124 Centralblatt f. d. Med. Wissensch., No. 15, 1875.
The arrest of development of the bones has been already mentioned, as well as that of their epiphyses and apophyses. The compact osseous tissue is atrophied: the medullary, on the contrary, abundantly developed and rich in fat.
PATHOGENY OF INFANTILE PARALYSIS.—In the pathological anatomy of infantile paralysis there are two principal facts to be correlated with its clinical phenomena—namely, the limitation of the myelitis to the anterior gray horns of the spinal cord; the destruction of the ganglionic nerve-cells in these gray horns. That the other lesions observed are subordinate to these is shown by their variableness as compared with the constancy of the anterior poliomyelitis. These lesions are, in the cord, the atrophy and sclerosis of the anterior nerve-roots and white columns; in the muscle, the fatty degeneration or simple atrophy of the fibre; in the nerve, breaking down, and finally atrophy of the myeline sheath, sometimes of the axis-cylinder; proliferation of the endoneurium.
Consequence of Limitation of Myelitis.—Limitation of the morbid process to a portion of the motor tract, the anterior cornua, and exclusion of the posterior horns and roots, readily explain the predominant positive symptom of motor paralysis, together with the absence of sensory disturbance. The absence of muscular rigidity, spasm, active contraction, and of exaggerated reflexes is similarly explained by the immunity from the morbid process of the posterior white columns and the portion of the lateral columns immediately adjacent to them. The motor paralysis resulting from destruction of the anterior ganglionic cells of the cord is much more complete than that which depends on simple interruption of the motor tracts passing from the brain. The manner in which the motor tracts are connected by a succession of arching fibres with these cells already indicates that the latter are dépôts for the reinforcement of the motor impulses. We must believe, indeed, that the centrifugal impulses reaching the anterior cornua are not yet motor in character, but to become so must sustain a new elaboration in the ganglionic cells of this region. Evidently, the network of gray fibres connecting the arcuate strands of the antero-lateral columns with the cells become, in virtue of that fact alone, essential to the process. But it is also probable that the multiplied transmission of impressions, which lies perhaps at the basis of the process of their higher elaboration in ganglionic centres, is carried on in the larger network of gray fibres as well as in the smaller network contained in the ganglionic cells. Destruction of a portion of this network would therefore interfere with the elaboration of the motor impulse, in the same manner, though to a relatively less extent, as destruction of the ganglionic cells themselves.
Trophic Lesions.—The rapid wasting of the paralyzed muscles, with their degenerative electrical reactions, seems, however, to be an effect altogether peculiar to lesions of the ganglionic bodies.125 According to Charcot, who has so especially formulated the laws of amyotrophic paralysis, all the ganglionic cells essential to the elaboration of motor impulses exercise a trophic influence upon muscles. The spinal cell, nerve-fibre, and muscle-fibre combine into a complex indissoluble unity or element. One part of this lesion of complex elements is necessarily followed by proportionate lesion of all its other parts.
125 The amyotrophic lateral sclerosis of Charcot exhibits in an exquisite manner the difference between paralysis without atrophy, caused by sclerosis of the antero-lateral columns, and paralysis with atrophy when the morbid process has extended to the anterior cornua.
According to Erb, however, who extends Samuel's doctrine of special trophic nerves, it is not the motor cells which influence the nutrition of the muscle-fibres with which they are connected, but special trophic cells lying among the others in the anterior cornua. This theory is principally based on the existence of muscular atrophies of central origin (progressive muscular atrophy, bulbar paralysis), unaccompanied for a long time by paralysis.126 Hammond cites as a converse example the anterior poliomyelitis “where the peripheric disturbance is, in the first place, solely one of motility; this is paralysis without atrophy. After a time, which may be as much as six months or even more, the trophic changes begin.”127
126 Ziemssen's Handbuch.
127 Loc. cit., p. 429.
But surely this is an exaggerated emphasis on the exception, rather than the true inference from the rule of rapid wasting in anterior poliomyelitis—a rule so general as to have originated the title atrophic paralysis. Erb gives an ingenious scheme (Fig. 55) of the mental relations of motor and trophic cells with cerebral and spinal nerve-fibres. It will be seen that isolated lesions of one or the other trophic apparatus might occur without paralysis of motor tracts, while simultaneous lesion of the trophic apparatus and of the ganglion-cells, or of the latter, involving the tracts coming from the trophic cells, would cause, as in anterior poliomyelitis, motor paralysis, muscular atrophy, loss of the reflexes, degenerative reaction in nerves and muscles.