The experimental production of deafness in young animals by diet / by Edward Mellanby.
- Edward Mellanby
- Date:
- [1938?]
Licence: In copyright
Credit: The experimental production of deafness in young animals by diet / by Edward Mellanby. Source: Wellcome Collection.
23/32 (page 393)
![In contrast to the great susceptibility of the cochlear nerve to compression and other injuries of its central branch, the resistance of the vestibular nerve to compression and elongation, which has been demonstrated above (Figs. 4, 5), is noteworthy. The experiments of other workers have also demonstrated this fact, for cutting the central branch of the vestibular neurone, as in the case of most other afferent nerves, produces only temporary derangement of Scarpa’s ganglion and no degeneration of the peripheral branch [Hallpike, 1937]. Thus the better preserved condition of the vestibular nerve in comparison with that of the cochlear nerve again supports the view that the nerve destructive changes are mechanical in origin and are due to bone overgrowth. The point under discussion, namely, whether bone overgrowth is directly responsible for the degeneration of the 8th nerve, is of fundamental importance and obviously cannot rest at the present point. The nerve degeneration produced by these vitamin A-deficient diets is widespread and includes not only the 8th nerve but also the optic and trigeminal nerves, the posterior roots of the spinal cord and many ascending fibres in the cord, including the endogenous nerve fibres of the anterior and posterior spino-cerebellar tracts. If, therefore, bone overgrowth is responsible for the death of the auditory nerve, it would be expected that the degenerative change in all the other nerves, peripheral and central, would have a similar cause. It is, therefore, desirable that the evidence that the auditory nerve has been killed in these experimental animals because of the overgrowth of bone should be as clear as possible, and that the possibility that the bone overgrowth is secondary to degeneration of the nerve or that both bone overgrowth and nerve degeneration are independent of each other but dependent upon some third factor should be excluded. On the whole, the evidence of the present experiment that the over¬ growth of bone of the labyrinthine capsule is responsible for the death of the nerves is as clear as can probably be expected. It is hoped that further experiments in which slight degrees of change are produced will help to settle the point at issue. Even so, however, the present results demanded that the investigation should be extended to see how the other nerves of the brain and spinal cord, which are also known to degenerate under these nutritional conditions, are affected by bone overgrowth in their immediate neighbourhood. This work is now being done and it is already clear that there is much bone hyperplasia in the neighbourhood of the optic and trigeminal nerves. Indeed the skull in immediate contact with the base of the brain,](https://iiif.wellcomecollection.org/image/b30631087_0023.jp2/full/800%2C/0/default.jpg)
