most common neurologic complication of diabetes mellitus (DM). The incidence of neuropathy increases with increasing duration of diabetes. Diabetes may be preceded by a long period of clinically silent impaired glucose tolerance, altering the nerve function by the time diabetes is diagnosed. Objectives: Assessment of early electrophysiological evidence of peripheral neuropathy in patients with newly diagnosed DM. Materials and Methods: Patients with newly diagnosed type 2 DM within 1 month of detection with or without clinical features of neuropathy were prospectively recruited. Nerve conduction studies were performed on the right upper and lower limbs. Sympathetic skin response and heart rate variability were studied. Results: Twenty-four patients (14 men and 10 women) with newly diagnosed DM were included in the study whose age was 57.66 ± 14.52 years. Eight patients had distal paresthesiae in the lower limbs of whom two had sensory deficit and two had mild motor deficit clinically. Thirteen patients (54.16%) had abnormal sensory conductions and nine patients had abnormal motor conductions. F-wave latencies were significantly prolonged in the upper and lower limbs. Sympathetic skin response was absent in four patients and R-R variation was subnormal in ten patients. Nerve conduction parameters showed correlation with increasing age and hyperglycemia values. Conclusion: Patients with newly detected diabetes have high incidence of clinically manifest and subclinical peripheral neuropathy.

Keywords: F-waves, nerve conduction studies, neuropathy, newly diagnosed diabetes mellitus

How to cite this article:
Kulkarni AP, Saroja AO, Naik KR, Ghatnatti V, Hesarur N. Nerve conduction abnormalities in patients with newly diagnosed diabetes mellitus. J Sci Soc 2018;45:30-3

How to cite this URL:
Kulkarni AP, Saroja AO, Naik KR, Ghatnatti V, Hesarur N. Nerve conduction abnormalities in patients with newly diagnosed diabetes mellitus. J Sci Soc [serial online] 2018 [cited 2022 Dec 5];45:30-3. Available from: https://www.jscisociety.com/text.asp?2018/45/1/30/237756

  Introduction Top

Peripheral neuropathy is the most common neurologic complication of diabetes mellitus (DM). It is a microvascular complication of DM and its incidence increases with increasing duration of diabetes and has a negative influence on morbidity and quality of life. Clinical scores that assess diabetic neuropathy including the diabetic neuropathy symptom score, diabetic neuropathy examination, and neuropathy disability score are used. The diagnostic efficacies of these scores were found to be 65.4%, 40%, and 66.7%, respectively, with nerve conduction study (NCS) as the gold standard.[1] Thermal quantitative sensory testing thresholds were reported to be abnormal in up to 27.5% of newly diagnosed type 1 diabetic patients.[2]

Age and duration of diabetes correlated with the degree of neuropathy whereas plasma glucose and body mass index (BMI) were not significantly associated.[3] Incidence of electrophysiological evidence of polyneuropathy has ranged from 8.3% to 15.2%.[4],[5] Reported electrophysiological abnormalities in patients with newly diagnosed DM have been variable. Ulnar motor conduction velocity was significantly slower in newly diagnosed diabetic group compared to controls.[6] Upper limb sensory conductions were found to be more sensitive in detecting neuropathy in newly diagnosed DM.[7] Motor conduction velocities were significantly abnormal than sensory nerve conduction parameters in an Indian study.[8]

This prospective study was conducted to evaluate the presence of clinical and electrophysiological abnormalities of peripheral nerve involvement in patients with newly diagnosed DM.

  Materials and Methods Top

Patients with newly diagnosed DM attending neurology and endocrinology outpatient clinic were prospectively recruited in the study from November 2016 to December 2017 after obtaining institutional ethical clearance. Diagnosis of diabetes was based on the American Diabetes Association criteria[9] and patients were recruited within 1 month of the diagnosis of diabetes after obtaining informed consent. Patients with known neuropathy due to other causes and radiculopathy were excluded from the study. Patients were evaluated for clinical evidence of peripheral neuropathy.

