Aphasia Due to Stib-dural Hemorrhage 
Without External Signs of Injury; 
Operation ; Recovery. 
BY 
L. BREMER, M.D., and N. B. CARSON, M.D , 
OF ST. LOUIS. 
FROM 
THE AMERICAN JOURNAL OF THE MEDICAL SCIENCES, 
February, 1892. Extracted from 
The American Journal of the Medical Sciences for February, 1892. 
APHASIA DUE TO SUB-DURAL HEMORRHAGE WITHOUT 
EXTERNAL SIGNS OF INJURY; OPERATION; 
RECOVERY. 
By L. Bremer, M.D., and N. B. Carson, M.D., 
OF ST. LOUIS. 
The history of the patient, H. T. K., a healthy and well-built man 
of about twenty-one years, is as follows: 
There is neither heart nor kidney disease. Two weeks previous to my 
seeing him he went to a wedding, got intoxicated, and on his way home 
fell between the joists of a new building. This was his statement sub- 
sequent to his recovery after the operation. He went home and was 
found asleep in the kitchen of his parents’ house the following morning. 
Except what appeared to be the effects of the liquor, he seemed in his 
usual health. In fact, nothing was mentioned by him as regards the 
fall. Being out of work, he stayed at home and rarely left the house, 
complaining off and on of a dull headache on the left side of the fore- 
head, with exacerbations in the afternoon. Occasionally he vomited, 
but had generally a good appetite. All this while there was not the 
slightest suspicion on the part of his family of any serious trouble. 
About one week after he had begun to stay at home, while walking 
on the street, one block away from his home, he suddenly became uncon- 
scious and fell. This attack did not last long, however, and he was 
assisted home by a person who happened to be near at the time. When 
he arrived at the house he was able to undress himself and went to bed. 
Shortly afterward it was discovered by his family that he had some 
difficulty in speaking. He now for the first time intimated to his family 
that he met with an accident on the night of the wedding. Dr. H. F. 
Hendrix was called in, who, in addition to the dysphasic disturbance, 
noted other symptoms, especially a slow, laborious pulse indicative of 
brain lesion. He observed that the patient was more or less speechless 
in the afternoon, when a moderate fever of about 101° would set in, 
whereas in the morning, when free from fever, the difficulty of speech 
would be much less, and he had many more words at his command than 
in the afternoon. 
When I saw him for the first time, thirteen days after he first com- 
menced to complain, it was stated that for the last three days he had 
been entirely unable to speak. On the day previous to my visit Dr. 
Hendrix had found his pulse to be 54. 
The patient seemed to be quite rational, judging from the looks of his 
eyes and the expression of his face. There was no trace of an injury 
to his head. He understood every word that was spoken to him, every 
question that was asked. Unfortunately, although not entirely illit- 
erate, the patient was not possessed of sufficient education to render the 2 
BREMER, CARSON, APHASIA. 
examination of this form of aphasia very profitable. Only the most 
elementary questions could be asked of him, the scope of his intellect 
being limited. 
In order to test his mental calibre and ascertain the nature of the 
trouble of speech, a number of questions were put to him. The prin- 
cipal ones were: 
Do you know what this is (showing him a glass) ? 
A ns. Zer— 
Q. Is it a glass ? 
Ans. Yes. 
When a pitcher is shown him, he calls it a“ tipper a“ pen ” he calls 
“ riglah a spittoon “ sempen a hat “ sem.” 
Q. Do you call this (the hat) “ sem ” ? 
Ans. No. 
Q. Is it a hat ? 
Ans. Yes. 
Q. What is this (showing him a match) ? 
Ans. “Ses.” 
In order to demonstrate that he knows what it is, he makes the move- 
ment of striking a match. A book he calls “ pokhandkerchief, 
“ sempence ;” suspender, also “ sempence ;” for pocket-knife he gives the 
correct name; but when shown a bunch of keys, he also says “ pocket- 
knife.” After this he calls everything that is shown him pocket, e. g., 
a watch and a button. 
When ordered to repeat a word that is spoken to him,,he is unable to 
do so. 
He understands perfectly what he reads. He is handed a newspaper, 
and an advertisement of an entertainment in the Exposition Building 
is pointed out to him. By putting a variety of questions, some of them 
misleading, I convince myself that he is familiar with the location of the 
building, and the purposes it is built for. 
