DISEASES OF THE SPINAL CORD
Acute Myelitis
Acute myelitis is an acute inflammation, with softening of the substance of the cord, giving rise to marked disturbances of motion, sensation and nutrition. When the whole thickness of a section of the cord is involved, the condition is termed transverse myelitis. When an extensive area is involved, it is termed diffuse myelitis. When the gray matter around the central canal is especially affected, it is termed central myelitis.
Etiology.—There can be no doubt that osteopathic lesions are very potent predisposing factors. Osteopathic lesions of the spine, even of a muscular nature, readily disturb the cord circulation. It may follow repeated exposure to wet, cold or exertion; or be a sequel to the infectious diseases, as smallpox, typhoid fever, typhus, puerperal fever or measles. It may be due to traumatism or disease of the vertebræ, as caries or cancer. Syphilis is a frequent cause.
Pathology.—To the untrained, naked eye, the cord may present little or no change. The nervous tissues are in various stages of degeneration. On section the substance of the cord is red and soft, the line of demarcation between the gray and white matter is lost or extremely indistinct, and minute hemorrhages are sometimes seen. In very acute cases, affecting the white and gray matter, after injury, when the membranes are cut, the substance of the cord may flow out as a reddish creamy fluid.
The nerve fibers are much swollen and the axis cylinders broken up. Blood discs, leucocytes, and numerous granular fatty cells may also be present. The blood-vessels are distended and dilated. There may be thickening and hyaline degeneration of the vessel walls and hemorrhagic extravasation.
Symptoms.—Acute Transverse Myelitis.—This is the type most frequently met with. The symptoms differ with the situation of the lesion, which is generally in the dorsal cord. At the onset there may be pain; numbness and tingling in the back, radiating into the limbs. There is usually moderate fever, malaise, chills, muscular pains, a coated tongue and constipation. Symptoms of motor paralysis soon develop, which may become more or less complete. Both motor and sensory symptoms vary to a marked degree, depending upon the pathologic involvement. The reflexes are lost at first. They may soon return and are exaggerated below the lesion. Following this the muscles often become rigid and contracted. Unless the lesion is in the lumbar or cervical cord, reaction of degeneration or much wasting of the muscles, as a rule, does not occur. A girdle sensation frequently occurs at the level of the disease. At first there is retention of the urine and feces, later incontinence. Bed-sores soon develop; also drying and hardening of the skin. The nails become thick and brittle. Death may occur from exhaustion, or heart or respiratory failure, but it is rare; segments of the cord may be completely and permanently destroyed, causing persistent paraplegia. H. A. Greene[126] reports a case, due to injury, which was greatly benefited by treatment.
Acute Diffuse Myelitis.—In the acute forms the course of the disease is rapid. The trophic disturbances are more marked than in the former type. This form is likely to follow exposure to cold, injuries, tumors, syphilis or one of the infectious diseases. There may be chills, fever, malaise, pain in the back and limbs, and occasionally convulsions. The reflexes are generally lost. The motor functions are rapidly lost. There is incontinence of urine and feces, rapid wasting of the muscles and bed-sores develop. The disease may prove fatal in from six to ten days.
Diagnosis.—Landry’s Disease.—In this the bladder and rectum are not affected. Trophic disturbances are absent. There is but slight loss of sensation, no reactions of degeneration and no girdle pains. Multiple Neuritis.—Both arms and legs involved, and slow onset. The bladder and rectum are rarely involved; the girdle pain is absent. Acute Poliomyelitis.—There are no sensory symptoms and the rectum and bladder are not affected.
Prognosis.—In very acute cases death occurs in from three to ten days. Milder cases generally recover with some loss of motor power, although in a few cases treated by osteopathy recovery was complete, due probably to the case being seen early and thus degeneration prevented.
Treatment.—Lesions of the vertebræ are usually readily found in cases of myelitis. Generally, deranged vertebræ are found in the upper dorsal region, and occasionally lesions are located in the lumbar and cervical vertebræ. The treatment of myelitis is chiefly to correct these lesions, so that the normal circulation of the cord may be reestablished. One has to be very careful when treating the lesions not to cause additional injury to the cord. An inhibitory treatment to the muscles about the lesion may be all the treatment that can be given at first; nevertheless, it aids nature just so much in overcoming the excessive irritation of the cord tissues. Nature has the curative means, provided they may operate unobstructedly. In a few cases the ribs in the region of the spinal lesion will be found deranged and interfering with trophic fibers, blood-vessels and lymph vessels of the cord. The patient should be kept in the prone posture at first.
Warm baths and massage will be found of additional value. The bowels and bladder should receive special attention. An ice-bag to the spine may be beneficial. If there is any danger of bed-sores, use alcohol to stimulate and harden the skin. Rest, liquid diet and good nursing are necessary. Later on careful exercising of the limbs will be beneficial.