All patients underwent detailed neurological examination and their BMI was calculated. Motor NCS and elicitation of F-waves were performed on median, ulnar, and common peroneal nerves. Sensory conduction study was performed on median, ulnar, superficial peroneal, and sural nerves on the right side. Sensory conductions were performed on median and ulnar nerves (orthodromic). Sensory conductions were performed on superficial peroneal and sural nerves (antidromic). Nerve conduction studies were done using Nihon Kohden MEB-9400 system at ambient temperature. Standard system settings were used for the study. Data from the patients were compared with normative data of the laboratory.

Data were entered and analysis was performed using SPSS software version 20.0 for Windows. Independent sample t-test was used to compare parametric variables in diabetic patients and controls. Karl Pearson's correlation coefficient was used to assess correlation between hyperglycemia (HbA1c), age, and BMI with the nerve conduction parameters of the patients. Differences were considered statistically significant at a P < 0.05.

  Results Top

Twenty-four consecutive patients, 14 men and 10 women, with an average age of 57.66 ± 14.52 years were included in the study. The interval from detection of diabetes to inclusion in the study ranged from 1 to 26 days (median 4 days). Eight patients had distal paresthesiae in the lower limbs of whom two had sensory deficit. Two patients had mild distal symmetrical weakness at ankle and toes. BMI of the patients was 26.18 ± 3.87 kg/m2. None had sensory symptoms in the upper limbs. Examination revealed loss of sweating and hair in distal lower limbs in two patients. One patient had presented with acute right lower motor neuron facial palsy. Fasting blood glucose values ranged from 99 to 275 mg/dl (170.79 ± 49.59 mg/dl), the postprandial blood glucose values ranged from 185 to 442 mg/dl (269.79 ± 86.12), and the HbA1c ranged from 6.8% to 16.6% (10.45 ± 2.86%).

Nerve conduction studies were normal in 11 patients. Thirteen patients (54.16%) had abnormal nerve conduction studies of whom nine had motor and sensory conduction abnormalities and only four had isolated abnormality in sensory conductions. Sensory nerve conductions revealed reduced velocity in six and decreased sensory nerve action potential (SNAP) amplitude in seven patients. Motor nerve conduction studies revealed reduced compound muscle action potential (CMAP) amplitude in nine patients and two of these patients had distal weakness. Two patients were found to have asymptomatic median neuropathy across the wrist. Sympathetic skin response was absent in four patients and R-R variation was subnormal in ten patients.

Distal motor latencies of the median and the common peroneal nerves were higher, and CMAP amplitude of the common peroneal nerve was significantly reduced. Motor conduction velocities of the median, ulnar, and the common peroneal nerves were significantly reduced in patients with diabetes. SNAP amplitudes were significantly reduced in superficial peroneal and sural nerves, and sensory conduction velocities were found to be significantly reduced in median, superficial peroneal, and sural nerves. F-wave latencies were significantly prolonged in median, ulnar, and common peroneal nerves [Table 1].
Table 1: The nerve conduction parameters in the patients compared with the normative data

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There was negative correlation with median motor conduction velocity, common peroneal distal motor amplitude, median sensory amplitude, superficial peroneal amplitude, and the sural nerve amplitude with increasing age of the patients (P < 0.05). Patients with higher HbA1c had prolonged distal motor latencies and reduced conduction velocities in the upper and lower limbs with reduction of CMAP amplitude in the ulnar nerve. Median nerve sensory amplitude and velocity were lower in patients with higher HbA1c (P < 0.05). Other nerve conduction parameters did not correlate with HbA1c level. There was no correlation between the BMI and any of the motor or sensory conduction parameters of the upper or lower limb nerves.

  Discussion Top

Patients with newly detected diabetes may have asymptomatic peripheral neuropathy and altered autonomic nerve function identified by electrophysiological and cardiovascular reflex methods.[5] Mechanisms of neuropathy in DM include increased endothelial vascular resistance and reduced nerve blood flow. There is depletion of nerve myoinositol and activation of polyol pathway through enzyme aldose reductase leading to accumulation of sorbitol and fructose in endoneurium. This induces nonenzymatic glycosylation of structural nerve proteins.[10]

Electrophysiological incidence of peripheral neuropathy has been generally about 30%.[11],[12] However, some studies have reported higher incidence going up to 82%.[7] The variation in prevalence may be attributable to the methodological differences, mean HbA1c levels, and duration of undiagnosed HbA1c. Our study identified electrophysiological abnormalities of peripheral neuropathy in 54.16% of the patients.