He is asked to read the advertisement of a boxing-match. I point 
out the name of the prize-fighter, and ask him : What is lie ? Is he a 
preacher ? This causes him to laugh. 
In short, there is no flaw in his perceptive and reasoning powers as 
far as can be ascertained by a necessarily limited conversation, and as 
far as a short acquaintance will permit. 
The most prominent of the other symptoms is a beginning obliteration 
of the naso-labial fold on the right side; on showing his teeth, the left 
naso-labial fold becomes much more marked than the right, and the left 
angle of the mouth is drawn considerably to the left; during an effort 
at whistling the right cheek puffs somewhat. The tongue deviates to 
the right. He cannot well draw the right angle of the mouth to the 
right, or make the right platysma muscle contract. On the latter symp- 
tom, however, not much stress is laid, because an effort on the other side 
is not very successful, and many people, even in absolute health, have 
not the power of contracting this muscle either singly or together with 
its fellow. 
The grip of the right and left hands seems to be almost equal ; he 
moves his arms with absolute freedom, and nothing abnormal can be 
seen in his walk. He stands on the right leg with the same ease as on 
the left. 
On being told to alternately flex and extend the right index finger, BREMER, CARSON, APHASIA. 
3 
there is an associated movement of the other fingers; and on trying to 
move the right thumb, the right index also moves in a rather clumsy, 
erratic manner. All such movements of the fingers on the left side are 
executed with precision, no associated movements of the others being 
noticeable. 
Sensation (tested with a pin) is somewhat dulled on the whole of the 
right side. The main dulness is in the fingers, the palm and back of 
the hand, and the wrist; it is less higher up to the elbow and shoulder, 
and much less in the face. But, as just stated, the whole of the left 
side, including the leg, shows a defect in common sensibility. The same 
is true of the sense of temperature and pain. Passive movements of the 
fingers of the right side are not so well perceived as those of the left, 
showing a lowering of the muscle sense. The passive movements of the 
toes on the right side, however, are correctly stated. There is no ataxia 
in the right arm or hand ; without hesitancy he carries his right index 
to the tip of the nose, the eyes being closed, and puts with precision the 
tip of the finger on the point of a pin. 
But on being told to write, he holds the pen in an awkward manner, 
and drops it repeatedly. He never has been much of a penman, but 
has been able to write simple letters. It is now impossible for him to 
express his thoughts in writing, and even the most commonplace and 
every-day expressions, when dictated, he fails to fix by letters. 
The effort at writing his name is more of a success. While his inability 
to write words, even the most familiar ones, is very marked, he puts 
figures with comparative ease. Thus in writing what is meant for “April 
28,1891,” he writes 28 and 1891 without the slightest hesitation. This 
facility of writing figures and difficulty, amounting often to impos- 
sibility, of penning words was tested in different ways, always with 
uniform results. There is no visible abnormality about the eyes; no 
inequality of the pupils, no hemianopsia. Nothing of a spastic character 
is observed in any of the muscles of the affected side. Patient is right- 
handed. 
From the foregoing data the diagnosis was made: Blood-clot (prob- 
ably extra-dural) pressing principally on the foot of the third frontal 
(Broca’s) convolution and the foot of the second frontal (probable centre 
for writing), impinging also on the face and tongue centres of the left 
hemispheres. 
The next day all the symptoms were more marked ; the grip of the 
right hand was weaker than that of the left; pulse 43. 
The operation of trephining was now set for the following day, and 
the patient transferred to the Mullanphy Hospital. While the prepara- 
tions for operation were in progress, the patient was once more examined 
as to the general and localizing cerebral symptoms. As regards the 
latter, it was found that they had become more vague and indistinct. 
The patient did not answer questions as readily as on the preceding 
days; it took him a longer time to comprehend their import. While 
during the first half-hour of the examination he tried to read from 
the questioner’s mouth, he grew listless and inattentive later on. 
Although there was no outspoken hemiplegia, he dragged the left foot, 4 
BREMER, CARSON, APHASIA. 
when told to walk, which had not been the case on the previous day. 
The grip of the right hand was also much weaker, the paresis of the 
right side of the face and the deviation of the tongue more marked. 
The dulness of sensation had increased in proportion to the motor weak- 
ness. How much, however, this was to be attributed to a want of atten- 
tion and increasing mental hebetude was difficult to decide. 
