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blood-state of which the cord disease is a result. This is probably the case in polio-myelitis. The temperature is sometimes raised in disease of the cord apart from the influence of morbid process. Disease of the upper cervical cord, like that of the medulla, may cause hyperpyrexia, and this may also result from acute central lesions that occupy a considerable vertical extent, such as a central hæmorrhage, although by what mechanism these act we do not know. Slight variable elevation of temperature sometimes occurs in disease of the dorsal cord, and is probably due, in some way, to the disturbance of its functions rather than to any influence of the morbid process. For instance, in one case of hæmorrhagic myelitis with damage from the third dorsal to the second lumbar segments, every application of electricity to the legs was followed by slight pyrexia.

Convulsions.-Lastly, convulsive attacks have been known to attend the onset of acute lesions in various parts of the cord, in adults as well as in children. They are most frequent in disease of the cervical cord, but I have known a convulsion to occur in an adult at the onset of myelitis in the lower dorsal region. The convulsions are general. Their mechanism is unknown, and in some cases, especially of infantile polio-myelitis, they may, like the mitral pyrexia, be the result of general disturbance of the system by an acute morbid blood-state.

COMBINATION OF SYMPTOMS.-Certain symptoms are frequently combined, and their combination has a definite localising significance. Loss of motor power occurs in two different associations, according to the position of its cause in the motor path. It may be combined with muscular wasting, loss of electric irritability, and loss of all reflex action. In this case the disease is in the anterior cornua or nerve-roots, the lower segment of the motor path. (But the same symptoms are produced by disease of the nerves themselves-in multiple neuritis.) On the other hand, there may be no wasting, no change in irritability, and, instead of a loss of reflex action, the myotatic irritability is increased. The interruption of the motor path is then in the upper segment, usually in the pyramidal tracts. It may be a focal lesion of the cord, or a primary degeneration of the tracts. The distinction is that, in the latter case, there is nothing more than the muscular weakness and increased myotatic irritability. In the former case there are, or have been, indications that the lesion has extended beyond the purely motor elements.

The symptoms caused by disease of the several elements of the cord have now been described, but it is necessary to consider further the combination of symptoms that results from a total transverse lesion of the cord, and from a unilateral lesion.

A total transverse lesion, however limited in vertical extent, separates from the brain all parts below it, and hence, so far as will and feeling are concerned, it produces the same effect as if the whole of the cord below the lesion were destroyed. Compression of the cord in the middle of the cervical enlargement, for instance, abolishes

motion and sensation in all parts below the distribution of the cervical plexus. A transverse lesion at the second dorsal nerve causes motor and sensory palsy of the trunk and legs, leaving the arms unaffected. But the same loss, motion and sensory, results from disease which damages the whole cord up to the level indicated. Hence the extent of the motor and sensory paralysis indicates only the upward limit of the lesion; how far it extends downwards is shown by the interference with the central and especially the reflex functions of the cord. The upward level is indicated not only by the loss of conduction, but also by the position of the girdle-pain, and radiating pains, or zone of hyperesthesia, which are due to the irritation of the lowest sensory nerves in the upper portion.

It is desirable to know the symptoms of impaired conduction that occur when a transverse lesion is at different levels in the spinal cord. They may readily be ascertained by an examination of the table given at p. 210. There is, however, some uncertainty as to the effect on sensation in the limbs produced by disease at different parts of the lumbar and cervical enlargements, since, as we have seen, the exact representation of sensation in the cord is still uncertain.

The upper limit of the lesion is shown by the upward extent of the motor and sensory loss, according to the first three columns. The lowest nerves supply the anus and perinæum. Those that supply the skin and muscles of the leg and foot arise from the fourth lumbar to the third sacral segments, and are damaged by a lesion involving the lower part of the lumbar enlargement. We must, however, remember that the skin of the inner part of the leg is not supplied from the sacral nerves, and so may escape when the outer part of the leg and back of the thigh have lost sensation. In the middle of the lumbar enlargement the nerves arise which enter the lumbo-sacral cord, and these are probably destined for the flexors of the knee, and for the hip-muscles supplied by the sacral plexus, the glutei, quadratus, and gemelli, and for the skin of the lower part of the gluteal region. These parts then will be paralysed by disease in the middle of the lumbar enlargement, while the muscles and skin in front of the thigh are unaffected. The latter suffer when the disease affects the upper part of the lumbar enlargement, the origin of the anterior crural (rectus, &c.), and obturator (adductors). The skin on the upper and outer parts of the thigh loses sensibility, with the part adjacent to the scrotum, and in the groin, only when the disease damages the highest part of the lumbar enlargement, from which the second and third lumbar nerves arise, and then the flexors of the hip become paralysed. In proportion as the disease is higher in the dorsal region, we have the symptoms ascending higher up the trunk, and marking accurately the height of the lesion by the loss of cutaneous sensibility, and by the impairment—first, of the abdominal muscles, and then of the intercostal muscles. The umbilicus corresponds to the tenth dorsal nerves, and the ensiform area to the

