Volume 5 — DISEASES OF THE NERVOUS SYSTEM. (continued 39)

A second cause of anterior poliomyelitis is, almost certainly, the presence of some poison circulating in the blood. The frequent occurrence of the accident in the course of one of the exanthemata is one indication of this; other indications are found in such cases as that related by Simon, where three children in one family were suddenly attacked—two on one day, one, twenty-four hours later.¹⁵¹ The same author relates a case of motor paralysis in an adult, followed by atrophy of left lower extremity, and which occurred during a fit of indigestion caused by eating mussels.¹⁵² The acute ascending paralysis of Landry, with its absence of visible lesion, has been said to strikingly resemble the effects of poison. Hydrophobia and tetanus are again examples of the predilection exhibited by certain poisons for the motor regions of the cord.

¹⁵¹ Journal de Thérap., 7, vii., 1880, p. 16. These children belonged to an American family, but were seen by several distinguished French physicians.

¹⁵² P. 357.

The evidence that infectious diseases may constitute the immediate (apparent) causal antecedent of acute poliomyelitis has led, not unnaturally, to the theory that all cases of acute infantile paralysis are due to a specific infecting agent, some as yet unknown member of the great class of pathogenic bacteria. It may be noticed, however, that the occurrence of the spinal accidents after the ordinary infectious diseases, as scarlatina and measles, should as well indicate that a specific agent proper to itself was at least not essential to its development.¹⁵³

¹⁵³ Perhaps the occurrence of diphtheria in the course of scarlatina and typhoid should indicate a similar lack of real specificity in the morbid agent of the former disease.

The influence of exposure to cold, which seems to have been sometimes demonstrated, must probably be interpreted, as in the case of rheumatism and pneumonia, as effective by means of some poison generated in the organism when cutaneous secretion, exhalation, or circulation has been suddenly checked.

DIAGNOSIS.—The diagnosis of the acute anterior poliomyelitis of childhood is usually easy, but unexpected difficulties occasionally arise.

Typical cases are markedly different from typical cases of cerebral paralysis, but in exceptional cases these differences disappear. This is shown in the following table:

SPINAL PARALYSIS. CEREBRAL PARALYSIS.

Paraplegic or monoplegic (rule). Hemiplegic, (rule). Monoplegic as residuum of hemiplegia or as consequence of solitary tubercle (exception).

Hemiplegic as residuum from paraplegia, or original and involving facial nerve (very exceptional).

Intelligence free (rule). Intelligence depressed (rule).

Intelligence depressed (when spinal paralysis has affected imbecile children). Intelligence free (exception, especially with solitary tubercle).

Disposition lively. Disposition apathetic or cross.

Initial convulsion unique; general symptoms of a few hours' duration (rule). Convulsions repeated; pyrexia prolonged several days or weeks (rule).

Convulsion repeated during two to three weeks before paralysis; fever a month (rare exceptions).

Sensibility intact (rule). Sensibility intact after initial period.

Occasional hyperæsthesia (exception).

Reflexes cutaneous, and tenderness lowered or lost (rule). Reflexes intact.

Reflexes preserved when only single muscles in groups paralyzed.

Associated movements of hand absent (Seeligmüller). Associated movements frequently observed in hand.

No rigid contractions of upper extremity. Extensive and rigid contractions of upper extremity very frequent.

Atrophy of paralyzed muscles and arrested development of limb, very marked. Atrophy very slight.

Faradic contractility diminished or lost; degenerative galvanic reaction. Electrical reactions normal.

Rather singularly, the diagnosis from transverse myelitis is less liable to error than that from cerebral paralysis:

ANTERIOR POLIOMYELITIS. TRANSVERSE MYELITIS.

Fever brief or absent. Persistent fever.

Sensibility intact. Hyperæsthesia, then anæsthesia.

Decubitus absent. Presence decubitus.

Reflexes lost. Reflexes increased.

Atrophy of muscles. Atrophy of muscles sometimes as intense.

Electrical muscular contractility lost. Loss of electrical contractility, but not proportioned to sensory and motor disturbance; less rapidly completed.

The diagnosis from hæmatomyelitis is almost impossible, and practically useless. For if the hemorrhage be severe, the child dies at once, as in Clifford Albutt's case. If less severe, it excites a myelitis, and the history becomes identical with that of the disease we are considering; or if the clot beyond the anterior cornua, it is identified with a vulgar myelitis of traumatic origin.

Progressive muscular atrophy is extremely rare in childhood, but is occasionally seen under hereditary influence (Friedreich's disease). In adult cases confusion is not only easy to make, but often difficult to avoid, especially with the rare, chronic form of poliomyelitis. The basis of distinction is as follows:

ANTERIOR POLIOMYELITIS. PROGRESSIVE MUSCULAR ATROPHY.

Onset sudden; maximum of paralysis at the beginning. March very gradual; maximum of disease not attained for years.

Faradic contractility lost almost at once. Faradic contractility not lost until atrophy complete.

Shortening of limbs and atrophy of limbs (in infantile cases). No arrest of development of limbs.

Functionally associated muscles frequently associated in paralysis: hand rarely affected. Capricious selection of muscles, but frequent wasting of these at eminences.

Paralysis from lesion of a peripheric nerve closely imitates anterior spinal paralysis.¹⁵⁴ It is distinguished by closely following the distribution of the injured nerve, and, usually, by concomitant lesions of the sensibility and of cutaneous nutrition.

¹⁵⁴ The importance of this fact has been shown in the section on Pathogeny. (See also quotations from Leyden and remarks on lesions of peripheric nerves.)

The pseudo-paralysis sometimes observed in syphilitic children as a consequence of a gummatous infiltration of the bones at the junction of the epiphysis and diaphysis¹⁵⁵ might easily be mistaken for a spinal paralysis. But it is an affection peculiar to the new-born; the electrical reactions of the paralyzed muscles are intact; careful examination will show that the movements of the muscles are not impossible, but restrained by pain; often other syphilitic affections are present.

¹⁵⁵ Parrot, Wagner.

The diagnosis from diphtheritic paralysis is embarrassed, from the fact that true anterior poliomyelitis may develop in the course of diphtheria as of other infectious diseases. The paralysis of the soft palate, preservation of faradic reaction, absence of atrophy, and the usually rapid recovery must establish the differentiation.

In spinal paralysis there is loss of the reflexes,¹⁵⁶ and also of faradic contractility, both of which are preserved in hysteria. In hysterical paralysis, also, there is no wasting of the affected muscles.

¹⁵⁶ See Gowers's monograph on “Spinal-Cord Diseases” for an excellent summary of the spinal reflexes.

Various diseases of the bony skeleton or articulations may simulate spinal paralysis. Congenital club-foot, caused by unequal development of the bones and cuticular surfaces, is to be distinguished from the paralytic variety by the date of its appearance,¹⁵⁷ by the deformity of the tarsal bones, and by the extreme difficulty of reduction.

¹⁵⁷ Though in some cases paralysis of the muscles of the foot seems to take place during fœtal life, and a club-foot result which is both congenital and paralytic.

Caries of the calcaneum, leading the child to walk on the anterior part of the foot to avoid pressure on the heel, may leave after recovery such a retraction of the plantar fascia as to cause a degree of equinus and varus, with apparent paralysis of the peroneal muscles. I have seen one such case.

Congenital luxation of the hip may simulate paralysis; indeed, by Verneuil, it has been attributed to an intra-uterine spinal paralysis. There is, however, no change in the electrical reactions of the muscles surrounding the joint.

In coxitis, however, Newton Shaffer¹⁵⁸ has demonstrated a moderate diminution of faradic contractility in such muscles, and a corresponding degree of atrophy; and this fact might complicate the diagnosis of paralysis from arthritis of the hip-joint. Gibney¹⁵⁹ has called attention to the facility with which this confusion may arise, and Sayre¹⁶⁰ relates cases of infantile paralysis mistaken for coxitis.

¹⁵⁸ Archives of Medicine.

¹⁵⁹ Am. Journ. Med. Sci., Oct., 1878.

¹⁶⁰ Orthopædic Surgery.

In a case observed by myself, which had been previously diagnosed as coxitis, the mistake was all the more interesting as the paralysis which really existed seemed to have been caused by a meningitis rather than primary myelitis of the cornua.¹⁶¹ It thus corresponded to the meningo-myelitic case related by Leyden.

¹⁶¹ The details of this case are as follows: C. P——, aged 11, ten months previous to consultation suffered from febrile attack, accompanied by retraction of head, severe pains diffused through body and intense at nape of neck; unconsciousness for thirty-six hours; vomiting; no convulsions. Case diagnosed as cerebro-spinal meningitis by attendant physician. Convalescence in a week, but with pain in lumbar region of back, predominating on right side, so aggravated by standing or walking that both acts impossible. Coincidently, pain in right calf; exquisite tenderness to pressure even from stocking. No complaint in recumbent position. Child could not get from floor to bed, nor raise right leg from ground. As pain subsided walking became possible, but right leg dragged. Chronic twitchings on left side, face, arm, leg. These symptoms lasted ten or twelve weeks, but at end of nine weeks patient could walk up stairs. In ten months power of walking almost recovered, but there remained a certain amount of lordosis and oscillation of pelvis, which is jarred on the left side while the right leg is swung forward. Recumbent, all movements executed equally well on both sides and passive motion of the hip-joint perfectly free. Circumference of right thigh and leg diminished from one-half to one inch as compared with the left. Faradic contractility diminished on the right side in the gluteal muscles, vastus externus, and rectus, and in the gastrocnemii. The sacro-lumbalis muscle was, unfortunately, not examined, but from the lordosis was probably affected. The remaining muscles were intact. Pain on pressure persisted over right side of second, third, and fourth lumbar vertebræ. Diagnosis was made of a limited meningeal exudation, with compression of anterior part of cord or of a portion of the lumbar and of the sacral plexus.

Scoliosis, which may be caused by the relatively rare unilateral paralysis of some of the muscles of the trunk, may also be simulated by paralysis with shortening of one lower extremity. To compensate the shortening, the trunk is bent over on the paralyzed side; hence a lateral curvature, easily reducible, but easily leading into error.