There could be no doubt that the pressure on the brain was rapidly 
increasing. During the last hour consumed in the examination, the 
patient grew more and more confused and listless; this was not en- 
tirely due to the fatigue attending upon keeping his waning mental 
faculties at work, for it could be distinctly ascertained that the grip of 
his right hand became more feeble, and that his right leg became 
unable to bear the weight of the body—so much so that he was unable 
to walk to the operating-room, and had to be carried there on a 
stretcher. 
The pulse when last examined was 56 as against 43 on the day pre- 
vious, this being the lowest figure ascertained. 
The operation, by Dr. N. B. Carson.—H. T. K. was admitted into the 
St. Louis Mullanphy Hospital, April 29, 1891, with the history given 
above, and the symptoms calling for an operation. 
The head having been rendered aseptic, a semicircular flap, with its 
base forward and its convexity backward, was raised together with the 
pericranium so as to expose the antero-lateral portion of the skull, with 
the pterion as a centre. The temporal vessels bled freely, and had to 
be clamped before the operation could be continued. 
An inch button was then removed with the trephine an inch and a 
quarter behind the external angular process, and the same distance 
above the base line. 
Upon exposing the dura, it presented a dark, cloudy appearance, and 
the vessels were empty and flattened. All evidence of pulsation was 
wanting ; the trephine opening was enlarged in every direction, more 
posteriorly, however, than otherwise, until an opening deemed suf- 
ficiently large had been made. The dura was then opened to full size 
of cranial opening, and a clot extending in all directions beyond the 
cranial opening was exposed to view. 
Upon raising the dura, a stream of dark, semi-liquid blood forced 
itself through the superficial layer of the clot, and spattered myself and 
assistants two and three feet distant. The thickest part of clot seemed 
to correspond to the centre of trephine opening, and was immediately 
under anterior branch of middle meningeal artery, between the dura 
and arachnoid.. With dull-edged curette the greater part of the clot 
was removed, and the smaller portions subsequently taken away with a 
very fine flat sponge held in forceps. In this way I wiped out the 
entire cavity occupied by the clot, which almost reached to the longi- 
tudinal sinus above, the base of the cranium below, and at least an 
inch and a half anteriorly and the same distance posteriorly. 
Being satisfied that there was no more bleeding, the dura was replaced 
over a horsehair drain, but not sutured. A rubber drain was then 
placed under the flap, which was replaced and sutured, and over all a BREMER, CARSON, APHASIA. 
5 
dressing applied, and the patient returned to bed in good condition. 
Before I left the hospital, an hour and a half later, the patient had 
returned to consciousness apparently none the worse for the operation. 
6 p.m. (day of operation). Temperature, 98.4° ; pulse, 86; reacted 
very nicely. 
April 30 (first day after operation). Temperature, 99.3°; pulse, 70; 
respiration, 22; clonic spasms in right side of face and right platysma 
myoides. Is stupid and unable to speak; complete motor aphasia. 
6 p.m., temperature, 99.3°; pulse, 70; conscious, but unable to use the 
right word. 
May 1 (second day). Temperature, 98.3°; pulse, 72; entirely free 
from spasms. In all efforts to speak prefixes “ shay ” to words. 6 
p.m., temperature, 99°; pulse, 76; brighter look; tongue slightly de- 
flected to the right when protruded ; elevation of lip improved. Can 
answer “ Yes ” and “ No ” correctly, yes having the “ sh ” sound very 
marked. A watch was pronounced “ swatch ;” keys, “ shkeys ;” half- 
dollar, “ shalf-dollar.” 
2d (third day). Temperature, 98.4° ; pulse, 66. In answer to ques- 
tions, said, “he felt well,” that “he liked the hospital.” Can speak 
words without sibilant sound. 6 p.m., temperature normal; pulse, 
68 ; doing well. 
3d (fourth day). Temperature normal; pulse, 66 ; dressed, horsehair 
removed. Union by first intention. All words spoken correctly. Re- 
plied to questions by answers of three words correctly. Sensation in 
right arm still impaired. Sharp points on right arm recognized as two 
points one and a half inches apart, on fingers two inches apart. Unable 
to feel blowing of breath on hands or arm. 6 p.m., temperature and 
pulse normal. Improving in all respects. 
4th (fifth day). Temperature normal; pulse, 54; 6 p.m., temperature 
and pulse unchanged. 
5th (sixth day). Temperature normal; pulse, 62 ; sensation improving. 
Can speak and write as well as before the accident. 
