ABSTRACTS FROM CURRENT LITERATURE. — Grant, Dundas.—Case of Emphysema of the Orbital Wall of the Anterior Ethmoidal Cells, Caused by blowing the Nose. — Jour. Lar., Rhin. and Otol. , March, 1900. — Lack, Lambert.—Case of Nasal Polypi, with Suppuration and Absence of Maxillary Sinuses. — Jour. of Lar., Rhin. and Otol. , April, 1900. — Lawson, Arnold.—Cicatrix Horn Growing from the Cornea. — The Lancet , February 3, 1900. — Lodge, Jr., M. D., Samuel.—A Case of Fatal Sphenoidal Suppuration. — The Laryngoscope , March, 1900. — Killian, Prof. Gustav.—Case of Acute Perichondritis and Periostitis of the Nasal Septum of Dental Origin. — Münch. med. Wochen. , No. 5, 1900. — Hawthorne, C. O.—The Eye Symptoms for Locomotor Ataxia, with a Clinical Record of Thirty Cases .— Brit. Med. Jour. , March 3, 1900. — I.— Cases in which Optic-Nerve Atrophy is the Primary or Dominating Condition. — II.— Cases with Argyll-Robertson Phenomenon. — III.— Cases in which an Ocular Paralysis is the Earliest or Dominating Symptom . — Menzies, J. Acworth.—Detachment of Corneal Epithelium (?). — British Med. Jour. , March 17, 1900. — Hines, M. D., Oliver S.—Iodide of Stannum in Tuberculosis. — The Amer. Hom. , March 15, 1900. — Kyle, M. D., D. Braddon.—Initial Forms of Tubercular Laryngitis. — Inter. Med. Mag. , March, 1900. — Ball, James Moores.—On Removal of the Cervical Sympathetic in Glaucoma and Optic-Nerve Atrophy. — Jour. A. M. A. , June 2, 1900. — CASE I.—EXCISION OF SYMPATHETIC FOR GLAUCOMA ABSOLUTUM. — CASE II.—DOUBLE SYMPATHECTOMY FOR GLAUCOMA SIMPLEX. — CASE III.—SYMPATHECTOMY FOR OPTIC-NERVE ATROPHY. — PATHOLOGIC CHANGES IN THE EXCISED GANGLIA. — TECHNIQUE OF THE OPERATION. — EFFECTS OF EXCISION OF SUPERIOR CERVICAL GANGLION. — HOW DOES EXCISION OF THE CERVICAL SYMPATHETIC REDUCE INTRA-OCULAR TENSION? — EXTENT OF SYMPATHECTOMY IN DIFFERENT DISEASES. — HISTORY OF SYMPATHECTOMY. — CONCLUSIONS. — Heath, M. D., Charles.—A Case of Sinuses in the Vault of the Naso-pharynx. — The Jour. of Lar., Rhin. and Otol. , May, 1900. — Roughton, B. S. (Lond.), F. R. C. S., Edmund W.—The Diagnosis and Treatment of Chronic Purulent Nasal Discharges. — The Jour. of Lar., Rhin. and Otol. , May, 1900. — Williamson, R. T.—Remarks on the Diagnosis and Prognosis in One Hundred Cases of Double Optic Neuritis with Headache. — Lancet , May 12, 1900. — Murrell, W.—A Case of Double Optic Neuritis from Serous Effusion (Quincke’s Disease). — Lancet , April 28, 1900. — Stephenson, Sydney.—Concussion of the Retina. — Brit. Med. Jour., January, 1900.
233
This case was shown to the British Laryngological, Rhinological
and Otological Association.
W. M., twenty-eight years, came under my care yesterday on
account of a sudden swelling of his eye which had taken place
two hours previously, and which had occurred suddenly as he was
blowing his nose without a handkerchief, and which gave him
the impression as if something were running out of his eye. The
swelling crackled in a manner characteristic of emphysema, and
the first suspicion was that he must have had some disease of the
orbital wall of the anterior ethmoidal cells, and that on examination
there would be found some evidence of ethmoidal disease.
None such was to be elicited, and the only history obtainable
was that he received several kicks on the nose and back of the
ear two months ago. This has probably resulted in a fracture of
the orbital wall of certain of these cells.
A man, aet. twenty-eight years, complains of nasal obstruction
and purulent discharge, with a disagreeable odor in the nose.
The polypi having been removed, the pus appeared to flow from
under the anterior ends of the middle turbinates. After wiping
the discharge away and bending the patient’s head forward, it
reappeared in large quantity. On transillumination the cheek on
both sides appeared quite dark, and the patient had no subjective
sensation of light. The diagnosis of antral suppuration was now
considered almost certain, and the patient was advised to have
234both antra punctured from the alveolar margins. This was
accordingly attempted under gas, but although the antrum drill
was forced in for its full length, no cavity was reached.
Puncture from the inferior meatus was next attempted, and
considerable force was used in two different points; but with no
better result. It would seem therefore that the antra must be
very small, if not entirely absent.
Discussion.—Mr. Spencer thought it might be one of those
convoluted inferior turbinals which form a gutter in which pus
collects. The majority considered it suppuration in the ethmoidal
region.
The patient was a female child, aged eight years, a hydrocephalic
idiot. The history given was that about one year previously
a white spot had appeared on the right eye and that the
eye began to project. Six months later a growth was first
noticed on the right cornea, and this had constantly increased in
size. Latterly a white spot had appeared on the left eye. On
examination of the eyes there was seen a large conical tuberculated
excrescence protruding between the lids of the right eye.
It was half an inch in length and its base attached to the cornea
covered about four-fifths of its surface. The left cornea
exhibited a yellowish infiltration just below the pupil, over
which the cornea was bulging; the anterior chamber was deep,
the iris was immobile, the tension was slightly raised, and the eye
was quite blind. Both globes were very anæsthetic, and there
was considerable muco-purulent discharge from a chronic inflammation
of both conjunctival sacs. The growth upon the right
eye was accidentally detached a few days after admission into
the hospital, and it was then seen to have been attached to the
cornea at the apex of a central staphyloma, which was left covered
by a fleshy soft core which had formerly been embodied in
the center of the growth. The cornea was entirely opaque, and
the eye was quite blind. After removal of the right eye a few
days later examination of the globe revealed a co-arct retina
with evidences of chronic degenerative changes in all the various
structures. The anterior chamber was completely abolished, the
iris throughout its extent being firmly adherent to the back of the
235cornea, which was bulging centrally. The apex of the corneal
staphyloma had evidently been the site of a large perforation,
which was closed by the fleshy granulations which formed the
core of the growth. The growth itself measured half an inch
from apex to base and one and a half inch around its base.
The interior portion was soft and crumbling, but the external
layers were hard and horny and cut with difficulty. A wedge-shaped
piece was cut away from the growth and specimens were
cut and stained with carmine. The microscope showed that the
external layers consisted of several faintly fibrillated strata of a
dense, homogeneous nature. The layers occupied about one-quarter
of the entire thickness of the walls, the rest being
entirely composed of small nucleated cells, those most external
being stratified. Adopting Mr. Bland Sutton’s classification of
human horns, this growth would be an example of a cicatrix
horn, the rarest of all varieties of horn, and one which had been
usually found in connection with cicatrices of burns and scalds.
The probable ætiology in this case was an overgrowth of granulation
tissue closing the perforation in the cornea, which, owing to
an unhealthy condition of the wound and eye, which was
anæsthetic and atrophic, had become exuberant, simulating
exactly the condition known as “proud flesh” elsewhere. By a
process of accumulation and heaping up, the granulations gradually
formed a cap over the cornea, whilst the external layers
gradually became stratified and horny from the pressure of fresh
growth from the central core and by the action of the air. The
nature of the growth was evidence that the corneal epithelium
bore no share in its production and discounted the possibility
that it might be due to a huge crust of inspissated conjunctival
discharges.
W. S., aet. thirty-one years, admitted to Royal Halifax Infirmary
May 15, 1899, complaining of pain in right ear and right
side of face of six months’ duration. For two months right side
face swollen and copious bloody, purulent discharge from right
nostril. Nine years ago had syphilis. Insomnia from pain.
On admission: Temperature 100°; skin over right superior
maxilla red and œdematous; thick purulent discharge from
236right superior meatus, sequestrum in region of right cribriform
plate; naso-pharynx, chest, and abdomen normal; urine, sp. gr.,
1014; trace of albumen. Fundi (of eye) normal.
May 16—No pus found in antrum on exploration and flushing.
Patient taking 60 grs. pot. iod. (t. i. d.) and mercurial inunction.
Temperature in ear usually higher than that in mouth until just
before death. June 8.—Mortuus est.
Post-mortem Examination.—Skull. Base of brain was bathed
in thick greenish pus, principally in the neighborhood of the
pituitary body, the pus extended back over the pons and medulla.
No brain abscess. Ventricles contained more than normal
quantity of fluid. Frontal sinuses and cribriform plate of ethmoid
and ethmoidal cells normal.
To right of the sella turcica there was some necrosis of the
walls of the sphenoidal sinus. Probe readily passed from base
of skull through sphenoidal sinus into the nose. Large free
opening from said sinus into nose, which sinus was full of
muco-pus. Cavernous sinus not thrombosed. Right antrum of
Highmore contained about a dram of thick glairy mucus.
There have been recorded two cases of perichondritis of the
septum due to alveolar periostitis. Suppuration of dental cyst was
cause in the following case.
A young man had pain in second left upper incisor; two days
after obstruction of nose supervened, with pain in forehead and
high fever. There was a sudden copious discharge of fetid pus
from right nostril seven days later. The entire mucosa of the
septum was raised from the cartilages, etc. It is considerably
swollen over right side of the triangular cartilage, but less so
posteriorly. Severe headache in forehead and frontal eminence,
and still little fever. The pus was escaping through a small hole
into the left nostril. It was freely incised. The triangular cartilage
was disintegrated, and the pus had burrowed between the
soft tissues and vomer and vertical plate of the ethmoid. The
choanæ were constricted by thickening of the septal mucous
237membrane. The wound healed in a fortnight without sequestrum,
while the toothache lasted but two days.
Six months later the patient had recurrence of pain in the
same tooth of two months’ duration; it was extracted and pus
continued to exude from the socket. A probe, passed 2½ centimeters
to the floor of the nose and septum, showed a cavity
covered with membrane in the anterior parts of upper jaw, which
was a cyst at the root of the tooth. The anterior cyst walls were
removed with bone forceps, and the remainder scraped. The
cavity gradually healed.
The cyst probably broke through under the septal mucous
membrane. In exceedingly few cases of perichondritis does the
process extend to the osseous septum. Only once has the
author seen record of a case which was as extensive as this. The
offensive odor also points to a dental origin.
It is now generally recognized that the disease known as
locomotor ataxia may include among its clinical manifestations
symptoms other than those which depend on pathological changes
in the spinal cord. A number of these are associated with the
functions of the eyeballs. The Argyll-Robertson pupil is universally
admitted as valuable confirmatory evidence of a diagnosis
of locomotor ataxia; ocular paralyses, if less frequent,
are certainly not less significant; and optic nerve atrophy is at
least so well known in connection with the disease that its occurrence
in any individual case would hardly call for comment.
