TERATOLOGY 41:239 (1990)
Letters
Comments on “Proposed Mechanisms of Action in Thalidomide Embryopathy” To the Editor: I wish to dissociate my name from the hypothesis stated by T.D. Stephens in his paper “Proposed Mechanisms of Action in Thalidomide Embryopathy” published in this journal (Stephens, ’88). Stephens writes that “the McCredie-McBride hypothesis states that neural tissues exert a n inductive influence on the development of the limb, that thalidomide damages neural tissues, and that, a s a result, the developing limb buds are growth retarded, resulting in limb malformations.” No source for this statement is quoted, so that its origin is obscure. I wish to state quite clearly that no such statement has ever been published in my name and that I disapprove of its content. Only one publication has ever appeared in the name of McCredie and McBride (’73). The conclusion of that paper is as follows: The radiological observations and certain other factors as outlined lead the authors to propose the following hypothesis: 1. The assumption that Thalidomide directly injures mesodermal cells is possibly incorrect. 2. The teratogenic action of Thalidomide is probably on the sensory neurone, specifically the neural crest and its derivatives (posterior root ganglia, autonomic nerves, cartilages of the face and spinal canal). 3. Mesodermal effects secondary to this are reduction deformities of the limbs (peripheral sensory neurone), visceral atresias, aplasias and other anomalies (autonomic nervous system), microtia, microphthalmia, cleft palate, spina bifida (cartilage).
0 1990 WILEY-LISS, INC.
This hypothesis has become known as the neural crest hypothesis. No eponym is needed. My research group has continued to explore this hypothesis, a s originally defined, with some 30 publications, sadly overlooked by Stephens in his review article. McBride introduced the terms “neural tissue” and “inductive influence” and has published numerous papers based on modifications of the neural crest hypothesis. He has never acknowledged my original X-ray observations and analyses as the source of the neural crest hypothesis. The radiology identified pathology in the neural crest, quite specifically. I do not know what is meant by the term “neural tissues,” and the hypothesis loses in specificity what it gains in breadth by substitution of this term. I have never used the term “induction,” and I do not approve the statement t h a t “neural tissues exert a n inductive influence on the development of the limb.” I have certainly never made such a statement. It is unreasonable, therefore, that my name should be attached to a conglomerate statement that I have never made and with which I strongly disagree. LITERATURE CITED Stephens, T.D. (1988) Proposed mechanisms of action in thalidomide embryopathy. Teratology, 38t229-239. McCredie, J., and W.G. McBride (1973) Some congenital abnormalities: Possibly due to embryonic peripheral neuropathy. Clin. Radiol., 24:204-211.
JANET MCCREDIE Department of Surgery University of Sydney Sydney, N.S.W. 2006, Australia
Letters
Comments on “Proposed Mechanisms of Action in Thalidomide Embryopathy” To the Editor: I wish to dissociate my name from the hypothesis stated by T.D. Stephens in his paper “Proposed Mechanisms of Action in Thalidomide Embryopathy” published in this journal (Stephens, ’88). Stephens writes that “the McCredie-McBride hypothesis states that neural tissues exert a n inductive influence on the development of the limb, that thalidomide damages neural tissues, and that, a s a result, the developing limb buds are growth retarded, resulting in limb malformations.” No source for this statement is quoted, so that its origin is obscure. I wish to state quite clearly that no such statement has ever been published in my name and that I disapprove of its content. Only one publication has ever appeared in the name of McCredie and McBride (’73). The conclusion of that paper is as follows: The radiological observations and certain other factors as outlined lead the authors to propose the following hypothesis: 1. The assumption that Thalidomide directly injures mesodermal cells is possibly incorrect. 2. The teratogenic action of Thalidomide is probably on the sensory neurone, specifically the neural crest and its derivatives (posterior root ganglia, autonomic nerves, cartilages of the face and spinal canal). 3. Mesodermal effects secondary to this are reduction deformities of the limbs (peripheral sensory neurone), visceral atresias, aplasias and other anomalies (autonomic nervous system), microtia, microphthalmia, cleft palate, spina bifida (cartilage).
0 1990 WILEY-LISS, INC.
This hypothesis has become known as the neural crest hypothesis. No eponym is needed. My research group has continued to explore this hypothesis, a s originally defined, with some 30 publications, sadly overlooked by Stephens in his review article. McBride introduced the terms “neural tissue” and “inductive influence” and has published numerous papers based on modifications of the neural crest hypothesis. He has never acknowledged my original X-ray observations and analyses as the source of the neural crest hypothesis. The radiology identified pathology in the neural crest, quite specifically. I do not know what is meant by the term “neural tissues,” and the hypothesis loses in specificity what it gains in breadth by substitution of this term. I have never used the term “induction,” and I do not approve the statement t h a t “neural tissues exert a n inductive influence on the development of the limb.” I have certainly never made such a statement. It is unreasonable, therefore, that my name should be attached to a conglomerate statement that I have never made and with which I strongly disagree. LITERATURE CITED Stephens, T.D. (1988) Proposed mechanisms of action in thalidomide embryopathy. Teratology, 38t229-239. McCredie, J., and W.G. McBride (1973) Some congenital abnormalities: Possibly due to embryonic peripheral neuropathy. Clin. Radiol., 24:204-211.
JANET MCCREDIE Department of Surgery University of Sydney Sydney, N.S.W. 2006, Australia