6th (seventh day). Temperature and pulse normal. 
1th (eighth day). Temperature, 98.4°; pulse, 56. .6 p.m., temper- 
ature and pulse normal. 
8th (ninth day). Temperature and pulse normal. 6 p.m., temperature 
and pulse normal. 
9th. Discharged cured May 18th, nineteenth day after operation. 
June 10. Returned to clinic to consult about a numbness or tired 
feeling in right foot, only after exertion and when fatigued. 
The question so often asked, In what cases of intra-cranial hemorrhage 
are we to operate, and what are the symptoms that should make us de- 
cide to interfere in these cases? is, in my opinion, still unanswered. 
Keen1 says: “ The importance of operative treatment is best shown 
by Wiseman, who collected 147 cases treated expectantly; out of this 
number 89.1 per cent, died, while, on the contrary, out of 110 cases 
treated actively only 32.7 per cent. died. This certainly points very 
decidedly in favor of active treatment.” 
1 Handbook of the Medical Sciences, page 227. 6 
BREMER, CARSON, APHASIA. 
But what surgeon is there that has not seen many cases where the 
symptoms pointed conclusively to an intra-cranial bleeding, that, after a 
varying lapse of time, had recovered as effectually as if the trephine had 
been applied ? 
A very interesting case bearing upon this subject was reported by 
Dr. Warren in a discussion following a report of a case of trepanation 
for sub-dural hemorrhage, reported by Drs. Homans and Walton re- 
cently.1 
In this case a diagnosis of clot having been made, and while prepara- 
tions for an operation were under way, the patient began to move the 
paralyzed limb, and eventually made a complete recovery without an 
operation. 
It is to be remarked, however, that although the diagnosis of clot was 
probably correct (the reasons for the diagnosis are not given), it was by 
no means certain. Without going into details, I will simply suggest 
that hemiplegia without focal lesions does not count among the impossi- 
bilities.2 
Again, in rapidly improving cases of hemiplegia without operation, 
with result of complete restoration, a diagnosis of clot, if it has been 
made, should be subject to reconsideration, and if the symptoms have 
not been cogent and unequivocal, the possibility of a transient throm- 
bosis (or embolism) of the sylvian artery should be thought of as being 
best calculated to explain such cases. 
I make this remark on general grounds, and without any special 
reference to the case which has given rise to it. 
Another case, nearer home, has just come to our knowledge, and is 
reported further on. Here, too, blood-clot was the diagnosis, by Dr. 
Bremer. For the reason that decided signs of improvement are demon- 
strable, operation was delayed. The patient is now making a good 
recovery. 
On the other hand we see cases—and I think most often—presenting 
not any more decided symptoms, that die because their friends will not 
consent to an operation. 
In our case there was no doubt as to the propriety of an operation : 
first, for the reason that the symptoms of hemorrhage were so very plain ; 
and, second, because the symptoms were rapidly growing worse. While 
two hours before being brought to the table the patient walked with 
only a slight halt, he could not move the limb when the time for the 
operation had come. 
1 “A Case of Successful Trephining for Sub-dural Hemorrhage produced by Contre- 
coup,” Boston Medical and Surgical Journal, February 12, 1891. 
2 Pillet: “ Ilemiplegie sans lesions en foyer de l’enc£phale,” Progres Medical, 1890, 
No. 7. . BREMER, CARSON, APHASIA. 
7 
In selecting cases for operation, we should not be too hasty in rushing 
into the cranial cavity, as we have seen some of these cases recover 
completely, and that, too, without the sequelse that are said to be 
dependent upon head injuries. 
Unless the condition of the patient demands immediate action, he 
should be treated with a view of controlling the hemorrhage and causing 
absorption of the clot. 
A careful watch ought to be placed over him, and so soon as there is 
an evident increase in the symptoms, then, and not until then, should 
the operation be undertaken. 
To one point of paramount importance in the management of intra- 
cranial hemorrhage I should like to call attention. It is based on the 
observation that patients of this class are prone to assume the horizontal 
position and go to sleep; often this is a sleep from wrhich there is no 
awaking. Owing to a simple mechanical law, renewed bleeding is apt to 
take place much more readily in the horizontal than in the erect posi- 
tion. The patient, therefore, as soon as the nature of the trouble has 
been established, or is only suspected, should be propped up by pillows, 
and kept in that position as long as possible. I am certain that many 
an unlooked-for catastrophe might be averted in this manner. My 
experience is, that this simple precautionary measure is only too often 
neglected by physicians and laymen. 
