which sensation, as well as motion, is lost. But such cases, which are most rare, differ from true transverse myelitis in the rapidity with which the damage restricts itself to its special seat, and the functions of the white columns are restored. The fact that these are diseased in only a secondary and trifling manner is emphasized by the fact that, even in these cases, there are never the acute bedsores that would surely ensue in a case of true transverse or total myelitis of corresponding seat.

The observations mentioned on p. 366 suggest that there are two varieties of the inflammation of the grey matter, such as we have recognised in myelitis generally; a parenchymatous inflammation consisting in a primary change in the nerve-cells, and an interstitial or general inflammation, as in the common forms of myelitis, involving the nerve-cells only as one of many structures equally damaged by a process that has no special relation to the nerveelements. The distinction is important, because we should expect to find, in the former cases, a wider slight initial affection than in the others, and finally a more definite relation to function in the parts diseased.

The true pathology of the malady, its relation to its causes, is still obscure. The one salient fact that we can discern, though scarcely define, is the evidence of a blood-state afforded by the general symptoms. That these symptoms are not the consequence of the local inflammation is shown by their disparity in degree and difference in time. It is probable, therefore, that the spinal lesion is not the cause of the constitutional disturbance, but is rather an effect of the cause of the latter. It seems impossible otherwise to understand the extreme variation in the two forms of disturbance. But we have no evidence as to the nature of the blood-state, and there are no other effects, commonly associated with the myelitis, to indicate the general pathological tendency of its cause. The closest analogy is with some forms of multiple neuritis, and this, as we have seen, may co-exist with the spinal lesion, as a consequence, at any rate, of exposure to cold. The variations, alike in the general symptoms, and in the inflammation of the cord, and especially the indications that the latter may be either parenchymatous or interstitial, suggest that the causal state also varies considerably in different cases. We have no indication of the way in which the remarkable relation to season is produced, whether by predisposing the individual or favouring the development of some toxic agent. We must, however, recognise as an essential element the predisposing influence of age, which we may associate with the facts that the structural development of the nervous system is complete, but the function of the nerve-elements must lack the stability that comes only from continued use, and that the period is one of the first serious demand on the functional energy of the grey matter of the cord. We may remember also the vascular activity that all function entails, and the readiness with which the vaso-motor system VOL. I.

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of children is disturbed. Such a glimpse of the pathological relations of the disease is all that we can at present obtain.

DIAGNOSIS. This rarely presents any difficulty except in the early stage. When the initial paralysis is passing away, and the wasting is distinct, the nature of the case is sufficiently evident, and is cor roborated by the electrical reactions, by the loss of reflex action, and by the absence of any impairment of sensibility. At the onset, however, the symptoms may readily be misinterpreted. The most common error is to attach too much importance to vomiting, and to regard the attack as simply gastric. General disturbance is naturally ascribed to some general cause until nervous symptoms manifest themselves. Even then there is risk of error. On the one hand, as we have seen, a diagnosis of a general disease is not always relinquished when paralysis appears, but the latter is regarded as secondary. On the other hand, especially in young children, the existence of paralysis is often overlooked at first, and it is supposed that the child does not move because it is prostrate. This error will not be made if it is remembered that mere prostration never causes total immobility, and à fortiori it does not produce local immobility. When the pyrexia ceases, and the loss of power persists and increases, the existence of paralysis is always unmistakable. The initial general disturbance must then be regarded as part of the disease unless there is the clearest evidence of its independent nature.

In adults, the danger of mistaking paralysis for prostration is considerably less, but, on the other hand, the general symptoms are as likely to be misinterpreted as in the case of children. The rheumatoid pains, which are so common, are usually regarded as evidence of acute rheumatism, especially when the affection follows exposure to cold. Whenever rheumatoid pains are not localised in the joints, and especially when they are spontaneous, and not influenced by movement, the possibility of their spinal (or nerve) origin should be remem. bered, and other indications of spinal mischief, such as local loss of power, tingling or formication, should be carefully watched for and receive due weight.

