FIG. 2.-Diagram to illustrate the distribution of the cutaneous nerves. Posterior view.

FIG. 3.-Diagram to illustrate distribution of the cutaneous nerves. Anterior view.

The dorsal nerves are distributed in belts around the body below the nipples and supply the entire abdomen. The 1st dorsal also supplies the inner side of the arms.

The cervical nerves are also distributed in belts, but the 5th, 6th, 7th and 8th also supply the arms from without inward except the portion supplied by the 1st dorsal.

Now, let us study the effects of injury to the various vertebrae: fracture of the coccyx is sometimes followed by coccygodynia when the coccyxigeal nerves are injured.

Fracture of the sacrum is rare and may be attended by absence of plantar reflex and anesthesia of the nates and genitals.

Fracture of the lower three lumbar vertebrae is rare; the injury is below the cord, but the nerves in the cauda equina may be injured, in which case there will be paralysis of the leg in proportion to the extent of the injury, together with anesthesia more or less complete. Patellar, gluteal and achilles reflexes may be absent. If the 1st or 2d lumbar be fractured, there will be in addition, loss of the cremaster reflex and disturbance of the vesical and anal centre. If the lesion is low, there is apt to be involuntary micturition, and if higher retention. But this rule is not absolute, and any lesion of the vesical and anal centre may be followed by incontinence of urine and feces.

In the dorsal region there is paralysis, both motor and sensory extending around the body somewhat lower than the injury. In the upper dorsal there is dyspnea, owing to paralysis of the muscles of respiration, and above the 7th there is likely to be frequent or continual priapism. If the lesion is from the 7th to the 12th there will be loss of the abdominal reflex; if from the 4th to the 7th of the epigastric, i. e, a stroke on the lower abdomen or epigastrium, respectively will be followed by no contraction of the abdominal muscles.

In the lower cervical reigon, there will be some paralysis of the arms, loss of reflexes of the arms and anesthesia extending from the elbow outward in proportion as the lesion is near the head. There is intense dyspnea, diaphragmatic breathing, dilatation of the pupil, and often hyperpyrexia sometimes as high as 112 degrees, and priapism is especially marked. The 4th or 5th vertebrae are fractured more often than any others, and produce quite different symptoms. The 5th cervical nerve makes its exit between the 4th and 5th vertebrae, so that a fracture to the 5th vertebra is below it and of the 4th is above it. It supplies the deltoid, brachialis anticus and the supinators, consequently when the fracture is below it, that is, in the 5th vertebra, all the other nerves of the brachial plexus being paralyzed, these muscles will contract and the patient assumes a peculiar position, the hands are supinated, the forearms flexed, and the elbows abducted. If the fracture is above the 5th vertebra, the paralysis will be complete.

Fractures above the 4th are practically always fatal at once or within

a few hours, and do not admit of much study.

One-sided lesions of the cord produce a complex of symptoms which is interesting and characteristic. On the side of the lesion, there is motor paralysis, loss of muscle sense, hyperesthesia, increased temperature

and at first a loss of reflex, but later an increased tendon reflex. At the physiological level of the lesion there is anesthesia, and just above this, hyperesthesia (Fig. 4).

The crossed paralysis and loss of muscle sense are easily explained. The motor fibres originate in the brain, pass down and decussate in the pons and medulla, then descend to their distribution. A lesion on that side produces motor paralysis on the same side which is followed later by loss of muscle sense. The sensory fibers originate in the peripheral and pass down to the cord and decussate immediatly and pass upward on the opposite side. A lesion to this side severs them, and no sensory impulse can reach the brain through them, consequently there is anesthesia where they originate, viz., on the opposite side.

FIG 4-Diagram to illustrate crossed paralysis due to a lesion to one-half of the cord.

Increased temperature is explained this way: Heat is produced everywhere in the body, and the tendency is to over-production rather than under-production. We find a fever a hundred times where we find a subnormal temperature once. In the brain there is a heat control centre the fibers from which pass down the cord to the periphery and control the production of heat. When there is a lesion to one side of the cord, this control is removed and the production of heat is unrestrained. This is as true. in complete lesions as in one-sided lesions and in fracture in the cervical region, as already mentioned, the temperature may be as high as 112 degrees.

