important to insist on the danger that the practitioner may be misled by the patient, who thinks that because he passes urine freely he necessarily empties his bladder perfectly.

Electricity has little influence on the chief symptoms of tabes. The voltaic current is powerless over either the pains or the ataxy, whether it be applied to the spine or the limbs. Faradisation of the skin by the wire brush has been recommended for the defect of cutaneous sensibility, but it has little if any influence. Temporary improvement in gait, and sometimes a little permanent improvement, may be obtained by faradisation of the muscles; the stimulation of the afferent muscle-nerves is probably the mechanism of its action. When the bladder or its sphincter is weak, faradisation from the hypogastrium to the perineum may be employed, and occasionally seems to do some good. In secondary wasting of the muscles an attempt may be made to maintain their nutrition by stimulating them with whatever current they respond to, but the central cause usually renders local treatment ineffective.

Nerve-stretching was fashionable a few years ago, the operation being usually performed on the sciatic nerve. In the first case in which it was employed (by Langenbuch) the procedure was followed by remarkable and mysterious improvement, not only in the pains, but also in the inco-ordination. The patient subsequently died under chloroform, administered in order that the nerves of the arms might be stretched. The spinal cord was found by Westphal to be healthy. Although the nerves were not examined, there can be little doubt that it was one of the cases in which the nerves alone are diseased. The operation has since been performed in a large number of cases, but without results that have secured its survival, and it is passing into merited disuse. Its place has been taken by extension of the spinal column. In this procedure the patient is suspended in such a manner as to allow the weight of the body to rest on the head and shoulders, and head alone, alternately, and the ligaments of the spinal column are supposed to be so stretched that the spinal cord and its nerve-roots are elongated. The chief effect is produced on the ligaments of the upper part of the spine, but the actual amount of elongation of the spine is exceedingly slight and insignificant, as has been proved by experiments on the dead body. It is difficult to conceive any mechanism by which it can do the good in tabes which was at first ascribed to it; and the careful observations by Russell and Taylor on a large number of cases at the Queen Square Hospital* seem te show conclusively that it has no real power of influencing the disease. It will also probably before long be forgotten.

Russell and Taylor, Brain,' Summer Number, 1890, vol. xiii, p. 206.

PRIMARY SPASTIC PARAPLEGIA

(PRIMARY LATERAL SCLEROSIS).

The morbid state thus designated is one that has been, and still is, the subject of much discussion. Its relations are complex, and a somewhat lengthy pathological introduction is necessary.

GENERAL PATHOLOGY.-We have seen that in every kind of transverse lesion of the spinal cord, provided this is situated above the lumbar enlargement, the paralysis of the legs is soon accompanied by excess of myotatic irritability (increased knee-jerk, foot-clonus), and that the muscle-reflex action, on which this irritability (and muscular tone) seems to depend, gradually increases to tonic spasm, so that a condition develops to which the term "spastic paraplegia" is applied. A condition quite similar to that which is thus secondary to a transverse lesion often develops gradually, without any indication of a primary focal disease, and without any sensory symptoms to indicate that the mischief extends beyond the purely motor elements of the cord. We have also seen that these symptoms indicate disease of the upper segment of the motor path, the cortico-spinal segment (p. 176), which extends from the motor cortex through the pyramidal tracts, and ends in the grey matter of the cord, doubtless by a subdivision and ramification of the nerve-fibres in the fibrillary network of the spongy substance. From the gradual onset and limitation of the symptoms in these cases, it has been assumed that the disease consists of a primary sclerosis of the pyramidal tracts, i. e. in a degeneration of the fibres of this upper segment. Since these tracts run chiefly in the lateral columns, the disease has been termed "lateral sclerosis." The clinical features presented by these cases, and their probable significance, were first pointed out by Erb.* Degeneration of the pyramidal tracts had been already observed, by Türck (1856) and Charcot (1865). Erb's inference as to the nature of these cases was supported by the independent (and indeed previous) researches of Charcot on cases of muscular atrophy; he showed that in such cases muscular rigidity coincides with degeneration of the pyramidal tracts. Pathologists have since been searching for confirmation of the hypothesis for evidence that the symptoms, in their pure form, without muscular atrophy, depend on degeneration limited to the pyramidal tracts. Such degeneration in slight degree, associated with slight symptoms, has been found in cases of general paralysis of the insane (by Westphal and others); but in all other cases that have been examined, either other parts of the white substance have been degenerated, or the disease has involved also the anterior cornua.t