Chronic Myelitis.—This defines the conditions when the inflammation is subacute with the paraplegia and other symptoms which then naturally appear, present, and also with the signs of both degeneration and repair. The symptoms develop slowly as compared with the acute form. It should not be confused with atrophy, pachymeningitis or tumors of the cord. Treatment is practically the same as in acute form. Surgical measures may be indicated. Loudon[127] reports a case due to injury which was greatly benefited.
Poliomyelitis
(Infantile Paralysis)
Definition.—An acute infectious disease occurring most commonly in young children, characterized by paralysis, rapid wasting of certain muscles, and fever. It is an acute myelitis that affects the anterior horns of the cord. There are no sensory symptoms.
Etiology.—It usually occurs in children under ten years of age, and the majority of cases occur before the fourth year. It is more common in summer than in winter. The infection seems to gain entrance through the nasal mucous membrane. Traumatism, exposure to cold and overexertion, are probably predisposing causes. It has occurred in severe epidemic form.
Morbid Anatomy.—The disease is most frequently seen in either the lumbar or cervical enlargement and is usually unilateral, though there is considerable variation in the extent of the lesions. In very early cases, the condition of acute hemorrhagic myelitis, with degeneration and rapid destruction of the large ganglion cells, has been found. In older lesions the anterior cornu in the affected region is atrophied and there is destruction of the multipolar ganglion cells. The anterior nerve roots are atrophied, the muscles are wasted and undergo a fatty and sclerotic change.
Symptoms.—The child may have a slight fever, malaise, muscular twitching, headache, some rigidity of the neck, and sometimes vomiting. This may last a day or several days or only a few hours, when paralysis sets in abruptly. The paralysis is rarely complete and groups of muscles only may be affected. As a rule, the paralysis comes on abruptly, but it may come on slowly, taking several days to develop. In a few weeks, atrophy sets in and the limb becomes flaccid, soft and wasted. The paralysis remains stationary for a time when improvement takes place, but complete recovery is rare. Sometimes the growth of the bone of the affected limb is impaired. Usually there are no sensory disturbances and the bladder and rectum are not affected. The condition of the reflexes is dependent upon the extent of involvement of the cornual cells. Occasionally the bulbar muscles are affected.
Diagnosis.—This is not difficult except in the early stages. Careful study of the case is commonly all that is necessary. Landry’s paralysis and peripheral neuritis are to be differentiated.
Prognosis.—Complete recovery is rare. Improvement is the rule. Ivie[128] tabulates sixteen cases, all showing good results. W. B. Davis[129] reports a case cured by six months treatment and still well after three years. T. M. King[129] one case cured and one greatly benefited and A. S. Craig[129] one much helped. Florence Gair, F. P. Millard, A. G. Walmsley and others report gratifying results in many cases.
Treatment.—In the treatment of chronic cases, F. P. Millard[130] says “Five minutes’ time is sufficiently long in treating a patient, and sometimes too long. * * * Start in and move every spinal joint. That takes about two minutes. Spring the sacro-iliac articulations just enough to get motion. Then give a specific cervical treatment. Do not stop to relax muscles in a child. Adjust as rapidly as possible. Make every spinal joint yield to motion. Spend only one minute, or possibly two, on the cervical vertebræ. So far we have consumed four minutes. The last minute we loosen up the wrist or ankle, according to the extremities that are involved.” This outline has been followed with gratifying success by Gair, Green, Bush and others in many chronic cases. The procedure in acute cases is condensed from A. G. Walmsley[130]: “Isolate, keep cool and absolutely quiet. Stop all food until the temperature drops to 100° F. or lower and until the pain subsides when fruit juices may be given followed by heavier foods. Give patient all the water he will drink. Where the spine is sensitive, and it will be in many, use hot fomentations until a specific treatment can be given. If the fever is running high cool compresses will be grateful and help reduce temperature. Irrigate the colon twice daily with saline water. Do this first thing when called. Later once daily will do and then discontinue. Look carefully to the nose and throat and wash with saline or boracic solution. Keep feet warm as they may be cold even with high fever. Treat the case over a long period. See that he does not overdo and observe all dietetic and hygienic measures.” Both these men lay great stress on the importance of specific adjustments and massage of muscle tissue has little place in their treatment. This, with drill at home can be attended to by the mother.
