Wang Ping-Hui, Yang Cheng-Chang, Su Wei-Ren, Wu Po-Ting, Cheng Shun-Chien, Jou I-Ming
Department of Orthopedics, Chi-Mei Medical Center.
Institute of Basic Medical Sciences, College of Medicine, National Cheng Kung University.
J Pain Res. 2017 Mar 20;10:643-652. doi: 10.2147/JPR.S125693. eCollection 2017.
To determine susceptibility to decompression surgery in diabetic and nondiabetic peripheral neuropathy using a chronic compression neuropathy model.
Twenty-four streptozotocin-induced diabetic rats were randomly divided into three groups: group I, chronic compression of the left sciatic nerve for 4 weeks with decompression; group II, similar without decompression; and group III, sham exposing the sciatic nerve only. The other 24 nondiabetic rats were assigned to groups IV-VI, which received compression-decompression, compression, and the sham operation, respectively. Mixed-nerve-elicited somatosensory evoked potentials (M-SSEPs) and compound muscle action potentials (CMAPs) were measured to verify the compression neuropathy in the posttreatment follow-up. Behavioral observations in thermal hyperalgesia tests were quantified before electrophysiologic examinations. Treated and contralateral nerves were harvested for histomorphologic analysis.
Chronic compression of sciatic nerve induced significant reduction of amplitude and increment of latency of M-SSEP and CMAP in both diabetic and nondiabetic rats. Diabetic group changes were more susceptible. Decompression surgery significantly improved both sensory and motor conduction, thermal hyperalgesia, and the mean myelin diameter of the rat sciatic nerve in both diabetic and nondiabetic groups. Near full recovery of motor and sensory function occurred in the nondiabetic rats, but not in the diabetic rats 8 weeks postdecompression.
Behavioral, electrophysiologic, and histomorphologic findings indicate that decompression surgery is effective in both diabetic and nondiabetic peripheral neuropathy.
使用慢性压迫性神经病变模型确定糖尿病性和非糖尿病性周围神经病变对减压手术的易感性。
将24只链脲佐菌素诱导的糖尿病大鼠随机分为三组:第一组,对左侧坐骨神经进行4周慢性压迫并减压;第二组,进行类似操作但不减压;第三组,仅对坐骨神经进行假暴露。另外24只非糖尿病大鼠被分配到第四至六组,分别接受压迫-减压、压迫和假手术。在治疗后的随访中测量混合神经诱发的体感诱发电位(M-SSEP)和复合肌肉动作电位(CMAP),以验证压迫性神经病变。在电生理检查前,对热痛觉过敏试验中的行为观察进行量化。采集治疗侧和对侧神经进行组织形态学分析。
坐骨神经的慢性压迫导致糖尿病和非糖尿病大鼠的M-SSEP和CMAP的波幅显著降低以及潜伏期延长。糖尿病组的变化更敏感。减压手术显著改善了糖尿病和非糖尿病组大鼠的感觉和运动传导、热痛觉过敏以及坐骨神经的平均髓鞘直径。非糖尿病大鼠在减压8周后运动和感觉功能几乎完全恢复,但糖尿病大鼠未恢复。
行为学、电生理学和组织形态学研究结果表明,减压手术对糖尿病性和非糖尿病性周围神经病变均有效。