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糖尿病患者における中枢伝導障害の検討
https://kindai.repo.nii.ac.jp/records/2001563
https://kindai.repo.nii.ac.jp/records/20015631c20669f-c07c-4987-826c-c09f37e33788
| 名前 / ファイル | ライセンス | アクション |
|---|---|---|
AN00063584-19951225-0175.pdf
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| Item type | ☆紀要論文 / Departmental Bulletin Paper(1) | |||||||||
|---|---|---|---|---|---|---|---|---|---|---|
| 公開日 | 2024-07-12 | |||||||||
| タイトル | ||||||||||
| タイトル | 糖尿病患者における中枢伝導障害の検討 | |||||||||
| 言語 | ja | |||||||||
| タイトル | ||||||||||
| タイトル | Delayed central conduction time in diabetes mellitus | |||||||||
| 言語 | en | |||||||||
| 著者 |
上山, 勝生
× 上山, 勝生
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| 言語 | ||||||||||
| 言語 | jpn | |||||||||
| キーワード | ||||||||||
| 主題 | central motor conduction time, diabetes mellitus, magnetic stimulation, short latency somatosensory evoked potential, brainstem auditory evoked potential | |||||||||
| 資源タイプ | ||||||||||
| 資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||||||
| 資源タイプ | departmental bulletin paper | |||||||||
| 版 | ||||||||||
| 出版タイプ | AM | |||||||||
| 出版タイプResource | http://purl.org/coar/version/c_ab4af688f83e57aa | |||||||||
| 出版者 名前 | ||||||||||
| 出版者 | 近畿大学医学会 | |||||||||
| 言語 | ja | |||||||||
| 書誌情報 |
ja : 近畿大学医学雑誌 en : Medical Journal of Kinki University 巻 20, 号 2, p. 175-188, 発行日 1995-12-25 |
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| ISSN | ||||||||||
| 収録物識別子タイプ | PISSN | |||||||||
| 収録物識別子 | 03858367 | |||||||||
| 内容記述 | ||||||||||
| 内容記述タイプ | Abstract | |||||||||
| 内容記述 | To elucidate clear the pathophysiological state of the central nervous system in diabetics, a systematic electrophysiological study was done, using motor evoked potentials (MEPs) by magnetic stimulation, short latency somatosensory evoked potentials (SSEPs), and brainstem auditory evoked potentials (BAEPs). Brain magnetic resonance imaging (MRI) was examined in diabetics for considering the vascular factor in the lesion. Twenty-seven healthy volunteers (mean age 53.2±9.8 years old) and 66 diabetics (mean age 56.8±11.3 years old) were enrolled. The diabetics were classified into two groups according to Dyck's criteria : one with asymptomatic neuropathy (stage 0 or 1, twenty-four patients, mean age 57.4±8.0 years old) and the other with symptomatic neuropathy (stage 2 or 3, forty-two patients, mean age 56.5±12.9 years old). The MEPs from the abductor pollicis muscle in the upper extremities were recorded after magnetic stimulation at the scalp (hand motor cortex) or neck (cervical nerve roots). The MEPs from the flexor hallucis muscle in lower extremities were also measured following magnetic stimulation at the scalp (foot motor cortex) or back (lumbar nerve roots). Central motor conduction time (CMCT) was determined by the difference of MEP latencies between the cortical and the spinal stimulation. Somatosensory evoked potentials after median nerve stimulation or posterior tibial nerve stimulation were measured according to previous reports by Nakamura and the central sensory conduction time (CSCT) was obtained by subtraction of the spinal evoked potential from cortical evoked potential. BAEPs were also evaluated using a routine technique. There was no significant difference in the CMCT in the upper extremities between diabetics and normal subjects. CMCT to the lower extremities in the diabetics with asymptomatic neuropathy was significantly prolonged than that in the normal subjects. Also the CSCT from the lower extremities in diabetics significantly showed more prolongation than that in the normal subjects. Latencies of greater than three standard deviations from the mean were defined as abnormal. The abnormal rate in the CMCT of the upper extremities was 10～13% in diabetics and that in the CMCT of the lower extremities was 7～13%. Impairment of central motor conduction in at least one muscle was found in 16% of the diabetics. The prolongation of the CSCT from the upper extremities was 0～2% and from the lower extremities was 7～8%. These findings showed that the conductivity concerning the lower extremities was greater than that with the upper extremities which had to conduct over a longer tract. Prolongation of interpeak latency I-III of BAEPs was detected in 6% in the asymptomatic neuropathy group and in 17% in the symptomatic group. The impairment of central conduction in diabetics was highly frequent with acoustic conduction and motor conduction but rare in sensory conduction. The distribution of these abnormally conducted tracts was sporadic. These central conduction changes did not correlate with other diabetic clinical parameters. The brain MRI in diabetics often showed multiple lacunae (38%) but these lacunae were not correlated to the conduction disturbance in the brainstem. On the other hand the abnormal rate of central conductivity in the symptomatic neuropathy group was higher than that in the asymptomatic group. These findings suggest that the conduction disturbance in the central nervous system of diabetics did not appear as often as in diabetic peripheral neuropathy, but might be induced by diabetic microangiopathy as in peripheral neuropathy. | |||||||||
| 言語 | en | |||||||||
| 内容記述 | ||||||||||
| 内容記述タイプ | Other | |||||||||
| 内容記述 | 本文データはCiNiiから複製したものである。 | |||||||||
| 言語 | ja | |||||||||