Ivie[131], among other good ideas on treatment, gives the following: “May I suggest that when such severe results (the acute stage) follow a slight infection, that we may expect to find a lesion located at such a point as will interfere with one or more of the anterior root arteries which join and supply the anterior spinal plexuses. As there are only five or ten of the anterior root arteries (Dana), the lesions affecting them can be located throughout a wide range of the spine. In a great many cases we find that the correction of lesions well up in the dorsal and even in the cervical region have increased the amount of the improvement well beyond that received in the correction of the lumbar lesions alone. To promote resolution, correct the lesions, both muscular and bony, and relax the muscles of the spine daily; move every vertebra to the limit of all its possible motions; use flexion, extension, rotation, and lateral flexion at least once every day for at least a week; and help to overcome stasis by keeping the child off its back, turning it from side to side, and letting it lie on its stomach as much as possible. The limb, to be kept in its best condition, should be kept warm; treated gently; held in a natural position by the use of sand bags and clothes cradle, thus beginning early the prevention of deformity; the paralyzed muscles should not be kept on a stretch, as that will retard any possible improvement; stimulating rubs and baths should be given frequently.” In the chronic stage he advocates: “Now that the nerve cells have been given a chance to regenerate (removal of lesions), the best thing to do is to force them to work if possible. To do this, the so-called resistance exercises or educational movements are to be strongly recommended; the idea being to place the limb in a given position and then ask the child to fix all its attention on the limb and to earnestly attempt to hold it there while you move it, or to keep making the attempt while you move the limb through its whole range of motion in that direction. These movements should be so calculated that the resistance of the child will exercise the group of muscles affected. The mother or nurse can give these exercises every night on going to bed.”
Acute Ascending Paralysis
(Landry’s Paralysis)
Definition.—An acute disease, characterized by an advancing paralysis, beginning in the legs, passing upward to the trunk and the arms and finally it may involve the centers in the medulla. Toxic and infectious influences that congest the nerve courses and ultimately destroy the cells seem to be the important factor. The anterior gray matter of the cord is involved, and it is probable that many cases are a form of acute poliomyelitis. The spleen is congested and in some instances the lymphatics.
Etiology.—A definite cause has not been found, although osteopathic lesions are important predisposing factors. A toxic cause seems probable. The disease is most common in males between twenty and forty years of age. It may follow traumatism, exposure, cold or the infectious fevers.
Symptoms.—Weakness of the lower extremities is generally the first symptom, though the arms may be involved first. This is shortly followed by paralysis. The paralysis then extends to the trunk and within a few days the arms are also affected. The muscles of the neck are next involved and finally those of respiration, deglutition and articulation. The reflexes are abolished. The muscles are relaxed, but generally do not waste or show electrical modification. Sensation is usually not affected, but there may be tingling, numbness, hyperesthesia and muscular tenderness. The sphincters are not involved as a rule. The spleen is usually enlarged. The course is variable. Death often occurs in from two days to a few weeks. When the improvement takes place, the part last affected recovers first.
Diagnosis.—This is not always easy. It is sometimes impossible to differentiate between this disease and multiple neuritis. The history, the motor paralysis, the absence of wasting and of electrical modification, as well as the absence of involvement of the sphincters, will definitely aid in the diagnosis.
Prognosis.—The prognosis is unfavorable. A large majority of cases prove fatal. In a few cases treated osteopathically, results were favorable if the patient was seen early. The muscles of the spinal column were markedly contracted.
Treatment.—The treatment of Landry’s disease consists principally of thorough treatment of the spine, especially of the lower dorsal and lumbar regions, and attention to the underlying toxic condition. The treatment should be most thorough; the vertebræ and ribs found disordered should be corrected and each vertebra should be carefully separated (if conditions permit) from its neighbor. When the paralysis has extended to the trunk and neck, a thorough treatment all along the spinal column should be given with a view to relaxing the contracted muscles and to render flexible the entire spinal column, so that the cord may be properly nourished and the progress of the disease checked. Careful relaxation of the contracted spinal muscles unquestionably has a potent effect upon the cord circulation, which tends to check and retard degenerative processes. Treatment of the limbs directly will be found a help, as well as direct treatment of all tissues paralyzed. If swallowing is impossible, the patient should be fed through the rectum, or by the stomach or nasal tube. See that the patient is carefully nursed. Massage is beneficial.
Locomotor Ataxia
(Tabes Dorsalis)
Locomotor Ataxia is frequently met with. It is a disease of the spinal cord wherein the ultimate effect is a sclerosis of a progressive character of the nerve courses of the posterior column. It is claimed that the origin is in the protoplasmic processes of the posterior spinal ganglion. The characteristic symptoms are incoordination, Argyll Robertson pupil, lightning pains and loss of knee-jerk.