It would seem easy to distinguish traumatic cases of subluxation of the humerus from those due to paralysis of the deltoid. Yet sometimes only the history will serve to establish, and that somewhat doubtfully, the diagnosis.¹⁶²

¹⁶² A child of four was brought to me with a stiffness and rigidity of the shoulder-joint which could only very partially be overcome by passive motion, and not at all by voluntary effort. The mother stated that several months previously the child had, without apparent cause, become suddenly unable to move the arm. After two months' delay it was taken to a dispensary, and told that the arm was out of joint, and had it reset under ether. From this date the stiffness had gradually developed. The deltoid was atrophied, with marked diminution of the faradic contractility. Question: Were these signs merely symptomatic of an arthritis consequent on a dislocation, or was the latter the result of a spinal paralysis of the deltoid?

THERAPEUTICS.—The treatment of anterior poliomyelitis embraces two stages. In the first it is directed against inflammation of the spinal cord and the paralysis of the muscles; in the second period the spinal lesion has run its course and the paralysis is considered incurable. Treatment is then directed to the prevention or palliation of deformities or toward facilitating the functions of the limb in spite of them.

These two periods are not, however, rigidly separated from each other in chronological order. From the very outset it is important to take certain precautions to prevent deformities, and while palliating these with orthopædic apparatus it is important for years to continue treatment of the paralyzed muscles in the hope that at least a remnant of them may be saved. To abandon the case to the orthopædic instrument-maker, or to neglect the problem of dynamic mechanics while applying electricity and studying the progress of fatty degeneration, are errors greatly to be condemned.

The treatment of the initial stage is necessarily purely symptomatic for the fever and convulsions, since the diagnosis cannot be made out until these have subsided.

As soon as the diagnosis is clear, however, certain measures should be adopted to diminish the hyperæmia of the spinal cord. Dally¹⁶³ recommends the ventral decubitus; almost all modern authorities advise ice to the spine and ergot internally or subcutaneously. Thus, Althaus¹⁶⁴ makes hypodermic injections of ergotin in doses of one-fourth of a grain for a child between one and two years old; one-third of a grain between three and five; and one half grain from five to ten; and these doses repeated once or twice daily. The only objection to this treatment is the degree of local irritation it can hardly fail to occasion. Hammond, who “affirms ergot to be of great service, the only medicine capable of cutting short the disease or of limiting its lesions,” recommends the internal administration of the fluid extract—ten drops three times a day for infants of six months, half a drachm for children between one and two years.¹⁶⁵

¹⁶³ Journ. Thérap., t. viii., 1880.

¹⁶⁴ On Infantile Paralysis.

¹⁶⁵ I have elsewhere quoted one case of early recovery under the use of ice and ergot; or was this a case of temporary paralysis?

The belladonna treatment, at one time so warmly praised by Brown-Séquard, retains to-day few adherents.

Simon advises cutaneous revulsives to divert the circulation to the surface; thus, hot-air baths, mustard powder sprinkled on cotton enveloping the limbs. Ross advises mercurial inunction along the spine, followed by iodine and blisters. At the same time, iodide of potassium should be given internally in large doses. The action of this drug upon inflammations of the nerve-centres seems, within certain limits, to be indisputable, but its mode of action is certainly very obscure. Where the lesion can be attributed to a meningo-myelitis,¹⁶⁶ the iodide may be expected to facilitate the absorption of the exudation. In these cases it should be continued for a long time.¹⁶⁷

¹⁶⁶ As in Leyden's first case, and my own.

¹⁶⁷ Binz explains the local action of iodine by an exudation of leucocytes which follows the dilatation of blood-vessels. These elements break down the exudation into which they are poured, and thus facilitate its absorption.

Electrical treatment may be begun by the end of the first week after the paralysis. At this stage Erb recommends central galvanization as an antiphlogistic remedy for the myelitis. For this purpose a large anode must be placed over the spine at the presumed seat of the lesion, while the cathode is applied over the abdomen. By a slight modification of the method the cathode is placed over the paralyzed muscles. The application is stabile, and, according to Erb, should last from three to ten minutes; according to Bouchut, several hours daily. Erb's method is intended exclusively as a sedative to the local inflammation. When the cathode is placed on the muscles it is hoped that the descending current, replacing the lost nervous impulses, may avert the threatening degeneration of the muscle and nerve.

Faradization cannot modify the inflammatory lesions of the cord. As a means of averting degeneration in completely paralyzed muscles it is inferior to galvanism, and should not therefore be used in those muscles which refuse to contract under its stimulus. Its immense utility, however, is as a stimulus to muscles imperfectly paralyzed, but liable to degenerate from inaction and to be overborne by their antagonists. The excitation of contractions in such muscles is a powerful local gymnastic, helping to maintain nutrition by artificially-excited function.

For the same purpose, muscles inexcitable to the faradic current should be, when this is possible, made to contract by the interrupted galvanic current. After this treatment has been prolonged during several months, the faradic contractility often returns, and the current then should be changed (Seguin).

The value of electrical treatment has been very differently estimated. Erb remarks that “its results are not precisely brilliant.” Roth, whose testimony perhaps is not above suspicion, since evidently prejudiced, insists that numerous cases fall into his hands which have submitted for months to electrical treatment without the slightest benefit. On the other hand, Duchenne, as is well known, has expressed almost unbounded confidence in the therapeutic efficacy of faradization, declaring that it was capable of “creating entire muscles out of a few fibres.”

The sensitiveness of children to the electrical current, and their terror at its application, seriously interfere with its persistent use; as, if the patience of the physician is maintained, that of the parents is very likely to fail in the presence of the cries and resistance of the child.

It is very probable that some of the failures of electrical treatment are due to the attempt to rely upon it exclusively, instead of suitably combining both electrical methods with each other and with other remedial measures. With our present knowledge it is safe to assert the desirability of persistent electrical treatment during at least the first two years following the paralysis. The currents must never be too strong—the faradic, at least, never applied for longer than ten minutes at a time. The muscles should be relaxed by the position of the limbs (Sayre). If the muscles continue to waste, and especially if they become fatty, the electrical response will grow less and less, and finally cease altogether.¹⁶⁸ In the contrary case the galvanic contraction will become normal in quality, and the faradic contractility will return and increase, while the atrophy is arrested and the muscle regains its bulk and voluntary powers. Sometimes, as already stated, the latter is regained, while faradic contractility remains greatly diminished.¹⁶⁹

¹⁶⁸ Passing through three stages: faradic contractility diminished, galvanic contraction increased; faradic response lost, galvanic degenerative; absence of contraction to either current.

¹⁶⁹ Sayre (loc. cit.) has noticed cases in which the muscle would contract several times under faradism, then refuse to do so for a day or two. This observation, if valid and not due to unequal working of the battery, is a most curious one.

A succedaneum to electricity that is highly prized by some authorities is strychnia, especially when subcutaneously administered. Pelione¹⁷⁰ relates the cure of two cases in children of four and five years, after three and four years' duration of the paralysis, by strychnia—one-half milligramme daily. None should be given to children under six months, but over that age one-ninety-sixth of a grain may be given (Hammond). It should not be given subcutaneously more than two or three times a week (Seeligmüller).¹⁷¹

¹⁷⁰ L'Union médicale, 1883.

¹⁷¹ Duchenne relates a case of a paralysis general at the outset and remaining so for six months. It was then treated by strychnine for five or six months, and at the end of that time had become limited to the lower extremities (Elect. local., ed. 1861, p. 278).

The incidental action of electricity in attracting blood to the paralyzed muscles may be sustained by several other methods.

Among these the external application of heat, either dry or in the form of hot douches, alternating with cold, is an adjuvant remedy of real importance. Beard has suggested tubing, malleable to the limbs, for the conduction of hot water. It is desirable to employ massage immediately after cessation of the hot applications.

On the value of massage and passive gymnastics opinion is even more variable than in regard to electricity. Roth, a specialist in orthopædics, places it at the head of all remedial measures, and denounces electricity in comparison. Many professional manipulators, ignorant of medical science, continually claim wonderful triumphs over regular physicians obtained by means of systematized massage. Volkmann, on the other hand, dismisses the pretensions of the Heilgymnastik with considerable contempt, declaring that faradization is the only method which can really secure exercise to paralyzed muscles.

The Swedish movement cure consists in passive movements imparted to a limb by the manipulator, at the same time that they are strenuously resisted by the patient. From the nature of this method, and its aim in stimulating the voluntary innervation of the muscles, it is admirably adapted to hysterical paralysis. Theoretically, it is difficult to perceive the applicability of this method in organic atrophic paralysis, especially in young children, whose voluntary efforts cannot be commanded. There are, however, several real indications for passive gymnastics in the treatment of infantile paralysis. Surface friction and deep massage have some influence in dilating the blood-vessels and causing an afflux of blood to the cold and wasting muscles. A probably more important effect may be produced upon the contraction caused by malposition and adapted atrophy of certain groups of muscles. It is these contractions which formerly constituted the special objection of the orthopædist, and were treated almost universally by tenotomy. They are in any case the proximate cause of deformities; and, generally existing on the side of the joint opposite to the most severely paralyzed muscles, they keep these over-stretched and prevent them from receiving the benefit of the electrical treatment. Muscles which will not contract to the faradic current while thus stretched will often begin at once to do so when the rigidity of their antagonists has been overcome.

Persevering stretching by the hands will often overcome this rigidity as completely, and even more permanently, than will the tenotomy-knife. It is in this part of the treatment that entirely ignorant and even charlatan manipulations do, not unfrequently, achieve remarkable results.¹⁷²

¹⁷² Of course many of those on record, and to some of which I have been a witness, relate to hysterical contractions, hysterical scoliosis, etc.

It is the retracted tendo Achillis and plantar fascia which most frequently require this manipulation. In the paralytic club-foot of young children all authorities agree in the value of repeated manipulations and restorations of the foot as nearly as possible to a position where it may be retained by simple bandaging. While turning the foot out it becomes perfectly white, but on releasing hold of it the circulation is restored, after which the manœuvre may be repeated (Sayre).

This principle of intermittent stretching by seizure of the segments of the limb above and below the joint applies to all forms of paralytic contraction. In the trunk the pelvis should be held by the mother, while the manipulator, seizing the thorax of the child between both hands, moves it gently but forcibly to and fro in the required direction. Great care is required in these manipulations—not merely to avoid exhausting the muscles, but even to avoid fracturing atrophied bones.