The present study revealed abnormalities in the nerve conduction parameters in patients with newly diagnosed diabetes which correlated with the HbA1c values and age. The most common type of neuropathy was length-dependent sensory neuropathy. This is being attributed to altered axoplasmic flow and accumulation of fructose and sorbitol. Tingling was the most common symptom similar to other study on Indian patients with newly diagnosed diabetes.[12]

Functional changes have been demonstrated in large fibers as well as autonomic fibers in patients with no clinical evidence of neuropathy. Hence, it is vital to conduct detailed electrophysiological evaluation of small and large fibers even in asymptomatic patients.[13] The Verona Newly Diagnosed Type 2 Diabetes Study reported the prevalence of confirmed cardiac autonomic neuropathy (CAN) as 1.8% whereas that of early CAN as 15.3% in the entire cohort of 557 patients with newly diagnosed type 2 diabetes.[14] Our study demonstrated electrophysiological evidence of autonomic neuropathy in the form of the absence of sympathetic skin response in four patients and subnormal R-R variation in ten patients. Thus, autonomic and large fiber sensory neuropathy predominates compared to motor abnormalities in newly detected diabetes.

F-waves evaluate the whole length of the motor axon and the excitability of the motor units. Adding F-wave latencies to motor and sensory conductions improved the sensitivity of detection of electrophysiologic abnormalities from 3% to 36% in asymptomatic patients of diabetes in one study.[15] We report significant prolongation of F-wave latencies in the median, ulnar, and common peroneal nerves in our patients of newly diagnosed diabetes.

Our patients had higher HbA1c which could probably indicate diagnostic delay in Indian patients due to the lack of awareness and periodic health checkups. Reducing mean HbA1c by 1% with treatment has been shown to reduce the risk of microvascular complications by 37%.[16]

de Souza et al. reported slowing of motor conduction velocity and reduction in amplitude of SNAP to be the earliest evidence of diabetic neuropathy in asymptomatic patients. This is followed by prolongation of sensory latencies, reduction of sensory velocity, and later by reduction in amplitudes of CMAP when patients are likely to manifest clinically.[17] This explains the clinical and electrophysiological evolution of diabetic neuropathy.

Rota et al. found NCS alterations of distal median motor neuropathy across the wrist in 42% of the patients with newly diagnosed diabetes.[7] In our study, distal motor latencies were significantly prolonged in the patients’ group, whereas ulnar distal latencies were normal. Two patients in the study were found to have asymptomatic carpal tunnel syndrome (CTS). The prevalence of CTS is reported to be 2% of general population, and studies have demonstrated CTS in 14% of participants of diabetes without polyneuropathy.[18] Ulnar nerve conduction parameters were not significantly altered in our patients of diabetes as opposed to those of the median nerve. Similar observation was reported by Rota et al. for the motor conductions although not for the sensory conductions (50% and 17% for median and ulnar motor conductions, respectively).[7]

  Conclusion Top

Electrophysiologic abnormalities of large-fiber and autonomic function are common in patients with newly diagnosed diabetes. Occurrence of electrophysiologic changes in nerve function correlates with age and degree of HbA1c. Nerve conduction studies in patients with newly diagnosed DM are required to identify patients with subclinical impairment of nerve function.

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  References Top

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Zoppini G, Cacciatori V, Raimondo D, Gemma M, Trombetta M, Dauriz M, et al. Prevalence of cardiovascular autonomic neuropathy in a cohort of patients with newly diagnosed type 2 diabetes: The Verona newly diagnosed type 2 diabetes study (VNDS). Diabetes Care 2015;38:1487-93.  Back to cited text no. 14
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