A further step forward in our knowledge of the clinical possibilities
of locomotor ataxia has been the recognition of the fact
that ocular disturbances may precede the evidences of any spinal
lesion. This advance necessarily means that the occurrence
of any one of the ocular events above mentioned must, unless otherwise
explained, generate the suspicion that the case may in its
later events display the phenomena known to depend upon
sclerosis of the posterior columns of the spinal cord.
It is very difficult to collect the evidence necessary to show in
what proportion of cases this suspicion is justified by the event.
For it is certain that ocular disturbances may long precede the
238manifestation of spinal symptoms. In the case of optic atrophy
the interval may, according to Gowers, extend even to twenty
years. Thus it can only be in very exceptional instances that
one and the same physician will have the opportunity of observing
at least a number of these cases through all the stages of
their progress. Yet, if true, it is of manifest importance, for the
sake both of exact knowledge and of accurate prognosis, that it
should be clearly recognized that an optic-nerve atrophy, an
ocular paralysis, or a loss of the pupil light reflex, unless capable
of other explanation, belongs in all probability to the order of
events incident to locomotor ataxia, and that any one of these may
well be the introduction to a more widely-spread manifestation
of the disease.
For reasons stated above, the collection of complete histories
necessary to afford actual demonstration of the truth of these
propositions is difficult; and all the more so as there is reason
to believe that in those cases in which the early stress of the disease
falls upon the nervous apparatus of the eyeball the spinal
symptoms are apt to be slight in degree as well as delayed in
development. This is certainly the case when the ocular disturbance
takes the form of optic-nerve atrophy. “In a large
number of such cases,” says Gowers, “ataxy never comes on, the
spinal malady becoming stationary when the nerve suffers.”
Of course, in a given case of optic-nerve atrophy without
spinal symptoms the question may fairly be raised whether it is
right to place such a case in the locomotor ataxia group. All
that can be said in reply is (1) that from cases of optic atrophy
pure and simple one passes by an unbroken series of steps
through cases with more and more distinct evidence of locomotor
ataxia to, at the end of the series, optic atrophy in association
with characteristic ataxic symptoms, and (2) that, as already
stated, a simple case of optic atrophy may remain unchanged
for many years, and yet in the end display undoubted evidence
of the development of a spinal lesion. But if optic-nerve
atrophy may be the primary symptom in the disease, if the occurrence
of spinal symptoms may follow it after an interval of many
years, and if again it may remain without at any time any existing
ataxia, it is not unreasonable to presume that both the Argyll-Robertson
pupil and an ocular paralysis may each have exactly
corresponding relations to the development of the spinal evidences
239of locomotor ataxia. The collection of evidence to support this
suggestion is even more difficult than in the case of optic-nerve
atrophy. The latter condition must ere long compel the patient
to seek medical advice, and thus the opportunity for a complete
investigation of the state of his nervous apparatus is afforded at
a relatively early date. But an Argyll-Robertson pupil may
exist, and presumably exist for years, without any inconvenience
to the patient. Such a patient, therefore, will not consult his
medical adviser until spinal or other symptoms display themselves,
and thus the precedence of the pupillary condition cannot
be determined. In the case of an ocular paralysis medical
assistance is, no doubt, usually promptly invoked. But such an
occurrence is open to a number of ætiological explanations, for
example, rheumatism, cold, etc., which it is difficult to exclude
with confidence. Hence it is much less precise in its significance
than either a double optic atrophy or the Argyll-Robertson
pupil. It must be by the collection of observations extending
over a long term of years that actual demonstration of the relationship
of the ocular disturbances now in question to the
occurrence of spinal disease can be established. But while
falling short of the merit of actual demonstration, the presentation
of the facts displayed by a number of cases which could
only be observed over relatively brief periods is not without
value. If no one case affords a complete history of all the stages
of the disease the picture presented may none the less be fairly
complete, provided the cases are sufficiently numerous, and they
are seen at different points of development. It is believed that
in the present series these conditions are fulfilled. The conclusions
they afford, as far as the present purpose is concerned, are:
(1) That an optic-nerve atrophy, an ocular paralysis, or an
Argyll-Robertson pupil may exist as an isolated symptom for a
considerable time, presumably for years; (2) that any two of
these may be associated together, with a correspondingly increased
presumption that the diseased process causing them is of
the locomotor ataxia order; (3) that any one of the three, or a
combination of two or all of them, may exist in conjunction with
a greater or less degree of evidence of spinal disease; and (4)
that occasionally a case which commences with purely ocular
symptoms may be seen to develop with comparative rapidity
characteristic symptoms of the spinal lesion of locomotor ataxia.
240The cases therefore may be held to justify the view that an optic-nerve
atrophy, an ocular paralysis, or the Argyll-Robertson pupil
(not capable of other explanation) must be regarded as affording
a definite basis for suspicion in reference to a possible development
of spinal disease. On the other hand, it must be admitted
that the prognostic indication, so far as spinal disease is concerned,
is not an absolute one, for the ocular defect may exist
certainly for many years without any evidence whatever of the
involvement of the spinal cord.
The cases here recorded have all been the subject of detailed
and in most cases repeated examination, and unless the contrary
is stated, it may be taken for granted that the thoracic and
abdominal viscera are normal, to physical and other methods of
examination. In all cases, too, in which no specific statement is
made, it is to be understood that the visual acuity, the visual
fields (both for white and colors), and the fundus oculi have
been proved to be normal. This last statement of course does
not apply to cases in which optic atrophy exists. Particular care
has been taken to be accurate in regard to the condition of the
pupils and the knee-jerks. In nearly, if not absolutely in every
instance where a departure from the normal is chronicled, the
record has been confirmed by more than one observer, and in
the case of a deficient knee-jerk the conclusion stated has never
been formulated until the conditions insisted on by Gowers,
Buzzard, and Jendrassik have been fulfilled. With a few exceptions
in which only a single observation was possible, the patients
have been watched for months, and in some instances for several
years. The cases are arranged in series, with a view to show
how, from a purely ocular condition, one may pass through
gradually accumulating evidence to the same ocular condition in
association with the characteristic signs of the spinal lesion of
locomotor ataxia.
(a) Optic Atrophy, without Other Evidence of Disease.
Case I.—W. T., aged twenty-five. Failure of vision extending
over two years, with reduction of visual acuity to the power
of counting fingers at three feet. Double optic atrophy; pupils
medium, with distinct light response; knee-jerks distinct and no
241evidence of spinal disease, and no cerebral symptoms other than
one or two attacks of giddiness. Urethritis, but no syphilis.
Case II.—F. R., aged thirty-eight. Double optic atrophy,
with almost complete loss of vision, the defective sight having
been observed for at least eighteen months; pupils dilated and
immobile; no evidence of spinal disease, unless possibly some
degree of failure of sexual power; no cerebral incidents; no
history or evidence of syphilis.
(b) Optic Atrophy, with Other Ocular Evidence Suggestive of Locomotor Ataxy.
Case III.—(By permission of Mr. Ernest Clarke, F. R. C. S.)
R. C., aged thirty-nine. Double optic atrophy, reducing right
visual acuity to the power to count fingers at four feet, and left
to mere perception of light; right pupil dilated and three times
the size of the left; neither any light response, but free movement
on convergence; entire absence of symptoms and objective
signs of spinal disease; “gleet” twenty years before, no syphilis.
Case IV.—A. S., aged twenty-five. Double optic atrophy,
with observed failure of vision for twelve months. V. A. right-hand
movements only; left, 6
18 part; pupils 2.5 mm., no light
response, but contract on convergence; knee-jerks difficult to
obtain, but movement, though possibly wanting in promptness,
is normal in extent; no ataxia or other evidence of spinal disease;
mother of three healthy children, no miscarriages.
(c) Optic Atrophy, with Some Evidence of Spinal Disease.
Case V.—W. A., aged thirty-seven. Double optic atrophy,
with reduction of visual acuteness to “hand movements;” pupils
dilated and immobile; knee-jerks absent, but no other evidence
of spinal disease; venereal sore when aged twenty; no recognized
secondaries, and father of four healthy children.
Case VI.—J. G., aged thirty-five. Failure of sight (six
months); optic atrophy, gradually increasing whilst under observation
of twelve months; pupils not definitely abnormal;
knee-jerks absent throughout, but no further appearance of
spinal disturbance; urethritis, but no history of syphilis; father
of two healthy children, wife no miscarriages.
Case VII.—F. L., aged thirty-nine. Double optic atrophy,
reducing visual acuteness to 6
24, pupils very small, and with
242Argyll-Robertson phenomenon; subsequent to failure of sight
(twelve months) has had shooting pains in thighs, and failure in
retention power of bladder; knee-jerks distinct; no ataxia or
sensory defect in lower limbs; venereal sore twenty years before;
no recognized secondary syphilis; wife healthy: seven pregnancies,
five miscarriages.
(d) Optic Atrophy, with Distinctive Evidence of Spinal Disease.
Case VIII.—C. H., aged thirty-eight. Failure of sight (two
years) from double optic atrophy; pupils medium, with Argyll-Robertson
phenomenon; moderate double ptosis, but no ocular
paralysis; shooting pains in lower limbs (eight years); knee-jerks
absent; considerable ataxia and failure of control over
bladder; syphilis at nineteen years.
Case IX.—G. S., aged forty. Pallor of disks and peripheral
contraction of visual fields; four months later loss of knee-jerks
and gradual development of ataxia; pupils normal throughout;
death at the end of twelve months with symptoms of meningitis;
syphilis at twenty-five years.
(a) Argyll-Robertson Phenomenon, without Other Evidence of Disease.
Case X.—A. L., aged thirty-three, the subject of slight hypermetropic
astigmatism. Pupils small, not quite circular, with
Argyll-Robertson phenomenon; no other ocular defect, and no
evidence of a spinal lesion. No history of syphilis.
Case XI.—K. S., aged forty-three. Pupils rather small, unequal,
quite destitute of light response, though moving freely in
convergence; no other ocular defect except some presbyopia;
no evidence of spinal disease, though left knee-jerk not easily
obtained. Unmarried; syphilis seems highly improbable.
Case XII.—G. G., aged sixty. Pupils small, with distinct
Argyll-Robertson phenomenon. Knee-jerks, not easily obtained,
but not definitely abnormal, and no other evidence of spinal disease.
Patient suffers from defective vision, probably from
tobacco poisoning (central scotoma for red); no history or
evidence of syphilis.
(b) Argyll-Robertson Phenomenon, with Other Ocular Disturbance Suggestive of Locomotor Ataxia.
Case XIII.—D. T., aged forty-two. Pupils below medium size,
243destitute of light response, with free movement in convergence;
had for seven days suffered from diplopia, and under observation
gradual development of complete paralysis of right external
rectus; no other ocular defect. Knee-jerks distinct, and no
suggestion of spinal disease; chancre of lip and secondary
syphilis nine years before.
(c) Argyll-Robertson Pupils, with More or Less Evidence of Spinal Disease.