sixth and seventh. When the disease reaches the lowest part of the cervical enlargement (the first dorsal nerves), we have the first symptoms in the upper extremity; but these are not, as might be expected, in the muscles moving the shoulder-joint, but in the hand. The first numbness is complained of in the little finger, and the first weakness is in the intrinsic muscles of the hand. Ascending higher, the symptoms pass up the arm with some uniformity, and without respect to nerve distribution. When the middle of the cervical enlargement is reached (the fifth, sixth, seventh cervical) the shoulder-muscles and the serratus magnus become paralysed, and there is general loss of power and sensation. (For details see table, p. 210, and also p. 192.) Above the level of the sixth pair, the trapezius and sterno-mastoid become somewhat weakened, for the fibres of the spinal accessory which supply them undoubtedly arise in part from this region of the cord. At the fourth and fifth cervical the low part of the neck becomes anæsthetic, and the diaphragm ceases to act. Here our localisation might cease, for total transverse lesions at this spot necessarily cause death. For a little time the sterno-mastoids and scaleni can still get some air into the chest, rarely in sufficient amount to maintain life for more than a few days. Lut limited lesions may occur higher up, and then we have complete powerlessness of the muscles moving the head, upper part of trapezius and sterno-mastoid, and other muscles attached to the occipital bone, and interference with sensation in the neck and parts of the head, which are not supplied by the fifth nerve.

The extent downwards of the lesion, its vertical extent, is thus not indicated by the impairment of the conducting functions, by the motor or sensory paralysis; to ascertain it we have to examine the functions of the cord as a central organ, and to ascertain how far they are impaired in the paralysed region-to examine especially muscular nutrition and reflex action. The state of muscular nutrition and irritability indicates how far the anterior cornua are injured. The relation of the several groups of muscles to the cord is shown in the first column of the table. The integrity of reflex action indicates the integrity of the reflex loops, and the study of the superficial reflexes of the trunk is especially instructive in this respect. The series of reflexes, and the relation of each to the cord, are shown in the third column of the table; the muscle-reflex contractions are printed in italics in the position which corresponds to the centres and nerve-roots which are essential for their production. Excess of superficial reflex action indicates loss of the cerebral control exerted on the reflex centres, and considerable excess of the muscle-reflexes implies impaired function of the lowest part of the pyramidal tracts, and generally shows the existence of a descending degeneration in the lateral columns. Reflex action in the legs may be abolished for a few hours by acute disease or injury above the lumbar enlargement, in consequence of inhibitory shock, but soon returns if the lumbar centres are intact. As already

explained (p. 220), if there is no return of reflex action or myotatic irritability, their absence shows that the lumbar region is involved in the primary lesion; secondary extension to this is indicated by loss of reflex action distinctly subsequent to the onset. If such loss occurs without wasting and loss of faradic irritability in the muscles it shows that the disease in the lumbar region is limited to the posterior columns or cornua.*

The fact of chief importance is that dorsal cord disease, the most common form, causes no persistent loss of reflex action in the legs, and that for such loss special causes must be sought.

