J. (John) Hymers.

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acute or more rarely chronic endocarditis ; occasionally it come.s
from the aorta or lungs. In typical cases we would expect —

An acute onset, acute attack of unconsciousness without warn-
ing, spasmodic twitching in affected limbs, coma never very pro-
longed, often only a few minutes.

Temperature normal or depressed one-half degree.

Aphasia, if right side is paralyzed.

Cranial nerves unaffected.

Reflexes at first inhibited ; later much increased.

Later we have attacks of Jacksonian epilepsy in affected limbs^
athetotic movements, contractures and retarded development.

As a rule, only one limb is permanently paralyzed.

The picture is one of an acute though fairly mild onset, followed



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802 The Atlanta Medical and Surgical Journal.

by perniaDeDt though limited symptoms of irritative paralysis
later.

Hemorrhage. — We have the same acute ouset, but the coma is
much deeper and more prolonged. A very small hemorrhage will
cause more severe symptoms at the onset than the largest embolus
possible.

As nearly all hemorrhages occur at the base from rupture of the
lenticulo-striate artery^ we do not have the symptoms of cortical
irritation. Though the limb is paralyzed and somewhat stiff there
is neither convulsions^ athetosis or spasm of the paralyzed part.
On the other hand, as the damage is in the internal capsule, the
paralysis is much more extensive, generally involving a whole aide.

The temperature falls in an hour from one to four degrees.

No aphasia.

After the coma disappears the condition is almost unchanged.

I^ter we have a persistent paralysis and stiffness.

The picture is one of an acute and severe onset followed by
extensive and permanent results of a passive, instead of irritative
nature.

In sinus thrombosis the picture is entirely different.

Thrombosis may be primary or secondary. Secondary thrombosis
occurs from extension of suppurative processes near the sinus, gen-
erally in the lateral or cavernous sinus, as a result of ear disease.
It gives no marked motor symptoms, so does not concern us here.

Primary thrombosis is the result of certain blood states, result-
ing in increased coagulability of the blood or diminished blood
pressure, such as the infectious fevers, tubercular disease, or exhaust-
ing intestinal disease. Hemorrhage has caused this condition by
reducing the volume of blood ; the rigid sinus walls are unable to
contract, so the blood current is very much slower.

In all cases of which I have notes the superior longitudinal
sinus was affected.

We first have a history of the exhausting disease, prolonged
diarrhea or bad health ; then some day general convulsions, slight
or severe, occur, followed by apathy, somnolence or coma. Vom-
iting is an early symptom, and if the child is old enough to talk,
headache and mental dullness may be noticed a day in advance.



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Acute Cerebral Palsies in Children. 803

In from a few hoars to a day there are developed internal stra-
bismus, stiffness of the neck mascles, rigidity of the limbs, either
both arms or both legs ; epistaxis, prominence of fontanelle and
edema of the scalp.

There are recurring convulsions through the whole acute pro-
cess, often every halt hour; these are general. Unilateral convul-
sions, when they exist, are due to the extension of the clot into
the surface veins of the cortex.

With even such severe symptoms there is little or no rise of
temperature ; it is either normal or that already existing.

The prognosis is bad ; fully 80 per cent. die. If recovery takes
place there is the same spastic paralysis that occurs with embolism
and the same irritative cortical symptoms, Jacksonian spasm and
•contractures, mental dullness and imperfections.

The whole picture is one of an acute cerebral process, very sug-
gestive of meningitis, supervening on some exhaustive disease,
having an onset of from an hour to a day and characterized by
repeated convulsions.

All these cases have been the result of vascular disease. They
are non-febrile in themselves, and inflammatory results are slight
and always secondary to them. There still exists a class of cases
decidedly different in onset, though resulting in the same variety
of paralysis, the etiology of which is yet involved in doubt.

A healthy child is suddenly taken ill with severe meningeal
symptoms; there is a rapid rise of temperature to 103 or more
degrees, vomiting, general convulsions, restlessness or stupor. In
twenty-four hours these symptoms diminish, and in forty-eight
have, as a rule, disappeared. In a day or so it is noticed that the
child is partially paralyzed on one side, face, arm and leg. This
increases for a week, and then slowly improves a little, and in a
year some use of the limbs is regained.

