Review of the autopsies recorded would indicate that the lesions in question are brought about sometimes in one, sometimes in another, of these ways—sometimes even, as in Leyden's case, by extension from a meningitis. That sclerosis of the white columns is most frequently a secondary degeneration is indicated by the frequency with which it appears below the lesion of the cornua, by the rarity with which it is found above, and also by the general proportion between its intensity and that of the disease of the gray matter.
We have devoted so much space to consideration of spinal-cord lesions, because they are by far the most constant and the most important; after these rank the structural alterations of the muscles, which received for a while such a preponderance of attention.
Hammond has studied the progress of these changes on the living subject by fragments of fibre successively removed with Duchenne's harpoon. In an incipient stage of degeneration the fibrillæ are found to be irregular and torn,116 the transverse striæ dim; oil-globules are seen arranged according to the long axis of the fibre. In a more advanced stage the transverse striæ nearly disappear, the oil-globules are in large numbers, and fat-corpuscles are also abundant. Finally, the whole specimen is seen as a mass of air-globules. Six weeks later, however, these had in turn disappeared, and there remained a mass of connective tissue.
116 Though, from the method of removal, this appearance cannot be considered as certainly pathological.
This series of changes, however, does not always take place, as Hammond himself recognizes. Laborde117 first described a granular form of muscle atrophy, where the muscular substance gradually wastes away without ever becoming fatty, and leaving a transparent and hyaline sheath. The two forms of fatty and of simple atrophy can be distinguished by the naked eye. In the latter the muscle begins by being thinner or lighter and softer than usual, ultimately turning light brown. The fatty muscle becomes a homogeneous yellowish-white, diversified by occasional remnants of reddish fibres.
117 Loc. cit., p. 131.
Proliferation of the interstitial connective tissue may be combined with either simple or fatty atrophy. A combination of abundant sclerosis and abundant fatty infiltration may lead to a pseudo-hypertrophy of the muscles.
“There cannot be the slightest doubt,” observes Erb, “that the lesions described constitute a degenerative atrophy similar to what may be caused by section or sense traumatism of a peripheric nerve.”
The peripheric nerves have been much less thoroughly studied than the spinal cord. Leyden first directed special attention to the nerves. He found the sciatic altered in two cases,118 in the first by an interstitial neuritis; in the second by partial atrophy. In 1880 the same writer, in an extensive article on poliomyelitis and neuritis,119 greatly extends his views as earlier expressed. Not only does he claim the coexistence of neuritis with spinal-cord disease in atrophic paralysis, but thinks that many cases of this, and also of other forms of paralysis, “lately supposed to originate in the spinal cord, may really begin in any part of the motor apparatus,” thence sometimes generalize throughout the whole apparatus, sometimes remain limited to the original portion affected. Thus, progressive muscular atrophy may sometimes begin in the nerves, sometimes in the muscles, and sometimes in the ganglionic cells of the cord; and this variety of origin explains the discrepancies of opinion which have been held upon the nature of this disease. Similarly, all forms of acute or chronic atrophic paralysis in either children or adults may begin in either the nerves or cord, thence become generalized to both, or remain limited to one part of the spinal motor system. Cases of atrophic paralysis which recover are probably not cases of poliomyelitis at all, but of multiple neuritis, rheumatic, traumatic, or infectious in nature. The regeneration of peripheric nerves is a well-demonstrated possibility, but not that of the cells of the cord. Lead-paralysis is usually confined to the nerves, but sometimes extends to the cord. In diphtheritic paralysis Buhl has found injection, thickening, and granular infiltration of nerves at the union of their anterior and posterior roots;120 and as long ago as 1876, Dejerine, in a case of atrophic paralysis in a syphilitic woman, found varicose swelling of the medullary sheath in the nerves of the paralyzed lower extremities, together with heaping up of the myeline into large drops, colored black in glycerin and osmic-acid preparations. Coincidently, in the cord, at the origin of the same nerves, the number of motor-cells was diminished, and of those that remained the prolongations, and even the body, of the cell were atrophied.121