* In 1875, Berlin. klin. Wochenschr.,' No. 26; 1877, Virchow's Archiv,' Bd. lx. In a case recorded by Stofella no other part than the pyramidal tracts could

In some cases, as one published by Dreschfeld (of which a figure is given at page 447), the change in the anterior cornua has been so slight that the required conditions are nearly fulfilled.

Although absolute demonstration has not yet been furnished, the indirect evidence of the correctness of the pathological hypothesis. is very strong, and the only open question is whether, when there is no disease of the motor nerve-cells of the anterior cornu, the degeneration is so limited to the pyramidal tracts as to constitute a system disease in the strict sense of the word. It is not surprising that demonstration of the nature of the pure cases is not forthcoming, since, as we shall see, the disease has little tendency to shorten life.

It should, moreover, be noted that cases which present this group of symptoms may be very various in nature. We have seen (p. 212) that, in each segment of the motor path, the same symptoms are produced by disease of any part of the segment. In the upper segment, with which we are now concerned, the symptoms are the same, whether the disease is in the cortex of the brain, the internal capsule, the pyramids of the medulla, or the pyramidal tracts of the cord; and they must also be the same if the disease is limited to the termination of the segment in the grey matter of the cord. In cerebral hemiplegia the state of the arm closely resembles that present when primary spastic paraplegia involves this limb. The leg in hemiplegia presents a less close resemblance to its condition in spinal disease, because the leg is innervated from both cerebral hemispheres, and the supplementary influence of the hemisphere of the same side lessens the effect of the disease of the hemisphere of the opposite side. But if there is disease of the leg-centres in both hemispheres, the state of the legs may be identical with that resulting from disease of the spinal cord. Such bilateral disease often results from injury during birth,-meningeal hæmorrhage over the upper part of the central convolutions. This resulting condition is termed "congenital spastic paraplegia." (See vol. ii.)

On the other hand, it is extremely probable that degeneration begins in the termination of the fibres in the grey matter, just as it does in the extremities of the peripheral nerves. It may even be limited to these terminal parts, as the extremity of the lower segment is paralysed alone by many agents. In such disease the white columns would be found normal, as in one recorded case in which the symptoms of spastic paraplegia existed during life, and no anatomical change was discovered after death. The detection of the disease of the terminal portion in the grey matter is extremely difficult, perhaps impossible, because the structure must consist of nerve-fibrillæ that interlace with others that are unaffected. This view is supported by the fact that in other cases some degeneration has been found in the lateral pyrabe seen diseased on naked-eye observation, but no microscopical examination was made.

midal tracts in the lumbar region, slighter than the intensity of the symptoms suggested, and gradually lessening, to cease higher up the cord. Such a condition is comparable to the degeneration of the lower portion of the second segment of the motor tract in some cases of peripheral (degenerative) neuritis, in which there is a degeneration of motor nerve-fibres, greatest in their extremities, extending for a variable distance up the nerves, but lessening long before the spine is reached. It is highly probable that the toxic agents which cause lathyrism and pellagra (q. v.) act on the extremities of the pyramidal fibres, as curara does on the nerves; among the spinal symptoms of lathyrism are paralysis of the legs with rigidity and contractures, and increase of myotatic irritability-foot-clonus, &c.*

Both clinical and pathological evidence shows that the morbid state often occurs also as part of a more extensive degeneration. Degeneration may occur in both lateral and posterior columns, giving rise to combined paralysis and ataxy-"ataxic paraplegia," sufficiently definite in its clinical characters and course to make its distinction convenient; it is therefore separately described. The following account of the clinical features of spastic paraplegia is founded on cases in which the motor paralysis and spasm existed alone, with no definite sensory loss, in which they came on gradually, with nothing in the state of the patient or the history of his symptoms to suggest either a focal lesion or an acute process.

