Ziegler D, Mühlen H, Dannehl K, Gries F A
Diabetes Research Institute, Heinrich-Heine-University, Düsseldorf, Germany.
J Neurol Neurosurg Psychiatry. 1993 Jan;56(1):58-64. doi: 10.1136/jnnp.56.1.58.
To determine whether central nervous conduction deficits are related to the degree of peripheral neuropathy somatosensory evoked potentials (SEP) were measured after tibial nerve stimulation in 51 healthy subjects aged 39.3 (SE 2.0, (range 21-71) years and 100 insulin dependent diabetic patients aged 37.3 (1.5, 18-73) years. Five criteria were used for staging of peripheral neuropathy: nerve conduction; thermal discrimination threshold; vibration perception threshold; tendon reflexes; and neuropathic symptoms. Thirty seven patients had fewer than two abnormalities among the first four criteria and no symptoms (stage 0 = no neuropathy), 37 had 2 or more abnormalities but no symptoms (stage 1 = subclinical neuropathy); 26 had 2 or more abnormalities in conjunction with symptoms (stage 2 = symptomatic neuropathy). Multiple regression analysis was used to define the age and height dependent limits of normal of SEP at the 97.5th and 2.5th centiles. In five patients with stage 1, seven patients with stage 2, but no patient with stage 0 the individual SEP components were unrecordable. The relative frequencies of abnormally prolonged or non-evokable popliteal N8 latency as well as cortical N33 latency and N33/P40 amplitude increased significantly from stage 0 (3-30%) to stage 1 (22-62%) and stage 2 (46-84%) (p < 0.05 for each component and stage). The numbers and percentages of abnormal recordable spinal N22-30 and supraspinal N30-33 interpeak latencies were two (6.3%) and four (11.8%) in patients with stage 0, but these rates did not increase in subjects with stage 1 or 2. The components of SEP were significantly associated with the indices of peripheral and autonomic function tests. There were no major relations between the latencies of SEP and duration of diabetes or prevailing glycaemic control. These findings suggest that the degree of dysfunction along the somatosensory afferent pathways in insulin dependent diabetic patients depends on the stage of peripheral neuropathy; is not related to the degree of glycaemic control or duration of diabetes; and can be characterized mainly by an alteration of the cortical sensory complex and peripheral transmission delay, while spinal and supraspinal conduction deficits are detected infrequently.
为了确定中枢神经传导缺陷是否与周围神经病变程度相关，对51名年龄为39.3（标准误2.0，范围21 - 71）岁的健康受试者以及100名年龄为37.3（1.5，18 - 73）岁的胰岛素依赖型糖尿病患者进行了胫神经刺激后的体感诱发电位（SEP）测量。采用五项标准对周围神经病变进行分期：神经传导；温度辨别阈值；振动觉阈值；腱反射；以及神经病变症状。37名患者在前四项标准中异常少于两项且无症状（0期 = 无神经病变），37名患者有两项或更多异常但无症状（1期 = 亚临床神经病变）；26名患者有两项或更多异常并伴有症状（2期 = 有症状神经病变）。采用多元回归分析确定SEP在第97.5和第2.5百分位数时年龄和身高相关的正常范围。在5名1期患者、7名2期患者中，但0期患者无一例，SEP的各个成分无法记录。异常延长或无法引出的腘窝N8潜伏期以及皮层N33潜伏期和N33/P40波幅的相对频率从0期（3 - 30%）到1期（22 - 62%）和2期（46 - 84%）显著增加（每个成分和分期p < 0.05）。0期患者中可记录到异常的脊髓N22 - 30和脊髓上N30 - 33峰间潜伏期的数量和百分比分别为2例（6.3%）和4例（11.8%），但在1期或2期受试者中这些比率并未增加。SEP成分与周围和自主神经功能测试指标显著相关。SEP潜伏期与糖尿病病程或当前血糖控制情况之间无主要关联。这些发现表明，胰岛素依赖型糖尿病患者体感传入通路的功能障碍程度取决于周围神经病变的分期；与血糖控制程度或糖尿病病程无关；主要表现为皮层感觉复合体改变和周围传导延迟，而脊髓和脊髓上传导缺陷很少见。