After recovery we have all the signs of a cortical lesion. Spastic
paralysis, athetotic movements and attacks of Jacksonian spasm.

There is no involvement of the cranial nerves, but if the left
»ide of the brain is affected aphasia is present.

These cases differ from the other types mentioned decidedly.



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804 The Atlanta Medical and Surgical Journal.

The picture is one of acute febrile disease runniug its course, fol-
lowed after a short interval by paralysis.

These symptoms have long been attributed in a vague way to a»
acute encephalitis, a localized primary inflammation of the braia
corresponding to a myelitis in the cord.

Striimpell has very decided ideas that are worthy of more atten-
tion than they have yet received. He believes these cases to be
due to an inflammation of the motor cortex cells, a polioencepha-
litis, a condition with the same etiology and pathology as polio-
myelitis.

This theory, though accepted in Germany, is not credited else-
where.

Gowers sums up the following objections to it:

1. A primary inflammation limited to certain cells in a certain
part of the cortex is theoretical and scarcely possible.

2. If it did occur we would have some pathological examples of
the disease in the acute stage, as diseases of the brain are more
fatal than those of the cord.

3. That the liability of the brain to disease is very much less,
than the cord, and we would expect infection to attack the cord by
preference.

These objections seem to me readily answered.

That the condition is theoretical is admitted, since no specimens
have been secured [during the acute stage. Autopsy in later life
has, however, shown the identical changes found in old poliomy-
elitis cases, disappearance of cellular elements, increase of connec-
live tissue, induration and shrinking of the affected part of the
cortex ; in each variety of tissue the same changes.

To the objection that as diseases of the brain are more &tal than
those of the cord, so, therefore, we should have some specimens
showing acute changes; the answer would be-that the far greater
frequency of cord disease more than evens this up, and that as an
actual fact this disease, whether in cord or brain, is very rarely
fatal.

As to the lesser liability of the brain, this disease, when it occurs
in the cord, does not affect the whole tract, but picks out situations
often widely apart. If it could affect in one person the lumbar



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Acute Cerebbai. Palsies in Childben. 806

segment and in another the cervical^ it might readily affect the
cortex in a third case.

The treatment must vary in each condition.

In hemorrhage we do absolutely nothing. Any interference is
dangerous; if the heart action becomes weak, strophanthus in small
doses to strengthen it. Never use digitalis or strychnine — absolute
quiet in a darkened room^ on a milk diet.

In embolism the symptoms are due to the cortical anemia, result-
ing from the plugging of the artery. If we can push the plug far-
ther along the artery we diminish the number of branches cut off.

To do this we give nitro-glycerine and caffeine, so dilating the
artery and stimulating the heart. Nitro-glycerine is not in itself a
heart stimulant. Quiet, with a simple and nourishing diet.

In thrombosis stimulation is of the greatest importance. In
secondary thrombosis opening and packing the diseased sinus has
given the best results, but I have never seen a case of primary
thrombosis in which surgical procedure was practicable. The
original disease has generally caused such great depression that
surgical interference was unwarranted. All the cases I have seen
so far have been fatal.

In polioencephalitis we evidently have an acute febrile disease
with an inflammation of the cortex as the characteristic lesion.
The management is that of other febrile conditions. Small doses
of aconite, belladonna and brandy, rest and tepid baths are best.

The resulting contractures, spasms and paralysis are best treated
by galvanism. Much is said against electrical treatment, princi-
pally by physicians who possess a small farradic battery, and who
are unacquainted with the difference between a primary and sec-
ondary current. The effects of proper electrical treatment are
often striking.

Massage and passive motion are subsidiary measures.

For the Jacksonian spasms bromides are best, but hot baths are
also useful.

Slight as the mortality is, it would be still smaller were it not
for the fiict that all these cases are generally mistaken for menin-
gitis, and depletive measures, assisted by cold to the bead, is the



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806 The Atlanta Medical and Subqioal Joubnal.

staple treatment. The weaker children promptly succumb, but
the stronger manage to pull through.

Counter irritation in any form is useless.

S02 Peachiree Street.



REMARKS ON PULMONARY TUBERCULOSIS.*

By W. S. KENDRICK, M.D.,
Atlanta, Ga.