It may be laid down as a positive rule that tenotomy should never be performed in the contractions of spinal paralysis until the resources of manipulation have been exhausted. It is to be remembered that the rigidity depends on no active contraction of the muscle, but on its elastic retraction. The manœuvre of stretching does not appeal to the force of contractility, which may have been lost, but to the force of elasticity, which remains and can be made to act in a reverse direction. Finally, in the cases where the retracted muscles have not been originally paralyzed, but have lost the power of contracting during the process of shortening, this power may be restored if the muscle regain its normal length.

The operation of tenotomy, apparently a far more heroic measure, is often a less efficacious means of arriving at the results. Unless followed by the application of apparatus which permits motion in the joint, section of contracted tendons is only of brief utility.

Though the edges of the cut tendon have been kept apart until the intervening space is filled by new tissue, union is finally effected by the latter, and retraction through elasticity is again imminent. Often, therefore, the deformity is repeated in spite of repeated operations; when it is not, the happy issue is due to the fact that, with increased freedom of locomotion immediately after the tenotomy, the patient has been enabled to bring the influence of weight to bear in such a manner as to fix the limb in a new and more convenient position. Thus, after section of the tendo Achillis for pes equinus, if the patient begins at once to walk on the paralyzed foot, the weight of the body, pressing down the heel, may keep the tendon stretched. So walking immediately after section of the hamstring muscles will have a tendency to produce genu-recurvation by the same mechanism which produces it in total paralysis, and the original deformity will not recur.

Besides the tendo Achillis, the parts which may be occasionally submitted to tenotomy are the plantar fascia, the peroneal muscles, very rarely the anterior tibial and extensors, the hamstrings, the thigh adductors. Section of the external rotators of the thigh or of the tensors of the fascia lata could hardly ever be required, and among these operations Hueter¹⁷³ rejects that on the plantar aponeurosis as inadequate. The excavation in the foot it is designed to remedy depends upon alteration in the form of the tarsal bones, and can only be cured by means of forcible pressure exerted on their dorsal surface. Section of the peroneal muscles, often recommended by Sayre, is considered by Hueter to be superfluous after section of the tendon achilleis. Paralytic contraction of the hamstrings or of the hip flexors is rarely sufficiently severe to demand tenotomy.

¹⁷³ Loc. cit., p. 416.

From what has preceded it is evident that maintenance of locomotion is of great importance, in order to avoid the deformities which are threatened by prolonged repose. Locomotion, however, can only be safely permitted with the assistance of apparatus capable of restraining the movements liable to be produced by the weight of the body. The supporting instrument which restrains movement in certain directions must, however, facilitate it in others: immovable apparatus, such as is not infrequently applied after tenotomy, is always injurious.

In young children unable to walk, the development of pes equinus may often be prevented by drawing down the foot to a sole splint made of thin wood, gutta-percha, or felt, and fastening it with a flannel bandage. The point of the foot may be drawn up toward the tibia by a strip of diachylon plaster. If the equinus has already developed, a splint of gutta-percha or of felt (Sayre) may be modelled to the leg and foot while the latter is held forcibly in dorsal flexion. The splint is attached by means of strips of adhesive plaster. It should extend as far as the knee, and be suitably padded (Seeligmüller).

In children able to walk a sole splint of thin metal, to which the foot had been previously attached by a flannel band, should be inserted in a stout leather boot. On the outer side of this boot should run a metallic splint, jointed at the ankle and extending to a leather band surrounding the leg just below the knee. A broad leather band, attached to the outer edge of the sole anterior to the talo-tarsal articulation, also passes up on the outside of the foot, gradually narrowing until, opposite the ankle, it passes through a slit in the side of the shoe, to be attached to the leg-splint. This band tends to draw the point of the foot outward, and thus correct the varus (Volkmann). Sayre¹⁷⁴ has improved on this shoe by dividing the sole at the medio-tarsal articulation, in which lateral deviation takes place, and uniting the anterior and posterior parts by a ball-and-socket joint, permitting movement in every direction.

¹⁷⁴ Loc. cit., p. 88.

The orthopædic boot for the treatment of calcaneo-valgus is constructed on the same principle. But the splint runs up the inner side of the leg, and the leather strap passing to it from the edge of the sole draws the point of the foot inward and raises its depressed inner border (Volkmann). Essential to the treatment of this deformity, however, is the elevation of the heel. This is effected by means of a gutta-percha strap which is attached below to a spur projecting from the heel of the shoe, and above to a band encircling the leg. If, by rare exception, a paralytic calcaneus exists in a child unable to walk, a simple substitute may be found for the shoe in a board sole-splint projecting behind the heel, attached to the foot by a strip of adhesive plaster, which finally passes from the posterior extremity of the board up the back of the leg, and is there secured by a roller bandage.

The device of the gutta-percha elastic band to replace the gastrocnemius muscle illustrates a principle of wide application in orthopædic apparatus. The suggestion to replace paralyzed muscles by artificial ones was first made by Delacroix¹⁷⁵ in an apparatus designed for the hand. The suggestion was repeated by Gerdy;¹⁷⁶ and in 1840, Rigal de Gaillac proposed to exchange the metallic springs hitherto used for India-rubber straps. Duchenne elaborated the suggestion in a remarkable manner,¹⁷⁷ using delicate spiral springs as a substitute for the lost muscles, and taking the greatest pains to make the insertion-points of these to exactly correspond with the insertions of the natural muscles. This was effected by means of sheaths, imitating natural tendinous sheaths, sewed to a glove or gaiter in which the hand or foot was encased.

¹⁷⁵ Article “Orthopédie,” Dict. des Sciences médicales, quoted by Duchenne.

¹⁷⁶ Traité des Bandages, 2d ed., Paris, 1837, quoted by Duchenne.

¹⁷⁷ See chapter on “Prothetic Apparatus” in his treatise De l'Électrisation localisée.

At the present day the prothetic apparatus the most employed is that contrived by Barwell.¹⁷⁸ The principle is the same as Duchenne's, but the artificial muscles are made of India-rubber, to which a small metallic chain is adjusted, and they are attached to the limb by means of specially-devised bands of adhesive plaster and pieces of tin bearing loops for the insertion of the muscle. In this apparatus the artificial muscles do not attempt to imitate the situation of the natural muscles with the precision which Duchenne claimed for his. Barwell's own dressing for talipes valgus consists of two rubber muscles which pass from the inner border of the foot, one to the inner, the other to the anterior, part of a band which encircles the leg just below the knee. For talipes calcaneus another band is required behind the leg, passing to the heel, as in Volkmann's apparatus, already mentioned. For talipes varus a rubber band should pass on the outside of the foot; for equinus, one or more from the anterior part of the leg to the sides of the anterior part of the foot.

¹⁷⁸ A tolerably minute account of the Barwell dressing is given by Sayre, loc. cit., p. 84.

Sayre endorses Barwell's dressing as entirely adequate for the treatment of any form of club-foot, but modifies it by substituting a ball-and-socket shoe for the adhesive plaster which should encircle the foot. The artificial muscles are then passed from the sides of the shoe to a padded leather girdle encircling the leg. A straight splint, jointed opposite the ankle, runs up from each side of the foot to this girdle, and from it two lateral upright bars, jointed at the ankle, pass to the heel of the shoe; and from below the joint passes forward on each side a horizontal bar reaching the point of origin of the artificial muscles and giving attachment to them.

In equinus it is necessary to bind the heel of the foot down firmly in the heel of the shoe; and this is accomplished by means of two chamois-leather flaps which are attached to the inside walls of the shoe and lace firmly across the foot.¹⁷⁹

¹⁷⁹ “The aim of the dressing or instrument is simply to imitate the action of the surgeon's hand; accordingly, any apparatus combining elastic force is far superior to any fixed appliance; and, moreover, that is to be preferred which is the most readily removable. Shoes, therefore, are better than bandages or splints. A proper shoe must have joints opposite the ankle and the medio-tarsal articulation; it must permit the ready application of elastic power; and it must not so girdle the limb as to interfere with the circulation” (Sayre, loc. cit., p. 91).

Sayre places so much confidence in the power of this elastic tension to overcome contractions that he rarely resorts to tenotomy in the treatment of paralytic talipes. Hueter, however,¹⁸⁰ considers tenotomy much the speediest, and therefore the most desirable, way of removing contractions.¹⁸¹

¹⁸⁰ Loc. cit.

¹⁸¹ Loc. cit.

Seeligmüller quotes with approval Böttger's method for the treatment of deformities, where the weight of the body is utilized to stretch the retracted tendons. Thus, for talipes equino-varus an over-reduction is effected under ether, and the foot forced into a position of moderate calcaneo-valgus. In this position it is retained by the immediate application of a plaster or silica bandage. After this has hardened the child should be encouraged to walk in the mould, with the addition of felt shoes having a slanting sole that is thickened like a wedge at the inner side of the foot and strapped on like a skate. Then, during the act of walking the body tends to constantly force down the heel and thus stretch the retracted tendo Achillis, while the bandage and felt sole (acting like a splint) prevent the inner side of the foot from slipping up.

For talipes valgus the method is analogous, but the foot is forced into an equino-varus position, so that the tendo Achillis is artificially shortened, and ultimately becomes a rigid band, capable, in spite of the sural paralysis, of sustaining the heel.

A cause of relapse in talipes not unfrequently overlooked is the presence of even slight contractions of the hip- and knee-joints. These by shortening the limb tend to the production of equinus, since the foot points itself in order to reach the ground. These contractions, whose rigidity is far inferior to that induced by chronic arthritis, may be overcome by forced extension under ether or gradually by manipulations, or by the weight-and-pulley apparatus, applied in the recumbent position, as in morbus coxarius. The obvious objection to the latter method is the confinement in bed which it necessitates in a child enjoying at the time perhaps robust general health.

The contraction once overcome, the limb must be placed in apparatus which shall both maintain suitable extension and assist in supporting the trunk during station and locomotion. The latter purpose is effected, as in apparatus for chronic joint diseases, by transferring the weight of the body to steel splints running up each side of the limb, the outer one as far as a girdle which encircles the hips; the inner to a band surrounding the upper part of the thigh. Thus is extended the support which in paralysis limited to the leg-muscles is given by the steel splints inserted in the side of the club-foot shoes.

