A Case of Type 1 Diabetes Mellitus Demonstrating Cerebellar Ataxia and a High Titer of Anti-GAD Antibody

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  • Dochi Yukari
    Department of Diabetes and Endocrine Medicine, Kagoshima University Graduate School of Medical and Dental Science
  • Deguchi Takahisa
    Department of Diabetes and Endocrine Medicine, Kagoshima University Graduate School of Medical and Dental Science
  • Arimura Aiko
    Department of Diabetes and Endocrine Medicine, Kagoshima University Graduate School of Medical and Dental Science
  • Oku Hiroko
    Department of Diabetes and Endocrine Medicine, Kagoshima University Graduate School of Medical and Dental Science
  • Shinohara Kazuya
    Department of Neurology and Geriatrics, Kagoshima University Graduate School of Medical and Dental Science
  • Arata Hitoshi
    Department of Neurology and Geriatrics, Kagoshima University Graduate School of Medical and Dental Science
  • Takashima Hiroshi
    Department of Neurology and Geriatrics, Kagoshima University Graduate School of Medical and Dental Science
  • Nishio Yoshihiko
    Department of Diabetes and Endocrine Medicine, Kagoshima University Graduate School of Medical and Dental Science

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Other Title
  • 小脳失調を呈した抗GAD抗体陽性1型糖尿病の1例
  • 症例報告 小脳失調を呈した抗GAD抗体陽性1型糖尿病の1例
  • ショウレイ ホウコク ショウノウ シッチョウ オ テイシタ コウGAD コウタイ ヨウセイ 1ガタ トウニョウビョウ ノ 1レイ

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Abstract

We herein review the case of a 71-year-old woman who was diagnosed with diabetes mellitus due to a plasma glucose level of 500 ml/dl at 59 years of age and was started on medication. At 61 years of age, she began to receive insulin therapy. At that time, her C-peptide level in the urine was 5 μg/day and her HbA1c level was around 8-9 %. At 70 years of age, she complained of weakness of the left upper and lower limbs, staggering while walking and dysarthria. A T1 high-intensity signal region was found in the basal ganglia on head MRI. The patient's abnormal MRI findings and weakness in the upper and lower limbs disappeared following treatment of the hyperglycemia. However, the symptoms of staggering while walking and dysarthria did not improve. In addition, the titers of serum and cerebrospinal fluid anti-GAD antibodies were 37,000 U/ml and 1,700 U/ml, respectively. Recently, we found several reports of cerebellar ataxia associated with a high titer of anti-GAD antibodies; many of the patients also had diabetes mellitus. We therefore speculate that this case may have been caused by the effects of anti-GAD antibodies. Many reported patients with cerebellar ataxia and a high titer of anti-GAD antibodies also showed hyperglycemia, suggesting that there may be a relationship between cerebellar ataxia with a high anti-GAD antibody titer and hyperglycemia.

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