Part 31

Sequel to acute. Result of sprains and spinal injuries. Symptoms: paresis on exertion, lameness in one or more limbs, knuckling, circumductive movement of feet, uncertain planting, dropping, worse if blinded, phenomena progressive. Lesions: sclerosis of cord; absorption of nerve cells and fibres, in gray horns, and columns, superior, lateral and inferior, cord, altered in color, unduly firm, in points softening. Stains deeply in carmine, lightly in osmic acid or hæmatoxylin. Meninges thickened, nerve roots atrophied. Diagnosis: previous acute myelitis; later muscular weakness, and paresis, under exercise; from embolism. Treatment: hopeless if advanced: progress delayed only. Good hygiene, tonics, open air, gentle exercise, pure water, grooming, succulent pasture, nourishing food, alkalines, common salt, phosphates.

Cases of this kind have not been satisfactorily diagnosed, and as a rule domestic animals affected with partial paralysis are rarely allowed to live in a condition in which they are offensive to themselves and owners, a source of constant expense with little or no hope of recovery nor profit. Again, in the case of the large mammals, the prolonged recumbency and the low grade of nutrition in the semi-paralyzed parts, usually entail unhealthy sores and septic poisoning which sooner or later prove fatal. It is only, therefore, in the slighter cases, in which a fair measure of control over the limbs remains, that these cases are likely to survive. Trasbot suggests that many cases which pass for lumbar sprains are really chronic myelitis and on careful examination will show spinal sclerosis.

Causes. These are largely speculative, yet doubtless the same causes which determine the acute form, will produce the chronic when acting with less force and greater persistency. The lesions that are left after an acute attack are calculated to keep up a measure of vascular and trophic disorder which will be found associated with more or less sclerosis.

Symptoms. In Weber’s case in the horse (Recueil de Med. Vet., 1884, p. 432) the advance was slow, so that for nearly a year the manifestations were not diagnostic. At first there was weakness of the hind limbs when worked to fatigue. Perfect rest led to improvement, and work, to aggravation which became steadily worse and worse. For a length of time the horse maintained good condition, glossy skin, elevated head, alert expression, keen sight and hearing, and normal breathing and pulse. Standing in the stall there was no abnormal position of the limbs, nor evidence of lack of perfect control.

But when moved all this was changed. He showed first lameness in the right fore limb and soon in all four members. The feet were swung and planted uncertainly, the animal swayed and staggered, the limb would knuckle over at the knee or fetlock, or bend at the hock, and be recovered with difficulty. After going slowly for a few steps he moved with greater freedom though still with difficulty, and the trouble was greatly aggravated when the eyes were blindfolded. Then every step threatened to precipitate him to the ground. The symptoms were essentially those of locomotor ataxy.

The tactile sensibility was unimpaired, the loins had the normal sensibility, urination and defecation were natural and the appetite remained good. After ten months he showed loss of condition, dullness of the special senses, stupor, and a special sensitiveness about the head, and resented its handling.

Lesions. Thirteen months after the commencement of the attack this horse was destroyed and the cord was found to be profoundly altered by fibroid degeneration of the neuroglia and absorption of the nerve elements (cells and fibres), the lesions affecting different portions of the gray horns, and the columns—superior, lateral and inferior. The affected portion of the cord usually shows in man a grayish, opaque or translucent appearance, with in some cases a shrunken aspect and undue firmness of texture, with at points, centres of softening. If hardened, the sclerosed sections take the carmine stain deeply, but the osmic acid or hæmatoxylin stain very slightly, contrary to what holds in health. In recent cases there is only slight thickening of the neuroglia, but when the disease is advanced the trabeculæ are thick, dense, and firm, and the nerve fibres have largely disappeared. The coats of the blood vessels adjacent to the sclerosis are thickened and their lumen is narrowed. Thickening of the meninges is not uncommon, either confined to those covering the diseased portion of the cord or extending completely around it. Atrophy of the nerve roots is often appreciable by the naked eye.