Case XIV.—T. F., aged fifty-five. Right pupil 2mm., left
3 mm., each with Argyll-Robertson phenomenon; no other
ocular defect except presbyopia. Ten years ago had difficulty
in passing urine, and since then occasionally voids it involuntarily,
and for eighteen years has been liable to seizures of pain in calves,
insteps, and heels; knee-jerks normal, and no objective signs of
spinal disease. Venereal sore when aged twenty, but no secondary
symptoms, and father of six healthy children.
Case XV.—H. W., aged thirty-eight, is the subject of hypermetropia,
4.5 D. Pupils very small, especially left; neither
moves under light, but distinct contraction during convergence.
Admits recent difficulty in descending stairs, saying he “frequently
misses the bottom step,” and has suffered from
“sciatica” for two years. No objective evidence of spinal disease,
and urinary and sexual functions undisturbed. Admits
gonorrhea, but denies syphilis. Wife miscarried eight months
after marriage; no further pregnancies.
Case XVI.—R. S., aged forty-three. Hypermetropic and
presbyopic. Pupils small, unequal, not quite circular, and with
definite Argyll-Robertson phenomenon. Knee-jerks cannot be
obtained (confirmed on three different dates), but no other sign
or symptom of tabes dorsalis, unless “rheumatic pains” in lower
limbs for several years. Unmarried; no history of syphilis. Four
years ago had, after “catching cold,” to have urine withdrawn
by a catheter, but no subsequent disturbance of bladder function.
Case XVII.—E. W., aged forty-eight. Myosis with Argyll-Robertson
phenomenon; right ptosis and crossed diplopia (one
month), without obvious ocular paresis; absence of right knee-jerk
(confirmed on two occasions), and failure in retention power
of bladder (six months), but no other evidence of spinal disease;
vulvar sores and skin eruption six years before.
244
(a) Ocular Paralysis, without Other Evidence of Disease.
Case XVIII.—(By permission of Mr. J. T. James, F. R. C. S.)
F. D., aged thirty-seven. Dilated and immobile pupils, without
any other ocular defect. No evidence of spinal disease; syphilis
nine years ago; no change while under observation for three
years.
Case XIX.—K. K., aged twenty-eight. Iridoplegia, double,
followed by paralysis of left external rectus, the condition being
under observation for nearly a year, but without the discovery of
any satisfactory explanation. No evidence of spinal disease.
Married, four healthy children, no miscarriage; during one
pregnancy very free loss of hair (now grown again), but no other
occurrence to suggest syphilis. No family or personal history of
gout or rheumatism.
Case XX.—G. H., aged thirty-three. Dilated and immobile
pupils, with incomplete ptosis and divergence of eyeball on each
side. Present condition of four years’ duration, and separated
by an interval of three years from venereal sore and skin eruption.
No other ocular defect; no evidence of spinal disease, and general
health good throughout. No change while under observation
for three months.
(b) Ocular Paralysis, with Other Ocular Evidence Suggestive of Locomotor Ataxia.
Case XXI.—E. S., aged forty-three. Diplopia from paralysis
right external rectus, pupils small, each with Argyll-Robertson
phenomenon; visual left acuity only 6
12, and small but distinct
central scotoma, with some contraction of the peripheral field;
knee-jerks distinct, and no ataxia or other evidence of spinal disease.
Three early miscarriages, no full-time child. No change
while under observation for nine months, but on two occasions
severe attack of vomiting and abdominal pain, extending over
several days and without recognized cause (? gastric crises).
Case XXII.—A. M., aged fifty-five. Left ptosis and paralysis
of external ocular muscles supplied by third nerve in 1887, the
pupils being normal, followed by incomplete recovery. In 1897
development of identical condition on the right side, and pupils
found to be small and with Argyll-Robertson phenomenon;
245knee-jerks very slight and with great difficulty, but no other
evidence of spinal disease. No history of syphilis.
Case XXIII.—H. F., aged thirty-seven. Right ptosis with
diplopia (seven days) and defective inward excursion of right
eyeball; pupils very small, not quite equal, and with Argyll-Robertson
phenomenon; optic disks pale and marked contraction
of visual fields, but normal central vision; knee-jerks
scarcely to be obtained, but no other evidence of spinal disease.
No history of syphilis. Father of four healthy children. Seen
after a month’s interval, paralysis of all external right ocular
muscles supplied by third nerve, and knee-jerks absent.
(c) Ocular Paralysis, with More or Less Evidence of Spinal Disease.
Case XXIV.—G. S., aged forty-one. Ptosis and complete
ophthalmoplegia externa on left side, with dilated and immobile
pupils and some degree of right ptosis, these conditions or some
of them having been present for five years. Knee-jerks distinct,
and no ataxic phenomenon, but imperfect control over bladder,
and failure of sexual power during last six months. No admitted
syphilis.
Case XXV.—J. L., aged forty-two. Diplopia and drooping
left upper eyelid for four years. Ptosis left side, and marked
defect of ocular movements in each eye; left pupil dilated and
immobile; right small, contracts during convergence, but no light
response; no other ocular defect. Knee-jerk scarcely obtained
on either side; no ataxia, but attacks of “twitching pains” in
lower limbs, and for some time difficulty in starting the flow of
urine. Venereal sore in 1882, and subsequent loss of hair, but
no other secondary symptoms. Patient watched for twelve
months without appreciable change.
Case XXVI.—L. D., aged forty-four. Crossed diplopia (one
month), without obvious ocular paralysis, and pupils small with
Argyll-Robertson phenomenon. Knee-jerks absent; no ataxia
to usual test, but has noticed tendency to stagger in the dark; is
troubled with pains in the knees, has difficulty in commencing
the act of micturition, and recent marked failure of sexual
power; venereal sore at twenty years, and subsequent sore
throat, but no skin eruption or loss of hair. Father of three
healthy children.
Case XXVII.—J. H., aged forty-seven. Double vision of two
months’ duration; similar attack three years ago, with complete
246recovery. Paralysis of right external rectus; pupils, visual
acuity, and visual fields normal. Knee-jerks absent, but no other
evidence of spinal disease. Patient the subject of albuminuria,
and presents physical evidence of an aneurism of the ascending
aortic arch. Youngest child has marked evidence of inherited
syphilis.
Case XXVIII.—W. M., aged thirty-five. Paralysis of left third
nerve, without iridoplegia or cycloplegia; pupils normal. Knee-jerks
absent, but no ataxia or other evidence of spinal disease.
Several venereal sores ten years ago, but no recognized secondary
syphilis. There is, however, evidence of a former iritis.
Case XXIX.—M. C., aged fifty-four. Paralysis of left external
rectus, with history of two previous attacks of diplopia during
last four years; no other ocular defect, unless some imperfect
light response in left pupil; knee-jerks absent, and complaint of
“sciatica” for two years, but no other evidence of spinal disease.
Albuminuria distinct, and physical signs of hypertrophy of left
ventricle. No history of syphilis.
Case XXX.—(By permission of Mr. N. M. MacLehose, M.
B.) H. Y., aged thirty. Homonymous diplopia observed over a
period of six months without appreciable ocular paralysis;
pupils of medium size, with definite Argyll-Robertson phenomenon;
knee-jerks absent, and in later months decided ataxia
and sensory defects in lower limbs; visual acuity unaffected to
ordinary test, but gradual contraction of visual fields, especially
on right side; chancre and secondary syphilis four years before.
There are in these series of cases many facts which might reasonably
be made the subject of remarks, and several of the cases
are certainly of great individual interest. But they are here
displayed in the above grouping for the purpose of illustrating
the clinical order and sequence in which, as a matter of actual
experience, the ocular disturbances of locomotor ataxia may
manifest themselves in relation to the spinal evidences of that
disease. Of course, in those cases in which there exists only a
single ocular symptom unaccompanied by any sign of spinal disease,
it may be objected that it has yet to be demonstrated that
such cases are of the nature of locomotor ataxia. It is doubtless
to be desired that such cases should be under exact observation
as long as the opportunity for further developments exists—that
is, for the entire life of the patient. But to insist upon such a
247condition is a mere counsel of perfection. One must make reasonable
use of such evidence as the brevity of life and the exigencies
of practice permit. And the evidence here set forth
affords at least a very strong presumption, to say the least of it, of
the truth of the doctrines stated in the earlier paragraphs of this
paper. Probably the particular proposition which is most likely
to be contested is the one which places the Argyll-Robertson
pupil equally with optic-nerve atrophy, and an ocular paralysis,
as a possible first event in the eruption of the phenomena of
locomotor ataxia. But on turning to the records it will be found
that the facts support this suggestion almost as strongly as they
support the corresponding suggestion in reference to optic-nerve
atrophy and ocular paralysis. Attention in this respect may be
particularly given to Case XIII. The man complains of a quite
recent diplopia, and he has undoubtedly had syphilis; the pupils
show the Argyll-Robertson phenomenon. It is in the highest
degree probable that, had the patient been under observation a
week or two earlier, the condition of the pupils would have been
the sole existing ocular abnormality. Yet in the light of the
development of an ocular paralysis, it can scarcely be doubted
that, whether he develop spinal symptoms or not, his nervous
system is the site of diseased processes of the locomotor ataxia
order. When to these facts there are added, as in Cases XIV. to
XVII., illustrations of the various forms and degrees of evidence
of spinal disease that may be associated with the Argyll-Robertson
pupil, it seems impossible to resist the conclusions that the
condition of the pupil so named may be the first evidence of
locomotor ataxia; that it may precede by varying intervals other
evidences of the disease; and that at least very probably, in a
certain number of cases, the symptomatology of the disease may
be permanently restricted to this one event. In some examples
of its spinal form locomotor ataxia is undoubtedly an extremely
chronic disease, with few and imperfectly developed symptoms;
and it is thus not unnatural to expect that similar limitations
may obtain in the ocular manifestations of the disease. That
evidences of grave nervous disease may be limited to the pupil is
well seen in Case XVIII., where a syphilitic patient was under
observation for three years without the discovery of any abnormality
other than paresis of each sphincter iridis. There is certainly
no obvious reason why a similar restriction should not
248determine the Argyll-Robertson pupil as a purely isolated phenomenon
with, it must be added, the same unfortunate possibilities
that are undoubtedly attached to the patient whose case
has just been quoted. The conclusions above adopted in reference
to the Argyll-Robertson pupil are applicable, mutatis
mutandis, to optic-nerve atrophy and to ocular paralysis, as is
abundantly demonstrated in the corresponding series of the
cases recorded in this paper.
