Bendszus Martin, Wessig Carsten, Solymosi László, Reiners Karlheinz, Koltzenburg Martin
Department of Neuroradiology, University of Würzburg, Würzburg, Germany.
Exp Neurol. 2004 Jul;188(1):171-7. doi: 10.1016/j.expneurol.2004.03.025.
Acute axonal nerve lesions cause a hyperintense signal on T2-weighted (T2-w) magnetic resonance imaging (MRI) at the nerve lesion site and distal to it. The aim of this experimental study was to investigate the spatiotemporal evolution and resolution of MR nerve signal changes following denervation and reinnervation, and to relate these findings to electrophysiology and histology. The proximal sciatic nerve of adult rats was ligated by a tight suture that was removed 1 week later to induce complete axotomy and nerve regeneration upon release. Serial electromyography (EMG) and motor nerve conduction studies were performed parallel to MRI at multiple points of time. Moreover, sciatic nerves were taken for quantitative histological evaluation. Nerve hyperintensity on T2-w MRI was present distal to the lesion at thigh level 24 h after denervation preceding the occurrence of spontaneous activity on EMG by 24 h. After 48 h, the entire sciatic nerve and its branches showed an increased signal down to the level of the lower leg. The increased nerve signal regressed with a proximo-distal gradient beginning from week 2 after onset of nerve regeneration in the thigh. On EMG, the first reinnervation potentials were detected at that time at the respective level. Compound muscle action potential (CMAP) in the foot muscle fully recovered 12 weeks after onset of nerve regeneration, that is, 2 weeks after resolution of the hyperintensity along the entire nerve on MRI. Histology revealed axonal degeneration in the acute phase and later nerve oedema parallel to the increased nerve signal on MRI. MR signal alterations occur as early as 24 h after an axonal nerve lesion and correlate with nerve fiber degeneration and later with nerve oedema on histology. MR findings in denervation and reinnervation parallel the electrophysiological changes. Thus, MRI is a promising diagnostic tool for the early detection of acute axonal nerve lesions and monitoring of nerve regeneration.
急性轴索性神经损伤在T2加权(T2-w)磁共振成像(MRI)上,神经损伤部位及其远端会出现高信号。本实验研究的目的是探究去神经支配和再支配后MR神经信号变化的时空演变及消退情况,并将这些发现与电生理学和组织学相关联。成年大鼠的坐骨神经近端用紧密缝线结扎,1周后移除缝线以诱导完全轴突切断并在松解后实现神经再生。在多个时间点与MRI并行进行连续肌电图(EMG)和运动神经传导研究。此外,取坐骨神经进行定量组织学评估。去神经支配后24小时,在大腿水平病变远端的T2-w MRI上出现神经高信号,比EMG上自发活动的出现早24小时。48小时后,整个坐骨神经及其分支在小腿水平以下均显示信号增强。从大腿神经再生开始后第2周起,增强的神经信号以近端到远端的梯度消退。在EMG上,此时在相应水平检测到首次再支配电位。神经再生开始后12周,足部肌肉的复合肌肉动作电位(CMAP)完全恢复,即MRI上整个神经高信号消退2周后。组织学显示急性期轴突变性,后期神经水肿与MRI上神经信号增强平行。轴索性神经损伤后24小时内即出现MR信号改变,与神经纤维变性相关,后期与组织学上的神经水肿相关。去神经支配和再支配时的MR表现与电生理变化平行。因此,MRI是早期检测急性轴索性神经损伤和监测神经再生的一种有前景的诊断工具。