CAUSES. An inherited neuropathic tendency is to be traced occasionally in this as in other chronic spinal diseases. Thus in one case there was a history of insanity in uncle, aunt, and two cousins. The disease affects both sexes in almost equal frequency, presenting in this a contrast to posterior sclerosis. The period of life at which it most frequently begins is between twenty and forty; about three quarters of the cases begin in these two decades, and about an equal number in each. Cases frequently commence, however, in the second decade of life, chiefly in its latter portion. After forty they become much less common; the latest age at which I have known a typical case to commence is sixty-one.

The disease sometimes follows syphilis in a way to suggest a causal relation, even when all cases are excluded in which there is any reason to suspect a focal lesion. In one case the symptoms commenced six months after the primary disease. But this antecedent is not frequent, and in this respect also the disease contrasts with posterior sclerosis. Proximate causes are to be traced only in a minority of the cases. The most frequent is concussion of the spine, such as a fall on the back. Some time, often two or three years, elapses between the fall and the first pronounced symptoms of the disease, and hence focal lesions due to the fall can be excluded. Next in frequency See Marie, Prog. Méd.,' 1883, No. 43.

The cord lesion was found to be sclerosis, but the direct cerebellar tract was also degenerated (Minkowski).

is repeated exposure to wet cold. Very rarely the symptoms have slowly followed some acute illness. In several cases the disease has succeeded prostration after childbirth or abortion, or has commenced during lactation. In one case an attack of arthritis in the knee and ankle of one leg was the immediate antecedent, and this leg was the first to become weak. In another case the symptoms followed subacute arthritis of both knee-joints, apparently rheumatic in nature. The possibility that a joint inflammation may be of spinal origin must be borne in mind in considering the significance of such cases, but it is on the whole probable that a primary joint affection is an occasional cause of the spinal disease. (Acute arthritis, certainly of spinal origin, has only been observed in severe myelitis.) The cause of the congenital form is always injury to the brain during birth, in most cases meningeal hæmorrhage, causing compression of the motor cortex.

SYMPTOMS.-Weakness of the legs, of very gradual development, is the first symptom. The patient finds that he gets tired more readily than before, and that the legs feel heavy; sometimes one leg becomes weak before the other. The progress of the weakness is very variable, but it is slow in all characteristic cases. In many instances the patient is still able to walk a mile or two, even after the disease has lasted for several years, slowly increasing. On the other hand, walking power may be almost lost at the end of six months. It is doubtful whether more acute cases belong to this category. The early weakness is often accompanied by slight unsteadiness, chiefly subjective. When the patient seeks advice, it will generally be found that there is very distinct loss of power in the flexors, often greatest in the flexors of the hip, but considerable also in those of the knee and ankle, and occasionally much greater in the last than elsewhere. The knee-jerk is excessive and quick; the rectus contraction can be obtained, as the patient lies, by tapping the depressed patella, and a rectus-clonus is often obtainable by sudden depression of the patella. The foot-clonus is usually also obtained with readiness. In rare cases, in which the upper part of the legs suffers most, there may be a rectus-clonus, but only slight indications of a foot-clonus, two or three movements quickly ceasing. The tendency to spasm is at first noticeable as slight stiffness of the legs on first rising in the morning, but it gradually increases in degree as power lessens, until at last the legs, whenever extended, pass into a condition of strong extensor spasm, rigidly fixing them to the pelvis, so that, as the patient lies, if one leg is lifted from the couch by the observer, the other leg is moved also. The spasm may be such that the knee cannot be passively flexed by any force that can be applied to it until the spasm has become less. When flexed the limb is comparatively supple; but if it is then extended, the spasm instantly returns, making the limb rigid, and often completing the extension, just as the blade of a knife opens out under the influence of its spring, " clasp-knife rigidity." See Arthritic Muscular Atrophy.'