Reflex disturbance on the side of the lesion is also easy to explain. The reflex is sometimes decreased, but this is of short duration, and is

probably due to shock. Naturally the impulse from a stroke on the patellar tendon is carried to the cord through the posterior root of a spinal nerve. This is connected with the multipolar cells in the anterior cornu and through them with the anterior or motor root, by which it is carried right back to the tendon as a motor impulse and causes a contraction of the muscle. The multipolar cells in the anterior cornu are also connected with fibers passing downward from the brain which have an inhibitory influence on the reflex, which inhibited reflex is known as normal. In a one-sided lesion these inhibitory fibers are cut off and inhibition is removed, and consequently the reflex is exaggerated (Fig. 5).

Hyperesthesia on the affected side has never received a satisfactory explanation. The same is true of the hyperesthesia at the upper border of the lesion.

Anesthesia at the physiological level of the lesion is caused by the fibers which should pass through the lesion being severed.

Inhibitory fibers

Lesion

FIG. 5.-Diagram to illustrate the exaggerated tendon reflex in a one-sided lesion of the cord.

In the prognosis and treatment we must remember that spinal injuries are fatal in proportion to their nearness to the head, and all operative procedures are more and more fatal as we approach the head. Operations are, laminectomy, reduction of displacement and removal of pressure. When called to such a patient we must determine the nature and location of the injury, but all interference with the injured spine to elicit crepitus or preternatural mobility must be avoided, and diagnosis made from other symptoms. If the cord is severed or severely crushed, all operative procedures will be useless, but if there is merely pressure from a clot or a spicula of bone or a dislocation operation is imperative, but often these points cannot be determined before operation. Then the patient may recover without operation, or die as a result of it. So it is a question of great complexity and requires good judgment and careful diagnosis for its solution. I take the ground that when there is doubt, it is better to oper

ate.

If he dies it will be better for him and for the community upon

which he will be dependent than for him to live and be permanently paralyzed. He may still be paralyzed after operation, but both he and the surgeon will always feel that everything possible had been done for his relief. But with all, there is but a small percentage of cases that demand operative interference.

Non-operative cases require absolute rest with sometimes extension and counter-extension. A smooth flat bed with the patient flat on his back is ordinarily sufficient extension. Great cleanliness and care of the bed are necessary, because of the tendency of such patients to develop bed No condition requires more diagnostic skill and judgment in treatment than traumatic lesions of the spine.

sores.

TENDON TRANSPLANTATION IN THE TREATMENT OF PARALYTIC DEFORMITIES.

Frank C. Davis, M. D., Des Moines, Ia.

NTIL within recent years, no chapter of surgery has been more unsatisfactory in its results than the treatment of paralytic deformities. From the beginning attempts have been made to supply by means of a great variety of apparatus the functions lost, as a result of paralysis or injuries of muscles, nerves and tendons. On the whole, these attempts. have been unsatisfactory and in many instances a decided disadvantage.

Albert made a great advance, when he proposed and practiced arthodisis, nevertheless his results were far from satisfactory.

The introduction of tendon transplantation in the treatment of paralytic deformities was unquestionably the greatest advance ever made in the management of this class of cases. The credit of this brilliant idea has usually been accorded to Ecolodom, but in reality belonged to Duplay, who in 1876, employed the procedure in the treatment of a case of traumatic loss of function of the arm.

Briefly I will sum up the literature on this subject: Hacher in 1886 reported a favorable result. Lipburger in 1889 sutured the tendon of the gastro-cnemius to the peripheral end of the traumatically severed tendons of the periven, and thus corrected a varus deformity.

In 1893 Brobint reported 7 cases, in which favorable results had followed the transplantation of tendons in the treatment of paralytic defor mities.

Winkelmann, in 1894, reported a favorable result in a case in which he sutured the tendon of the gastrocnemius to the peripheral end of the paralyzed longus, and then sutured the tendon of the paralyzed peroneus brevis to that of longus.

Phocas, in 1893, reported a favorable result in a case of talipes calcamus paralytcus in which he transplanted one of the peroneal tendons to the tendo achilles.