The 2-stage neuroskeletal pathomechanism of developmental deformities of the limb skeleton. A contribution to the discussion on the McCredie-McBride hypothesis.

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.