Peripheral Nerve Function Is Increasingly Impaired During Puberty in Adolescents With Type 1 Diabetes

  1. Päivi H. Riihimaa, MD1,
  2. Kalervo Suominen, MSC2,
  3. Uolevi Tolonen, MD2,
  4. Ville Jäntti, MD2,
  5. Mikael Knip, MD13 and
  6. Päivi Tapanainen, MD1
  1. 1Pediatrics and
  2. 2Clinical Neurophysiology, University of Oulu, Oulu
  3. 3Hospital for Children and Adolescents, University of Helsinki, Helsinki, Finland

    Abstract

    OBJECTIVE—To evaluate the impact of puberty on peripheral nerve function in adolescents with type 1 diabetes.

    RESEARCH DESIGN AND METHODS—Of 138 eligible patients with type 1 diabetes, 100 patients (age >9 years and diabetes duration >2 years) attending an outpatient diabetes clinic and 100 age- and sex-matched healthy control subjects took part in this cross-sectional study. Peripheral motor and sensory nerve conduction tests, cardiovascular reflex tests on the autonomic nervous system, and measurements of vibration-perception threshold (VPT) were performed.

    RESULTS—Nerve conduction velocity (NCV) in the distal motor and sensory nerves, the motor nerve distal latency, and the sensory nerve action potential (SNAP) amplitude were impaired in the adolescent patients with type 1 diabetes. The deterioration in motor NCV, H-reflex latency, and SNAP amplitude became more conspicuous in late puberty and postpuberty and was related to poor metabolic control. A total of 10 patients had distal diabetic polyneuropathy (DP) neurophysiologically, and these patients had significantly lower heart-rate variation in the deep breathing test than the other patients. Three of the patients with DP had peripheral neurological signs or symptoms. A slight difference in the VPT between the patients and control subjects was observed after puberty.

    CONCLUSIONS—Increasing subclinical motor nerve impairment can be detected during late puberty and after puberty, and sensory NCV and SNAP amplitude are reduced in adolescents with type 1 diabetes. Poor metabolic control during puberty appears to induce deteriorating peripheral neural function in young patients with type 1 diabetes.

    Footnotes

    • Address correspondence and reprint requests to Päivi H. Riihimaa, Department of Pediatrics, University of Oulu, P.O. Box 5000, FIN–90014 University of Oulu, Oulu, Finland. E-mail: priihima{at}cc.oulu.fi.

      Received for publication 5 September 2000 and accepted in revised form 5 March 2001.

      A table elsewhere in this issue shows conventional and Système International (SI) units and conversion factors for many substances.

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