The following case seems to be worthy of record because of
the long duration of the symptoms and the immediate relief
ultimately obtained. Mrs. W. consulted me on August 4, 1899,
and gave the following history: Five years previously the right
eye was struck and “cut” by a cricket ball. Since that time
there had been pain exactly as if there was a foreign body under
the lid or embedded in the cornea. There was a pricking feeling
on winking, and the patient could not bear to have the upper lid
touched in its outer half. She could only obtain ease by keeping
the eyes closed and perfectly still, or wide open with the lids
motionless. On examination no foreign body could be seen, and
the lids were normal. In the lower outer quadrant of the cornea
careful observation showed that the epithelium was ruffled and
freely movable over a small area, and in part of the same area
was a tiny circular, slightly opaque, raised patch of the corneal
tissue. Nothing more could be made out. I prescribed a bandage
and some boric lotion with cocaine. Two months later, on
October 6, I again saw the patient, who was then in precisely
the same condition as before, and had been so during the two
months’ interval. She was in such misery that I decided to
adopt surgical measures at once. Accordingly, after instilling
cocaine, I carefully explored the painful area with a needle,
but could detect no foreign body. I then scraped the part
thoroughly with a sharp spoon, removing the epithelium for some
little distance around, and a fair amount of corneal tissue in the
affected area. The following day there was some smarting, but
the eye could be moved freely under the lid, and there was no
pain on pressure over the previously tender spot. Progress was
uninterrupted. The epithelium grew over the denuded surface,
249and no opacity resulted. The eye now is perfectly right and
the vision is normal.
I should have put the difficulty I had in making a diagnosis
down to my having overlooked some detail, had it not been that
the patient was for a considerable time under treatment at an eye
hospital. The explanation I am inclined to adopt, for want of a
better, is this, that the original blow caused the anterior elastic
lamina with the epithelium to become detached. The nutrition
of the epithelium might thus be kept up, and every movement
which pressed upon the surface would bring the detached membrane
down on the corneal nerve filaments. But it must be
confessed it is not easy to understand how this condition could
remain stationary for five years.
The author thinks iodide of stannum often preferable to stannum
in tuberculosis. He uses it when the patient has a clear
complexion and long eyelashes and where the progress of the disease
is rapid. He reports a case for which the 2x trituration
was given, in which there was “a marked tubercular affection
of the chest, increased vocal fremitus, an abundance of thick
yellow and sweetish sputum, sweat at night, and rapid emaciation.”
The result was encouraging.
The enumeration and exact description of these prodromal
symptoms are so important that we copy them in full.
The following, which is a translation of an article by Monsarrat
of Paris (Rev. Hebdom. Laryngol., d’Otol., et de Rhinol., No.
43, October 28, 1899), covers the ground so thoroughly that it is
worthy of repetition:
“Laryngeal phthisis completely developed presents multiple
and varied symptoms, some more characteristic than others. In
one patient are found symptoms functionally grave, out of proportion
to the lesions relatively benign. In another, physical signs
take first place; there may be an ulceration completely obliterating
one cord, or considerable œdema of the arytenoids and
vestibule, which closes the opening of the glottis. Having
250reached the period when tuberculosis is easily recognized, the
various patients are able to date their laryngitis from diverse
pathologic beginnings. This one will present solely the history
of a cough, the other a raucous voice, in another pain will take
precedence. In mentioning these various modes of commencement
we insist on the connection which may exist between each
of them and the localization at the beginning of tuberculosis, on
one or the other parts of that complex organ known as the larynx.
Let us divide the symptoms into the functional and the laryngoscopic.
The connection or antithesis between them will be
noticed.
“An initial symptom, quite frequent in tubercular laryngitis, is,
without a doubt, cough. This symptom, common to all maladies
of the respiratory tract, would have no diagnostic value, except
that it is characteristic. On it alone the diagnosis of laryngeal
phthisis could never be based. At the beginning, cough puts us
on our guard, especially when it is causeless; that is to say, when
auscultation of the chest fails to reveal anything abnormal. This
cough is always persistent, sometimes violent, hawking, and
provoking.
“The physical signs of the chest do not correspond to the
tenacity of the cough; it is therefore possible for the larynx to be
accused. As regards this cough, the ‘hemming’ so often described,
and which draws attention most often to a possible
rhinopharyngitis, may cause us to think at the beginning of
tuberculosis, but only after examination of the rhinopharynx has
established its integrity. There is a cough, well known at the
beginning of tubercular laryngitis, a little dry cough, commencing
insidiously, often at the moment when the patient is about to
speak, which the individual himself does not notice, but to which
his friends attach an importance too often justified by the outcome.
The cough may be hacking, followed or not by expectoration,
and often accompanied by vomiting. It is certainly
right to consider it as a symptom of the beginning of the disease.
“The speaking voice is often altered, dysphonia appears, and
the patient who is attacked presents little alteration in his larynx;
no ulceration, the cords accurately approximate, and they are
very slightly congested; the laryngeal image does not reveal anything
by which this profound alteration in the voice can be
explained. There is no cough. There will come a time in the
251disease, however, which will cause us to see that this, too, is an
initial form, and oblige us to give a prognosis exceedingly
guarded.
“The voice may be eunuchoid. Castex has noted it among
the tuberculous. The raucosity of the voice should also recall
the statistics which demonstrate the fact that a fifth of the cases
of this condition are tubercular. But these three symptoms,
dysphonia, raucosity, eunuchoid voice, are also found in other
maladies of the larynx; conditions, however, easily diagnosticated
by the laryngoscope. If nothing justifies these affections of the
voice, one should think of tuberculosis. It is these initial forms,
apparently paradoxical, but analogous to that, which we are going
to mention under the subject of pulmonary lesion not sufficient to
provoke cough in the beginning if the larynx has not been initially
affected. The forms that are recognized in the mirror are
evidently very numerous. We will mention some: Congestion of
the cords, monocorditis, recurrent laryngitis, and a nodular form
at the free border of the vocal cords. We do not take into consideration
any variety of ulceration, no matter how insignificant,
as for the most part the velvety aspect of the cords leads us to
think at once of laryngeal phthisis. But this has not appeared at
the beginning, and we are only considering initial forms. The
symptoms which we are attempting to describe are those suggestive
of tuberculosis, and we only say that tuberculosis of the
larynx may begin by a nodule, by a congestion, by a monocorditis,
etc.
“Congestion of the vocal cords, whose ætiology is difficult to
explain, often coincides with slight dysphonia, with cough. This
congestion, fugacious, if not tuberculous, disappears with rest, if
it is not aggravated by a chronic rhinopharyngitis. In the majority
of cases the patient returns. Despite a treatment, properly
instituted, the congestion persists; it extends on the cords; it may
remain there, or it may reach over the ventricular bands to the
arytenoidal apophyses; this is a form of commencing laryngeal
phthisis, especially if, after a period of calm, there is found in a
patient a new congestion. It is recurrent laryngitis, another form
of initial tuberculosis more grave than the first. Against laryngitis
of this form treatment is of no avail.
“Another variety of initial tuberculosis is monocorditis. The
patient becomes suddenly aphonic; laryngoscopic examination
252shows a cord perfectly red, congestion of which is evident, not
only by the color, but by its altered volume. Contrast with the
sound cord is often striking. Movements of the affected cord
may be observed, but it is generally paretic. Acute monocorditis
should cause us to think that it is an initial form of tuberculosis.
This monocorditis often corresponds to the side of the lungs
which is afterward or at that time attacked by the bacillus. Certain
authors admit that this relation is absolutely constant, and
their statistics allow no exception to the rule. On the other
hand, Bayle’s theory, setting forth the direct penetration of the
tubercular infection, becomes less often justified. It is the
lymphatic route which most often produces bacillary infection.
“Tubercular laryngitis may often begin by a nodule situated
on the border of the vocal cords. It is important not to confound
it with singers’ nodules, these latter being more conical and more
rounded. The tuberculous nodule may grow slowly, not ulcerate
for a long time; interfering so little with the speaking voice that
the patient often refuses any intervention. But the day comes
when we see this nodule desquamate, and we may observe the
evolution of the tuberculous ulceration which displaces it. We
make no mention of the other forms of commencement characterized
by a congestion of the entire organ, by œdema of the epiglottis,
by a lividity quite characteristic which invades the entire
endolaryngeal mucosa, forms most usual for the tubercular
involvement of the larynx. A form especially noticeable is that
which begins with a sensation of a lump in the throat. It is true
that this variety is not observed except in the nervous; it is not,
however, to be compared to the globus hystericus. Tuberculous
patients, in whom the tuberculous process in the larynx begins
with a sensation of a lump in the throat, may be in very good
health, but this particular impression is often the first symptom
which they observe in a laryngitis, which finally becomes tuberculous.
At the moment when the patient complains of this
symptom it may happen that laryngoscopic examination fails to
detect any lesion. It is useless to add that this form is especially
met with in the female. It most nearly resembles that form that
begins with a dysphagia that persists to the end; but at the beginning
of tubercular laryngitis this dysphagia alone is noted without
any other symptoms.” So it can be seen that laryngeal phthisis
may begin by a variety of symptoms, some common, the others
253rare. It is needless to insist upon the importance of an early
diagnosis.
Palmer.
I propose to consider the surgery of the cervical portion of
the great sympathetic nerve in certain ocular diseases. European
oculists and surgeons have performed sympathectomy for
glaucoma and exophthalmic goiter. I have gone further, and in
one instance removed the superior cervical ganglion for simple
atrophy of the optic nerve. I have performed sympathectomy
four times up to July 20, 1899. First the cases will be reported;
then the conclusions will be drawn.
Mrs. B. S., aged thirty-six, has had pain in and around the right
eye for two months, and examination showed vision in this eye
reduced to light perception; tension + 3, and the pupil widely
dilated. The anterior chamber was shallow, the cornea cloudy
and slightly anæsthetic, the media slightly cloudy, still allowing
the fundus to be seen. The episcleral vessels were enlarged.
Circumcorneal injection was present and the optic nerve cupped.
A diagnosis of chronic irritative glaucoma was made. The left
eye presents immature cataract, and vision in this eye is 20/70.
Knowing of the flattering results obtained by Jonnesco and
others, by excision of the superior cervical ganglion in absolute
glaucoma, I explained the operation to the patient, and
obtained permission to operate. On May 15, 1899, the patient
was anæsthetized, chloroform being employed. An incision four
inches in length was made on the right side downward from the
mastoid process, extending along the posterior border of the
sterno-cleido-mastoid muscle. The external jugular vein was cut
and tied. The sterno-cleido-mastoid was then separated from
the trapezius muscle, and the spinal accessory nerve was cut. A
deep dissection was then made, exposing the carotid sheath.
This was opened to enable us to locate the pneumogastric nerve
beyond question. The carotid, internal jugular vein, and pneumogastric
nerve were then pulled forward, enabling us to see the
rectus capitis anticus major muscle, on which the superior cervical
254ganglion rests. Tearing through the fascia, the ganglion was
found and stripped. The ganglion was then cut high up with
curved scissors and all its branches severed. About one inch of
the trunk of the sympathetic below the ganglion was removed.
The wound was closed with interrupted sutures and the neck
placed in a plaster cast. The time required for operation was
fifteen minutes, and immediately after it was noticed that the
right eye was suffused with tears, the right conjunctiva much
injected, and the right nostril moist. The intra-ocular tension
was + 2. The patient slept well all night, without medicine,
being free from pain for the first time in over two months. Tension
had steadily decreased to + 1.