In the simplest form of apparatus locomotion is expected to be accomplished by the action of muscles inserted above the seat of the paralysis. Thus, when the muscles passing over the ankle-joint are paralyzed, the foot is moved as a dead weight by means of the quadriceps extensor, popliteus, and hamstring muscles inserted at the upper extremity of the leg. If the quadriceps cruris is paralyzed, the rotators of the thigh, ilio-psoas, sartorius, and adductor muscles, passing from the pelvis to the thigh, and which are so frequently intact in atrophic paralysis, are enabled to move the limb if the weight of the body is borne by steel splints, if these be light and properly jointed at the hip, knees, and ankle.¹⁸²

¹⁸² Or the joint of the knee may be kept locked while the patient walks, when extension of the limb is mainly required, during both the active and passive movements of locomotion, the necessary flexion being supplied at the hip and ankle. By means of a key the knee-joint can be flexed during the sitting positions.

But an important aid to locomotion may be obtained from the artificial muscles, whose elastic tension is of such value in overcoming contractions. The quadriceps extensor, the most frequently paralyzed, may be supplemented by an India-rubber band and chain passing down the front of the thigh from a point on the pelvic girdle corresponding to the anterior iliac spine to a point on a leg-band, imitating the tibial insertion of the quadriceps tendon. Analogous bands stretched on the posterior aspect of the thigh simulate the hamstring muscles. When the external rotators are paralyzed, the artificial muscle must stretch from the pelvic girdle to a band encircling the upper part of the thigh.

The action of these muscles, apart from their elastic tension of repose, is thus explained by Duchenne: When any effort is made to move a paralyzed limb, the intact antagonists to the paralyzed muscles contract; thus, the flexors of the leg. But this contraction, being constantly opposed by the elastic tension of the artificial quadriceps, is restrained and gradual, instead of being brusque, jerking, and excessive, as it otherwise would be. This is the first result obtained. In the second place, contraction of the antagonist having ceased, the artificial muscle which has been stretched returns upon itself in virtue of its elasticity, and restores the limb to the position of normal equilibrium.

For the act of walking, however, the artificial quadriceps would require to be made tense enough to resist flexion, and thus keep the limb in extension. An artificial anterior tibial muscle, however, would require to yield to the intact gastrocnemius while the heel was being raised from the floor; then its elastic force should be sufficient to retract the point of the foot in dorsal flexion during the pendulum movement which passively swings the leg forward. The tension of the artificial muscle should therefore be so adjusted that it can only be overcome by the active contraction of the gastrocnemius, and at the moment of greatest tension, immediately after stretching, it should be able to quite overcome the gastrocnemius, then relatively¹⁸³ relaxed.

¹⁸³ We say relatively, believing that the simultaneous contraction of antagonist muscles has been well established as a constant normal phenomenon.

The anterior tibial, gastrocnemius, and many other of the artificial muscles devised by Duchenne are still in use in the modified form given to them by Barwell. On the other hand, the action of the long peroneus in pronating the foot, and which Duchenne imitated by an elaborate artificial tendon following the exact course of the natural one, is to-day generally supplemented by the jointed shoe and laced bandage.

In paralysis of all the muscles surrounding a joint, when the limb is placid and no retractions by adapted atrophy have taken place, the artificial muscles can only serve to oppose the malpositions which are threatened from mechanical influences.

In the upper extremities prothetic apparatus has been principally used for progressive muscular atrophy. Paralysis of the wrist extensors is perhaps the only case in which the artificial muscle is required in anterior poliomyelitis. A string may be necessary to support the arm in paralysis of the deltoid, to avert luxation of the humerus.

Duchenne's ingenuity did not shrink from the difficult task of supplementing the muscles of the trunk. This he did by inserting the elastic spirals in corsets in a direction following that of the muscles paralyzed. Thus, a unilateral paralysis of the sacro-lumbalis may be met by a spiral splint running up one side of the spine; below, to the lateral posterior portion of a pelvic girdle. In bilateral paralysis two springs are used to antagonize the action of the abdominal muscles.

In Barwell's apparatus for the trunk¹⁸⁴ India-rubber bands are again substituted for spiral springs. No attempt is made to imitate the direction of muscles, but the force is applied in any direction required to antagonize the pressure producing the deformity.¹⁸⁵

¹⁸⁴ Especially designed for habitual scoliosis, but applicable also to the paralytic deformity.

¹⁸⁵ Volkmann (loc. cit., p. 778) thinks that the force of Barwell's India-rubber straps, whether for scoliosis or club-foot apparatus, is inadequate, and much inferior to metallic springs.

It is always important to remember the rarity of scoliosis caused by spinal paralysis of the trunk-muscles, and the much greater frequency with which this deformity occurs as a consequence of the paralytic shortening of a leg. A high shoe, equalizing the length of the lower extremities, is then the simple and efficient remedy.

In cases of long standing, even when the scoliosis is due to this cause, certain muscles on the concave side of the curve may become so retracted and rigid as to require tenotomy. Before this operation it is necessary to put the rigid muscles on the stretch as much as possible; and this may be done, if necessary, by means of Sayre's hanging apparatus. After this operation the spine may be straightened out with ease—an important distinction from advanced habitual scoliosis, where the alteration in the shape of the vertebræ defeats all attempts at rectification. The position may be maintained by elastic straps or corsets and by removing the condition which has led to the deformity.

Seeligmüller criticises too unfavorably the entire system of elastic tension in the prophylaxis and treatment of paralytic deformities. He quotes Duchenne's admission, that in certain cases traction upon rigidly-retracted tissues becomes insupportably painful, and must be abandoned. It is in these cases that tenotomy becomes an indispensable preliminary to the use of apparatus. Sayre insists that the necessity for tenotomy is indicated when pressure on the rigid muscle is followed by instantaneous spasmodic contraction in the affected or neighboring muscles. He declares that such contractions indicate reflex irritations, show that the muscle has undergone structural change, and that any attempt to stretch or lengthen it would be followed by an excess of irritation and pain.

This explanation can hardly be accepted, since muscles, whether imperfectly or not at all paralyzed, which from position and adapted atrophy have become retracted, have necessarily undergone structural changes. The greater these changes, the greater the diminution of reflex excitability; and in any muscle completely paralyzed and degenerated this is entirely lost. If, however, the afferent nerves retain enough vitality, if the muscle be slightly paralyzed or altogether intact, then irritation of its tendon by stretching may serve to excite contractions in the belly of the muscle. The possibility of such spinal reflexes is demonstrated by the now familiar phenomenon of the tendon reflex in various spinal diseases.¹⁸⁶ The contractions must be painful from the impediments offered to the progress of the contracting nerve, and from the exaggeratedly vicious position into which they tend to force the limb. Under these circumstances prothetic apparatus must be deferred until section of the tendons has been made.

¹⁸⁶ “Passive muscular tension excites tonic contraction in a muscle, and this action may, in abnormal conditions, be excessive, as in the myelitic contractions (so-called tendon reflexes).... The afferent nerves commence in the fibrous tissues of the muscle, and seem to be especially stimulated by extension” (Gowers, On Epilepsy, 1881, p. 97).

DISEASE OF ONE LATERAL HALF OF THE SPINAL CORD.

BY H. D. SCHMIDT, M.D.

SYNONYMS.—Unilateral lesion of the spinal cord; Spinal hemiplegia and hemiparaplegia; Unilateral spinal paralysis.

INTRODUCTION.—This disease remained unnoticed until twenty years ago, when Brown-Séquard, observing that certain lesions of the spinal cord were accompanied by symptoms resembling those which he witnessed in animals after section of one lateral half of the cord, recognized it as a special affection. Although some of the accompanying phenomena of such a section had likewise been observed by Stilling, Budge, Eigenbrodt, Tuerk, Schiff, Von Bezold, and Van Kempen,¹ nevertheless this whole group of symptoms, as belonging to the same disease, was first clearly recognized and anatomically demonstrated by Brown-Séquard.² According to this physiologist, a section or a destruction of a small portion of a lateral half of the spinal cord in its cervical region gives rise to the following phenomena: namely, on the injured side is observed a paralysis of voluntary motion, of the muscular sense, and of the blood-vessels; the latter, manifesting itself by a greater supply of blood and a higher temperature of the parts, may continue to exist for some years. There is, furthermore, an increased sensibility of the trunk and extremity to touch, prick, heat, cold, electricity, etc., owing to vaso-motor paralysis, though in some cases a slight anæsthesia may exist in a limited zone above the hyperæsthetic part, and also in certain parts of the arm, breast, and neck. Besides these symptoms, vaso-motor paralysis of the corresponding side of the face and of the eye, manifested by an elevated temperature and sensibility, partial closure of the eyelid, contracted pupil, slight contraction of some of the muscles of the face, etc., may also be present. On the opposite side of the injury an anæsthesia of all kinds of sensation, excepting the muscular sense, is observed in both extremities; there is also an absence of motor paralysis. The anæsthesia on this side is owing to the decussation of the sensory nerves in the spinal cord.

¹ Eckhard, “Physiologie des Nervensystems,” in Handbuch der Physiologie, edited by L. Hermann, 2d part of vol. ii. p. 165.

² “On Spinal Hemiplegia,” Lancet, Nov. 7, 21, and Dec. 12, 26, 1868, reported in Virchow and Hirsch's Jahresbericht for the year 1868, vol. ii. p. 37.

If the hemisection of the cord is made in the dorsal region, the functional disturbances are limited to that part of the body below the point of division, and a hemiparaplegia, or paralysis of the corresponding lower extremity, will be the result.

From these facts it will be readily understood that a lesion occurring in any portion of one lateral half of the spinal cord of man must be followed by some or all of the above-mentioned symptoms, and that the phenomena produced by physiological experiments on animals constitute, in reality, the pathological basis of unilateral spinal paralysis in man. They will be more clearly understood by calling to mind the course of the musculo-motor, vaso-motor, and sensitive tracts in the spinal cord. Thus, the musculo-motor tracts, after having descended to the crura cerebri, cross one another in the pyramids of the medulla oblongata and adjoining upper portion of the spinal cord, forming the so-called decussation of the pyramids; they then descend through the spinal cord to supply the muscles of the same side of the body.³ A section of one lateral half of the cord therefore causes motor paralysis on the same side. The vaso-motor tracts remain uncrossed, and pass, each, through one lateral half of the cord to supply the vessels on the same side; some regions of the body are stated to make an exception to this rule. According to Brown-Séquard, the sensitive tracts conducting the different kinds of sensation, with the exception of the muscular sense, on the contrary, cross over to the opposite half of the spinal cord soon after their entrance into it, and thence pursue their further course to the brain. A section of one lateral half of the cord, therefore, will be followed by a loss of sensation of touch, pain, heat, tickling, etc. on the other side of the body.

