some nausea, but to be brief, the ejections of the matter vomited were made without effort. Things went thus for seven or eight days, all treatment was impotent, and I did not know to what cause to attribute these obstinate vomitings, when there arose certain peculiar new phenomena to dissipate all uncertainty. On the next day the voice was hoarse, and the patient was seized with a most painful panting; there was no appreciable lesion of the respiratory apparatus to account for these new accidents; soon the continued trouble of respiration was complicated with an access of dyspnoea, during which asphyxia was imminent, the voice was no longer raucous, but was extinguished; I diagnosticated a compression of the pneumogastrics. Two days afterwards the orthopnoea was continuous, and the patient succumbed. On autopsy I found in the lungs general sero-sanguinolent infiltration and emphysema, such as had been pointed out as following experimental section of the vagi nerves; hence I did not doubt the justness of my diagnosis; and when it was evident to me that there was no compression of the pneumogastric at any point, I took away the nerves themselves. to study them microscopically. This examination shows us on FIG. 1.-The nerve is much thickened; it is formed of fibrous tissue, circumscribing vacuoles which contain numerous fatty globules.

the two sides an atrophic degeneration of the nervous fibres; not simply a fatty degeneration such as I pointed out to you in the two preceding forms, but the fatty transformation with connective proliferation, that is to say, fibro-fatty degeneration or sclerous atrophy. The figures which I present you have been designed by M. Renault, interne of the service, and they faithfully represent this alteration; figure 4 is borrowed from Rokitansky; it exhibits fatty atrophy of the facial nerve; you can easily appreciate the analogies and the differences between these two lesions.

FIG. 2.-A point in the periphery of the pneumogastric after removal of the neurilemma. There is nothing remaining but the fibrous tissue.

In this case it was impossible for me to discover the cause of atrophy of the vagi nerves; to the naked eye the bulb appeared sound, and committing the same fault with Wachsmuth, in the observation I cited you, I neglected to examine it with the microscope. Despite these defects, this case is nevertheless an example clearly marked of atrophy of the pneumogastrics, it is a landmark in the as yet little known history of the alterations of these nerves.

As to the spinal nerves many authors, and especially Kierulf, Hebra, and Löberg, have observed spontaneous atrophy in spe

dalskhed, the anesthetic form of Norwegian leprosy. The lesion in this case partially affected the mixed nerves of the limbs, and it extended itself up to the posterior nervous roots; in certain cases the cords corresponding to the marrow have also been affected.*

FIG. 3.-Central part of the pneumogastric. Much fibrous tissue; certain nervous tubes, the cylinder of which is invisible, and which have a slightly nodulated aspect.

FIG. 4.-(Taken from Rokitansky), sclero-fatty atrophy of the facial nerve.

* Kierulf, Ueber die norwegische Spedalskhed, (Archiv. für path. Anatomie, 1852.)

Such are the principal facts which demonstrate our third form of nervous atrophy; to put it in clear opposition to the two first, I will call it spontaneous atrophy. It results from the preceding analysis that this atrophy, although rare, has already been seen in the vegetative nerves, and in the cranial and spinal nerves. It is not only by its spontaneity that this atrophy differs from the others, but it is also distinguished by its anatomical characteristics. Whilst the two first forms are principally if not entirely made up of a fatty degeneration, the third generally presents along with the fatty organization a hyperplasia of connective elements and amyloid deposits.

It seems from certain analyses of Bibra that they are very poor in water. According to this observer, the proportion of water in the sound nerves is, on the average, 69.5 in man and 63.8 in woman; now, in a woman of sixty-eight, he found in the upper portion of the sciatic 32.4, and in the lower part 39.3, and in the crural only 15. This observation was made upon the atrophied nerves of a limb which had been for a long time paralyzed; we do not know if the mortification also exists in other forms of atrophy. The results indicated by Bibra are the more remarkable, that in cholera, where there is such a considerable loss of water, the proportion of this principle in the nerves appears scarcely diminished. Voit has found in the sciatic of a man 62.9, and in the same nerve of a woman 63.1*.

Spontaneous atrophy of the nerves being anatomically characterized by fatty deposit and connective proliferation, it may be asked if these lesions are not the result of a nevritis. This question, it seems to me, does not allow of an unequivocal response; the situation is the same as for sclerous atrophy of the

Hebra, Skizzen einer Reise in Norwegen (Zeitschr. der k. k. Gesells. der Aerzte zu Wien, 1853.

Löberg, Die Spedalskhed in St. Jürgenhospital Zu Bergen (Norsk. Mogazin-Schmidt Jahrbucher, lxxx).

Compare: Virchow, Remak, Séance de la Soc. Méd. de Berlin, du 2 févier,

1861.

Jaccoud, Les Paralysis, etc., Paris, 1864.

* Birkner, Das Wasser der Nerven, etc. Augsburg, 1859---Hasse, loc. cit.

marrow and brain. The sclero-fatty lesion may be, it is true, the last expression of an inflammatory work, but can also constitute a purely passive process; consequently sclerous atrophy of the nerves, like those of the marrow, and like that of the brain, ought not, in all cases, to be attributed to one and the same origin; as on the one hand there is no constant anatomical criterion which will at once permit the denial or affirmation of the inflammatory character of the alteration, it is less in the anatomical particulars than in the clinical phenomena that we must seek a response to this question; so, only to speak of the atrophy of the nerves, it sometimes presents from its beginning more or less lively pains, whilst under these circumstances it is absolutely silent, and reveals itself only by successive paralyses resulting from degeneration of the nervous cords; when the painful phenomena are very well pronounced and persistent, they reveal an active process, irritative or phlegmasial, which nothing authorizes us to admit when the disease is perfectly indolent and torpid. The importance of the pain in this point of view has already been noticed by Professor Hasse, and like him I hold this clinical criterion as the best test. In certain cases however, the consideration of the lesion itself is not entirely. sterile ; there are sometimes found vestiges of inflammatory injection which have marked the beginning of the pathological work. This is what happened in the very remarkable observation of Duménil, of which I will soon speak to you more fully. Now, gentlemen, that we have cleared up the characters and forms of atrophy of the nerves, I can apply this knowledge to the patient we have before us; the paralysis, the study of the symptoms of which has enabled us to localize it in the separate branches of the spinal nerves, has its cause (atrophy of the nervous branches) which squares marvellously well with the precise diagnosis; the dissemination of the paralyses in the sphere of certain nerves to the exclusion of others, results from the fact that all the branches of the same plexus, and all the twigs of the same trunk, are not atrophied at the same time; precocious atrophy of the muscles, the loss of reflex movements,