On May 16, slight ptosis was noticed on the right side. This
symptom is yet present. On May 19 the circumcorneal injection
was much less; the conjunctival hyperæmia and lachrymation were
still present, while the ptosis was slightly increased and tension
was + 1.
At the present date—July 23, 1899—this patient has no pain.
The retinal arteries are increased in size. Tension is + 1.
Vision has increased from light perception to ability to count
fingers at three feet. The conjunctival injection which followed
the operation has disappeared; the optic nerve has a color more
approaching the normal. The ptosis is less.
This was the first sympathectomy made in America for
glaucoma.
Miss M. E., a German, aged forty-three, was sent to me on
June 14, 1899. For two years sight had been failing, until at this
time vision was as follows: R. E. = 0; L. E = light perception.
Tension was + 3. Both optic nerves showed marked cupping of
the disk; the vessels were pushed to the nasal side. She stated
that she had never had pain in the eyes, and had not consulted
an ophthalmic surgeon.
I advised her to submit to an excision of the left superior cervical
ganglion; she consented, and on June 15 the operation was
performed by myself, assisted by Dr. E. C. Renaud, at St.
Joseph’s Sanatorium, in the presence of Drs. J. C. Murphy, A. R.
Kieffer, and S. A. Grantham. The operation was difficult, owing
to the abnormal position of the vagus nerve. This was outside
255of and external to the carotid sheath, and was much smaller than
normal; it was not larger in diameter than the head of a pin. It
was identified by irritating it and watching the effect on the heart.
The superior cervical ganglion was removed and one-half inch of
the trunk of the sympathetic below. Shortly after the operation
there were lachrymation, ocular congestion, and contraction of the
pupil on the corresponding side. On the second day she counted
fingers at 2½, and on the third at 3½ feet. Slight ptosis was
present.
She left the hospital on the eighth day. At this time she counted
fingers at four feet. There was only slight, if any, reduction of
tension during the eight days she was in the hospital. In counting
fingers she saw with the nasal side of the retina—temporal
field. I did not see her again until June 30, and she was then
counting fingers at five feet. Tension on that day was normal.
She had light perception in the right eye.
On July 16 I excised the right superior cervical ganglion without
difficulty, and on July 7 she counted fingers at seven feet
with the left eye, and could see the hand at four inches with the
right. I examined her on July 20, when vision remained the
same, the tension of the right eye was + 1, and of the left + 2.
She was well pleased to have the small amount of vision she
possessed.
T. J., aged forty-six, an inmate of the St. Louis City Hospital,
a laborer, was admitted on account of blindness. There was no
history of syphilis, rheumatism, nor any systemic disease. The
patient was of limited mentality. No history of his family could
be obtained. He claimed to have had good health all his life, with
the exception of an attack of malarial fever several years ago.
The patient had been a moderate drinker of alcoholic beverages.
In appearance he was robust, and he complained only of loss of
vision which, in the left eye, had been failing for eleven months,
in the right for seventeen weeks, according to his statement.
Until seventeen weeks before this he could see enough with the
right eye to get around. Since then vision had steadily declined
until he had light perception only—and this only apparent when
light was concentrated on the eye by the ophthalmoscopic
mirror. Vision of the left eye = 0.
256The pupils were widely dilated. The ophthalmoscope showed,
in the right eye, a white disk, particularly on the temporal side;
the arteries slightly reduced in caliber, veins normal. There
was shallow, atrophic cupping of the nerve head. The retina
and choroid were normal, the vitreous and lens clear. The left
eye showed a disk of a dead white color throughout the whole
area, arteries very small, atrophic excavation pronounced, veins
reduced in caliber, and choroid normal. The macula was not
visible in this eye, owing to the much-reduced blood-supply.
The vitreous and lens were clear. Vision was as follows:
R. E. = perception of concentrated light. L. E. = 0.
Diagnosis.—R. E. = optic-nerve atrophy. L. E. = complete
atrophy of optic nerve and retina.
Treatment: Resection of the right superior cervical ganglion
of the sympathetic was done. The operation was followed by
conjunctival congestion, lachrymation and contraction of the
pupil, slight ptosis and hypotonia.
No appreciable change in the patient’s vision followed, and
ophthalmoscopic examination made two weeks after operation
showed no change in the appearance of the fundus, except that a
cilioretinal artery in the upper part of the disk had doubled in
caliber.
So far as I know, Case III. is the first instance in the history
of medicine of an excision of the superior cervical ganglion, or
of any part of the sympathetic system, for the relief of optic-nerve
atrophy. Although the operation was not of benefit in this
particular instance, yet I am not willing to concede that it will
prove valueless in cases of non-inflammatory atrophy in which
vision is not entirely lost. In truth, I expect it to prove
beneficial in such cases, sufficiently often to justify the procedure.
I was led to make this experimental operation for several
reasons: 1. The use of glonoin is often followed by an improvement
in vision in cases of simple atrophy of the optic nerve.
2. Glonoin enlarges the retinal vessels, as has been proved by
ophthalmoscopic examination. 3. There is no question that in
glaucoma simplex—a disease in which there is an atrophy of the
optic nerve—improvement in vision follows sympathectomy. 4.
Excision of the cervical sympathetic is followed by an increase
in the blood-supply of the orbital contents.
257
The microscopic examination of three of the excised ganglia
was made by my friend, Dr. Carl Fisch, of St. Louis. The
specimens were those from Cases I., II., and III. Of the two
ganglia removed from Case II. only the first one—the left—was
examined.
Transverse and longitudinal sections of the three specimens
were studied microscopically, by means of a great number of
different staining methods. Owing to the method by which the
ganglia had been preserved—weak formalin solution—the
employment of the Golgi—Marchi—and the more delicate Nissl
stains was rendered impossible. In general it may be said that
the pathologic changes found were the same in the three cases,
although a little less pronounced in No. 2 than in 1 and 3.
Most striking of all was a very marked hyperplasia of the
connective tissue, which in some places resulted in dividing up
the ganglion into small groups of nervous elements separated by
broad bands of fibrous elements. The walls of the vascular
structures showed decided sclerosis; the connective-tissue
sheaths of the ganglionic cells were much increased in thickness.
In Case I. small foci of round-cell infiltration were seen in this
hyperplastic growth, of an inflammatory character. No plasma
nor mast cells could be demonstrated.
The ganglionic cells were markedly pigmented. Together
with a number of cells normal to all appearance there were great
numbers showing different stages of degeneration. As a rule
the nucleus, besides having lost part of its peculiar staining
property, had assumed the parietal position; the nucleus was
reduced in size or even missing in a large percentage of the cells.
While in some cells the chromatic elements were well preserved,
in others the process of chromatorhexis and chromatolysis could
be followed up through all of its stages. Only comparatively
few cells were seen showing the normal dendriform processes;
very often the processes were short, ending bluntly, or they had
even disappeared altogether. The general peripheral network of
processes was much reduced in volume and compressed by the
pressure of the connective-tissue formation. Only very few
medullated fibers were seen. Unfortunately it was impossible
to study their structure with the Marchi method.
The general pathologic aspect was that of a decided sclerosis,
258originating in inflammatory processes going on in, and starting
out from, the walls of the vascular structures. The changes of
the nervous elements were most likely not idiopathic, but due to
pressure and inhibited nutrition.
The plates accompanying this paper have been made from
drawings of sections of superior cervical ganglia.
The ordinary precautions for surgical cleanliness are to be
observed, and general anæsthesia employed. The incision
should be made along the posterior border of the sterno-cleidomastoid
muscle, starting at the mastoid process and running
downward to within an inch of the clavicle. The sternomastoid
is separated from the adjacent muscles, the spinal accessory
nerve cut, and the carotid sheath reached. This dissection is
made with the fingers. The carotid sheath should always be
opened in order to locate the pneumogastric nerve. I consider
this very important because: 1. The nerve is sometimes outside
the sheath, as happened in my second case, in which the pneumogastric
was much atrophied and was external to the sheath. 2.
Differentiation of the cervical sympathetic from the vagus is
sometimes difficult. Often, in operating on the cadaver, I have
found both nerves inclosed in the same fascia. It is needless to
say that excision of the vagus instead of the sympathetic would
not only defeat the object of the operation, but would add a
serious complication. Differentiation of these nerves after opening
the carotid sheath is not usually difficult, for in working
upward the operator comes upon the ganglionic expansion of the
sympathetic. The ganglion is seized with forceps and stripped.
Its branches are cut first, then the cord passing below is severed,
and lastly the ganglion is cut above, as high as possible. It is
best to use curved scissors and to have the finger under the
ganglion while traction is made, thus cutting on the finger and
avoiding injury to the underlying structures.
If the middle ganglion is to be removed, it will be best to
excise it first and then work upward. If the entire chain of the
sympathetic is to be removed, as is done for epilepsy, and as is
now advised in exophthalmic goiter by Jonnesco, the operation
is one of great difficulty, owing to the location of the inferior
ganglion. This is situated near the neck of the first rib. One of
my friends, who is a skillful surgeon, in removing this ganglion
259ruptured the vertebral artery near its origin and was obliged to
tie the subclavian to check the hemorrhage. After the latter has
ceased the wound is closed with superficial sutures. The
hemorrhage in removal of the superior ganglion is usually
trifling, only a few small vessels being cut. The external
jugular vein was cut in my first case, but not in the others. The
patient leaves the hospital on the eighth or ninth day.
Jonnesco’s method, according to his latest communication on
the subject, is different. He always employs the premastoid
route where only the superior ganglion is to be removed, reserving
the postmastoid for the excision of the entire chain. The
carotid sheath is split, the internal jugular vein and sternomastoid
drawn outward by a retractor; a second retractor draws the
vagus and internal carotid inward. In the space made the
superior ganglion is found. The deep vertebral fascia is opened,
all the branches of the ganglion isolated and cut by blunt, curved
scissors; when this has been done the ganglion is attached only
by nerve strands above, a strong pull is made, and the ganglion
gives way. The excision is then completed by cutting the
inferior strands. In closing the wound, he uses both deep and
superficial sutures.
He mentions a transient dysphagia and pain in the cranio-mandibular
joint as occurring after this operation.
The effects of removal of this ganglion are immediate and
remote: The immediate are relief of pain, lachrymation and
conjunctival injection, together with a discharge from the
corresponding nostril, unilateral sweating, and contraction of
the pupil. Often there is an immediate reduction in intra-ocular
tension. These effects are noted within five minutes after the
excision.
The remote effects are ptosis, which appears on the third or
fourth day, improvement of vision, and in some instances a tardy
contraction of the pupil and a tardy reduction of the intra-ocular
tension. To these there must also be added a slight sinking of
the eyeball into the orbit, and a feeling of heaviness in the head.
What I have just written applies particularly to cases of
glaucoma.
In exophthalmic goiter, after the excision of the ganglia, the
260exophthalmus and tachycardia are said to improve almost
immediately and a reduction of the goiter soon follows.
