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Vibratory perception in diabetics during arrested blood flow to the limb.肢体血流阻断时糖尿病患者的振动觉
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2
Effects of treatment with myo-inositol or its 1,2,6-trisphosphate (PP56) on nerve conduction in streptozotocin-diabetes.肌醇或其1,2,6-三磷酸酯(PP56)治疗对链脲佐菌素诱导的糖尿病大鼠神经传导的影响
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Aldose reductase inhibition, nerve perfusion, oxygenation and function in streptozotocin-diabetic rats: dose-response considerations and independence from a myo-inositol mechanism.链脲佐菌素诱导的糖尿病大鼠中醛糖还原酶抑制、神经灌注、氧合及功能:剂量反应考量以及与肌醇机制无关
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Impaired recovery in diabetic rat nerve following anoxic conduction block.缺氧性传导阻滞后糖尿病大鼠神经恢复受损。
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Subclinical nerve dysfunction in children and adolescents with IDDM.患有胰岛素依赖型糖尿病的儿童和青少年的亚临床神经功能障碍。
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Changes in nodal function in nerve fibres of the spontaneously diabetic BB-Wistar rat: potential clamp analysis.自发性糖尿病BB-Wistar大鼠神经纤维中节点功能的变化:电压钳分析
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Effects of acute experimental diabetes on composite energy metabolism in peripheral nerve axons and Schwann cells.急性实验性糖尿病对周围神经轴突和施万细胞复合能量代谢的影响。
Diabetes. 1981 Nov;30(11):967-74. doi: 10.2337/diab.30.11.967.
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The effect of ischaemia on the excitability of human sensory nerve.缺血对人感觉神经兴奋性的影响。
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Ischemic conduction failure and energy metabolism in experimental diabetic neuropathy.实验性糖尿病神经病变中的缺血性传导衰竭与能量代谢
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Resistance of the diabetic rat nerve to ischemic inactivation.糖尿病大鼠神经对缺血失活的抗性。
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糖尿病患者缺血性阻滞后神经传导和振动觉的延迟恢复

Delayed recovery of nerve conduction and vibratory sensibility after ischaemic block in patients with diabetes mellitus.

作者信息

Lindström P, Lindblom U, Brismar T

机构信息

Department of Neurology, Karolinska Hospital, Stockholm, Sweden.

出版信息

J Neurol Neurosurg Psychiatry. 1997 Sep;63(3):346-50. doi: 10.1136/jnnp.63.3.346.

DOI:10.1136/jnnp.63.3.346
PMID:9328252
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2169712/
Abstract

OBJECTIVES

To determine if the recovery of nerve function after ischaemic block is impaired in patients with diabetes mellitus relative to healthy controls.

METHODS

Median nerve impulse conduction and vibratory thresholds in the same innervation territory were studied in patients with diabetes mellitus (n = 16) and age matched controls (n = 10) during and after 30 minutes of cuffing of the forearm.

RESULTS

Cuffing caused a 50% reduction of the compound nerve action potential (CNAP) after 21.9 (SEM 1.6) minutes in patients with diabetes mellitus and after 10.6 (0.7) minutes in controls. After release of the cuff the half life for CNAP recovery was 5.13 (0.45) minutes in patients with diabetes mellitus and <1 minute in controls. At seven minutes after release of the cuff CNAP was fully restored in the controls whereas in patients with diabetes mellitus CNAP had only reached 75.1 (4.1)% of its original amplitude. After onset of ischaemia it took 14.6 (1.9) minutes in patients with diabetes mellitus before the vibratory threshold was doubled, whereas this took 5.8 (0.8) minutes in controls. After release of the cuff half time for recovery of vibratory threshold was 8.8 (1.0) minutes in patients with diabetes mellitus and 2.6 (0.3) minutes in controls. Ten minutes after the cuff was released the threshold was still raised (2.0 (0.3)-fold) in the diabetes mellitus group, whereas it was normalised in controls. Among patients with diabetes mellitus the impaired recovery correlated with older age, higher HbA1c, and signs of neuropathy, but not with blood glucose.

CONCLUSION

After ischaemia there is a delayed recovery of nerve conduction and the vibratory sensibility in patients with diabetes mellitus. Impaired recovery after ischaemic insults may contribute to the high frequency of entrapment neuropathy in patients with diabetes mellitus.

摘要

目的

确定与健康对照相比,糖尿病患者缺血性阻滞后神经功能的恢复是否受损。

方法

对糖尿病患者(n = 16)和年龄匹配的对照者(n = 10)在前臂袖带绑扎30分钟期间及之后,研究同一神经支配区域的正中神经冲动传导和振动阈值。

结果

在糖尿病患者中,袖带绑扎21.9(标准误1.6)分钟后复合神经动作电位(CNAP)降低50%,在对照者中为10.6(0.7)分钟后。松开袖带后,糖尿病患者CNAP恢复的半衰期为5.13(0.45)分钟,对照者<1分钟。松开袖带7分钟后,对照者的CNAP完全恢复,而糖尿病患者的CNAP仅达到其原始幅度的75.1(4.1)%。缺血开始后,糖尿病患者的振动阈值加倍需要14.6(1.9)分钟,而对照者需要5.8(0.8)分钟。松开袖带后,糖尿病患者振动阈值恢复的半衰期为8.8(1.0)分钟,对照者为2.6(0.3)分钟。松开袖带10分钟后,糖尿病组的阈值仍升高(2.0(0.3)倍),而对照者的阈值已恢复正常。在糖尿病患者中,恢复受损与年龄较大、糖化血红蛋白较高和神经病变体征相关,但与血糖无关。

结论

糖尿病患者缺血后神经传导和振动感觉恢复延迟。缺血性损伤后恢复受损可能导致糖尿病患者卡压性神经病的高发。