(By Dr. Bremer.) 
Considering the present advanced state of cerebral localization, the 
diagnosis was comparatively an easy matter. The case presented a 
group of the clinical focal symptoms which form, so to speak, the 
very groundwork of local diagnosis in brain disease. That a blood- 
clot w7as the cause of the trouble could not be doubted considering 
the manner of development of symptoms and the history of the case. 
Although there was no external injury, no fracture of the bone, not 
even a lesion of the scalp, to point to the seat of the trouble, there were 
the more exact and unfailing localizing brain symptoms. Compared 
with these, the visible external injury plays nowadays an inferior role. 
This is well illustrated by cases in which the external injury exists but 
the site of the symptom-producing clot is opposite to that of the injury. 
Such a case has lately been reported by Homans and Walton,1 in 
which a hemorrhagic clot was diagnosticated on the opposite side of the 
injury (this being on the right side). Aphasia was also one of the 
localizing symptoms. Contrary, however, to our case, the brain sub- 
stance itself was involved, which gave rise to Jacksonian epilepsy. This 
was, as remarked above, entirely absent in our case. In Homans’ and 
1 Loc. cit. 8 
BREMER, CARSON, APHASIA. 
AValton’s patient it was probably a branch of the middle cerebral 
artery that was ruptured, implicating the cerebral cortex directly and 
causing discharging symptoms; whereas, in our instance, the smooth 
and shining arachnoid intervening between the clot and dura could be 
made out very plainly. 
Keen1 says: “ No diagnosis can be made at present between hem- 
orrhage from the middle meningeal and the middle cerebral.” This is 
probably true for most cases. It is the generally accepted opinion 
among competent observers. Possibly, however, the presence or absence 
of irritative (spastic) phenomena may enable us, in a limited number of 
cases, to differentiate between cerebral and meningeal hemorrhage. In 
the former, localized and serial spastic disturbances are most likely to 
appear, owing to the direct involvement of the cortex; in the latter, 
provided the arachnoid is not torn, as in our case, the paralytic symp- 
toms will be the first to appear. General epileptic convulsions, as the 
result of diffuse brain pressure, will, of course, not count as a differential 
diagnostic factor. 
The extent of the clot covered a larger area than had been expected. 
It is outlined in the accompanying figure, and shows the various centres 
pressed upon, and the outline is, ot course, approximate. It did not 
extend to the top part of the Rolandic region—the leg centre. The 
fact that the latter became implicated is probably to be explained by a 
pressure through the brain matter on the corresponding part of the 
internal capsule. It is seen that the clot extended down to the first 
1 Reference Handbook of the Medical Sciences, vol. viii. p. 226. BREMER, CARSON, APHASIA. 
9 
ternporo-sphenoidal convolution, which would account for the difficulty 
on the part of the patient, on the morning before the operation, to under- 
stand what was said to him (word-deafness). The darkest shade denotes 
the greatest thickness of the clot, and is over Broca’s convolution, the 
foot of the second frontal and the lower end of the anterior central, which 
is in keeping with the prominent symptoms—motor aphasia, a gradual 
paralysis of the face and tongue. The arm and wrist centres are less 
implicated. 
A brief allusion to a few points bearing on this and similar cases will, 
perhaps, not be out of place. How is the fact to be explained that, 
during the first week after the supposed occurrence of the hemorrhage, 
there were almost no symptoms of brain pressure, and that suddenly, a 
week later, alarming cerebral symptoms developed, which gradually 
grew in intensity almost to a fatal issue ? 
The concurrent testimony of observers of this class of cases goes to 
show that the bleeding has ceased before the operation has been resorted 
to. Whether arterial or venous in origin, the blood is found in the 
coagulated, not in the fresh or fluid, state. 
In our case the clot was old ; no distinct layers could be made out. 
Such layers, if present, would indicate different successive hemorrhages. 
There was a discharge of tarry blood breaking through the clot on open- 
ing the dura, but nowhere was there any evidence of recent hemorrhage 
or a recent coagulum. The anterior main branch of the middle menin- 
geal artery was empty, and pressed flat like a ribbon. The same was 
true of two of its anterior subdivisions that came within the field of 
operation. The probability, therefore, is that the hemorrhage was 
stopped long before the operation ; that the clot had acted as a sort of 
tampon, compressing the ruptured branch and the main artery, and 
that by this “auto-tamponade” any further hemorrhage was prevented. 
