Early Electrophysiological Abnormalities and Clinical Neuropathy

A prospective study in patients with type 1 diabetes

  1. Jeanette Wahlberg-Topp, MD, PHD3
  1. 1Section of Neurology, Department of Clinical Neuroscience, Karolinska Institutet, Karolinska Hospital, Stockholm, Sweden
  2. 2Section of Clinical Neurophysiology, Department of Clinical Neuroscience, Karolinska Institutet, Karolinska Hospital, Stockholm, Sweden
  3. 3Department of Medical and Health Sciences, Linköping University and Östergötland County Council, Linköping, Sweden
  4. 4Department of Women’s and Children’s Health, Uppsala University, Uppsala, Sweden
  5. 5Division of Paediatrics, Department of Clinical and Experimental Medicine, Linköping University and Östergötland County Council, Linköping, Sweden
  1. Corresponding author: Lars Hyllienmark, lars.hyllienmark{at}karolinska.se.

Abstract

OBJECTIVE The aim of this study was to elucidate whether subclinical nerve dysfunction as reflected by neurophysiological testing predicts the development of clinical neuropathy in patients with type 1 diabetes.

RESEARCH DESIGN AND METHODS Fifty-nine patients were studied twice with neurophysiological measurements at baseline and at follow-up. At baseline, patients were 15.5 ± 3.22 years (range 7–22 years) of age, and duration of diabetes was 6.8 ± 3.3 years. At follow-up, patients were 20–35 years of age, and disease duration was 20 ± 5.3 years (range 10–31 years).

RESULTS At baseline, patients showed modestly reduced nerve conduction velocities and amplitudes compared with healthy subjects, but all were free of clinical neuropathy. At follow-up, clinical neuropathy was present in nine (15%) patients. These patients had a more pronounced reduction in peroneal motor nerve conduction velocity (MCV), median MCV, and sural sensory nerve action potential at baseline (P < 0.010–0.003). In simple logistic regression analyses, the predictor with the strongest association with clinical neuropathy was baseline HbA1c (R2 = 48%, odds ratio 7.9, P < 0.002) followed by peroneal MCV at baseline (R2 = 38%, odds ratio 0.6, P < 0.006). With the use of a stepwise forward analysis that included all predictors, first baseline HbA1c and then only peroneal MCV at baseline entered significantly (R2 = 61%). Neuropathy impairment assessment showed a stronger correlation with baseline HbA1c (ρ = 0.40, P < 0.002) than with follow-up HbA1c (ρ = 0.034, P < 0.007).

CONCLUSIONS Early defects in nerve conduction velocity predict the development of diabetic neuropathy. However, the strongest predictor was HbA1c during the first years of the disease.

  • Received October 30, 2012.
  • Accepted March 30, 2013.

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This Article

  1. Diabetes Care
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