Of other spinal cord diseases, all chronic lesions are distinguished at once by the onset. From other acute diseases, moreover, the distinction is only difficult in the early stage. As soon as the initial palsy begins to lessen, and the muscles in one part lose faradic irritability and begin to waste, the nature of the case admits of no doubt. The diagnosis may be thus made with certainty after the end of the first week by the electrical reaction. If we find loss of faradie irrita bility, it is certain that the characteristic alteration in vcltaic irrita. bility will follow. The isolated induced shocks should be used, instead of the induced "current," because any harmful stimulation of the sensory nerves is thereby avoided.

Acute transverse myelitis is only simulated when the inflammation of the grey matter is bilateral and so intense as to extend to the

white columns, but the age of the patient generally suggests correctly the nature of the disease. The myelitis of childhood is polio-myelitis. The pseudo-transverse variety-polio-myelitis, transverse through its intensity is seated in one of the enlargements; the true transverse form usually occurs in the dorsal region. Real difficulty is confined to adults, in whom there is extensive cervical or lumbar myelitis involving the grey matter. In young adults, polio-myelitis is more likely; this is indicated also by what is best described as a regressive onset in contrast to one that is progressive. In the former, a wide extent is quickly reached and the symptoms then tend to lessen; in the latter, the morbid process is a longer time reaching its height: in the former, the symptoms clearly show that the most severe affection is of the anterior grey matter; in the latter, severe anesthesia or trophic disturbance may point to an equally intense lesion of the other parts of the cord. If attention is paid to the character and significance of the symptoms, the difficulties will soon vanish; and the cases that present them are really few. Most perplexities will, indeed, be prevented by the recollection of the fact just mentioned, that primary myelitis in children is always polio-myelitis. The separation of subacute from acute myelitis of the grey substance is, to a large extent, arbitrary. The symptoms are similar, but the onset is less rapid and occupies more than a week. The distinction of diphtheritic paralysis and of multiple neuritis is from the subacute rather than the acute spinal atrophies, and is considered in the next section.

The diagnosis from paralysis of cerebral origin is usually easy. In cerebral palsy there is never loss of faradic irritability or extreme muscular wasting, or loss of the muscle-reflex action. In the spinal affection there is no trace of the mobile spasm that is common in infantile hemiplegia. Any cerebral symptoms which may attend the onset of polio-myelitis are subordinate in significance to the state of the muscles, as evidence of the permanent lesion. Convulsions at the onset of infantile spinal paralysis are general; those that result from a cerebral lesion are usually unilateral or commence locally.

The exceedingly slow onset of pseudo-hypertrophic paralysis, developing gradually, as it does, with the child's growth, ought to render its confusion with polio-myelitis impossible. A reasonable doubt can only arise in a slight case in which the onset was unnoticed or forgotten. I have once known slight atrophic palsy of the extensors of the knee to induce the habit of putting the hand on the knee in rising from the ground-an action often thought to be peculiar to the pseudo-hypertrophic disease, but acquired when weakness of the extensors occurs in early childhood from any cause. If this is not known, it may puzzle the observer.

Diseases outside the nervous system which have been mistaken for infantile paralysis are chiefly those in which local pain interferes with the movement of the limbs, and the child is young. I have known, for instance, the mistake to be made in the case of hip-joint disease,

necrosis of the femur, and the affection termed "scorbutic rickets," in which there is enlargement of the shafts of the long bones, extreme pain on movement, and spongy gums. In all these cases, a careful examination will show that movement is interfered with only by the pain; there is no actual paralysis, and there is no interference with reflex action. The preservation of the knee-jerk is often of great significance; it at once excludes atrophic palsy in any case in which the extensors of the knee are weak.

The points above described will always enable the diagnosis to be made. It is impracticable to enumerate the distinctions from every disease with which confusion is possible, for experience shows that there is no form of palsy with which a common disease, such as this, is not at some time confounded.