Unilateral lesions interrupt the motor path to the muscles on the same side as the lesion, causing one-sided palsy, termed " spinal hemiplegia" when the disease is so high as to affect both arm and leg, “hemi-paraplegia" when it is lower, and affects one leg only. There is often some loss of power on the opposite side, which may be due either to slighter damage to the other side of the cord (since few lesions are strictly unilateral) or to damage to non-decussating or re-decussating fibres. Conversely, the paralysis of the leg may be incomplete when that of the arm is complete, owing to the escape of the fibres for the leg which cross lower down the cord. Sensation is affected on the opposite side, but not quite up to the level of the lesion, because the decussation of the sensory tract is not immediate, but occurs somewhat above the entrance of the nerves. The upper level may vary for different forms of sensibility, in consequence probably of the level of crossing (in relation to entrance) being different for the several paths. A lesion in one side of the lumbar enlargement often affects sensation on the same side as motion, because it damages the sensory path before it has crossed. In all cases of crossed motor and sensory paralysis, the sensibility of the muscles differs from the other forms of sensibility, and if it is affected on one side, this is the side of the motor palsy and not of the cutaneous anesthesia.†

A few cases have been met with in which a transverse lesion of the dorsal cord, especially a transverse concussion-myelitis, without post-mortem signs of lumbar inflammation, has caused a persistent loss of reflex action in the legs. In these cases, however, there has been not only loss of the muscle-reflex action, but also of the skin reflexes, a clear indication of an exceptional condition. Moreover, there has also been loss of faradic irritability and rapid muscular wasting-in short, there have been all the indications of a lumbar myelitis. The most probable explanation of these cases is that the descending degeneration of the pyramidal tract has been more than usually irritative in nature, so as practically to amount to a parenchymatous inflammation, and that this has invaded the motor structures as a nutritional change, sufficient to abolish their function, without, however, destroying their form. In one such case it was noted that the lumbar nerve elements were extremely granular in aspect. For a different explanation of these cases, see Bastian, Med.-Chir. Trans.,' 1890. also 19.55°2

This was first pointed out by Brown-Séquard in his important study of these cases. Scepticism has been expressed as to the fact, based on a denial that the test commonly employed, recognition of posture, is significant. Experiments on animals, even monkeys, are inconclusive, but the evidence from cases in man is very

The crossed affection of cutaneous sensibility may involve all forms of sensation or only some of them. Sensibility to pain is almost invariably impaired. The temperature sense is usually affected with that for pain; in only two of twenty recorded cases (in which the affection of sensibility was carefully noted) was the sense of temperature normal, and that of pain impaired, and in neither of these cases was the sensibility to pain actually lost. On the other hand, in one third of the cases tactile sensibility was unaffected, and in about one tenth of the cases it was impaired on both sides.

Cutaneous sensibility is sometimes impaired in a zone at the level of the lesion, and on the same side, in consequence of the damage to the nerve-roots entering the cord, and above this there may be a narrow band of hyperesthesia from irritation of the roots at the upper part of the lesion. On the side of the lesion, below the anaesthetic zone, there is, in most cases, a remarkable hyperesthesia, corresponding in distribution with the anesthesia on the opposite side. Painful impressions are felt most acutely, and even a touch on the skin, or warm or cold bodies, produce pain. The cause of this hyperesthesia is obscure. Both it and the opposite loss of sensibility may last for twenty years, and it cannot be ascribed therefore to any irritation by the morbid process. It is perhaps due to an altered action of the cerebral centres on the opposite side of the brain. There is much evidence of an intimate connection between the sensory centres on the two sides, and it is conceivable that the altered functional state of the centre on the side of the lesion, to which impressions cease to come, may induce in the opposite hemisphere a condition expressed as hyperesthesia. The condition may be thought of in relation to the peculiar phenomena of transfer in hysterical hemianææsthesia.

Reflex action is increased in all its forms on the side of the lesion, but the increase only occurs after some days. At first it is lessened or even abolished, no doubt from the inhibitory influence of the irritation of the morbid process.

The side below the lesion is at first, for some days or even weeks, warmer than the other, the difference being usually about a degree Fahrenheit. In the course of time this difference passes away, and the side may even be colder than the other.

These symptoms may be shown in the form of a table:

strong, not only of the occurrence of the loss, but of the significance of the test. In some cases, moreover, the muscles were insensitive to pressure. One recorded instance is the following:-A stab in the dorsal region caused loss of cutaneous sensibility in the right leg and motor palsy in the left. On this left side, on which cutaneous sensibility was normal, the sense of posture was absolutely lost, while it was present on the right side on which cutaneous sensibility was impaired. The patient often thought the left leg was flexed when it was extended. Ultimately this leg presented distinct ataxy. (Gilbert, Arch. de Neurologie,' 1882, p. 275.)

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