Diagnosis. This depends largely on the fact that the condition follows an acute attack of myelitis, on the supervention of muscular weakness and lack of muscular control, whenever the animal is exercised to fatigue, the morbid symptoms subsiding promptly when he is allowed to rest, the aggravation of these symptoms when the patient is blindfolded and a gradual though slow advance of the symptoms with the lapse of time. From arteritis and embolism it is to be distinguished by the absence of the local symptoms of pain and tenderness, and by the absence of pulsation in the same artery distal of the obstruction and of improvement by the lapse of time or a run at grass.

Treatment: Unless in the very early stages even a partial recovery is not to be looked for. By a run at grass or by gentle well regulated exercise the impaired nerves and muscles may be educated to a better control for a limited period but the progress of the disease is not really arrested and the final issue is likely to be ruinous. Even in man, where 90 per cent. of the cases are connected with syphilis, the fibroid hyperplasia (sclerosis) is not remedied asgummata are, by mercury and iodides. In the soliped, where no such specific disease can be charged, the repair of the structural changes is no more hopeful. The many different methods of treatment in man,—electricity, blisters, firing, stretching of the spine, stretching, of the sciatic and crural nerves,—though inducing transient improvement in many cases, produce no real permanent benefit, and are to be remanded to the region of psychic inferences which have little or no place in the therapeutics of the lower animals. Strychnia, veratrin and other spinal stimulants are of little permanent value. A general hygienic and corroborative treatment may be used with the view of retarding the progress of the disease rather than of curing it. Open air exercise, sunshine, succulent pasturage, an ample supply of pure water, and active grooming are valuable. Nourishing food is all important. Lecithin or the hypodermic injection of spermin or other rich albuminous animal product is useful. A course of bicarbonate of soda and carbonate of iron with or without bitters may be tried. When the animal must be kept on dry winter food, he should have free access to common salt and water. This favors at once absorption, assimilation, and elimination, and by fostering nutrition and the removal of waste matters, it contributes to keep the disease in abeyance. Phosphoric acid and the various phosphates have been largely used and largely rejected, their main value being in the tonic effect on the spinal centres. Trasbot especially recommends the neutral gelatinoid phosphate of lime as having proved especially valuable in his hands. He gave from 1 grain upward to dogs twice a day.

ARTERITIS (THROMBOSIS, EMBOLISM) OF THE SPINAL CORD AND MEMBRANES.

Conditions of spinal circulation favorable to embolism and microbian invasion. Slow currents. Blood stasis. Free anastomosis a compensation. Symptoms. Treatment.

Facts are wanting with regard to these lesions in the domestic animals, but anatomical, physiological and pathological consideration are strongly suggestive of their occurrence. The vascular network of the spinal cord favors a tardy circulation, and this in turn is favorable to the arrest of solid bodies and the delay, proliferation and colonization of microbes. The median spinal artery receives a supply of blood by two trunks, right and left, entering by the intervertebral foramina at each intervertebral articulation. It has not, therefore, one continuous, equable, onward flow, but rather numerous independent currents corresponding to the entering vessels, and with intervening eddies or areas of comparative stagnation. The nervous material of the cord admits no large arteries but only capillary trunks which anastomose freely in its substance. This would seem to entail a sluggish flow, which would favor microbian arrest and colonization, even if the small size of the vessels serves to shut out clots of any material size. Finally the abundant venous plexus, and especially the two lateral venous sinuses, communicating freely with each other and, through each intervertebral foramen, with the extra spinal veins determine a similar tardy flow that should be favorable to morbid processes. If we pass back of these vessels, we find the posterior aorta to be at once the largest and the most direct channel for the entrance of emboli coming from the left heart or lungs. This danger is counteracted in greater part by the fact that the greater part of this blood passes into the large vessels which supply the liver, spleen, kidneys, stomach, bowels, and hind limbs, and while embolism is well known in these parts it has not been demonstrated as yet in the spinal cord. The toxins produced in infectious diseases and circulated in the blood can often lead to destruction of the endothelium, and inflammation of the deeper structures. In this way any circulating microbes find a ready infection atrium. Hektoen seems to have demonstrated this in the case of tubercular meningitis. By pressure of the neoplasm on the vessel or by fibroid thickening and contraction of the walls of the vessel, the subsidiary cord is denied its full supply, and degeneration of the nervous substance is invited. In the human subject degeneration of the cord has been shown to follow the line of such diseased arteries. Thrombosis follows in every case in which the serous coat is involved, and embolism can easily occur from clots small enough to enter the capillary vessels. Lamy’s experiment of blocking the small arteries with inert powder, shows that this will give rise to foci of hemorrhagic softening, which commence in the gray substance. The blocking, however, must be multiple to produce any material effect, as the free anastomosis of the spinal capillaries otherwise secures an abundant blood supply to adjacent parts. In case of an infective embolism the disease will advance even if the obstruction is single.