Osteopathic Etiology and Pathology.—Most cases develop between the ages of thirty and forty, although it is occasionally seen in young men, and rarely in children from hereditary syphilis. Males are much more frequently affected than females (10 to 1, Osler), and the disease is much more frequent in cities. Predisposing causes are given as syphilis, prolonged exposure to wet and cold, and sexual excesses, although there is a disposition on the part of neurologists to confine the cause of true tabes to syphilis, some records showing as high as 90 per cent. of the cases from that cause. Tabetic symptoms develop in from five to fifteen years after syphilitic infection. There are no data to show the probable proportion of syphilitic cases which later develop tabes, but it is undoubtedly small. As all cases of tabes examined by osteopaths show spinal lesions, it is reasonable to suppose that by interfering with the nutrition to the spinal cord, they allow consequent degeneration. It is also quite probable that osteopathic treatment for syphilis would, for the same reason, prevent sclerosis and resultant tabes. That syphilis is not the only cause, is also held by some authorities. Starr cites a true case from a severe blow in the dorsal region. Osteopathic observation would lead to a differentiation of tabes, according to the cause. Cases have been recorded, which simulated true tabes in most symptoms, which did not have a history of syphilis. J. Knowles makes the point that probably certain cases simulating tabes have reached what might be called an irritation stage (pathologically) of the nerves and their centers, sclerotic changes not having taken place; and he believes these cases would naturally yield to osteopathic treatment. Teall confirms this view by being of the opinion that these cases are the ones largely due to traumatism, exhaustion or exposure, and the probabilities are that in time sclerotic changes would take place, resulting in true tabes. In such cases there can be no question as to the osteopathic lesion, which would be sufficient to materially interfere with the peripheral sensory nerves and disturb the protoplasmic processes to the spinal ganglia and sensory tract. As a rule they are in the lower dorsal and lumbar regions. Cases are reported which had marked sacral and coccygeal lesions.
Pathologically, Dana speaks of locomotor ataxia, “as a post-infective degeneration, which first attacks the posterior spinal ganglia or corresponding cells of the special senses, due to a prolonged poisoning of these parts by the toxins of the infection.” The first change is in the posterior roots. Without doubt osteopathic lesions can readily affect the nutrition of these roots. This is shown upon examination in cases where the vertebral lesions impinge the tissues surrounding the spinal nerve at its exit, (or otherwise damage nervous stimuli and circulation) and also where the displaced head of the rib crowds upwards against the spinal nerve and again where the rib impinges the corresponding sympathetic ganglion which lies anterior to the head of the rib. Very likely in many cases the syphilitic infection is an exciting factor, but it seems plausible that osteopathic lesions, traumatism, cold, exposure and excesses predispose by disturbing the circulation to involved areas. The changes are at first inflammatory, followed by degenerative changes in the nerve courses which cause connective and neuroglia overgrowths to take the place of fibers in the sensory tract, and finally in the motor tract. Thus from the posterior ganglia, a section between the columns of Goll and Burdach is involved, and the progress of the sclerotic change is upward in the cord. The pia mater and coats of the vessels are thickened. The principal changes in the cord are in the lower dorsal and upper lumbar segments and the cord may be changed in shape. In long standing cases there is degeneration of the ascending antero-lateral tract, of the direct cerebellar tract, and of the pyramidal tract. The cerebral changes in some cases consist of sclerosis in the restiform bodies in the inferior peduncles of the cerebellum, and of certain cranial nerves, especially the third, optic, vagus and auditory nerves, and also cortical changes may occur.
Symptoms.—Authorities divide the symptoms into three stages—the preataxic, ataxic and paralytic. This division is largely an arbitrary one. Motor symptoms are usually the most prominent. There is inability to coordinate the muscles. The patient first notices that he cannot walk steadily when in the dark or when he has his eyes closed. Later he finds that he cannot maintain his equilibrium even in daylight; this is ascertained when the patient places his feet together and the eyes are closed (sign of Romberg). As a rule this is unaccompanied by muscular wasting, so there is no loss of motor power. Soon the gait becomes characteristic; in walking the feet are lifted high and are brought down heavily on the heel; the ball of the foot comes down last, producing what is called the “double step;” the walk is straddling: the limbs are thrown about, and there is staggering, due to incoordination. Incoordination also develops in the hands, but usually later in the disease. Sudden involuntary movements and palsies are other motor symptoms. The latter occur in about twenty per cent of cases and as a rule are of short duration. Paralysis and muscular atrophy do not develop until after a few years.
Pain is an early symptom and always present; it is of a darting, shooting or stabbing character and appears in paroxysms. It is most common in the legs, lasting but a second or two, and often accompanied by a hot, burning feeling. Herpes may appear along the course of the nerve. Anesthesia and hyperesthesia of certain areas may occur. A girdle sensation may be a noticeable symptom. The muscular sense is more or less impaired; there is a feeling as if there were cotton between the patient’s feet and the floor. Retardation of tactile sensation is a common symptom. The power of localizing pain is often lost. The knee-jerk is lost early in the disease. Occasionally, however, cases are met where it is retained. The skin reflexes are also impaired; in some cases they may be increased at first, but later are sure to be involved with the deep reflexes. The pupil does not respond to the light, but still accommodates for distance, constituting the Argyll Robertson pupil. Ptosis may develop with or without strabismus. Optic atrophy, which may lead to blindness, paresis of the ocular muscle, and contracted pupils, may occur. The ocular symptoms may appear early in the disease.
The visceral pains or crises are chiefly gastric and are sometimes accompanied by obstinate vomiting. Laryngeal, rectal, urethral and nephritic crises may occur, and at times are exceedingly severe. Laryngeal crises may be manifested by intense dyspnea and noisy breathing. Constipation is common. There may be retention of the urine resulting in cystitis. Sexual power is generally lost early.