It will be remembered that the diagnosis of extra dural clot had been 
made. This was done on account of the insignificance of the initial 
symptoms and of the comparatively slow development of the graver 
ones. A priori, it stands to reason that a hemorrhage between the 
skull-bone and the tough and unyielding dura is apt to be more limited, 
and to produce less rapidly cerebral symptoms than sub-dural hemor- 
rhage, although it is a well-established fact that just in the neighbor- 
hood of the meningeal arteries the dura is less firmly attached to the 
bone than elsewhere. Besides, in the vast majority of ruptures of a 
middle meningeal artery or its branches the hemorrhage takes place 
upon the dura. For these reasons the diagnosis of extra-dural clot 
seemed to be the more likely one. This was a mistake, and, I believe, a 
mistake that could have been avoided on the ground that probably all 
meningeal hemorrhages due to indirect violence are sub-dural. This point 
will be enlarged upon further on. 10 
BREMER, CARSON, APHASIA. 
Now, taking the sequence and course of the symptoms into considera- 
tion, one would, basing one’s reasoning upon simple mechanical laws, be 
apt to conclude that, one of the smallest anterior branches having 
burst, the hemorrhage was at first extremely limited and insignificant, 
and pressing moderately on the left frontal lobe, anteriorly to the well- 
known centres, no positive symptoms developed, and that only the gen- 
eral ones of mental dulness (the pulse was not examined during the 
first week) and vomiting were present; that gradually, or in turns, 
slight fresh hemorrhages ensued, pressing successively upon the centres 
for articulate and written speech ; on those of the angle of the mouth, 
tongue, arm; then upon the centre for the interpretation of words heard 
(first temporo-sphenoidal convolution). Thus, e.g., the fall and short attack 
of unconsciousness one week after the accident might be due to a recur- 
rent hemorrhage. Again, in this manner might the inability of the 
patient to understand what was said to him shortly before the opera- 
tion be accounted for, if one does not prefer to ascribe it to a lowering 
of the intellect preceding a gradually approaching coma. 
Much more likely, however, to my mind, is another explanation. 
In meningeal, as in cerebral hemorrhage, there are two factors which 
have to be considered as productive of brain pressure. The one is the 
mass of blood extravasated, the other is the amount of reaction which is 
bound to arise in consequence of pressure-irritation. 
The brain will tolerate a certain amount of local pressure, according 
to the nervous make-up of the individual, as has been established by 
the clinical histories of a number of cases of cerebral tumors which may 
exist without symptoms, regardless of their size, until suddenly their 
presence becomes manifest by paralytic or discharging symptoms. For 
there is a limit of tolerance in cases of clot as well as of tumor. 
Thus, in our case, the at first gradual, and afterward rapid, superven- 
tion of paralytic symptoms might be explained in this way: There is a 
clot extending over a large part of the left hemisphere, covering a 
number of cortical centres. The brain mass accommodates itself to the 
pressure when gradually developed, and there are only slight symptoms 
until the branches of the vessels that enter at the base of the brain—viz., 
the anterior perforated space—respond to the irritation coming from 
above. It is, to my mind, conceivable that after a certain amount of 
pressure has been borne by the cortical and sub-cortical substance, the 
branches of the lenticulo-striate artery and other neighboring ones react 
according to the old pathological maxim, ubi irritatio ibi ajfluxus. 
This afflux of blood means increased pressure from the opposite 
(under) side of the clot—a pressure which not only bears upon the 
cortex, but also on the conducting fibres below, including the internal 
capsule. The rapidly-developing complete hemiplegia involving the 11 
BREMER, CARSON, APHASIA. 
leg, which for a long time was intact, may be accounted for in this 
way. 
Considering this rapid progress of alarming symptoms, the operation 
was performed in the nick of time, and may, without doubt, be set down 
as a life-saving act. 
The establishment of the exact source of inter-meningeal hemorrhage 
is often a matter of impossibility. Whenever there is a fracture of the 
skull, the trunk of the middle meningeal artery or vein may, of course, 
be lacerated, together with other soft parts, by direct violence. It is 
also said that hemorrhages of the middle meningeal artery have been 
observed without injury either to scalp or bone. Merkel' points out 
that it is principally the anterior branch of the artery that is ruptured. 