I must offer an apology for having no paper this evening, but
my work has lately been such as to render it impossible for me to
prepare one. But I shall make some remarks upon the subject
assigned me.

The trend of recent investigations goes to prove that tuberculosis
is an infectious disease due to the presence of the tubercle bacillus.
This attacks almost any portion of the body. The danger of infec-
tion is not from the moist state but from the expectorations of the
persons having the disease. These expectorations become dry and
are blown about in the air, and it is the inhalations of these that
give rise to the most frequent forms of phthisis pulmonalis. We
have several forms of this, but the form which I propose to discuss
is the chronic ulcerative phthisis. That is the general form which
we meet with in tuberculosis, and in which the process is slow, as
the disease may run over a number of months or years, or may
remain quiescent for a length of time. The inhaled bacilli usually
attack the apex of the lung, and this is generally supposed to be
due to the fact that the expansion here is less vigorous. Conse-
quently the bacilli gain a vantage point there and set up the inflam-
mation which we find accompanying tuberculosis. The disease is
manifested by nodular bodies called tubercles, which we find in the
bronchioles and elsewhere in the air passages. They excite a cer-
tain amount of inflammation wherever located, and this accounts
for the fact that however small an area may be infected we never
have a case without a case of secondary pneumonia. They are

^Atlanta Society of Medicine, December IS, 1896.



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Remarks on Pulmonary Tuberculosis. 807

foreign bodies and give rise to secondary solidification of the lung
tissue^ as they excite a certain amount of inflammation^ and whether
as large as my finger or as small as a pin head we have the two
forms of pneumonia. When the tubercles have existed for a certain
length of time they die and produce softening and caseation ; and
in this breaking down of lung tissue the cavity is produced. We
have two processes ; one is caseation and the other is sclerosis. The
life of the patient will depend upon which of these processes super-
venes. In caseation we have softening and destruction of the lung
tissue until we have the cavity, and this process repeats itself. The
process of sclerosis is much more common than we usually think,
and we would be surprised at the large number of persons over 45
years of age who have the sclerotic patches; forty or fifty per cent,
of the people on whom post-mortems are made are found with these
patches, and yet there was no evidence of tuberculosis during the
patients' lives. As before stated, it is due to one or the other of
these processes as to whether4he patient will die early after the in-
vasion or whether he will live longer.

Now as to the invasion of the tubercle. It is not suspected by
the patient until he is notified. We have certain symptoms accom-
panying this; we sometimes have dyspepsia and derangement of the
stomach, loss of flesh, loss of strength, emaciation, and a dry, hack-
ing cough. One of the first signs is hemoptysis, or hemorrhage from
the lungs. This is supposed to be nearly always due to the presence of
the tubercles, which produce an erosionof some bloodvessel andcause
hemorrhage. Where we have a profuse hemorrhage it is usually
due to the rupture of one of the large blood vessels in a cavity and
results in the death of the patient. At first the cough is dry and
hacking, for the reason that the destructive process has not yet be-
come sufficiently advanced. The most characteristic sign is the
fever. We may have a patient with night sweats and loss of flesh
and yet not suspect phthisis, but, if, upon taking the temperature,
we find the patient has a slight increase of temperature, particularly
in the evening, which continues for weeks (ruling out other condi-
tions) and he have the other symptoms, we can reach but one con-
clusion. The fever is pathognomonic and is the most reliable ; if



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808 The Atlanta Medical and Suhoical Journal.

there is no typhoid fever or anything else, we can almost make out
a perfect diagnosis, which will be confirmed by finding the bacilli.

We divide tuberculosis into three stages, whether acute or chronic.
The first stage is the stage of acute pneumonia, that is, the stage of
tuberculization; this is the irritative or congestive stage. The
second stage corresponds to the second stage of acute pneumonia,
that is, the stage of solidification. The third stage of acute pneu-
monia is the stage of resolution, and it is at this point that these
two diseases separate. In acute croupous pneumonia we have res-
olution and the walls return to the normal condition. In ordinary
croupous pneumonia we have no destruction of lung tissue. The
two diseases diverge at this point, for instead of tuberculosis termi-
nating in resolution we have the other process which is directly op-
j)08ite, and we have caseation, softening and destruction of lung
tissue, however small or large the affected area may be, and thereby
giving rise to cavities.