The general symptoms of these conditions would depend on the exact seat of the lesion, and treatment would have to proceed on general principles, the object being to check the inflammatory conditions, and trust to the vis medecatrix naturæ in connection with rest and good hygienic conditions.

HEMORRHAGES INTO THE SPINAL MEMBRANES. MENINGEAL SPINAL APOPLEXY. HÆMATORRACHIS. HEMORRHAGE INTO THE SPINAL CORD. SPINAL APOPLEXY. HÆMATOMYELIA.

Definition. Causes: violent exertion, blows, falls, morbid blood, fractures, caries, tumors, tubercle, aneurisms. Lesions: Clot between or outside membranes in meningeal hæmorrhage, in gray matter and even in white in myelon bleeding. Cord bulges. If survives, nervous matter absorbed. Symptoms: Sudden stiffness or palsy of given areas; spasms more common in meningeal extravasation. Rapid muscular wasting. No fever at first. Treatment: cold to part; slings; atropia, ergot, lead acetate. Later as for myelitis. Large clot may warrant surgical interference.

In the first of these forms the bleeding takes place between the arachnoid and the two contiguous membranes—pia and dura, or outside the dura. In the second it takes place into the substance of the cord though it may encroach on the pia mater. Both conditions have been attributed to violent muscular efforts or contractions as in draught, racing, fighting, leaping, tetanic convulsions, also to blows on the back, or falls from a height. Morbid states of the blood in which there is a hemorrhagic tendency (scurvy, purpura, hæmophilia, anthrax) may be contributory causes. Spinal fractures, aneurisms, caries, tumors, and tubercle may be additional causes.

Lesions. In meningeal bleeding the clot is found outside the dura, or between the dura and arachnoid which may or may not be ruptured. A clot on the pia mater may press seriously on the cord or may cause rupture of the arachnoid. In hemorrhage of the cord, the effusion usually begins in the gray matter, though it may extend far into the white. It may be circumscribed to half an inch in diameter or affect almost the entire length of the cord. The cord may be distinctly enlarged at the point of effusion, and in exceptional cases the blood may have broken through to the membranes. If the patient survives, absorption and degenerations of the cord are inevitable.

Symptoms. In both forms there is a sudden attack, with stiffness or paralysis of given muscles and without hyperthermia. Rigidity and spasms of the muscles are more characteristic of meningeal hemorrhage, and early paralysis of the spinal. An early hyperæsthesia is also most significant of an effusion in the cord. Rapid muscular atrophy is also characteristic of this. The two conditions resemble meningitis and myelitis but come on much more suddenly and are unattended by fever.

Treatment. Such cases are not hopeful. Cold to the affected part of the spine, keeping the patient in slings to solicit the good effect of gravitation, and giving ergot or lead acetate internally are among the first indications. Later, the treatment would be practically the same as for meningitis or myelitis. In case of complete paralysis from the sudden formation of a large clot, it has even been advised to cut down on the seat of the injury and evacuate the blood, using antiseptic precautions.

SPINA BIFIDA.

