The presence of hypertrophied fibres in wasting muscles lends a special significance to the cases of true muscular hypertrophy described by Auerbach56 and Hitzig.57 Auerbach's observation related to a soldier aged twenty-one, whose upper arm became rather rapidly hypertrophied and paretic. In a fragment excised from the enlarged biceps the fibres were seen to have a diameter of from 96 to 180 µ. (the normal diameter being 33 to 67 µ.). The other arm was not enlarged, and yet examination of fibres obtained by means of a similar excision found them also enlarged. Auerbach suggests that this hypertrophy constituted a preliminary stage in the general process of pseudo-hypertrophic paralysis. In it, as when the excessive volume is known to depend upon the presence of non-contractile tissue, the arm, far from increasing in strength, was paretic.58
56 Virch. Arch., Bd. liii., 1871.
57 Berlin. klin. Wochen., Dec. 2, 1872.
58 Mobius (loc. cit.) declares that neither of these cases bears any relation to pseudo-hypertrophy.
Connective Tissue.—Far more conspicuous than the alterations in the contractile fibre of the muscles are those of its connective tissue. The perimysium internum, between the primitive bundles, proliferates abundantly, and the hyperplasia gradually extends correlatively with the wasting of the muscular fibres, until the hypertrophied mass is mainly composed of connective tissue. Broad bands replace the thin lamellæ normally present between the primitive bundles; the parenchyma of the muscle seems stifled in a sclerosis. It is then that it offers the feeling of stony hardness so often noticed in the clinical history.
Charcot, Knoll, Müller, and Barth describe a rich development of nuclei and of spindle-shaped cells in this new connective tissue, this being especially abundant in the neighborhood of the small vessels and in their adventitia. Eulenburg and Leyden, however, affirm that the connective tissue is unusually poor in nuclei, and thence infer that the hyperplasia is compensatory, and not due to inflammation.
In some cases, as in those of Duchenne examined by Ordonez, the sclerosis and atrophy of contractile tissue constitute the entire lesion of the muscle. Only a few fat-cells are interspersed among the bands of connective tissue or penetrate between the primitive bundles. The fatty infiltration tends constantly to increase, apparently by the same process as governs the growth of normal adipose tissue—namely, the deposit of fat in connective-tissue cells; and ultimately not only muscular fibre, but the hyperplastic connective tissue, is concealed in a yellowish glistening mass indistinguishable from a lipoma.59
59 See case of Billroth.
The growth of fat contributes to the apparent hypertrophy of the diseased muscles, but much less so than does the hyperplasia of connective tissue which invariably precedes it. Great rapidity of fatty infiltration marks a more rapid and irresistible progress in the disease, a lower stage of nutritive degradation. Fat-cells are found penetrating between the primitive bundles of fibres in the atrophied as well as in the hypertrophied muscles; but there the fatty substitution is always much less complete.
In contrast with this fatty infiltration true fatty degeneration of the muscular fibre is as rare in pseudo-hypertrophy as in progressive muscular atrophy. This fact is emphasized by Pepper from observation of the harpooned fragment examined by him,60 also by Cohnheim.61 In Meryon's first case,62 however, the post-mortem examination of the muscular fibres found them "totally degenerated, their substance changed into a mass of granules and oil-globules, while the sarcolemma was destroyed." In Brieger's case63 the fibres were filled with fat-globules.