³ Though, in the majority of cases, a complete decussation of the motor tracts probably takes place in the pyramids, the researches of Flechsig have shown (Die Leitungsbahnen im Gehirn und Rückenmark des Menschen, p. 273) that there are a number of others in which the decussation is not complete, but where a part of these tracts passes to the spinal marrow uncrossed on the inner surface of the anterior white columns.

The symptoms above mentioned must of course vary according to the extent, the intensity, and the particular nature of the lesion, as well as the height at which it is located in the spinal cord.

DEFINITION.—The chief characters of unilateral spinal disease are motor paralysis, hemiplegia, or hemiparaplegia, paralysis of the muscular sense and of the blood-vessels on the side of the lesion, and paralysis of sensation with preservation of the muscular sense on the other side of the body. These symptoms may vary, and be accompanied by other phenomena according to the particular seat, extent, and depth of the lesion.

SYMPTOMS.—According to the nature of the lesion, the symptoms of unilateral disease of the spinal cord may be developed suddenly, as, for instance, when caused by traumatic injuries; or in a gradual and slow manner, when they may be preceded by premonitory symptoms, such as vertigo, pain on the side of the lesion, etc. The most prominent clinical phenomena, as before mentioned, are motor paralysis on the side of the lesion, and anæsthesia on the opposite side of the body. The motor paralysis on the side of the lesion may, according to the seat of the latter, manifest itself in either the form of a hemiplegia or hemiparaplegia, and even extend in a light form to the opposite side of the body. In typical cases, however, in which the injury or disease is strictly confined to one lateral half of the cord, the motor power on the other side of the body remains entirely undisturbed. At the same time, the muscular sense on the injured side is paralyzed or considerably diminished, and in some cases (Fieber, Lanzoni, Allessandrini) the electro-muscular excitability also has been found lowered, while in others it has remained normal. There is furthermore observed, on the side of the lesion, a vaso-motor paralysis, manifesting itself by a greater supply of blood to, and a higher temperature of, the paralyzed trunk and limbs, giving rise to an increase of sensibility (hyperæsthesia) of touch, prick, heat, cold, electricity, etc. in these parts. If the seat of the lesion is sufficiently high up in the cord, this paralysis extends, moreover, to the corresponding side of the face and eye, where it also causes an elevation of temperature, increase of sensibility, partial closure of the eyelid, contracted pupil, slight contraction of some of the muscles of the face, etc. In a number of cases at the boundary of the hyperæsthetic region a narrow anæsthetic zone is observed to exist on the breast, neck, or arm. This anæsthesia is owing to the division, at the level of the section, of some nerves of sensation on their way to the other half of the spinal cord. An increase of the reflex irritability of the tendons has in some cases (Erb, Schulz, Revillons) been observed, while in one case (Glaeser) the reflex was found to be absent. Swelling and œdema of the paralyzed limbs have also been met with (Glaeser), and in one case (Allessandrini) even swelling and pain in all the joints of the injured side were observed before death, while masses of coagulated blood in these joints, particularly in the knee, were revealed by the autopsy. The inflammatory affection of the knee-joint of the paralyzed leg has, moreover, been observed by Viguès, Joffroy, and Solomon.⁴ Frequently, atrophy of the paralyzed muscles takes place, especially in chronic cases. In one case (Fieber) even atrophy of the upper extremity of the uninjured side of the body was observed.

⁴ Erb, “Diseases of the Spinal Cord, etc.,” Cyclopædia of the Practice of Medicine, edited by H. v. Ziemssen, Amer. ed.

The most prominent symptoms observed on the side of the body opposite to the seat of the lesion are anæsthesia of every kind of sensation, preservation of the muscular sense, and absence of motor paralysis. Reflex action and electro-muscular contractility generally remain normal, though in one case (Fieber) the latter was found increased. Although the anæsthesia of the skin generally comprises every kind of sensation, three cases were observed (Fieber) in which the sensation of heat remained unimpaired, while the electro-cutaneous sensibility appeared to be lost. As a general rule, there is no vaso-motor paralysis on the uninjured side, though in some cases (Erb, Allessandrini) an elevation of temperature has been observed.

Besides the above symptoms, some others, less characteristic in nature, are now and then observed in individual cases. They are painful sensations on one or the other side, or even simultaneously on both sides of the body, and also a feeling of constriction at the level of the lesion (Erb). Disturbances of the functions of the bowels or bladder are also met with, though in other cases they are absent.

PATHOLOGICAL ANATOMY.—The pathological changes taking place in the spinal cord of patients affected with unilateral spinal paralysis must vary in different cases according to the particular nature of the lesion giving rise to the characteristic symptoms. In those cases reported to have terminated by a gradual disappearance of the symptoms with or without therapeutic interference it is very probable that the exciting cause was a hyperæmia or a myelitis of a small portion of one lateral half of the spinal cord, sufficiently high in degree to impair the conducting power of the nerve-fibres passing through it. In some cases the myelitis may lead to a degeneration of the nerve-fibres, or even extend to the other half of the cord, and by calling forth additional symptoms render the case more complicated. In syphilitic cases the disease depends upon syphilitic deposits or neoplasms in the affected portion of the spinal cord; these cases, however, generally yield to treatment. In the same manner may circumscribed sclerosis give rise to the disease. Another cause may be found in the compression of the cord caused by meningeal tumors or by the fractured portions of some of the vertebræ. Chronic disease of the vertebral bones themselves (Pott's disease) may also, by encroaching upon the spinal cord, become an exciting cause.

The most typical cases, however, are those depending upon traumatic injuries, by which one lateral half of the spinal cord is forcibly divided. These lesions resemble in nature the division of the cord in the physiological experiments on animals, and are most frequently caused by a stab from a knife penetrating to the cord through the intervertebral spaces.

DIAGNOSIS.—In those cases in which the symptoms of unilateral spinal paralysis appear soon after an external injury to the spine, it becomes obvious that the latter is the exciting cause. In cases of a more chronic character, in which the symptoms appear gradually, the nature of the exciting cause can only be correctly determined by the observation of certain collateral symptoms characteristic of such causes as might give rise to the symptoms of the disease in question. As regards the diagnostic symptoms of unilateral spinal paralysis themselves, they are sufficiently characteristic to be easily distinguished from those of other forms of hemiplegia or hemiparaplegia. Thus, cerebral hemiplegia may be distinguished from the disease under discussion by the sensory disturbances being either absent or on the same side as the paralysis; furthermore, by the one-sided paralysis of the face and of the tongue and by the affection of various cranial nerves. The hemiplegic form of spasmodic spinal paralysis is distinguished by the absence of sensory disturbance, etc. Lastly, hemiplegia depending upon lesion of one side of the cauda equina is distinguished from unilateral spinal disease by the paralysis and anæsthesia being confined to the same side, and by generally affecting certain nervous districts of the lower extremities.

PROGNOSIS.—In unilateral spinal lesions the prognosis depends obviously on the particular nature and intensity of the exciting cause. On the whole, there are quite a number of cases reported, even of traumatic origin, which have terminated favorably.

TREATMENT.—The treatment of unilateral spinal paralysis depends, like the prognosis, upon the nature of the exciting cause. The principles upon which it is to be pursued of course are the same as those upon which the treatment of the various lesions causing the disease—such as hyperæmia, myelitis, sclerosis, wound of the spinal cord, etc.—is based.

PROGRESSIVE LABIO-GLOSSO-LARYNGEAL PARALYSIS.

BY H. D. SCHMIDT, M.D.

SYNONYMS.—Chronic progressive bulbar paralysis; Progressive muscular paralysis of the tongue, soft palate, and lips.

HISTORY.—Although the particular group of symptoms constituting this disease must have been met with and known to the older medical observers, they were nevertheless first recognized as a special variety of paralysis in 1841 by Trousseau,¹ who named the affection labio-glosso-laryngeal paralysis. But as the memorandum prepared by this distinguished physician at the time when, in consultation with a medical colleague, he had observed the particular symptoms of this affection, unfortunately remained unpublished, twenty years more elapsed before the first accurate and detailed description of the symptoms and progressive nature of this disease under the name of progressive muscular paralysis of the tongue, soft palate, and lips was rendered by Duchenne. The writings of this author directed at once the attention of other medical men to this disease, and since that time a large number of cases have been reported and discussed,² while the microscopical examination accompanying the autopsies of many of them finally revealed that the seat of the lesion giving rise to the phenomena of this disease was to be sought in the nervous nuclei of the medulla oblongata. Hence at the present time the pathology of this disease is thoroughly understood.

¹ Clinique médicale de l'Hôtel Dieu de Paris, vol. ii. p. 334.

² A very considerable number of cases of this disease, and discussions thereon, will be found reported in Virchow and Hirsch's Jahresbericht über die Leistungen und Fortschritte der Gesammten Medizin, for the years 1866-80, vol. ii., section “Krankheiten des Nervensystems.”

DEFINITION.—That form of labio-glosso-laryngeal paralysis to be treated in the following pages is characterized by a progressive paralysis and atrophy of the muscles of the tongue, lips, palate, pharynx, and larynx, interfering in a greater or lesser degree with the articulation of words and sounds and with the functions of mastication and deglutition—affecting, furthermore, in the later stages of the disease, the voice and the function of respiration. The paralysis is caused by a progressive degeneration and atrophy of the ganglion-cells of those nerve-centres in the medulla oblongata from which the muscles of the above-named organs receive their supply of nervous energy, though in most cases the pathological process extends to, or even beyond, the roots of those nerves which originate in these centres and terminate in the respective muscles. In many cases the pathological process extends to the spinal marrow, and there causes paralysis and atrophy of the muscles of the trunk, and, generally, of the upper extremities. Almost in every case the disease, as its name indicates, slowly progresses until it terminates in death.

There are, however, a number of cases observed which, though exhibiting the same or similar symptoms, do not, in reality, depend upon a progressive degeneration and atrophy of the centres and nerve-roots of the medulla, but, on the contrary, owe their symptoms to other causes; as, for instance, to tumors, hemorrhages, syphilitic neoplasms, etc., which, either by pressing upon the medulla from without, or, if situated within, by deranging in various manners the individual nervous elements of that part, may give rise to some or even all of the symptoms of true labio-glosso-laryngeal paralysis. These symptoms, however, according to the character of the lesion, may, after remaining stationary for some time, retrograde, and even disappear, as has been observed in syphilitic cases; or they may progress, and finally end in death. In order to distinguish these cases from the chronic or progressive bulbar paralysis some authors have attached the term retrogressive to this form of the disease.