This is an elastic swelling consisting of the spinal meninges enclosing a liquid, and in some cases the spinal cord as well, and protruding between the unclosed laminæ of the vertebral rings, usually in the region of the sacrum or loins. It is essentially an arrest of development on the part of the vertebræ and enveloping muscles and skin, and an extension of the cord and effusion of the meningeal and central spinal liquids, in the absence of their bony and muscular support. Hydrocephalus is no uncommon complication.

The diagnosis may be based on the presence of an elastic, somewhat transparent tumor, projecting from the vertebral spines, at birth. If it contains a segment of the cord it is usually flattened, depressed on the summit and often associated with paralysis.

As occurring in the lower animals this need not be treated. In man, careful antisepsis and evacuation followed by injection of a solution of iodine 10 grs., iodide of potassium 30 grs., and glycerine 1 oz., have, in favorable cases, secured obliteration of the sac, but even then the recovery has rarely been complete and permanent. Paralysis and death have usually supervened.

SPINAL CARIES. TUBERCULAR OR OTHER INFECTIVE DISEASE OF THE VERTEBRÆ.

Spinal caries in old horses, sprains, fractures, infections; caries often confined to articulating processes: anatomical form: Axoido-atloid caries from poll evil, concussions, fights, rachitis. Tubercle of bone and intervertebral cartilage in cattle. Symptoms: distortion, stiffness, rigidity; stands day and night, sensory and motor paralysis: localization of lesion; dyspnœa; spastic palsy back of lesion; effect on tail, sphincters. Diagnosis: progressive tenderness and stiffness of spine, distortion, localized exaltation or depression of nervous function, osteoporosis, rachitis, caries, tubercle, melanoma, abscess, infectious disease. Treatment: Sling in narrow stall, good food, pure air, sunshine, tonics, phosphates.

As seen in the human subject spinal caries is usually tubercular and is known as “Pott’s disease.” As seen in old horses it appears to be rather a result of other infections, especially purulent, and may have started in connection with traumatic or mechanical injuries to the bones and ligaments. In such cases I have seen it repeatedly in hollow backed horses in which the line of the spine descended abruptly and extremely from the withers and rose again to the sacrum. The distortion was so great that the back appeared as if it could barely sustain the weight of the animal and yet the patients were kept at work and proved useful for light driving. Post mortem examination showed extensive caries and suppuration of the vertebral bodies, confined, however, to one or two segments as if due to a mechanical lesion. In the region of the loins it is much more likely to affect the articulations of the vertebral rings, because of the manner in which these are wedged into each other when the spine is pressed downward. In the neck where the normal movement is so much freer such injuries are much less common. Caries affecting the articular surfaces of the axoido—atloid joint is by no means uncommon. It may follow poll evil, or injuries sustained when a horse runs against a wall, or in the fights of bulls or rams. Disease of the vertebræ may be of the nature of rachitis occurring in this case in early life.

In cattle the disease is liable to be tubercular in which case, not only is the bone invaded but the morbid process extends to the intervertebral cartilage and projecting, presses on the spinal meninges and cord. It may even encircle the entire spinal cavity and strangle the cord. If the pus should extend downward it may form abscess under the spine, and rupture into an internal cavity or externally.

Symptoms. Injuries and disease of the vertebræ may last for a length of time without implicating the spinal cord or nerves. They may then cause only distortion, with stiffness or rigidity of the spinal column. When, however, the displacement of the injured, carious or tubercular bones, the distension of the abscess or the increase of the hyperplasia leads to pressure on the nerve roots, the meninges or cord, nervous symptoms are likely to be developed. Compression of the nerve roots—sensory or motor—may cause sensory or motor paralysis or both, limited to particular areas the outline of which will point to the precise seat of the lesion. If in the recti of the head and other muscles of the neck, it points to the anterior cervical vertebræ. If in the fore limbs, it points to the posterior bones of the neck. The implication of the diaphragm would incriminate the fourth and fifth cervical vertebræ. If in the crural muscles or those of the quarter and thigh, the lumbar vertebræ must be looked to. The implication of the nerves of the back, while impairing the functions of the intercostal and abdominal muscles, produce less marked symptoms than when the limbs are involved.