Trophic changes occur later in the disease. The so-called arthropathies, or joint lesions, may occur at any period of the disease. It consists of an enlargement of the joints, associated with serous exudations, which rarely become purulent; atrophy of the heads of the bones; destruction of the bones and cartilages; or spontaneous fracture or dislocation may occur, owing to the brittleness of the bones. There is no pain and the large joints are most frequently affected; these may be excited by an injury. Herpes, skin ecchymoses, edema, local sweating, alterations in the nails, perforating ulcer of the foot, onychia, decay of the teeth and atrophy of the muscles may occur. The auditory nerve is rarely affected, but in some cases there may be deafness. There may be attacks of vertigo. Olfactory symptoms are rarely met with. Cerebral symptoms are rare. Paralysis may develop and the patient becomes bed-ridden. The disease itself does not prove fatal; the patient may live for years until some intercurrent disease causes death.
Diagnosis.—This is usually easy when the characteristic symptoms are developed. The presence of lightning pains, absence of the knee-jerk, early ocular palsies, a squint, ptosis and Argyll Robertson pupil make the diagnosis conclusive. Care has to be taken in making diagnosis from peripheral neuritis, paresis, ataxic paraplegia, cerebral disease and some diseases in which the posterior columns are disturbed.
Prognosis will depend largely on the exciting cause, as it is least hopeful from syphilis, but the earlier the case is treated the better the chance. The progress of the disease can sometimes be arrested and occasionally cases presenting symptoms of the first and second stage are entirely relieved with persistent treatment.
Treatment.—Experience in the treatment of locomotor ataxia has been that often the disease can be checked and the symptoms relieved; but curing a case of locomotor ataxia, except in the early stages, is seldom possible. When there is degeneration of nerve centers, there is no hope for a cure. Those with a syphilitic history are by far the hardest to relieve. Antisyphilitic treatment should be considered. Cases with a syphilitic history presenting preataxic symptoms, Argyll Robertson pupil, lightning pains and loss of patellar reflex have been cured; unfortunately these cases are not always diagnosed.
The treatment consists of thorough correction of the spinal derangements found, especially through the lumbar and lower dorsal regions. If the disease has involved the arms or brain, thorough treatment should be given the entire length of the spine with a view to increasing the circulation in the spinal cord and brain, and thus checking or preventing the tissue degeneration. “In the early stage, deep massage to the muscles of the back promotes the flow of venous blood through the spinal vessels and their anastomotic branches, and is the best means of relieving the congestion which is supposed to exist.” (Starr) The lower spine will be found to be rigid and should be well sprung to get mobility.
Careful treatment of the limbs should be given, but be exceedingly cautious in the treatment of the limbs of advanced cases, as there is considerable danger of producing fractures. Stretching the thigh muscles and internal and external rotation treatment of the legs should be given. See that the bowels are moved daily and be positive that there is no retention of the urine in the bladder. A catheter has to be used in some cases. The patient should be careful about taking too much food, and especially beware of indigestible food, as it irritates or excites gastric crises.
During painful attacks the patient should rest in bed, and with careful treatment the attack can generally be relieved. Hot applications are of considerable aid.
At all times excesses should be avoided. Occupation of some character should be given the sufferer. Do not promise to cure the patient, and make it plain at the start that it will probably require a long time to show much improvement. Systematic exercises to reestablish coordination should not be neglected.
Hereditary Ataxia
(Friedreich’s Ataxia)
This is a rare hereditary disease, due to sclerosis of the columns of Goll and Burdach and the pyramidal tracts. There are ataxia, muscular weakness, nystagmus, speech disorders and loss of knee flex. Almost invariably there will be found a neuropathic history. Alcoholism, syphilis and insanity in the parents are predisposing causes. Tuberculosis may be a factor. Acute diseases, especially infectious fevers, dentition and injuries to the spine may be exciting causes. It occurs most frequently in males about the seventh or eighth year and very seldom after puberty. Several members of the same family are apt to be affected. The disorder is transmitted by the female. “The degeneration of the posterior and pyramidal columns seems to occur at the time of cord development, when malnutrition or hereditary dyscrasia would disturb it most.”
Pathologically, “the spinal cord is smaller throughout than normal; we have also a combined disease of the posterior and lateral tracts (Schultze), a degeneration of Goll’s tract in toto, of Burdach’s almost entirely, and of the direct cerebellar, the crossed pyramidal (?), and of Clarke’s columns, in which we find not only atrophy of fibers, but also a degeneration of the ganglion cells. Gower’s tract may likewise be involved.” (Oppenheim).
Symptoms.—Impaired coordination, beginning in the legs and later extending to the arms, is the first marked symptom. The gait is peculiar; it is swaying and irregular and it lacks the pronounced stamping gait of locomotor ataxia. There is a loss of reflexes, while no sensory symptoms are present as a rule. The sphincters are normal. Nystagmus is present and is a characteristic symptom. The speech is scanning. Talipes and lateral curvature of the spine are common. The mind becomes sluggish in later stages. The course is always very slow.
