A new compression syndrome of the deep branch of the radial nerve is described, in which a sudden anterior displacement of a part of this nerve under maximal tension is followed by an axonotmesis. This happens in an area in which the deep branch of the radial nerve crossed some narrow structures which are unyielding and have more compression strength (tense cords of connective tissue Fig. 3). The operative finding of a torsion of the injured fascicles justifies the correctness of the immediate operative revision; otherwise the nerve regeneration would be impaired by the torted empty endoneural tubes. This description is a further constribution not observed before to the compression syndromes of the radial nerve, since in 1970 the author was able to give an explanation for the pathogenesis of compression palsies of the radial nerve, unclear up to that time but observed after forceful muscle contractions again and again since the beginning of this century. This observation gives the evidence that the occurrence of a peripheral compression lesion of nerves is not bound absolutely on the existence of a "physiological narrowness" (fibrous or osteofibrous tunnel etc.). This is also true for the median nerve.
本文描述了一种新的桡神经深支卡压综合征，在此综合征中，该神经的一部分在最大张力下突然向前移位，随后发生轴索断裂。这种情况发生在桡神经深支穿过一些狭窄、坚硬且具有更强压迫力的结构（结缔组织的紧张索带，图3）的区域。手术中发现受损束支发生扭转，这证明了立即进行手术修复的正确性；否则，扭曲的空神经内膜管会损害神经再生。这一描述是对桡神经卡压综合征的进一步贡献，此前未曾观察到，因为在1970年作者能够对桡神经压迫性麻痹的发病机制做出解释，在此之前其发病机制尚不清楚，但自本世纪初以来，在强力肌肉收缩后反复观察到这种情况。这一观察结果证明，神经外周压迫性病变的发生并不绝对取决于“生理性狭窄”（纤维性或骨纤维性隧道等）的存在。正中神经也是如此。