Although Jonnesco speaks of the immediate reduction of the
intra-ocular tension, yet this does not always occur. In my
second case, at the end of eight days the tension was + 2. On
the sixteenth day the tension was normal. In my first case
reduction of the tension was immediate. The relief from pain
in the first case was immediate and lasting. This patient had
not been free from pain for two months previously. The slight
ptosis following sympathectomy is to be attributed to paralysis
of Müller’s muscle. Sinking of the eyeball is no doubt due to
paralysis of the unstriped peribulbar fibers found in Tenon’s
capsule. Contraction of the pupil is usually an immediate
result; it may, however, appear tardily. Thus in my first case
the pupil was unchanged until the fourth day after the operation;
and it did not become at any time as markedly contracted
as in the other two patients. In the third case—that of optic-nerve
atrophy—the pupil was markedly contracted within five
minutes after the excision.
The lachrymation, conjunctival injection, and nasal moisture
are transient symptoms which are usually absent after the first
day.
In this connection it is interesting to note that Mr. Jonathan
Hutchinson, as early as 1866, recognized many of the ocular
symptoms of paralysis of the cervical sympathetic, and wrote a
paper thereon.
This is a question difficult to answer—difficult for the reason
that we are not sufficiently acquainted with the physiology of
the production of aqueous humor under normal surroundings.
Panas and Duvigneaud have assumed rightfully that “If the
nervous mechanism of intra-ocular secretion or, to speak without
hypothesis, the action of the nervous system on intra-ocular
tension can be known, the pathology of glaucoma will be cleared
up, iridectomy will be explained, and perhaps a new and scientific
basis for the treatment of glaucoma will be established.”
Many observers have sought to solve the problem. Donders
attributed the hypertension to a neuro-secretory cause and believed
261the trigeminus to be the agent of excessive secretion. He
held that section of the trigeminus should relieve intra-ocular
tension, while section of the cervical sympathetic could have no
particular influence.
His views were overthrown by experiments made by Wegner
in 1866, on rabbits. By means of manometers placed in the
anterior chamber, he sought to record variations in the intraocular
tension. He proved to his own satisfaction that the
trigeminus takes no part, while section of the cervical sympathetic
produces hypotonia, and irritation of its upper end and causes
hypertonia. He held that section of the cervical sympathetic
enlarges the blood vessels of the eye; the blood then flows
under reduced pressure, and intra-ocular secretion is lessened.
Almost identical results were obtained by Adamück—1866‒68—who
experimented on cats.
Von Hippel and Gruenhagen believed that the cervical sympathetic
contains vasoconstrictor fibers for the eye. Their
experiments were made on cats and dogs. They found that
irritation of the upper end of the cervical sympathetic causes in
the cat hypertonia, while its extirpation increases intra-ocular
tension. While, according to Wegner, the hypertonic action
proceeds from the enlargement of vessels caused by cutting the
cervical sympathetic, and the contraction of the blood vessels
caused by the irritation of the nerve causes a hypertonic action,
the contrary view is held by Adamück, Von Hippel, and Gruenhagen.
However this may be, there is no doubt that the trigeminus
plays no great part in the production of ocular tension. Furthermore,
the inefficiency of Bedal’s operation—stretching the nasal
nerve—is explained by the fact that it is the cervical sympathetic,
and not the trigeminus, which influences intra-ocular tension.
Jonnesco believes that the ocular sympathetic fibers from the
brain and spinal cord pass through the superior cervical ganglion;
permanent or intermittent irritation of these is accompanied by
dilatation of the pupil, narrowing of the small intra-ocular
arteries, contraction of the peribulbar muscular fibers, and probably
an increased action of the elements which produce the
aqueous humor. “As a matter of fact,” says Jonnesco, “any
increase of the blood pressure will produce a permanent or intermittent
narrowing of the arteries and cause the extravasation
262and increase in aqueous humor; then it is probable, although
not definitely settled, that a permanent or intermittent irritation
of the excito-secretory fibers is followed by an increase in the
secretion of aqueous humor; the permanent or intermittent
dilatation of the pupil pushes the iris into the iris-angle, closes
the canals of the filtration zone, and hinders or prolongs the
exit of aqueous humor from the eye; the permanent or intermittent
contraction of the unstriped peribulbar muscular fibers
closes the efferent veins of the eyeball, and hinders the venous
circulation of the eye—hence the dilatation of the intra-ocular
veins.”
He holds that excision of the superior cervical ganglion
destroys all vasoconstrictor fibers of the eye. The arteries relax,
the blood pressure is lowered, and extravasation is reduced.
This operation destroys the excito-secretory fibers, thus limiting
the amount of aqueous produced. The fibers which dilate the
iris are destroyed, hence the contraction of the pupil reopens
the iris-angle and removes the obstacle to the outflow of aqueous.
The nerve-fibers supplying the unstriped muscular apparatus
contained in Tenon’s capsule are destroyed, hence the pressure
on the efferent veins is removed and ocular circulation is reestablished.
Jonnesco believes that the starting-point of the nervous
derangement producing glaucoma is central: “When one removes
the ganglion the point of origin of the influence will not
be removed, but the communication between this center and the
eyeball is destroyed.”
Regardless of the differing views of physiologists concerning
the mechanism of the reduction of ocular tension, based on
experiments made on the lower animals, there can be no difference
of opinion concerning the effect of excision of the superior
cervical ganglion in the human subject. The operations made
by Jonnesco and others on the Continent, and by myself in
America, prove that removal of the superior cervical ganglion
causes a marked reduction of intra-ocular tension in glaucomatous
cases. That the same effect occurs in eyes with normal
tension is evident from my third operation—that done for
optic-nerve atrophy.
Up to the present time excision of the cervical sympathetic
263has been performed for the following diseases: epilepsy, exophthalmic
goiter, glaucoma, and optic-nerve atrophy. The question
naturally arises: How extensive an operation is necessary
in these affections? This I will attempt to answer:
In epilepsy it is necessary to excise the entire cervical chain
on both sides for the reason that, according to Jonnesco’s theory,
it is necessary to convert a state of cerebral anæmia—which he
assumes is the condition in epilepsy—into one of cerebral
hyperæmia. Since the carotid plexus is formed by branches
from the superior ganglion, and the vertebral plexus arises from
branches which have their origin in the inferior cervical ganglion,
it is evident that the entire cervical sympathetic must be removed.
In exophthalmic goiter, although Jonnesco in his first operation
excised only the superior and middle ganglia, he now
believes it necessary to remove the inferior as well, for this
reason: from the superior ganglion the ocular fibers arise;
from the inferior the vasodilator, cardiac-accelerator, and, probably,
the secretory nerves of the thyroid gland. If eye, thyroid,
and cardiac symptoms are to be relieved the entire chain must
be excised.
In glaucoma removal of the superior ganglion alone is necessary.
All of the sympathetic fibers of the eye, with the exception
of those which pass directly from the cerebrum by way of
the trigeminus, are connected with the superior ganglion.
In optic-nerve atrophy, if it should be proved that noninflammatory
atrophy of the optic nerve can be improved by
sympathectomy, removal of the superior ganglion alone will be
necessary, for reasons already given.
If the glaucoma is unilateral, it is necessary to remove only
the corresponding ganglion.
In 1889 Alexander of Edinburgh resected the superior
ganglion on both sides. In 1892 Jacksh resected the vertebral
plexus and cut the cord connecting the middle and inferior
ganglion. The third operator was Kummel, who excised the
superior ganglion on one side only. In 1893 Bojdanik made a
bilateral resection of the middle ganglion. In 1896 Jaboulay
made a bilateral section of the sympathetic cord, above and
below the middle ganglion. These operations were all made for
epilepsy.
264In regard to exophthalmic goiter, Jaboulay made a simple
section of the sympathetic early in 1896. In September of the
same year Jonnesco excised the superior and middle ganglia.
Jonnesco was the first, in 1896, to do a bilateral resection of all
three cervical ganglia, though it is claimed by a Polish surgeon,
Baracz, that he proposed the same in 1893. To Professor
Jonnesco furthermore belongs the credit of having first excised
the superior ganglion for glaucoma in September, 1897.
Ball of St. Louis was the first to remove the superior cervical
ganglion for optic-nerve atrophy. The date of this operation was
June 24, 1899.
Terrier, Guillemain, and Malherbe, in their “Chirurgie du
Cou,” 1898, were among the first to give the surgery of the
sympathetic a place in a text-book.
Among those who have operated on the cervical sympathetic
for the relief either of glaucoma or exophthalmic goiter, or both,
are Abadie, Réclus, Gerard-Marchant, Chauffand and Quénu,
Jeunet, Bled, Ball, Renaud, and Bartlett.
Panas is opposed to sympathectomy in glaucoma. He reports
seeing a patient in whom, three months after the operation,
vision was still declining.
François-Frank, at a meeting of the Paris Academy of Medicine,
held May 22, 1899, spoke of the effect of sympathectomy
on the circulation of the thyroid gland, brain, and eyes, and on
the heart. He believes that the operation can easily produce good
results.
Doyon has described the trophic changes produced in the
rabbit by excision of the cervical sympathetic.
From a study of the cases of sympathectomy made by Jonnesco
and others, and from the observation of my own cases, I offer
these conclusions:
1. Excision of the superior cervical ganglion is a most valuable
procedure in glaucoma.
2. It is of more value in glaucoma simplex than in inflammatory
glaucoma.
3. In inflammatory glaucoma, on which iridectomy has been
done without benefit, excision of the superior cervical ganglion
should certainly be tried.
2654. In cases of absolute glaucoma with pain, sympathectomy is
to be tried before resorting to any operation on the eyeball.
5. In cases of simple optic-nerve atrophy, sympathectomy may
possibly be beneficial if done before vision is entirely lost.
6. In cases of exophthalmic goiter, which do not improve
under hygienic medicinal and electric treatment, excision of the
cervical sympathetic on both sides is to be advised.
7. In unilateral glaucoma excision of the sympathetic ganglion
is to be done only on the corresponding side.
8. In the hands of a careful operator, excision of the superior
and middle ganglia is a safe operation, but removal of the inferior
ganglion can be done safely only by the most skillful surgeons.
9. The postmastoid route is to be preferred in excision of any
part, or all of the cervical sympathetic.
10. The fact that glaucoma is improved by sympathectomy
and the finding of pathologic changes in the excised ganglia
suggest the conclusion that this affection is due either to a permanent
irritation of the cervical sympathetic, or to an irritation
located elsewhere and transmitted by means of the cervical
sympathetic.
I wish to extend my thanks to Drs. E. C. Renaud and Willard
Bartlett for valuable assistance in the preparation of this paper;
to Dr. Carl Fisch for the pathologic report.
Case shown at the Lar. Soc. of London:
A woman, æt. thirty-one years, had suffered several years with
discomfort in nose, throat, and mouth, with dyspepsia. Mucosa
of nares and pharynx markedly atrophied. Atrophied condition
made post-rhinoscopy easy. “The eustachian eminences were
seen to be enormous, filling the fossæ of Rosenmüller, and reaching
nearly to the pharyngeal roof. Just behind the upper edges
of the choanæ, on each side, there appeared a transverse elliptical
opening, which was about half an inch long and a fifth of an
inch across at the widest part on the left side, and slightly less in
each dimension on the right; a probe apparently extends about
a quarter of an inch into the cavity.” In the discussion following
some thought them to be small recesses formed by cicatricial
266tissues, other formed by peculiar distribution of adenoid tissue,
and still genuine sinuses.