Diagnosis.—This is not difficult as a rule, owing to the usual family history presented. The spinal curvature, nystagmus, incoordination, scanning speech, irregular gait, and deformity of the feet are symptomatic. In locomotor ataxia the gait, sharp pains, anesthesia and Argyll Robertson pupil will differentiate between the two. Differentiation will also have to be made from chorea, ataxic paraplegia and multiple sclerosis.
Treatment.—The same treatment as in locomotor ataxia is followed. Lesions presented have been found at the tenth and eleventh dorsals, and at the second and third cervicals, although, as a rule, the entire spinal column is quite debilitated. Some improvement will be noted in these cases, but not much can be expected from treatment; contractures may be prevented.
Spastic Paraplegia
Spastic paraplegia begins as a stiffness in the legs, with no sensory symptoms, but finally the muscles become rigid and slowly paralyzed. The reflexes are exaggerated.
It may occur, in a few instances, as a primary disease, “being a degeneration of the motor neurone, whose body lies in the brain cortex and whose axone lies in the lateral pyramidal tract.” Usually it is secondary to tumors, inflammation and softening of the brain. Multiple sclerosis, hemorrhage, transverse myelitis, syringomyelia and other diseases of the cord, injury, exposure and overexertion are exciting causes. Syphilis may be a cause. It generally develops between the ages of twenty and forty.
Pathologically, the degeneration involves the lateral pyramidal columns of the cord. It begins at the periphery and extends upward until finally the axones atrophy and neuroglia overgrowth takes place and sclerosis of the motor tracts results.
Symptoms.—Muscular stiffness in one leg is usually the first symptom, which gradually disturbs both sides. The muscular stiffness increases to a rigidity, and even cramps, so that it is with considerable difficulty that the patient moves about. The reflexes are exaggerated. The joints, as well as the muscles are stiff, so that the toes are dragged upon the ground and the legs are kept close together, abduction of the limbs being difficult. On the whole, there is much tiredness, stiffness, rigidity and hardness of the leg muscles, so that all motions with them are performed with great effort. Sensory and trophic symptoms are lacking; control of the bladder and rectum is usually normal. The progress of the disease is slow. The upper extremities may be involved in after years, but the common extensive disturbance is with the legs, so that they may be entirely useless and the muscles atrophy from disuse, although rigidity and contractures remain.
Treatment.—The prognosis is usually unfavorable, though frequently the patient may be considerably benefited. A few cases that have been caused by traumatism, cold or exposure have yielded to osteopathic treatment and all symptoms disappeared. The treatment is largely that of locomotor ataxia. The lesions are readily located in the spinal column. In a few cases a slight posterior curvature of the dorso-lumbar region is found, but the majority of the lesions are in the lower dorsal region. Special care should be given to the bladder and bowels. Prolonged warm baths are beneficial. Treatment of the legs is always secondary to that of the spine. The diet should be nutritious and one easily digested. Give the patient plenty of fresh air and sunlight with cheerful surroundings. E. C. Link[132] reports two cases, one of over one year’s standing, completely recovered, and another much improved.
Ataxic Paraplegia
In ataxic paraplegia there are ataxic and spastic symptoms, due to both posterior and lateral sclerosis. Traumatism, cold and exposure are etiologic factors. It is found in diffuse myelitis, general paresis, leptomeningitis and in toxic conditions as in pernicious anemia. The posterior and lateral columns are degenerated, so that in the former there is an ascending degeneration and in the latter a descending.
Symptoms.—These comprise those of tabes and spastic paraplegia. Incoordination, ataxia, lightning pains, anesthesia, rigidness of muscles and exaggerated reflexes are the principal symptoms. The muscles easily fatigue; sensory symptoms are not so troublesome as in tabes; there may be visceral crises, sometimes Argyll Robertson pupil; and possibly spasms of the upper extremities and jaw. The course of the disease is slow.
Diagnosis.—This is not difficult as a rule. First, there is ataxia; then increased reflexes, fatigue of the muscles and paraplegia. Tumor of the cerebellum may confuse the diagnosis.
Treatment.—There is frequently a chance to greatly benefit these cases, and even in some instances a cure may be performed, provided the case is seen early. Thorough treatment of the spine to relax the muscles and to adjust the ribs and vertebræ is the indication. Stretching the spine, if carefully done, is beneficial. Muscular manipulation improves the spinal cord circulation, and osseous correction removes probable impingements to nutrient channels and nervous influences induced by cold, exposure, traumatism and secondary disturbances. Care of the general health, hygiene, diet, etc., are important.
Syringomyelia
Definition.—A chronic affection of the spinal cord in which there is an embryonal neurogliar overgrowth about the central canal, with cavity formation. It is characterized, clinically, by progressive muscular atrophy, peculiar disturbances of sensation and various trophic and vasomotor disorders. The onset generally takes place before the thirtieth year. Males are much more commonly affected than females. It is claimed by some that the disease is infectious. It frequently follows trauma.