Now we come to the physical signs. In the incipient stage the
physical signs are absent to such an extent that we cannot say
whether it is tuberculosis or not. After the disease has reached a
certain point, we value inspection, percussion, palpation and aus-
cultation ; especially auscultation and percussion, and percussion is
the more valuable of the two. Inspection gives us very little; if
we get anything at all it is a certain amount of lost expansion at
the apex, but in many cases we will not get even this. Of course,
if the disease is well advanced we get on palpation an increase of
vocal fremitus. This is tvpical : if we lay our hands on both lungs
and ask the patient to speak we perceive the difference in the frem-
itus on the two sides. If, in the first or second stage we get great
loss of expansion, we know exactly what is going to follow ; we
know that we will get an increase of vocal fremitus and have dull-
ness upon percussion, and upon auscultation we will get broncho-
vesicular breathing. We will get harsh inspiration and prolonged
expiration. If we listen at the beginning of the invasion of the
disease we will nearly always get prolonged expiration. We get
this because the alveoli are congested ; the lungs lose their elasticity
and it takes the air longer to escape.

The second and third stages run so close together that one dc-



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Remarks on Pulmonary Tuberculosis. 809

scription will answer for both, except when we have ctlvities. In
the second stage of tuberculosis, which is the pneumonic stage, we
get loss of expansion. I will say just here that in making exami-
nations, it is impossible to do this thoroughly if the patients are
allowed to retain any of their clothes around the thorax ; they
should be stripped to the waist. The loss of expansion is due to
the inflammatory changes in the lungs and also due to pleurisy.
We know that we will get dullness on percussion after loss of ex-
pansion, and then when we listen we get the strongest sign, which
is bronchial breathing. What we hear we get on expiration, be-
cause the inspiration is active and the expiration passive. In nor-
mal conditions the pitch of inspiration is higher and of expiration
lower, and the reverse is true in all conditions of solidified lungs.
In solidified lungs the pitch is higher and longer in expiration and
gets higher until respiration ceases.

In the third stage we get practically the same signs ; we get soft-
ening of lung tissue and cavities. All three stages are going on at
the same time. The third stage differs from the second upon,
auscultation, as we have various sounds in the third stage. These
sounds are indicative of cavities filled with air or filled with fluid,
or partly filled with air and partly filled with fluid. These are
some of the physical signs. Of course, I have left out a great deal,
of it, as it is something that one could talk on for hours, but these
are what we find in ordinary cases of tuberculosis. One thing
especially, we do not find all these signs on the anterior surface of
the chest, and we hardly get them at the apex, but usually below
the clavicle, not at the apex itself, but a little lower down. We
may get well marked solidification and cavities on the posterior
portion before any signs appear on the anterior surface of the chest..

As regards prognosis we cannot say in all these cases that death
will be the result, for many cases are retrogressive and the patient
will live for a number of years and go on discharging his duties.
Death, of course, comes to a number of cases from many causes.
In the latter stages the disease becomes a septic disease in which the
tubercle may not play an important part, but a general septic condi-
tion is produced and death is due to sepsis.



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810 The Atulitta Medical and Surgical Journal.



PUERPERAL CONVULSIONS, AND THEIR
PREVENTION*

By JOHN N. UPSHUR, M.D., Richmond, Va.,
Profeasor of the Priictice of Medicine in the Medical College of Virginia, etc.

A firm conviction of the great responsibility resting upon as in
the care of the puerperal woman, and the skilful guidance through
the perils of thb period to its happy consummation in a safe deliv-
ery, is the motive prompting to the discussion of this condition —
80 ft*ightful in its manifestations and so dire often in its conse-
quences.