We ascertain by interrogation, (a) if the discharge is purulent or
muco-purulent; (b) whether it is unilateral or bilateral; (c)
whether it is continuous, intermittent, or influenced by change of
posture; (d) if there is offensive smell perceived by the patient or
by others; (e) pain is not usually complained of unless there is
obstruction to drainage, and consequently retention of pus under
pressure. Unilateral discharge suggests a foreign body in a child
or sinus involvement in an adult. If it is intermittent or influenced
by position probably originates in a sinus. Subjective fetor
suggests sinusitis; while objective fetor, ozena; and combined
subjective and objective is the rule in syphilitic necrosis. Location
of pain is of very little, if any, use in diagnosis.
Rhinoscopy.—Attention directed to (a) situation of the pus; (b)
polypi; (c) atrophy of the mucous membrane; (d) crusts; (e)
ulcerations; (f) adenoids; (g) nasal obstruction; (h) foreign
bodies. Under (a) beside usual cleansing of nasal cavities and reexamination
to ascertain situation, he recommends “tamponading,”
i. e., by blocking up first one part, then another, with
pledgets of wool, and noticing whence the discharge reappears.
(e) Ulceration may be syphilitic, simple, tubercular, or lupoid in
origin. “It must not be forgotten that a perforation” of the
septum “may be entirely the work of a misused finger-nail.”
(g) The normal mucoid discharge damned up by nasal obstruction
frequently becomes purulent.
Special methods of diagnosis as follows are mentioned:
transillumination; examination of upper teeth; catheterization
of the ostium, maxillares, naso-frontal canal, and outlet of the
sphenoidal sinuses; external examination of antrum and frontal
sinuses; exploratory puncture of the antrum through the inferior
meatus, alveolar process, or canine fossa. Diagnosis of ethmoiditis
is principally by exclusion.
Treatment of the accessory sinuses may be summed up
under the following indications: (a) removal of the cause; (b)
267evacuation and drainage of pus; (c) antiseptic irrigation; (d)
removal of morbid material, when present. PALMER.
The detection of optic neuritis is of the greatest importance in
the diagnosis of cerebral affections. Nevertheless, in certain
cases of double optic neuritis with headache considerable caution
is necessary before coming to a conclusion as to the exact nature
of the disease. Though these two symptoms are present in the
majority of cases of brain tumor and are so frequently due to
this cause they are also met with in other diseases. In some
cases of granular kidney, for example, the patient comes under
treatment for headache and failure of vision; and ophthalmoscopic
examination may reveal intense optic neuritis like that
of cerebral tumor (neuritic form of albuminuric retinitis). At
first the symptoms appear to indicate cerebral tumor, but a careful
examination of the urine and cardio-vascular system will
clearly reveal the cause. Limited space does not permit an
enumeration of all the causes of double optic neuritis with headache.
The results of the examination of one hundred cases
presenting these two symptoms reveal, however, several points
of interest. Most of these cases have been seen by us conjointly;
some were seen separately, whilst others (in Groups I. to VIII.)
were examined by one of us (R. T. W.) whilst holding the post
of medical registrar at the Manchester Royal Infirmary. For
permission to include the latter amongst our cases we are
indebted to the medical board of that hospital.
With respect to the diagnosis and termination these one hundred
cases may be grouped as follows:
I. Brain tumor, verified by necropsy, 27.
II. Cases terminating fatally; probably, majority due to brain
tumor; but no necropsy obtained, 27.
III. General symptoms of brain tumor; but necropsy revealed
distention of the ventricles of the brain with fluid; no tumor
(serous meningitis of ventricles), 2.
IV. Cerebral abscess (fatal), 3.
V. Tuberculous meningitis (fatal), 2.
268VI. Chronic interstitial nephritis; neuritic form of albuminuric
retinitis (fatal), 3.
VII. Toxic conditions and blood diseases:
Chronic lead poisoning, 3.
Ulcerative endocarditis, (fatal), 1.
Purpura hemorrhagica (fatal), 1.
Henoch’s purpura (fatal), 1.
Chlorosis with cerebral symptoms (recovery), 3.
VIII. Headache and double optic neuritis (without localizing
symptoms); probably syphilitic (recovery, with blindness, 2;
with impaired vision, 4), 6.
IX. Headache and double optic neuritis (without localizing
symptoms); no evidence of syphilis; duration six and two and a
quarter years, respectively. Termination still uncertain, 2.
X. Headache and double optic neuritis (without localizing
symptoms); no evidence of syphilis; recovery with blindness, 8;
with impaired vision, 3; with good vision, 8, 19.
The following are brief abstracts of the notes of the cases in
Group X. which have come under our observation and which we
have followed for a considerable period of time. The number
of years during which each case has been followed is given in
parentheses after the brief note.
1. A boy, aged ten years. Double optic neuritis, headache,
and vomiting; slight internal strabismus of the left eye. Recovery
with normal vision. (Seven years.)
2. A young woman, aged seventeen years. Headache, vomiting,
and double optic neuritis. Recovery, but with impaired
vision in one eye and blindness in the other. (Five and a half
years.)
3. A young woman, aged eighteen years. Double optic neuritis,
headache, and vomiting; several epileptic fits. Recovery,
with useful vision in one eye; vision in the other is very defective.
(Seven years.)
4. A young woman, aged eighteen years. Double optic
neuritis, headache, and vomiting. Recovery, but complete blindness
followed. (Four years.)
5. A young woman, aged nineteen years. Double optic neuritis,
headache, and vomiting. Recovery with good vision.
(Three years.)
6. A man, aged twenty years. Double optic neuritis, headache,
269and vomiting. Recovery, but complete blindness followed.
(Two and a half years.)
7. A girl, aged ten years. Double optic neuritis, headache,
and vomiting; knee-jerks were absent. Recovery, but complete
blindness followed. (Three years.)
8. A boy at the age of thirteen years had double optic neuritis
and headache; recovery ensued. At the age of fifteen years he
had a return of headache and double optic neuritis; also vomiting.
At a later date there was partial anæsthesia in the distribution
of the right fifth cranial nerve; the right cornea was opaque;
there was complete blindness in both eyes. Partial anæsthesia
of the face and blindness remained, but otherwise the patient
recovered and felt quite well nine months after the second
attack.
9. A girl, aged sixteen years. Double optic neuritis, headache,
vomiting; slight internal strabismus of the right eye. Recovery
with normal vision. (Four and a half years.)
10. A boy, aged ten years. Double optic neuritis, headache,
and vomiting. The head had increased in size. Recovery, but
with complete blindness. (Three years.)
11. A woman, aged nineteen years. Double optic neuritis,
headache, and vomiting. Recovery with normal vision. (Three
years.)
12. A boy, aged fifteen years. Double optic neuritis, headache,
and vomiting. Recovery. (Two and a half years.)
13. A woman, aged twenty-one years. Double optic neuritis,
much swelling of the disks, headache, and vomiting. Complete
recovery with normal vision. (Four and three-quarter years.)
14. A girl, aged fifteen years. Double optic neuritis, headache,
and vomiting. Recovery with good vision. (Five and a
quarter years.)
15. A boy, aged twelve years. Double optic neuritis, headache,
and vomiting; slight internal strabismus of the right eye.
Recovery with good vision. (Four years.)
16. A man, aged forty years. Double optic neuritis, headache,
and vomiting. Recovery, but with complete blindness.
(Eighteen months.)
17. A youth, aged seventeen years. Double optic neuritis,
headache, and vomiting. Recovery, but with total blindness.
(Five years.)
27018. A woman, aged twenty-two years. Double optic neuritis,
headache, and vomiting. Recovery, but with total blindness.
(Two and three-quarter years.)
19. A girl, aged fourteen years. Double optic neuritis, headache,
and vomiting; internal strabismus (left) for fourteen days.
Recovery, with normal vision. (Two years.)
The following are brief notes of the cases in Group IX.:
20. A girl, aged twelve years. Headache, vomiting, and
double optic neuritis in December, 1893. Recovery in twelve
months, but vision was much impaired. She remained well with
the exception of occasional headache until December, 1899.
Then the severe headache returned. She became ataxic and
optic neuritis reappeared. In April, 1900, the headache was much
less and the patient felt much better, but she was completely
blind. (Six and a half years.)
21. A young woman, aged seventeen years. Headache, vomiting,
and double optic neuritis. Vision was impaired. Vomiting
ceased; the headache continued for over two years, but
recently disappeared after lumbar puncture. (Two and a quarter
years.)
In all cases of double optic neuritis a systematic and careful
examination of the patients should be made. The urine and
cardio-vascular system should be examined for signs of chronic
interstitial nephritis; the gums should be examined for the lead
line and other indications of lead poisoning should be sought
for; the question of chlorosis or other “blood disease” should
be considered; and the ears should be examined for signs of
otitis. But when all these conditions have been excluded and
when the symptoms are apparently due to a cerebral affection,
there is one group of cases in which localizing brain symptoms
are absent and in which the chief indications of disease are
headache, double optic neuritis, and often vomiting. In most
of these cases syphilis can be also excluded. A diagnosis of
brain tumor is given, and the growth is thought to be situated in
some region in which the localizing symptoms are at first indefinite—cerebellum,
temporo-sphenoidal lobe, or prefrontal
region. Such a diagnosis often proves to be correct. Localizing
symptoms may develop later and a necropsy may show the
accuracy of the opinion expressed. But sometimes, to the surprise
of the medical man, a fatal termination does not occur;
271the symptoms sometimes disappear and the patient recovers,
though very often impairment or loss of vision remains. The
patient may continue in good health for years or for a lifetime
afterwards. Most medical men who have paid much attention
to cerebral diseases will have met with a case or cases of this
kind. The chief object of our article is to call attention to this
class of cases and to indicate the frequency of their occurrence.
Nineteen out of one hundred cases of double optic neuritis with
headache in the table just given could (after careful examination)
be placed in this group (X.).
What is the cause of the symptoms in this group of cases?
Possibly in some cases the symptoms are caused by a non-malignant
tumor (or tuberculous mass) which ceases to extend and
becomes quiescent and encapsuled. One of us has recorded
a case in which symptoms of cerebral tumor (including Jacksonian
epilepsy and hemiplegia) gradually subsided and temporary
recovery ensued; but three years later symptoms of
cerebellar tumor developed and death occurred. The necropsy
revealed a recent large tuberculous mass in the cerebellum
and an old capsuled tuberculous mass just beneath the motor
cortex in the right cerebral hemisphere. The latter had evidently
been the cause of the early cerebral symptoms from which
the patient had recovered. An instructive case has been recorded
by Dr. T. K. Monro of Glasgow. The patient, at the age of
sixteen years, suffered from severe headache with failure of
vision which passed on to complete blindness. For thirty-three
years he was an inmate of a blind asylum, ophthalmoscopic
examination showing double optic atrophy. He died at the
age of sixty-three years, from cancer of the stomach, and the
post-mortem examination also revealed a large myxomatous
tumor in the left half of the cerebellum. In all probability the
early cerebral symptoms had been associated with optic neuritis
which had passed on to optic atrophy and the cause had been
the myxoma in the cerebellum which had remained quiescent for
forty-six years.
