Armauer Hansen, Neisser and Leloir have not been able to find any leprous affection of the cord. The cases with changes in the cord, described by Langerhans and Steudener, were, in our view, not leprosy. Tschiriew’s case, Lepra tubero-anæsthetica, presented no marked changes.
Looft has found, in two cases of maculo-anæsthetic leprosy, degeneration of the posterior columns, atrophy of the posterior roots and fibrous degeneration of the spinal ganglia, with disappearance of the medullary fibres, and changes in the nerve cells. In these two cases the affection appeared to be primary in the ganglia, and secondary in the cord. Lepra bacilli were not found in either case, but Chariotti found them once in the cord, and Suderkowitsch in the spinal ganglia.
From all this we can only conclude that the cord is affected in some cases, in others not; definite clinical symptoms are absent, and where they suggest a central cause, they may be equally well ascribed to a peripheral neuritis.
The lymphatic glands related to the affected skin are swollen, but not nearly so much so as in nodular leprosy. After death one usually finds the glands but little swollen, and their appearance presents nothing characteristic. In only one case of maculo-anæsthetic leprosy have we found the inguinal glands distinctly leprous, and that two years after the disappearance of the macules. This indicates in the first place that the affection of the glands is due to the same cause in this as in the nodular form, and secondly, that the leprous affection of the glands may last longer than that of the skin. In the same case we found indefinite traces of leprous affection of the liver and spleen, unfortunately so indefinite that we cannot say with certainty whether the liver and spleen are affected with leprosy in this form of the disease. The case occurred in the pre-bacillary era.
The muscular affections, paralysis and atrophy, play a prominent rôle in the maculo-anæsthetic form of the disease, and the anatomical examination of the muscles is of great interest since some (Neisser)[5] regard it as a specific leprous process, while G. and E. Hoggan[6] had previously described it as secondary, and due to the neuritis. In our[7] examination of various stages of muscular atrophy, we have found that the changes begin with a multiplication of the nuclei of the Perimysium intern., which becomes thicker and thicker; at the same time the muscle fibres become thinner, they retain their transverse striation, and some break up into discs. The greater the thickening of the perimysium the thinner become the muscle fibres, so that one must regard the process as an atrophy due to pressure. The intra-muscular nerves showed interstitial neuritis.
Where the atrophy was very pronounced, as in the small muscles of the hands and feet, the muscular fibres had completely disappeared, and only fat and connective tissue remained. We found no bacilli, not even in sections of very early stages of the process, where the larger nerve branches, relating to the part, contained numerous ones, either in so-called mixed or in true tuberous cases. We must therefore with Hoggan regard the muscular affection in leprosy as a secondary one, caused by neuritis. We have tabulated at the end of this work the results of thirty-six post-mortems on maculo-anæsthetic lepers (see [Table II], page 138).
In those thirty-six cases we find simple meningitis twice, tubercular meningitis once, solitary tubercle in the cerebellum once, and hydrocephalus internus twice. The protocol notes nothing further.
The spinal cord twice showed macroscopic changes (thin and atrophic once, thickening and hyperæmia of the lumbar cord once).
The most of these brains and cords, which are entered as normal, were unfortunately only examined macroscopically.
Two cords thoroughly examined by Weigert’s method showed degeneration of the posterior columns.