I cannot emphasize too much the importance to the patient of an
early engagement of her medical attendant, that she may be closely
in touch with him, and that he, by extraordinary diligence, may be
keenly alive to every circumstance which may be to her a souroe
of peril. Giving to his patient advice as to personal care, of diet^
exercise, rest, bowels and kidneys ; making regular, oft;en frequent,
analyses of the urine, to determine the presence of albumen or the
lacking elimination of excrementitious solids. Often there is dan-
ger ahead when urinary analysis is negative in its results, and the
nervous system is ripe for a dangerous explosion so soon as some-
thing occurs to excite the requisite reflex. I cite the following
•oases for sake of illustration :

Case 1. Mrs. T., a woman of fine physique and robust health,
«ame under my care in 1885; she would never permit me to see
her until labor came on, though reported by her husband as being
very dropsical. Frequent examination of her urine fiiiled to show
any albumen, though the amount of urine was scanty. Treatment,
through the medium of her husband was, of course, very unsatis-
factory. When labor came on, I found her the most dropsical
^oman I ever saw at term. She was kept under chloroform,
until delivered with instruments, afler a protracted labor. In four
succeeding pregnancies she was never so dropsical again, but each
period of pregnancy was filled with symptoms of threatened eclamp-

^Bead before the Ricbinond A c ademy ot Medicine and Surgery, November 34, 1890.



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Prevention of Pcjerpbral Convulsions. 811

eia. The patient was a hearty feeder^ her urine was usually scanty^
albumen apparent on analysis, but not marked.

In her third pregnancy she had an attack of vertigo, followed by
a period of insensibility; she has always suffered with her head.
Her treatment during each pregnancy consisted of low diet, abund-
ant drinking of lithia water, and keeping bowels in a condition of
mild diarrhea. She has usually taken chloroform during the lat-
ter part of the second stage of labor, and has been safely delivered
five times without a single convulsion, and is now doing well in
her sixth pregnancy, having reached the end of the sixth month.

Case 2. Mrs. W., of delicate build, in her second pregnancy,
-during the ninth month, had agonizing headache, which failed to
respond to remedies; saw flashes of light and other objects contin-
ually before her eyes. When labor came on, she was kept under
-chloroform until delivered ; her skin was so dry as to feel parched.
Repeated examination of urine failed to detect any albumen.
Within an hour after delivery, she complained of not being able to
•see (she had had no undue amount of hemorrhage) and began to
talk wildly and incoherently. Chloroform was given to control
•excitement, followed by full doses of potassium bromide and pilo-
•carpine ; skin acted freely and all untoward symptoms subsided;
urine showed large percentage of albumen. Convalescence un*
•eventful until fourteenth day, when marked symptoms of septicemia
<leveloped ; but she passed safely through a most dangerous illness.

Case 3. Mrs. H. had been carefully watched during second
pregnancy, urine frequently analyzed, with negative results. About
the time she reached the fifth and a half month I was called to see
her with a sharp attack of cholera morbus ; a day or two of treat-
iment was sufficient to restore her to health. She was discharged
with caution as to imprudence in diet, and every other respect. On
the evening of next day, she went out to supper, eat very heartily
•of almonds and raisins. I was called early the following morning
to see her in what her husband called a trance. When I reached
her she talked to me rationally, and manifested no symptoms of
special gravity. At 4 p. m. she was seized with a violent puer-
peral convulsion, quickly followed by a second, and for a few mo-
ments I thought her dead. I bled her freely from the arm, labor



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812 The Atlanta Medical and Surgical Journal.

was brought on, and after delivery she made an uneventful recov-
ery — urine for the first time loaded with albumen. Her next preg-
nancy progressed satisfactorily to the ninth month, when she com-
plained of distressing head symptoms, urine scanty, but free from
albumen ; some disturbance of vision. She was freely purged with
calomel gr. vj., croton oil gtt. j, with complete relief of head symp-
toms. The week following, head symptoms again returned, and
the dose of calomel and croton oil was repeated with as prompt re-
lief as at first. Labor came on a few days after, and she was safely
delivered, without any complication; convalescence speedy and un-
eventful.

Case 4. Mrs. D., primipara, age 22, stout and plethoric. I was
retained six weeks before confinement. Frequent analysis negative,,
except once a trace of albumen, until October I2th, when urine was
found loaded with albumen, being almost solid on boiling. Was
called at 10 p. m.; found she had had three convulsions, cervix
rigid, dilated size of a nickel. She was bled freely from the arm^
manual dilatation persisted in for five hours; child turned and de-
livered; a serious convulsion during the labor, which looked as



Online LibraryJ. (John) HymersAtlanta medical and surgical journal → online text (page 72 of 80)