Pathologically, the condition begins with an overgrowth of embryonal neurogliar tissue. This is followed by degeneration of the gliomatous tissue with a formation of cavities, or this cavity formation may be the result of hemorrhage. The disease, in most cases, involves only the cervical or dorsal regions, and is usually in the posterior or postero-lateral tracts. The cavity may prevail throughout the entire cord, but usually only the cervical and dorsal regions are involved. The cavities lie in the gray matter outside of the canal.
Symptoms.—The onset is slow. The symptoms depend upon the situation and extent of the cavity. As the disease most frequently involves the cervical region, the neck and arms are usually affected. At first neuralgic pains may develop in the muscles. Later there is progressive muscular atrophy and loss of painful and thermic sensations. Tactile and muscular senses are usually intact. The reflexes are increased and a spastic condition is present. The lower limbs usually escape, but when they are involved the clinical picture may be that of amyotrophic lateral sclerosis. A lateral curvature is present. When the disease extends into the medulla, there will be various bulbar symptoms. Trophic changes and vasomotor disorders are common.
A form of syringomyelia, known as Morvan’s disease, is characterized by neuralgic pains, cutaneous anesthesia and painless felons.
Diagnosis.—The progressive muscular atrophy, the retention of muscular and tactile senses, and the loss of thermic and painful sensations are typical symptoms. The diseases with which it may be confounded are: Cervical Pachymeningitis. The pain is usually greater, the tactile sense is lost and it runs a more rapid course. Anesthetic Leprosy. The trophic changes are more marked, tactile sensation is lost and the phalanges often drop off. Progressive Muscular Atrophy and Amyotrophic Lateral Sclerosis. Sensory symptoms are wanting.
Prognosis.—The prognosis is unfavorable. Duration is from five to twenty years.
Treatment.—Little can be done except attending to the diet and hygiene of the patient and meeting urgent symptoms. Probably, continued treatment along the spinal column would influence to some extent the circulation of the cord in the region of the involvement. Hot applications are of value in relieving pain and cramps. The X-ray has proven of some benefit in checking the progress of the disease.
Amyotrophic Lateral Sclerosis
“This is a chronic, progressive form of spinal paralysis, characterized by the symptoms of progressive muscular atrophy in the arms and by lateral sclerosis or spastic paraplegia in the legs.” (Starr). It is similar to progressive muscular atrophy, except, in addition, there is sclerosis of the pyramidal tract. (See Progressive Muscular Atrophy.) Osler classes progressive muscular atrophy of spinal origin, amyotrophic lateral sclerosis and progressive bulbar paralysis as diseases of the whole efferent or motor tract, wherein these disorders may simply be various stages in the same case. He says, “A slow, atrophic change in the motor neurones is the anatomical basis, and the disease is one of the whole motor path, involving, in many cases, the cortical, bulbar, and spinal centers.” There can be no question that for the student, a classification of spinal cord diseases according to the whole motor tract, the upper motor segment, the lower motor segment, etc., is a scientific classification from our present knowledge of the histology and physiology of the neurone, but for clinical purposes the usual classification is given. Osteopathically, we are greatly in need of a new nosology, either according to the cause of the disorder or to the physiological disturbance.
Amyotrophic lateral sclerosis does not occur so frequently as progressive muscular atrophy. Heredity plays a part, and it affects older people. Injury to the spinal column is undoubtedly an important factor. Exposure and cold may be exciting causes. Infectious diseases and syphilis are probably important causes.
Pathologically, there are atrophy in the anterior cornu and sclerosis of the crossed and direct pyramidal tracts. There is sclerosis of centers in the medulla.
Symptoms.—Atonic atrophy, muscular weakness and fibrillary contractions, of varying degrees, are characteristic. The reflexes are exaggerated; the arm and leg muscles become weak and finally rigid and atrophied. This results in deformity. Disturbances of sensation are not pronounced. The sphincters may be slightly affected.
Diagnosis.—The disease is not so prolonged as progressive muscular atrophy. Differentiation has to be made from multiple arthritis and transverse myelitis and syringomyelia.
Treatment.—The same treatment as outlined for progressive muscular atrophy is indicated. The disease may be retarded and life prolonged.
Progressive Muscular Atrophy
A disease characterized by a slow, but progressive, loss of power and by muscular atrophy. Anatomically, it is characterized by degeneration of the ganglion cells of the gray matter in the cord. This atrophic affection develops just opposite to that of chronic anterior poliomyelitis. It is commonly a disease of males in middle life. Syphilis, rheumatism and lead poisoning predispose. It sometimes follows cold, wet, exposure, traumatism, mental worries, overuse of certain muscles, or prolonged emotional excitement. Hereditary influences are present in some cases. In all cases lesions are detected in the vertebræ and ribs, corresponding to the innervation of the diseased areas. Very likely these lesions are the starting point of the disease, by impairing nutrition to the motor cells of the anterior cornu, and thus resulting in atrophy.
