超声对周围神经慢性卡压损伤引起神经形态学变化的实验研究

目的探讨周围神经慢性卡压损伤后不同时间的声像图变化,以及卡压时间与病理变化之间的关系。方法健康家兔20只,随机均分为5组。4只分离坐骨神经不进行卡压,作为对照组;16只分为4组,分离坐骨神经后,分别神经卡压2,4,6,8周,作为卡压2周组、卡压4周组、卡压6周组、卡压8周组;各组分别去除卡压后即取材行组织形态学观察和病理学检查。超声观察坐骨神经的直径、连续性、外膜边缘整齐与否及内部回声情况;诱发电位仪测定运动神经传导速度(MNCV)和感觉神经传导速度(SNCV)。结果对照组在观察时间段内未见明显改变。各卡压组随卡压时间的延长,神经卡压段及两端内径逐渐增粗,卡压两端局部形成瘤样改变,内部回声逐渐减低,线性回声连续性差,神经外膜逐渐增厚,MNCV和SNCV随着卡压时间延长而减慢。各卡压组神经卡压区域均发生不同程度的轴突肿胀和阶段性脱髓鞘改变,卡压时间越长病理变化越重。卡压2周组神经束内髓鞘轴索和神经束膜纤维出现明显水肿,余各卡压组可见髓鞘崩解,轴突变性,纤维结缔组织增生逐渐明显。各卡压组坐骨神经远端、近端直径较对照组增大,MNCV和SNCV较对照组减慢,差异均有统计学意义(P0.05)。各卡压组坐骨神经直径与MNCV和SNCV均呈负相关(r分别为-0.76和-0.69,P0.05)。结论超声可实时、准确地反映神经慢性损伤后形态的动态变化,周围神经卡压损伤程度与卡压时间成正相关,及早去除卡压有利于损伤神经再生与修复。

Study of nitrasonography on neuromorphology changes of sciatic nerve caused by chronic compression

Objective To explore ultrasonographic changes of peripheral nerve caused by chronic compression in different time and the relationship between compression time and pathological changes. Methods A total of 20 rabbits were randomly divided into 5 groups. One group was selected as control group（n=4）, only having nerves been separated without compression, the other four groups were selected as 2 weeks group, 4 weeks group, 6 weeks group, 8 weeks group after the nerves had been compressed for 2, 4, 6, 8 weeks, respectively. The sonographic characteristics and changes of sciatic nerve in rabbits were observed for each group respectively after compression was relieved. The diameter, continuity, outer membrane and internal echo of sciatic nerve were observed using uhrasonography. Motor nerve conduction velocity （MNCV） and sensory nerve conduction velocity （SNCV） of sciatic nerves were detected using evoked potential instrument. Results No obvious changes were observed in control group on sonographic characteristics and pathological feathers. With the extended compression, the inner diameters of the compressed section and the two terminals were gradually thicken, internal echo of nerves decreased gradually, internal linear echo of nerves was poor continuity and epineurium was gradually thicken. The tissue morphology and pathological examination showed axon swelling and staged demyelination at varied degrees at the compression area of each group. Pathological changes were aggravating as the compression period extended. The obvious edema of myelin sheath axons and membrane fiber of nerve tract were shown in 2 weeks group. Myelin disintegrating, axonal degeneration and obviously generating connective tissue proliferation were found in other compression groups. Compared with control group, proximal and distal diameters of sciatic nerve in eachcompression group were enlarged. MNCV and SNCV decreased with prolonged compression time （P〈0.05）. With prolonged compression time, proximal and distal diameters of sciatic nerves in each compression group were enlarged and both compression ends of nerves were shown as tumor-like shapes. MNCV and SNCV were slowed with prolonged compression time. The diameters of sciatic nerves were negative correlated with MNCV and SNCV （r=-0.76,-0.69, P〈0.05）. Conclusion Morphological and functional changes of the compressed nerve can be observed using uhrasonography. There is a positive correlation between compression injury degree and compression time. Compression releasing early is beneficial for regeneration and repair of injured nerves.