(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.