To appreciate the full significance and gravity of such a process, it is only necessary to realize the complex and widely radiating rela tion of the great epigastric or solar plexus. It supplies all the ab dominal viscera. It receives the great splanchnic nerve on both sides of the body, part of the lesser splanchnics and the termination of the right pueumogastric nerve. Its semilunar ganglia are the largest in the body, and they lie close to the adrenal glands. Ten different nervous plexuses issue from the solar plexus. One of them, the ad renal plexus, is formed by branches from the solar plexus, from the semilunar ganglia, and from the splanchnic and phrenic nerves, a ganglion being situated at the junction of the latter nerve. This plexus is remarkable for its large size in relation to the smallness of the organ it ministers to. The other plexuses are the phrenic, coeliac, gastric, hepatic, splenic, renal, superior mesenteric, spermatic, and inferior mesenteric. We may now comprehend the magnitude of the interference with due performance of nervous function which is neces sarily entailed by the fibro-sclerosing process already described, and find explanation therefrom for many of the specific features and symp toms pertaining to Addison's disease. So markedly is this the case, that some observers regard the essential nature of the malady as de pending rather on the nerve-changes entailed by the disease of the adrenals than on the specific lesion in those organs. It is at all events certain that some examples of Addison's disease have been met with in which no primary changes were observable in the adrenal bodies, but solely in the semilunar ganglia.
This brings us face to face with the conflicting theories that have been advanced respecting the etiology of the disease, and these must now receive attention. Much difficnity has arisen from the fact that aberrant forms of Addison's disease have been met with. Addison believed that the train of symptoms he described would ensue in any form of destructive lesion which involved the adrenals, and in his me moir he gives the particulars of four cases in which these organs were destroyed by cancer. At a later period, his pupil Dr. Wills pointed out that in these cases the true symptoms of Addison's disease were not really present, and it is now generally recognized that cancer of the adrenals does not produce this disease. We are therefore con fronted with the strange fact that mere destruction of the adrenals is not in itself a necessary cause of true Addison's disease. The doc trine of Guy's Hospital School has generally supported the view that the destructive changes are practically specific in this disease, and are of the nature already described. In other words, the lesion is a tubercular one.
There is sufficient evidence now to prove that the adrenals may be gravely diseased without inducing Addison's disease. Death may ensue from other causes or complications such as phthisis or nephritis before melasma sets in. As will be shown later, malignant growths may occur in the adrenals of primary or of secondary character, sometimes of large size, and death ensues without the characteristic concomitants of Addison's disease. In such instances, we may fairly
believe that the processes are too rapid to lead to the involvement of the adjacent nervous structures in the manner characteristic of pro gressive and sclerosing tuberculosis. In this connection it was noted by Moxon that even large cancerous growths in the liver often fail to set up jaundice.
Further difficulties, however, await us, and we have to account for cases in which melasma occurs, as a leading symptom, without any obvious disease of the adrenals. We have already discussed the vari eties of melasma which may often simulate the specific adrenal form, and it is quite certain that many of the examples brought forward in support of the view now under consideration may be safely relegated to other categories of pigmentation.
By far the most important class of cases to excite doubt as to the special nature of Addison's disease is that in which obvious symp toms of the malady occur, leading to death, and in which no gross changes are found in the adrenals, but instead atrophy, sometimes to the most extreme degree, is discovered. Some of the most careful and competent pathologists are agreed upon these facts, and they must be accepted and reckoned with (Coupland): I am myself well satisfied on the point. The adrenals may thus be most difficult of detection in making an autopsy, and entire absence of any remaining structure has been noted. Small thin masses or relics of the gland may be found, little more than collections of pigmented granules, or organs shrunk to one third or less of their natural size and weight. Both glands may be absent in cases of this nature. We have no knowledge whatever respecting the occurrence of congenital absence of one or other of the adrenals. We have already pointed out that a gland may exist in its proper situation in cases of congenital ab sence of one kidney. But in the cases now before us we have to deal with a definite train of symptoms sufficiently recognized as indicating Addison's disease as a whole, in which, during life, we decide that the adrenaLs are unquestionably involved. Death occurs, and we ex pect to find, almost certainly, that the adrenals are the seat of gross lesions and enlargement. On the contrary, we find atrophic condi tions more or less pronounced. In most of the recorded cases illus trating the latter condition, there have been found associated changes in the adjacent nervous ganglia and sympathetic fibrils. This fact is of prime importance in the case, and we are at once led to inquire whether these remarkable trophic changes in the adrenals may not be the result of primary disease in these nervous structures so remarka bly associated with the glands in question. This is Dr. Coupland's interpretation of the difficulty. He thus conceives that the adrenals waste under the same influences that evolve the symptoms and the fatal cause of the malady.