In some cases of double optic neuritis with headache and
general cerebral symptoms, when recovery occurs the cause is
probably distention of the ventricles of the brain with fluid—serous
meningitis of the ventricles (Quincke). This condition
was present at the necropsy, and no tumor growth could be
272found in two out of the one hundred cases tabulated. It is
probable that a number of the cases in which a diagnosis of
cerebral tumor has been made, but in which recovery has occurred,
have been due to this condition—serous meningitis of the ventricles.
Probably the two cases in Group IX. and possibly some
of the cases in Group II., in which death did not occur for
several years after the onset of symptoms, were of this nature.
Other cases which recover may be due to a basal meningitis.
The table given above is instructive both as regards the
diagnosis and prognosis in cases of double optic neuritis with
headache. It shows the necessity for careful examination before
giving either a diagnosis or prognosis, and the clinical group of
cases No. X. ought always to be borne in mind whenever the
diagnosis is obscure and localizing symptoms are absent.
There are two other points to which we would draw attention.
In ten out of the one hundred cases the patient recovered completely
from the headache and general cerebral symptoms and
regained perfect health, but the optic neuritis was followed by
atrophy and complete blindness. In the face of this terrible
termination we cannot help thinking that simple trephining of
the skull and the removal of bone, without any interference with
the brain, as suggested and practiced by Mr. Victor Horsley for
the relief of optic neuritis and pressure symptoms, is a method
of treatment worthy of more frequent trial when vision is failing
markedly. Dr. James Taylor has published cases which appear
to show that this method of treatment may be of service in
checking the optic neuritis and failure of vision. In the class of
cases in Group X. if there should be a suspicion that the symptoms
may be due to serous meningitis of the ventricles, lumbar
puncture appears to be worthy of trial, since several cerebral
cases are now on record in which this treatment appears to have
been of great service, and in which the cause of the cerebral
symptoms was probably that just mentioned.
A schoolboy, aged seven years, was admitted into Westminster
Hospital on January 28, 1900, the only history obtainable being
that on the previous morning he had been brought home in a
“fit,” which lasted the greater part of the day. On admission he
273was perfectly sensible and talked freely, but on being put to bed
he passed into a condition of semi-consciousness which lasted
for many days. He took no notice when spoken to, and remained
absolutely mute. The face and upper extremities exhibited
choreiform movements of a slow and coarse type. These movements
were apparently purposive in character, and at times he
endeavored to clutch at objects within his reach. Sometimes the
arms were widely extended, and then slowly flexed, as if performing
the act of embracing. Sometimes the movements conveyed
the idea that he was feebly endeavoring to strike those
around him. There was no paralysis of the face or of the muscles
of the limbs. The movements were, as a rule, bilateral,
although sometimes the facial movements were unilateral, but not
always on the same side. There was no rigidity of the muscles,
retraction of the head, or opisthotonos. There was nothing to
indicate that the patient suffered from headache, although at
times the brows were contracted and the face wore a worried and
anxious appearance. The bowels were open twice a day and
urine and fæces were passed in bed. The motions were normal
in character. The patient was unable to swallow, and had to be
fed by the nasal tube. There was no nystagmus, the pupils were
normal in size and contracted well to light. There was well-marked
double optic neuritis. The temperature was 99.8° F.,
and the pulse was 108. There was no tenderness or swelling of
the joints, and there was no rash on the skin. No tache cérébrale
could be obtained. There was a little cough, but there was
no expectoration. The breath and heart-sounds were normal.
The urine was acid, had a specific gravity of 1018, and contained
neither albumen nor sugar. The spleen was not enlarged. The
patient showed no signs of anæmia, but the blood was not
examined. There was no wasting of the muscles, and the knee-jerks
were present, although somewhat sluggish. The tongue was
clean, and presented no sign of having been bitten. The patient
would not protrude it voluntarily, and it had to be examined with
the spatula.
The condition of the patient remained practically unchanged
for twelve days. The highest temperature recorded was on the
second day, when it reached 100°; on the following day it was
99.8°, and from that time onward it was normal. The double
optic neuritis continued, and the disks were observed to be getting
paler. On February 13 (the seventeenth day of the illness)
274the patient was much more sensible, and recognized his mother,
putting his arms round her neck. He was still unable to talk,
although apparently he endeavored to do so, from time to time
uttering a few unintelligible words. On being asked if he would
like an orange he nodded his head, and he showed some signs of
interest in a watch which was shown to him. The incontinence
of urine and fæces continued, but food was taken with less difficulty.
The movements gradually subsided. On the 17th the
patient could say his own name, but beyond that could utter only
inarticulate sounds, and failed to recognize letters or words,
either written or printed. On the 20th he was able to speak
plainly, although incoherently. He endeavored to get out of
bed, and during the night was so noisy that he had to be removed
from the ward. Urine and fæces were still passed under him.
On the 22d he was quieter, and for the first time indicated
that he wanted the bed-pan. The optic neuritis was less marked.
On March 1 the patient was able to get up, and seemed to be
quite well. On the 8th the following note was furnished by Mr.
G. Hartridge, who had frequently examined his eyes during the
course of his illness: “Pupils five millimeters each. React well
to light, to convergence, accommodation, and consensually.
Right vision 6
6, left vision 6
9. Right disk getting white; not much
swelling of the disk; edges clearing. Retinal vessels, specially
veins, very full and tortuous. Left disk pale (less so than
right), dim; edges blurred.” The only medical treatment adopted
was the administration for a few days of 15 minims of liquor
arsenicalis three times a day.
Several years have elapsed since Dr. R. Berlin described a
series of cases in which he had observed a peculiar retinal
change after the eye had been struck with a blunt object, as, for
example, a stick or a stone. Under those circumstances he
noticed a cloudiness of portions of the retina, not involving the
retinal blood vessels. The milky appearance reached its height
in twenty-four to thirty-six hours, and disappeared in two or
three days. Berlin pointed out that the rapidity with which the
cloudiness developed, and the length of time that it persisted,
stood in direct relationship with the severity of the original
injury. This curious condition, which Berlin called commotio
275retinæ, was associated with some reduction of sight, episcleral
congestion, and a difficulty in getting the pupil to dilate when
atropine was dropped into the eye. Small retinal hemorrhages
were sometimes present. Berlin explained the ophthalmoscopic
picture by supposing that a rupture of the choroid was followed
by bleeding and œdema of the retina. This theory has recently
been opposed by Denig. That observer, as the result of experiments
upon rabbits, believes that the blow upon the eyeball
causes the vitreous to impinge upon the retina, to tear the internal
limiting membrane, and to force the vitreous into the nerve-fiber
layer. The alternate elevations and depressions thus
brought about in the nerve-fiber layer of the retina are, according
to Denig, the cause of the ophthalmoscopic appearances.
Since the publication of Berlin’s original paper few cases of
commotio retinæ have been recorded. Indeed, the retinal changes
are of so fleeting a nature that an opportunity for observing them
must occur comparatively seldom. This fact leads me to place
upon record brief notes of a somewhat interesting case:
E. S., aged eleven years. First seen on July 25, 1899.
History.—At 6.45 P. M., on July 24, the patient was struck in
the right eye with a cricket ball, made of cork and covered with
rag cloth.
Present State.—Right eye: Small abrasion of the skin of the
lower lid, with a surrounding area of redness. Some general
conjunctival congestion, with a definite ecchymosis in the ocular
conjunctiva, opposite the lower-outer quadrant of the cornea.
Tension minus 1. The pupil distinctly sluggish and a trifle larger
than the other one. Anterior chamber deep. A narrow line of
blood clot lay at the bottom of the anterior chamber. V. 5
9 (ii.
letters). Pupil dilates imperfectly to a mydriatic. With the
mirror alone some parts of the fundus oculi were seen to be
unduly white. When examined more closely with the ophthalmoscope
there was found a wide but defective zone of whitish
fundus, situated peripherally upward, inward, and outward. No
such appearances could be made out in the lower part of the
fundus. The retinal vessels, which lay anterior to the affected
areas, showed no changes. In most places it was possible to get
beyond the whitish patches so as to see the edges of the latter.
These margins were irregular, and showed white, tongue-like projections
running into normal fundus. Some small islands of
cloudiness lay, however, beyond the area of general haziness.
276Around the yellow-spot region was a white radiating appearance,
but no definite white mass was present in that place. Left eye:
No fundus changes. V. 5
5 (iv. letters). Tension normal.
Treatment.—Vaseline to abrasion of skin of lid; atropine
drops (2 grs. to the ounce—to each eye twice a day); rest in bed.
Progress.—July 26. R. V. 5
12; tension still rather low. The
blood clot present in anterior chamber and also on anterior capsule
of lens renders it difficult to see the fundus clearly; but no
white patches can be made out in the fundus.
July 27. A little blood is still present in the lower part of the
anterior chamber. The parts of the retina that were milky have
resumed almost their natural appearance, and the changes above
mentioned are now represented merely by a faint, whitish, ill-defined
stippling of the areas in question. Around the yellow
spot is a system of fine radiating lines, which extend for some
distance into the surrounding fundus. This is doubtless due to
œdema of the retina.
July 28. R. V. 5
6 (i letter); tension still slightly minus. Ecchymosis
present in ocular conjunctiva, but the blood has disappeared
from the anterior chamber. Pupil not so wide as that of
the left eye, although atropine is being used to both. Faint
cloudiness lower third of the cornea, made up of almost transparent
dots, as may be seen with a +20 lens in certain positions
of the eye. Fundus changes have disappeared; faint radiating
lines, however, may still be seen around the yellow-spot region.
July 29. R. V. 5
6 (ii letter) T—I. Pupil now as large as that of
the other eye. Yellow-spot region still surrounded by a wide
band of fine, closely set, radiating gray lines. It may be noted
that the corresponding region of the left (unaffected) eye is encircled
by an ordinary oval reflex.
August 1. R. V. 5
6; (Tn.). A small ecchymosis still present in
the ocular conjunctiva on the outer side of the cornea. No blood
in anterior chamber; no corneal cloudiness. Radiating appearance
still present around yellow spot of fundus.
August 9. R. V. 5
9, L. V. 5
9; (Tn.).
August 12. Vision unaltered. Radiating lines still present
around yellow-spot region of affected eye.
September 5. The right pupil rather larger than its fellow, but
no break in the continuity of the edge of the iris can be discovered
to account for this. The action, both to light and to accommodation,
of the pupils is equal. The radiating lines formerly
present around the yellow spot of the right eye have been replaced
by an ordinary oval reflex, like that present in the other fundus.
Tn.; R. V. 5
6 (i letter), L. V. 5
6 (i letter); No. 1 Jaeger read easily.
September 7. Under atropine. R. V. = 5
18 + 1.5 D. Sph.
= 5
5. L. V. = 5
12 + 1.0 D. Sph. = 5
5.