SYMPTOMS.—As the degeneration of the nerve-centres in the medulla oblongata, upon which the disease depends, does not proceed in a regular fixed order, the order in which the clinical symptoms successively appear also varies in different cases. In the majority of cases, however, the symptoms appear gradually, manifesting themselves generally in the form of a greater or lesser impediment in the articulation of certain sounds or letters depending upon the movements of the tongue, such as e, i, k, l, s, and c, while at the same time a difficulty of mastication and deglutition may be experienced by the patient, due to the progressive development of the paralysis, which deprives the tongue of its lateral and forward movements. To this cause also, at this period, the apparently increased secretion of saliva, running from the corners of the mouth, must be attributed. With intelligent patients these symptoms are rendered less prominent by the special effort which they make to pronounce slowly for the purpose of hiding the deficiency in their speech. But as the disease advances the difficulty of articulation increases on account of the paralysis extending to the orbicularis oris, thus affecting the mobility of the lips and interfering with the pronunciation of the labial sounds p, b, f, m, and w. With the loss of power of articulation the patient's speech becomes gradually reduced to monosyllables, or even, finally, to incomprehensible and inarticulated grunts, by which he expresses his wants to his friends. In consequence of the paralysis of the lips the patient becomes unable to whistle or blow or to perform any movement depending upon these organs, while at the same time, through the disturbance created in the co-ordination of the facial muscles by the paralysis of the orbicularis oris, the mouth becomes transversely elongated and drawn downward by the action of the remaining unparalyzed muscles upon its angles. With the mouth partially open and the lower lip hanging down, the face of the patient has a peculiar sad and painful expression, while the voice assumes a nasal sound on account of the paralysis of the palate.

After a while the difficulty of deglutition, caused by the inability of the tongue to properly assist in the formation of the bolus of food and its propulsion into the pharynx, increases on account of the paralysis extending to the muscles of the pharynx. The failure of these muscles in the performance of their special function of grasping the food and carrying it to the œsophagus obliges the patient to push it down the pharynx with his fingers. In some cases the difficulty of swallowing rests with solids, in others with fluids. The defective deglutition furthermore gives rise to spells of coughing and suffocation by portions of food getting between the epiglottis and larynx, while the paralyzed muscles of the palate allow the fluids to pass through the nose and enter the posterior nares.

As the case slowly proceeds the symptoms grow worse. The paralysis of the orbicularis oris reaches a point when this muscle is no more able to close the oral cavity; the mouth of the patient therefore remains open. The tongue, having now entirely lost its lateral, forward, or upward movements, rests motionless upon the floor of the mouth, evincing no other signs of life but occasional slight muscular twitchings. In some cases a diminution of the sense of taste, and also of that of touch in the tongue, pharynx, and larynx, has been observed. Atrophy of the tongue and lips now sets in, and the function of speech is almost entirely lost. The only letter which the patient is still able to pronounce is a (broad); all other sounds are indistinct and can hardly be understood. The paralysis of the tongue and other muscles of deglutition gives rise, furthermore, to an accumulation of the now excessively secreted saliva, which, being retained in the oral cavity, assumes the form of a viscid mucous liquid dripping from the mouth, extending, in the form of strings or ribbons, between the surfaces of the lips. Finally, when, through the progressive paralysis of the orbicularis oris, the patient can no more close the lips, the flow of saliva from the mouth becomes continuous; he is then seen engaged in the constant use of his handkerchief for removing the secretion.

In the latter stages of the disease the pathological process extends to the centres of respiration, paralyzing not only the muscles of respiration, but diminishing at the same time the contractile power of the lungs. A great difficulty of breathing—consisting not only in the want of depth of the inspirations, but, moreover, in a feebleness of expiration (manifested by weak, powerless coughing)—then ensues, and the patient is no further able to blow his nose or clear his bronchial tubes from the accumulating mucus. The paralysis of the muscles of the larynx, also occurring at this stage, not only increases the difficulties of deglutition, but most seriously affects the voice of the patient by decreasing the innervation of the vocal cords; the voice then becomes hoarse and weak, to be finally entirely lost.

The decrease in the innervation of the heart—which, lastly, also occurs—gives rise to irregularities in the action of this organ, followed by irregularity of the pulse, attacks of syncope, feelings of extreme weakness, and fears of death; whilst simultaneously the insufficient performance of the respiratory function renders the breathing of the patient weaker and weaker. Feelings of great oppression in the chest then arise, and the patient may die during one of the now frequent attacks of dyspnœa and suffocation.

No fever or pain is observed during the course of this disease; sensation remains unaffected and the mind is perfectly clear. It is owing to these circumstances that frequently the patient walks about and attends to the duties of life, until shortly before death he becomes confined to bed by the great weakness caused by the want of nutrition. The appetite also remains good, but, unfortunately, in consequence of the difficulties attending the act of deglutition, the patient cannot satisfy the demands of his stomach. In the latter stages of the disease, therefore, when feeding can only be accomplished by the aid of the stomach-tube, every attempt to relieve the terrible gnawings and pains of hunger ends in a failure. With starvation staring in his face, the unhappy victim of the disease finally sinks into a state of extreme inanition, which, if life is not suddenly extinguished by an attack of suffocation, slowly leads to final dissolution.

The symptoms above described are those generally observed in uncomplicated cases of labio-glosso-laryngeal paralysis. There are, however, a number of cases reported in which the degenerative process has passed from the medulla oblongata to the spinal cord, and given rise to paralysis of the muscles of the neck, especially of the trapezius, and to those of the shoulders, and even to those of the upper extremities. Atrophy of the interosseus muscles of the hand, with those of the ball of the thumb, is not unfrequently observed. In other cases the disease has been found associated with progressive muscular atrophy, and in others, again, with paralysis of the lower extremities, accompanied by contractures and depending upon amyotrophic lateral sclerosis.

Labio-glosso-laryngeal paralysis is, as before mentioned, slow but progressive in its course, the duration of which is from one to three, or even five, years. It always terminates in death within the limits of this time, either from suffocation, inanition, paralysis of the heart, or some other intercurrent disease.

PATHOLOGICAL ANATOMY.—The macroscopical and microscopical examinations made during the last fifteen years of the cerebro-spinal axis in quite a number of cases of progressive labio-glosso-laryngeal paralysis show that this disease depends upon a degeneration of the nervous elements of the nuclei or nerve-centres in the medulla oblongata, involving also the roots of the nerves arising from the latter, and supplying with nervous energy the muscles of the different organs paralyzed in this disease. The exact nature of this degeneration—that is, whether it represents the sequel of a previously existing myelitis or originates in a so-called parenchymatous inflammation—appears to be as yet not definitely settled, though a number of pathologists entertain the view that it is preceded by a chronic myelitis. This view appears to be corroborated by the fact that frequently portions of the medulla oblongata and cervical portion of the spinal cord are found in a state of sclerosis. The uncertainty in the determination of the exact nature of the pathological process here concerned chiefly depends upon the diverse conditions in which the blood-vessels of the medulla are found. For while, in some cases, perhaps the majority, they have been found empty and in a normal condition, they have in others been met with congested with blood—a condition pointing to a chronic inflammatory process. In other cases, again, their walls have been found thickened or undergoing fatty degeneration.

At any rate, whether inflammatory or not, the now numerous microscopical examinations have revealed that the main features of the process are a degeneration and atrophy, not only of the ganglion-cells of the respective nervous nuclei with their plexuses, but also of the fibres of the roots of the peripheral nerves arising from these centres; frequently the degeneration extends to some distance upon the nerves themselves. The microscopical changes in the ganglion-cells consist of an increase of yellow pigment, a gradual disappearance of their nuclei, terminating in an atrophy of the ganglionic bodies themselves, the pathological process leaving, finally, nothing but irregularly-shaped masses of pigment in the places of these bodies. The degeneration of the nerve-fibres appears to consist, as elsewhere, in a swelling of the axis-cylinder, accompanied by atrophy of the medullary sheath—a condition which finally leads to the complete destruction of these elements of the nerve-fibres, so that, at last, the whole nerve is only represented by the connective tissue of its neurolemma. Besides these changes, certain pathological products, such as conglomerations of fatty granules or globules, amylaceous bodies, etc., are also found in the degenerated nerve-centres and nerve-fibres.

Although in different cases the route which the degenerative process pursues is not the same, a certain general order, in which the nerves and nerve-centres are successively affected, and corresponding to the clinical symptoms, appears, nevertheless, to exist. It is thus that the nucleus of the hypoglossus has been observed to degenerate before the other nerve-centres. The nuclei of the spinal accessory and pneumogastric nerves, and also that part of the facial nucleus from which the inferior division of the facial nerve arises, appear to be affected next. The glosso-pharyngeal nucleus appears not to be affected in all cases, and still less frequently the nuclei and roots of the abducens, auditory, and trifacial nerves. The fibres forming the anterior pyramids have frequently been found degenerated throughout the medulla oblongata and pons; sclerosis also has been met with in this locality. In many cases, as has been remarked before, the pathological process descends into the spinal cord. Here, as in the medulla oblongata, the degeneration is principally confined to the motor centres located in the anterior horns, while the posterior horns, together with the lateral and posterior white columns, remain free from disease. The degree of degeneration taking place in the fibres of the respectively paralyzed muscles also corresponds to that of the elements of the nerve-centres from which they are supplied. The microscopical changes observed in the muscular fibres consist in a decrease of their diameter, accompanied by an increase in the number of their nuclei, as well as in the quantity of the connective tissue surrounding the primary bundles; some authors have observed amyloid degeneration of the muscular fibres.

ETIOLOGY.—The causes which give rise to the pathological process above described are but little known. Nevertheless, in a number of cases the disease has been traced back to taking cold, to physical as well as cerebral over-exertion, mental excitement, sorrow caused by misfortunes, poverty of nutrition, excessive use of tobacco, etc. In some cases the disease commences in the spinal cord in the form of progressive muscular atrophy or amyotrophic lateral sclerosis, and gradually extends to the medulla oblongata; in many other cases no particular cause can be found. The disease is rarely if ever met with in persons under twenty years of age, but is confined to adult life and old age. It occurs in both high and low walks of life, attacking more frequently men than women.

