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 [in Japanese] Prolonged Diabetic Peroneal Nerve Palsy Resulting in Muscle Atrophy [in Japanese]
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腓骨神経麻痺は，比較的短期の経過で自然軽快する糖尿病性単神経障害として知られている．今回われわれは，同麻痺が持続し筋萎縮をきたした症例を経験した．症例は55歳，男性．1994年に糖尿病と診断されたが放置し，1998年から経口血糖降下薬を開始されたがHbA<sub>1C</sub> 9%台と血糖コントロールは不良であった．2003年1月，右大腿部のしびれと鈍痛に続き右下腿のしびれと歩行時のつまずきが出現したため，2004年5月当科を初診し，同年6月精査目的で入院した．入院時HbA<sub>1C</sub> 5.4%であった．深部腱反射低下，四肢末梢のしびれに加え，腓骨神経領域のTinnel徴候陽性，筋力低下，神経伝導速度の著明な低下，前脛骨筋萎縮を認めた．退院後もHbA<sub>1C</sub>は5～6%であったが，腓骨神経麻痺はわずかな改善にとどまった．過去の大量飲酒による神経障害や糖尿病性筋萎縮症の合併も疑われ，それらにより腓骨神経麻痺が遷延した可能性が推察された．
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 (HbA<sub>1C</sub>) 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 HbA<sub>1C</sub> 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 HbA<sub>1C</sub> 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 HbA<sub>1C</sub> 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.
- Journal of the Japan Diabetes Society
Journal of the Japan Diabetes Society 49(5), 337-341, 2006-05-30
THE JAPAN DIABETES SOCIETY