Pathologically, the muscles are wasted, the fibers undergo fatty degeneration and there is an overgrowth of connective tissue. The peripheral motor fibers are degenerated. The anterior nerve roots leading to the horns are atrophied. The large ganglion cells of the anterior horns are atrophied, or even entirely removed. The neurogliar tissue is increased. There is sclerosis of the anterior and lateral pyramidal tracts of the cord in the majority of cases. (See Amyotrophic Lateral Sclerosis). The pyramidal tracts have been found degenerated through the pons and internal capsule, even up to the motor cortex. When bulbar symptoms are present, there is degeneration of the motor nuclei of the medulla. The posterior columns are not involved.
Symptoms.—Irregular pains, numbness or exhaustion are usually felt in the region that is soon to become wasted. The upper extremities are first affected. The muscles of the ball of the thumb waste first, then the interossei. From atrophy of the interossei and lumbricales and contraction of the long extensor and flexor muscles, the deformity known as “claw hand” results. The wasting creeps up from the forearm, arm and shoulder. The muscles of the trunk are gradually affected. The muscles of the lower extremity may escape entirely. The platysma myoides does not waste and is often hypertrophied. The face muscles are attacked late or not at all. The affected muscles often twitch. Deformities and contractures develop, notably lordosis. Sensation is not impaired although the patient may complain of numbness and coldness. The bladder and rectum are not affected, but sexual power may be lost. The paralysis is flaccid and the reflexes absent in the so-called atonic cases. In atonic atrophy there is more or less spasm, the reflexes are greatly increased, there are often contractures and the wasting is usually trifling.
Diagnosis.—Differential diagnosis has to be made from syringomyelia, chronic anterior poliomyelitis, lead palsy and muscular dystrophies.
Prognosis.—The prognosis of progressive muscular atrophy is not favorable, although a number of cases have been greatly helped by an extended course of treatment.
Treatment.—The treatment consists of a thorough, stimulating treatment of the innervation of the affected regions, with manipulation of the muscles and parts diseased. Correction of the lesions to the vertebræ and ribs, which are involving the innervation to the diseased tissues, is of primary importance. A cure cannot be expected when degeneration of the nerve centers has occurred; still, the progress of the disease may be checked in many cases, and the patient occasionally gain considerable strength. When atrophy starts in the muscles of the ball of the thumb, the lesion is to the median nerve, and derangements of the cervical vertebræ, from the fifth to the seventh, may be found. Attention to the general health is important. Outdoor life is preferable and gymnastic exercises are of value, but do not overtax the strength.
Bulbar Paralysis
(Labioglossolaryngeal Paralysis)
A progressive atrophy and paralysis, invading the lips, tongue, pharynx and larynx, due to involvement (sclerosis) of the motor nuclei of the medulla oblongata that supply these tissues. It is rarely primary, more frequently secondary to tabes, amyotrophic lateral sclerosis and diseases involving the motor nuclei of the medulla. Diphtheria, syphilis and lead poisoning are said to predispose. Osteopathic lesions of the upper cervical are also important factors in many cases. Halbert says: “The nuclei of the hypoglossal, the spinal accessory, the facial and the motor part of the trifacial nerves suffer most decidedly from the sclerotic degeneration. The nerve trunks and the muscles which they supply gradually show the effects of a similar degeneration.”
The acute form results from hemorrhage, embolism or inflammatory softening. The onset is usually sudden. The speech is difficult or entirely lost. There are dribbling of saliva, difficult swallowing, flabbiness and flaccidity of the lips and frequent choking spells occur. These cases may prove rapidly fatal.
The chronic form may result from progressive muscular atrophy, insular sclerosis, amyotrophic lateral sclerosis, acute ascending paralysis or chronic poliomyelitis. The paralysis starts in the tongue, the first symptom being a slight defect in the speech. When the lips become involved, the patient cannot whistle and speech is rendered still more difficult. The lips are prominent and the lower one drops. The saliva is increased in amount and there is drooling. Mastication of the food becomes difficult. The tongue becomes atrophied and the mucous membrane wrinkled. Fibrillary tremors of the lips and tongue are present. Sensory symptoms are not present. Taste is normal. Paralysis of the larynx is not so pronounced as of the other parts.
Diagnosis.—This is generally easy as the symptoms are well marked. The prognosis is unfavorable.
Treatment.—Little can be done in the majority of cases. Only in those cases where the paralysis is caused by cervical lesions can much hope be given. Derangements of the cervical vertebræ, especially the atlas and axis, occasionally influence the circulation in the medulla to such an extent that the motor nuclei are greatly involved. The subluxated vertebras may interfere with the blood-vessels directly or through the vasomotor and trophic nerves. When the onset is not abrupt, the prognosis is more favorable. When deglutition is impaired, the stomach tube should be used in feeding the patient to prevent the food passing into the trachea.