DIAGNOSIS.—The symptoms of progressive labio-glosso-laryngeal paralysis are so characteristic in themselves as to exclude any mistake in the formation of a diagnosis. There are, nevertheless, some pathological conditions, such as hemorrhages in the medulla oblongata or thrombosis and embolism of the arteries supplying the latter with blood, which may give rise to the same or very similar phenomena, and thus render a correct diagnosis difficult. In such cases it must be remembered that the cause of true labio-glosso-laryngeal paralysis, depending upon degeneration and atrophy of the nervous nuclei along the floor of the fourth ventricle, is very gradual, while the symptoms produced by the causes before mentioned generally make their appearance in a more acute and sudden manner. The latter also, if not remaining stationary for some time, have rather a tendency to improvement, wanting, therefore, the progressive character of the former.

Tumors at the base of the brain also, by pressing upon the roots of the cerebral nerves or upon the medulla oblongata itself, may produce similar symptoms, which, on account of their comparatively slow and gradual development, may prove more difficult to distinguish from those characterizing genuine, progressive labio-glosso-laryngeal paralysis. Errors of diagnosis, however, may here be avoided by taking into consideration the special symptoms which generally accompany the presence of tumors of the brain, such as vertigo, headache, vomiting or even hemiplegia, and local paralysis. The sensory nerves also may become affected by the pressure of the tumor upon them. Thus, pressure upon the trifacial nerve may give rise to neuralgic pains, feelings of tingling and numbness, or even anæsthesia; while pressure upon the optic nerves or their tracts, or upon the olfactory and lingual nerves, will be followed by derangements of vision, smell, and taste. The symptoms produced by the pressure of a tumor at the base of the brain, moreover, are not strictly progressive, but may for some time appear, and disappear again before becoming permanent.

Facial diplegia, in which the expression of the face somewhat resembles that of a patient affected with labio-glosso-laryngeal paralysis, is distinguished from the latter disease by the paralysis affecting both divisions of the facial nerve, while the tongue remains free and deglutition is undisturbed.

There are still other affections of the cerebro-spinal axis, such as paralysis of the insane, disseminated sclerosis, etc., which in their course present some or perhaps all of the symptoms characterizing labio-glosso-laryngeal paralysis; these may be distinguished from the latter disease by taking their own special symptoms into consideration.

TREATMENT.—Although almost all cases of progressive labio-glosso-laryngeal paralysis terminate fatally, some cases have been reported by several observers in which a temporary improvement in the symptoms of the disease, or even a total cure, had been obtained by treatment. Of course such favorable results can only be obtained in the initial or earlier stages of the disease. Thus, Kussmaul recommends in the initial stage, when pains in the head and neck are present, wet cupping of the nape of the neck in strong persons, also the use of the shower-bath, while nitrate of silver may be given internally. The application of galvanism in an alternate direction he also recommends—first, through the neck, and later on through the whole spinal column—and at the same time currents in an alternating direction from the neck and hypoglossus nerve to the tongue. Dowse reported a case of bulbar paralysis which he cured by the application of the constant current upon the paralyzed parts, subcutaneous injections of atropine and strychnine, with the internal administration of cod-liver oil, quinine, and phosphorus. He attaches great importance to the careful feeding of the patient through a tube passed through the nose, and to the strict application of the galvanic current; for excessive salivation he recommends atropine. Erb recommends to regulate the diet and the habits of life of the patient in such a manner as to avoid every irritation of the nervous system; furthermore, to generally stimulate the nutrition in order to produce a tonic effect upon the nervous system. For this purpose he principally relies upon a cautious hydropathic treatment, to be continued for a long time and with great regularity. The greatest importance, however, he attaches to electricity, considering the best method of galvanism as follows: “Galvanize with stabile application transversely through the mastoid processes and longitudinally through the skull, the so-called galvanism of the cervical sympathetic (anode on the nuchus, and cathode at the angle of the lower jaw), and then induce movements of deglutition (twelve to twenty at each sitting); besides this, apply, according to circumstances, direct galvanic or faradic currents to the tongue, lips, and palate.” The electric treatment must be continued for some time, with from four to seven sittings a week. Of the medicines taken internally, Erb recommends nitrate of silver, iodide of potassium, iodide of iron, chloride of gold and sodium, ergotin, belladonna, and preparation of iron and quinine.

DISEASES OF THE PERIPHERAL NERVES.

BY FRANCIS T. MILES, M.D.

The nervous system of the higher animals is the apparatus by which stimuli coming from the external world or originating in the interior of their own bodies are perceived (its sensitive functions), or cause muscular contraction (its motor functions), or, lastly, cause molecular changes in tissues (its trophic functions).

Besides this power which the nervous system possesses of receiving impressions originating outside of itself and actively replying to them, it appears also to possess the power of originating within itself changes the result of which are sensations, movements, and trophic alterations. In other words, it can act automatically.

The apparatus for the performance of these various functions consists of the end-organs, the nervous centres, and the nerves.

The end-organs are peripheral mechanisms for the reception of impressions. The structure and mode of action of some of them, as the eye and the ear, are pretty well understood, while others, as those connected with the sense of touch, temperature, etc., are but imperfectly known. It is probable that there are also peripheral mechanisms which facilitate the delivery of the impulses coming from the nerve-centres to the organs, tissues, muscles, glands, etc.

The nervous centres are made up of nerve-cells variously connected with each other. They are immediately concerned in receiving impressions conveyed to them by the nerves and transforming them into sensations, or transmitting them to other organs, causing reflex actions, or in originating sensations and impulses.

The nerves are organs which, connected at one extremity with the end-organs and at the other with the nervous centres, convey peripheral impressions to the centres, and impulses and influences from the centres to the various organs of the body.

As it is with diseases of the peripheral nerves that we are now concerned, let us begin by looking more closely into their structure and functions.

The nerves appear to the naked eye as white strands of variable size, which a close inspection shows to be made up of threads or fibrils (best seen when the cut end of a nerve is examined) bound together by fine connective tissue and scantily supplied with blood-vessels. A microscopic examination shows that each of the fibrils visible to the naked eye is made up of a great number of fibres. These are the medullated nerve-fibres, and they extend unbroken between the nerve-centres, with the cells of which they are connected, to the various organs and tissues, with which they also enter into organic union.

If we examine the structure of a medullated nerve-fibre, we find it to consist of a central thread called the central axis or axis-cylinder, in which close microscopic investigation shows a longitudinal striation, indicating that it is made up of fibrillæ. Surrounding the central axis like a sheath is the white substance of Schwann, composed of an oleo-albuminous substance, myeline, to which the nerves owe their white appearance. According to some observers, the white substance of Schwann is pervaded by a meshwork of fibres. Surrounding the white substance of Schwann is the sheath of Schwann, a structureless membrane having at intervals upon its inner surface nuclei, around which is a small amount of protoplasm.

At intervals along the course of the nerve-fibres are seen constrictions which involve the sheath and white substance of Schwann, but which do not affect the central axis, which passes unbroken the points of constriction. These are the nodes of Ranvier. Each space on the fibre beneath the nodes of Ranvier contains one of the nuclei of the sheath of Schwann, and probably, together with the white substance of Schwann, represents a cellular element. Diseased conditions sometimes respect the limits of these cellular elements.

The central axis is the true conducting part of the nerve-fibre, and it is probable that each of the fibrillæ of which it is composed has a separate peripheral termination and possesses the power of isolated conduction. The white substance of Schwann and the sheath of Schwann protect the central axis and seem to be connected with its nutrition.

The fibres in a nerve are bound together by loose connective tissue, the endoneurium, into the primitive bundles, which are again united by the perineurium, a membrane of laminated connective tissue, into more definite funiculi seen by the naked eye, the secondary bundles.

The secondary bundles are tied together by connective tissue, in which are found fat-cells and in which run the fine blood-vessels supplying the nerves. This connective tissue has been named the epineurium, and its condensed outer layers constitute the sheath of the nerve. It is important to observe that the connective tissue of the nerves is permeated by lymphatics which penetrate to the nerve-fibres, so that these are brought in contact with, and as it were, bathed in, the lymph.

Each nerve-fibre runs an isolated course from end to end, without anastomosing with other fibres, and near its peripheral termination it usually divides into two or more branches.

The fibres of the peripheral nerves depend for their integrity and nutrition upon their connection with central organs. The large multipolar cells of the anterior horns of gray matter of the spinal cord preside over the nutrition of the motor fibres; the ganglia on the posterior roots of the spinal nerves over the nutrition of the sensitive fibres.

If a nerve be severed from its connection with these centres of nutrition, it in a short while undergoes degenerative changes which result in complete destruction of its fibres.

The nerve-fibres when in a state of functional activity conduct impressions along their length to the end-organs or to the nerve-centres with which they are in connection. This property of the fibres we call their conductivity. Each fibre conducts impressions in an isolated manner, not communicating them to other fibres with which it may be in contact. The rapidity of this conduction in human nerve-fibres is estimated at 33.9 meters (about 38 yds.) per second. This rate may be diminished by cold or by the anelectrotonic condition which is induced in the nerve by the passage through it of an electric current.

The nerve-fibres are irritable; that is, the application to them of stimuli excites their functional activity, and the impression made by the stimulus is transmitted to their extremities.¹

¹ The nerve-fibres in man do not appear to attain their full irritability until the fifth or tenth month after birth (Soltman).

The natural or physiological stimuli of the nerves act upon their extremities. Either they act through the peripheral mechanisms, giving rise to impressions which are conducted centripetally to the cells of the nerve-centres and there cause sensations or reflex actions, or they act upon the nerve-centres, giving rise to impulses which are conducted centrifugally and cause the various phenomena of contraction of muscles, inhibition of contraction, secretion, etc. Besides the physiological, there are other stimuli which excite the functional activity of nerve-fibres when applied at any point along their course.

Mechanical stimuli, blows, concussions, pressure, traction, etc., excite the nerves, causing sensations when applied to sensitive nerves, or contraction of muscles when applied to motor nerves. When mechanical stimuli are pushed farther, the irritability of the nerves may be destroyed. The gradual application of mechanical stimuli may destroy the irritability of nerve-fibres without any exhibition of excitation, as in paralysis from pressure. In nerve-stretching it is probable that many of the results depend upon the mechanical stimulation of the nerve-fibres by the traction. With a certain amount of force used the irritability of the nerve may be increased; carried farther, both the irritability and the conductivity may be diminished, and finally destroyed. As the centripetal fibres are soonest affected in the stretching, we can see how this proceeding is most beneficial in neuralgias, where a potent factor, if not the cause of the disease, is an abnormal excitability of the nerve-fibres. It is to be observed, nevertheless, that in cases of continued pressure upon mixed nerves the motor fibres are the first to suffer loss of their conductivity.

