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Our asylum superintendents, who are busy men, have not the time necessary to study this subject thoroughly, and it is well that we have men who are scientifically equipped, and of good general education, who can take up this subject and study it in the manner in which it ought to be studied. Kreplin psychiatry is modern psychiatry.
Dr. E. B. Block, of Atlanta; I wish to express my interest in Dr. Mobley's paper, which was an able one on this subject. I desire to call attention to one feature peculiar to the disease which he did not mention, and that is the peculiarity of the hand-shaking of these patients; the limp, loose, extending of the hand, which is given without any grasp, such as ordinarily takes place in greeting. This is a rather characteristic feature of this dis
Dr. Mobley (closing the discussion): While I have said nothing particularly new in my paper, I made an attempt to cover the subject as thoroughly as possible in the time allotted me. It is well for the general practitioner to take this class of patients, especially young children, and place them under the most favorable circumstances. A child with inherited stigmata or mental weakness should not be subjected to anything that will irritate, or at least be trying to him.
That is the only respect in which I thought this paper would excite the interest of the general practitioner, throwing a safegurd around this class of children, when this disease, at or before puberty, is so likely to develop. Of course, it may develop later, even at the age of twentyfive years, but that is still a mooted question.
BY J. CHESTON KING, M.D., ATLANTA.
Acute diseases of the anterior gray cornua are known as acute anterior poliomyelitis or anterior cornual myelitis, or acute atrophic paralysis, or sometimes simply as infantile paralysis. It differs from chronic myelitis or transverse myelitis in that it is selective, limiting itself to the anterior horns of the grey matter.
From one of its names, it might seem that it occurs only in childhood, but it occasionally occurs between ten and twenty years of age, or over that. It is most frequent in children of three years and under, and affects either sex about equally. The time of the year is a most significant factor for the occurrence of this class of cases. They are found to be most numerous in the hot months—June to September.
This might be explained as due to violent heat, followed by sudden chill, as getting wet and exposure to cold produce the disease. But its causes are practically unknown.
Generally the child is taken suddenly ill, with more or less fever, vomiting and perhaps convulsions. It is put to bed, passes a restless night and perhaps no diagnosis can be made at first. The following morning, perhaps, one, two, or even all four, limbs may be completely paralyzed.
Sometimes the trunk muscles are involved. The tem
perature is not very high, but remains stationary for four or five days.
In many cases the onset is very sudden, the paralysis coming on in a few minutes (which is suggestive, that these cases are likely due to hemorrhage or thrombosis of the cord).
Sometimes the paralysis takes one or two days to develop. Sensation is not affected and the power over the bladder and the rectum is not impaired as a rule. There are exceptions to this.
The maximum paralysis is reached either at once or within a very short time. Then it remains stationary for a few days, after which certain muscles will improve in power.
Motor power gradually returns in one part after another, until paralysis is narrowed down, it may be, to one or more limbs, or even to a part of one limb.
One leg, one arm, both legs, arm and leg of the same side may be affected. Within the limbs, certain groups of muscles may be picked out in a manner that is suggestive of spinal cord disease; for instance, in the upper limb the muscles of the hand and forearm, or the deltoid spinati and flexors of the elbow; in the lower limb, the anterior tibial group, or the calf muscles, or the thigh muscles. Within a fortnight, or earlier, the electro-contractility begins to alter and the muscles waste. This wasting marks out the localized character of the disease and these wasted muscles become flaccid at the end of two or three weeks, and if tested electrically they give the reactions of degenerations, viz.: they do not react to a faradie current, or only to a very strong one, and they show increased irritability to the constant current, and especially to the positive pole.
In most cases, but not all, these muscles, which lose
their faradic contractility and rapidly waste lose also, in the course of six months, their excitability to the constant current, and are permanently paralyzed; while in the muscles which ultimately recover the reaction to the two currents is diminished, but not completely lost for both. The distribution of the paralysis is more often seen in the legs than the arms, and it is not, as a rule, symmetrical. The whole limb may be paralyzed, but more commonly certain muscles, which will be seen to correspond to the groups of muscles assigned to the different segments of the brachial and lumbar enlargements of the cord. Even in mild cases, it is probable that some permanent disability will be left. In severer cases, as time goes on, not only do the muscles waste, but the bones of the affected limb are checked in their development, so that it becomes shorter than the opposite. Vasomotor paralysis is seen, the skin becomes cold, purplish and subject to chilblains. Deformities of the foot arise, mainly from the unbalanced action of non-paralyzed muscles; this disease is a fruitful source of club-foot. Where the extensors and flexors of a limb are paralyzed, it is quite flaccid, like a snail.
In cases described by Ferrier-Drummond and Oppenheim, the spinal cord shortly after death was red and softened, and from microscopical examination showed extreme vascularity, especially in the anterior horns, and also in the white columns and the middle and the anterior parts of the posterior horns, the arteries being intensely conjested with minute hemorrhages.
The neuroglia was swollen and in the anterior cornua the changes were most marked, the cells being granular and ill-defined, and processes often absent.
In cases of longer duration softening of the cord has
been found. In the muscles, the muscular fibres in part completely disappear and are replaced by fibrous tissue.
The primary lesion is vascular, in most cases inflammatory, and in some hemorrhagic, but in the absence of an injury, the cause of the lesion is not known.
The destruction of a cell in the anterior horn is followed by atrophy of the muscle fibril, which it supplies; and as the cell is not regenerated, the fibril remains permanently paralyzed and atrophied.
It is not fatal, except where the muscles of respiration are involved.
At the expiration of two weeks the muscles that react to faradism will recover, and those that do not react will either be permanently paralyzed or partially so; in the latter case, as long as the retention of reaction to the constant current remains there is some hope that the faradic reaction may return, and with it the power of the muscle.
At the onset of the attack the patient should be kept absolutely quiet in bed and lie on the face or on one side, and hot applications made to the spine.
We can not repair the destruction of cells, but we can facilitate recovery by maintaining the nutrition of the paralyzed parts. When the attack is due to cold the limb should be kept warm from the first; diaphoretics, as liquor ammoniae acetatis and citrate of potash, should be given; ergot and belladona are also recommended.
After the disease has assumed a stationary condition, cod-liver oil and tonics are used. Local treatment should not be used until at least a month has elapsed. The limb should then be bathed in hot salt and water and rubbed