Roth M
Radiodiagnostic Clinic, Medical Faculty, J. E. Purkynĕ University, Brno, Czechoslovakia.
Anat Anz. 1988;167(4):271-9.
Experimental skeletal deformities produced in laboratory birds and in frog tadpoles and examined with Williams' technique (1943) suggest a selective inhibitory effect of various teratogens upon the vulnerable growth of peripheral nervous trunks. The exaggerated osteoneural growth differential resulting therefrom is compensated for by adaptive deformities (buckling, achondroplasic stunting, dislocation) of otherwise normally growing bones which, though independent of innervation under normal conditions, have to "respect" the growth insufficiency of the nervous trunks and to accommodate along them during the proximo-distal development of the limb, even at the cost of a gross deformity. The McCredie-McBride hypothesis, on the other hand, is aimed at explanation of skeletal defects by an early neuroskeletal (neurotrophic) disturbance within the limb bud. Aneurogenic limbs produced experimentally do not necessarily militate against the existence of neuroskeletal relations in the early limb bud postulated, above all, by the McCredie-McBride hypothesis. These relations have been firmly established during the phylogenetic history so that artificial aneurogenic limb, never evolved by Nature, may grow up by (phylo)genetic inertia even without any neural involvement during the individual ontogenesis.
在实验室鸟类和蛙蝌蚪身上制造的实验性骨骼畸形，并采用威廉姆斯技术（1943年）进行检查，结果表明各种致畸剂对外周神经干的脆弱生长具有选择性抑制作用。由此产生的骨骼与神经生长差异过大，会通过原本正常生长的骨骼出现适应性畸形（弯曲、软骨发育不全性发育迟缓、脱位）来补偿，这些骨骼在正常情况下与神经支配无关，但在肢体由近及远的发育过程中，不得不“顺应”神经干的生长不足，并沿着神经干生长，即便以严重畸形为代价。另一方面，麦克雷迪-麦克布赖德假说旨在通过肢芽内早期的神经骨骼（神经营养）紊乱来解释骨骼缺陷。实验产生的无神经肢体不一定会对上述麦克雷迪-麦克布赖德假说所假定的早期肢芽中神经骨骼关系的存在构成挑战。这些关系在系统发育史上已经牢固确立，以至于自然界从未进化出的人工无神经肢体，可能会因（系统）发育惯性而生长，即使在个体发育过程中没有任何神经参与。