Sudden alterations of temperature act as stimuli to nerves. Heat increases their irritability, but its prolonged application diminishes it. Cold in general diminishes the nervous irritability, and may be carried to the point of completely destroying it temporarily.²

² But at a certain age in freezing the ulnar nerve Mitchell found its irritability notably increased.

Many substances of widely-different chemical constitution, as acids, alkalies, salts, alcohol, chloroform, strychnine, etc., act as stimuli when applied directly to the nerves, apparently by causing in them rapid molecular changes. Also may be enumerated as chemical stimuli to the nerves substances found naturally in the body, as bile, bile salts, urea. The rapid withdrawal of water from nerve-tissue first increases, and then diminishes, its irritability. The imbibition of water decreases nervous irritability.

An electric current of less duration than the 0.0015 of a second does not stimulate the nerve-fibres. It would appear that more time is required for the electric current to excite in nerve-tissue the state of electrotonus which is necessary to the exhibition of its functional activity. The electric current stimulates a nerve most powerfully at the moments of entrance into and exit from the nerve, and the more abruptly this takes place the greater the stimulation. Thus the weak interrupted currents of the faradic or induced electricity owe their powerfully stimulating effects to the abruptness of their generation and entrance into and exit from the nerves. At the moment of the entrance of the electric current into the nerve—that is, upon closing the circuit—the stimulating effect is at the negative pole or cathode; when the current is broken—i.e. leaves the nerve—the stimulating effect is at the positive pole or anode. A current of electricity very gradually introduced into or withdrawn from a nerve does not stimulate it. But if while a current is passing through a nerve its density or strength be increased or diminished with some degree of rapidity, the nerve is stimulated, and the degree of stimulation is in proportion to the suddenness and amount of change in the density or strength of the current. Although with moderate currents the stimulation of the nerve takes place only upon their entrance and exit, or upon variations of their density, nevertheless, with a very strong current the stimulation continues during the passage of the current through the nerve. This is shown by the pain elicited in sensitive nerves, and the tetanic contraction of the muscles to which motor nerves are distributed.

An important factor in electrical stimulation is the direction of the current through the nerve. A current passed through a nerve at right angles with its length does not stimulate it. Currents passing through a nerve stimulate in proportion to the obliquity of their direction, the most stimulating being those passing along the length of the nerve. Motor nerves are more readily stimulated by the electric current the nearer it is applied to their central connection. Experiments on the lower animals would seem to indicate that the motor fibres in a nerve-trunk do not all show the same degree of irritability when stimulated by the electric current.

The irritability of the nerve-fibres may be modified or destroyed in various ways. Separation of nerves from their nutritive centres causes at first an increase of their irritability, which is succeeded by a diminution and total loss, these effects taking place more rapidly in the portions nearer the nerve-centres. It is important to observe that an increase of irritability preceding its diminution is generally observed in connection with the impaired nutrition of nerves, and is the first phase of their exhaustion.

Prolonged and excessive activity or disuse of nerves causes diminution of their irritability, which may go to the extent that neither rest in the one case nor stimulation in the other can restore it. If a galvanic current is passed through a nerve in its length, the irritability of the fibres is increased in the region of catelectrotonus—viz. in the part near the cathode—and diminished in the region of anelectrotonus—viz. in the part near the anode. Certain substances, as veratria, first increase and then destroy the irritability of the nerves; others, as woorara, rapidly destroy it.

The fibres of the peripheral nerves are divided into two classes: first, those which conduct impressions or stimuli to the nerve-centres, the afferent or centripetal fibres; and, secondly, those which conduct impulses from the centres to peripheral organs, the efferent or centrifugal fibres. Belonging to the first class are (1) sensitive fibres, whose stimulation sets up changes in the nerve-centres which give rise to a sensation; (2) excito-motor fibres, whose stimulation sets up in the nerve-centres changes by which impulses are sent along certain of the centrifugal fibres to peripheral end-organs, causing muscular contraction, secretion, etc. Belonging to the second class are (1) motor fibres, through which impulses are sent from the nerve-centres to muscles, causing their contraction; (2) secretory fibres, through which impulses from nerve-centres stimulate glands to secretion; (3) trophic fibres, through which are conveyed influences from the centres, affecting the nutritive changes in the tissues; (4) inhibitory fibres, through which central influences diminish or arrest muscular contraction or glandular activity. No microscopic or other examination reveals any distinction between these various fibres.

Every nerve-fibre has the power of conducting both centripetally and centrifugally, but the organs with which they are connected at their extremities permit the exhibition of their conductivity only in one direction. Thus, if a nerve-fibre in connection with a muscle at one end and a motor nerve-cell at the other be stimulated, although the stimulus is conducted to both ends of the fibre, the effect of the stimulus can only be exhibited at the end in connection with the muscle, causing the muscle to contract. Or if a fibre in connection with a peripheral organ of touch be stimulated, we can only recognize the effects of such stimulation by changes in the nerve-cells at its central end which give rise to a sensation.

When we consider the extensive distribution and exposed position of the peripheral nerves, their liability to mechanical injury and to the vicissitudes of heat and cold, we cannot but anticipate that they will be the frequent seat of lesions and morbid disturbances. It may be that not a few of their diseased conditions have escaped observation from a too exclusive looking to the central nervous system as the starting-point of morbid nervous symptoms. This occurs the more readily as many of the symptoms of disease of the peripheral nerves, as paralysis of muscles, anæsthesia, hyperæsthesia, etc., may equally result from morbid conditions of the brain or spinal cord, and not unfrequently the peripheral and central systems are conjointly affected in a way which leaves it doubtful in which the disease began or whether both systems were simultaneously affected.

The elucidation of such cases involves some of the most difficult problems in diagnosis, and requires not only a thorough acquaintance with the normal functions of the peripheral nerves, but also the knowledge of how those functions are modified and distorted in disease.

The symptoms arising from injuries and diseases of the peripheral nerves are referable to a loss, exaggeration, or perversion of their functions, and we often see several of these results combined in a single disease or as the result of an injury.

The fibres may lose their conductivity or have it impaired, causing feebleness or loss of motion (paralysis), or diminution or loss of sensation (anæsthesia). Or there may be induced a condition of over-excitability, giving rise to spasm of muscles and sensations of pain upon the slightest excitation, not only from external agents, but from the subtler stimulation of molecular changes within themselves (hyperæsthesia). Or diseased conditions may induce a state of irritation of the nerve-fibres, which shows itself in apparently spontaneous muscular contraction or in sensations abnormal in their character, and not corresponding to those ordinarily elicited by the particular excitation applied, as formication or tingling from simple contact, etc. (paræsthesiæ), or in morbid alterations of nutrition in the tissues to which the fibres are distributed (trophic changes).

If we could recognize the causes of all these varied symptoms and discover the histological changes invariably connected with them, it would enable us to separate and classify the diseases of the peripheral nerves, and give us a sound basis for accurate observation and rational therapeutics. But, although the progress of investigation is continually toward the discovery of an anatomical lesion for every functional aberration, we are still so far from a complete pathological anatomy of the peripheral nerves that of many of their diseases we know nothing but their clinical history. We are therefore compelled in treating of the diseases of the peripheral nerves to hold still to their classification into anatomical and functional, as being most useful and convenient, remembering, however, that the two classes merge into each other, so that a rigid line cannot be drawn between them, and that such a classification can only be considered as provisional, and for the purpose of more clearly presenting symptoms which we group together, not as entities, but as pictures of diseased conditions which may thus be more readily observed and studied.

It is well to begin the study of the diseases of the peripheral nerves by a consideration of nerve-injuries, because in such cases we are enabled to connect the symptoms which present themselves with known anatomical alterations, and thus obtain important data for the elucidation of those cases of disease in which, although their symptomatology is similar, their pathological anatomy is imperfectly or not at all known.

Injuries of the Peripheral Nerves.

If the continuity of the fibres of a mixed nerve be destroyed at some point in its course by cutting, bruising, pressure, traction, the application of cold, the invasion of neighboring disease, etc., there will be an immediate loss of the functions dependent on the nerve in the parts to which it is distributed. The muscles which are supplied by its motor fibres are paralyzed; they no longer respond by contraction to the impulse of the will. No reflex movements can be excited in them either from the skin or the tendons. They lose their tonicity, which they derive from the spinal cord, and are relaxed, soft, and flabby. As the interrupted sensory fibres can no longer convey impressions to the brain, we might naturally look for an anæsthesia, a paralysis of sensation, in the parts to which they are distributed, as complete as is the loss of function in the muscles. Such, however, is not the fact. Long ago cases were observed in which, although sensitive nerves were divided, the region of their distribution retained more or less sensation, or seemed to recover it so quickly that an explanation was sought in a supposed rapid reunion of the cut fibres. Recent investigations, moreover, show that in a large number of cases where there is complete interruption of continuity in a mixed nerve the region to which its sensitive fibres are distributed retains, or rapidly regains, a certain amount of sensation, and that absolute anæsthesia is confined to a comparatively small area, while around this area there is a zone in which the sensations of pain, touch, and heat are retained, though in a degree far below the normal condition; in short, that there is not an accurate correspondence between the area of anæsthesia consequent upon cutting a sensitive nerve and the recognized anatomical distribution of its fibres. We find the explanation of this partly in the abnormal distribution of nerves, but principally in the fact of the frequent anastomoses of sensitive nerves, especially toward their peripheral distribution, thus securing for the parts to which the cut nerve is distributed a limited supply of sensitive fibres from neighboring nerves which have joined the trunk below the point of section. This seems proved not only by direct anatomical investigation, but also from the fact that the peripheral portion of the divided nerve may be sensitive upon pressure, and that the microscope shows normal fibres in it after a time has elapsed sufficiently long to allow all the divided fibres to degenerate, in accordance with the Wallerian law. Some of the sensation apparently retained in parts the sensitive nerve of which has been divided may be due to the excitation of the nerves in the adjacent uninjured parts, caused by the vibration or jar propagated to them by the mechanical means used to test sensation, as tapping, rubbing, stroking, etc.³ It is to be observed that this retained sensation after the division of nerves exists in different degrees in different regions of the body; thus it is greatest in the hands, least in the face.