Prolonged Diabetic Peroneal Nerve Palsy Resulting in Muscle Atrophy

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  • Kanai Akiko
    Department of Medicine, Diabetes Center, Tokyo Women's Medical University Department of Medicine, Kidney Center, Tokyo Women's Medical University
  • Teno Shinichi
    Department of Medicine, Diabetes Center, Tokyo Women's Medical University
  • Ohya Junko
    Department of Medicine, Diabetes Center, Tokyo Women's Medical University
  • Ishii Akiko
    Department of Medicine, Diabetes Center, Tokyo Women's Medical University
  • Kanno Hiroko
    Department of Medicine, Diabetes Center, Tokyo Women's Medical University
  • Nakagami Tomoko
    Department of Medicine, Diabetes Center, Tokyo Women's Medical University
  • Takeuchi Megumi
    Department of Neurology, Neurological Institute, Tokyo Women's Medical University
  • Iwamoto Yasuhiko
    Department of Medicine, Diabetes Center, Tokyo Women's Medical University

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Other Title
  • 腓骨神経麻痺が長期化し筋萎縮をきたした2型糖尿病の1例
  • 症例報告 腓骨神経麻痺が長期化し筋萎縮をきたした2型糖尿病の1例
  • ショウレイ ホウコク ヒコツ シンケイ マヒ ガ チョウキカ シ キン イシュク オ キタシタ 2ガタ トウニョウビョウ ノ 1レイ

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Abstract

Peroneal nerve palsy is a type of diabetic mononeuropathy that usually results in self-limited symptoms. We experienced a type 2 diabetic patient who suffered from peroneal nerve palsy for more than one year, resulting in crus muscle atrophy. The patient was a 55-year-old Japanese man who had no remarkable past medical history except for a habit of drinking 720 ml of sake a day for 30 years. He was diagnosed as having diabetes mellitus in 1994, but he did not receive regular treatments. Although he started to take an oral hypoglycemic agent in 1998, his glycohemoglobin (HbA1C) level remained at 9-10%. In 1999, the patient was pointed out diabetic retinopathy for the first time. Since then, he started medical nutrition therapy. His HbA1C immediately fell to 7-8%. He suddenly felt paresthesia and a pricking in his right femoral region, and right crus numbness, hypersthenia and drop foot soon appeared thereafter. He visited our hospital in May 2004 and was admitted for further examinations for peroneal nerve palsy. On admission, his HbA1C was 5-6%, deep reflexes were absent or reduced, and pallanesthesia and numbness in limbs, a Tinnel sign for the right peroneal nerve, atrophy in the anterior tibial muscle, and right drop foot were observed. A nerve conduction study (NCS) revealed right peroneal nerve palsy. Although his HbA1C level was maintained within 5-6% for 6 months after discharge, nerve conduction studies performed at 3 and 6 months after discharge showed that his peroneal nerve palsy had only slightly recovered. Peroneal nerve palsy may have persisted for a long period, resulting in muscle atrophy, in the present patient because of the presence of not only diabetic mononeuropathy, but possible alcoholic neuropathy and proximal diabetic neuropathy.

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