PROGNOSIS.-The danger to life is probably greatest when there is severe constitutional disturbance, and is in consequence of this, often before the development of the characteristic paralytic symptoms. In the stage of paralysis, there is peril only when the chief disease is in the cervical region, and respiration is interfered with; but this danger is small unless an attack of bronchial catarrh is intensified by the palsy. Definite cerebral symptoms involve danger proportioned to their character and degree, bat it is generally less in reality than in appearance. In the vast majority of cases the disease involves no immediate danger to life. But children are left with little power of resistance to other morbid influences, and occasionally succumb to some other illness, as an acute specific disease, or an attack of bronchitis, a few weeks or months after the onset of the paralysis.

As soon as the paralysis has become stationary, i. e. has not increased for twenty-four hours, the danger of further extension is small. But the question at once arises, and is anxiously asked,What will be the permanent condition? Will there be lasting paralysis? An answer cannot be given until the end of the first week or ten days, and then only by means of an electrical examina tion. Whatever muscles, at the end of that time, have lost faradic irritability, will certainly waste, will remain for a long time paralysed, and will probably be permanently affected in some degree, slight or On the other hand, if there is no loss of irritability at the end of ten days, but it is apparent at the end of a fortnight or three weeks, the wasting will be slighter in degree, and some ulti mate recovery may be anticipated even in the most affected part. Where there is no loss of irritability, the paralysis will pass away in the course of a few weeks, or at most of a few months. Where faradie irritability is lost early and completely, the wasting will be rapid and great, and it is unlikely that there will be much recovery of power or nutrition, although some use may be regained. The return of faradic irritability that has been lost is a favorable indication; it signifies nerve-regeneration, and will be followed by an increase in voluntary power. Without an electrical examination it is

necessary to wait longer before a prognosis can be given, until distinct wasting on the one hand, and improvement on the other, indicate the regions in which the paralysis will persist and in which it will pass away. Even then the prognosis must be much less definite.

In the chronic stage, the prospect of ultimate recovery depends on the rate at which wasting developed, on the electrical reaction, and on the duration of the case. Where there is no sign of returning power at the end of three months, very little recovery will occur; the nerve-cells are destroyed and their renewal is impossible. The preservation of voltaic irritability (of the muscular fibres) is so far satisfactory that it shows there has been no destructive degeneration of the muscles; and if voluntary power is increasing, it indicates favorable conditions for its exertion, but it does not lessen the grave significance of persistent palsy and the absence of faradic irritability that indicates persistent nerve-degeneration. On the other hand, if, at the end of one or two months, some faradic irritability can be still detected, although low in degree (i. e. elicited only by a strong current), improvement is probable, and may be considerable in the course of a few months. It is necessary, in the case of children, to remember, and to warn the friends, that the growth of the most affected limb will be hindered, and that this, in the case of the leg, may render the effect of the paralysis more obtrusive by its interference with the gait. Otherwise they are distressed by what seems to them an increase in the disease, but is really compatible with continued improvement.

TREATMENT. The treatment of the acute stage of the disease is essentially the same as that of myelitis, already described, and the rules and principles already stated need not be here repeated. In the initial stage it should be that of the general state, guided by any special causal indications that may be detected; such as free sweating, followed by salicylate of soda or salicin, in a case distinctly due to exposure to cold. We may hope that future observations will afford us some indications regarding the means of counteracting other blood-states that apparently exist at the onset, and are concerned in the production of the lesion. At present we are without this help, and can only treat the initial stage as we should any other local inflammation, directing our treatment to the symptoms that may be present, and the conditions that apparently underlie them. The child should be kept at perfect rest, on the side, and warmth applied over the affected part of the cord by poultices or fomentations. The marked relief these give when there is spinal pain, make it probable that they exert a beneficial influence in all cases.

In such a disease-in which there is a natural tendency for the morbid process to cease to spread, and then to lessen in extent-the difficulty of ascertaining the effect of treatment on the lesion of the spinal cord is very great. Full doses of belladonna or ergot have