But it is hard to understand how an artery or vein of the dura mater 
can be ruptured by concussion due to indirect violence, unless there is a 
hemorrhagic diathesis, a disease of the vascular wall, a miliary aneurism, 
for instance. Such abnormal vascular state we have no right to assume 
in a young man of twenty. 
Judging from the clinical course of our case we must, I think, dismiss 
the idea of arterial hemorrhage, whether of a smaller or a larger branch, 
at once. The sudden increase of pressure such as would be likely to 
result from arterial bleeding would make more pronounced and violent 
symptoms at the start. A slow oozing from a vein and the gradual for- 
mation of the clot, allowing the brain sufficient time to accommodate 
itself in a measure to increased pressure, is the more probable process. 
But how are we to conjecture the cause and nature of venous menin- 
geal hemorrhage ? Is it probable that from indirect violence, from 
mere concussion (for it is not at all likely that in the fall the head of 
our patient was struck) a healthy vein should burst ? 
Perhaps the interesting researches and observations of Dr. Mittenzweig2 
will, if enlarged and confirmed, throw some light on this vexed question. 
Mittenzweig quotes Bergmann, who, in his book on Injuries of the 
Head, says (§ 260) : 
“ The hemorrhages into the so-called arachnoidal sac are principally 
derived from those veins which pass from the upper and lateral parts of 
the cerebral hemispheres out of the pia to the longitudinal sinus. 
These are simply torn off, a tearing which, of course, can take place only 
by a considerable displacement of the brain in toto. Since it has been 
observed in some cases even without injury of the bone, it proves the 
very considerable change of form the bony cranial capsule is capable of, 
before its limit of elasticity is passed.” 
1 Handbuch der topograph. Anatomie, 1885, vol. i. p. 68. 
2 “ Subdurale Blutungen aus abnorm. verlaufenden Gehirnvenen,” Neurolog. Cen- 
tralbl , 1889, p. 193. 12 
BREMER, CARSON, APHASIA. 
Now, from a series of observations Mittenzweig arrives at the conclu- 
sion that in a number of persons abnormal anastomoses between cerebral 
and dural veins exist, being the remnants of foetal conditions which are 
normal. It is easy to understand how such abnormal venous anasto-1 
moses will tear on even slight displacements of the brain mass, and that 
an absolutely healthy and young individual may suffer from sub-dural 
hemorrhage as a result of comparatively little violence. 
This probably happened in our case, and if anatomical research and 
clinico-pathological experience should bear out Mittenzweig’s investiga- 
tions and conclusions, an additional differentially diagnostic point may 
have been furnished us as to extra- and sub-dural hemorrhages. 
In Dr. Carson’s report it is stated that on the day following the 
operation muscular twitchings about the face and mouth were observed. 
I believe that these post-operative spastic phenomena are to be ascribed 
to capillary hemorrhages in the cortex of that part of the brain pre- 
viously compressed by the clot. Continued pressure will produce a 
weakened, possibly a more or less atrophic condition of the cortical 
capillaries, or possibly venules and arterioles. The sudden removal of 
the pressure and the sudden rush of blood will then give rise to minute 
hemorrhages referred to. In a case (to be published by us in the near 
future) of a large sarcoma of the dura mater, pressing upon the motor 
area, such hemorrhage took place throughout the cortex directly and 
indirectly involved by the pressure as could be demonstrated by a post- 
mortem held two weeks after the operation. That capillary hemorrhage 
will result from even so slight an insult as light pressure of the surgeon’s 
finger for the purpose of ascertaining the consistence of underlying cere- 
bral structures, I could demonstrate in a case of epilepsy operated upon 
by Dr. Prewitt, of this city. The wrist centre was excised and the 
ablated piece of cortex showed throughout recent hemorrhages into the 
perivascular lymph spaces, and the brain substance itself. Thus, I 
think, the twitching, which was absent before the operation, might be 
accounted for after it. 
The long interval between the accident and the appearance of any 
decided pressure symptoms is noteworthy. In one of Wiseman’s cases 
the interval was still greater, being eleven days. 
Owing to the shortness of time allowed for examining into the dys- 
phasic troubles of the patient, and chiefly owing to his want of educa- 
tion, the yield in this respect is rather meagre. 
In conformity with the topical lesion, the aphasia was of the ataxic 
variety, combined with agraphia. The latter was somewhat obscured 
by clumsiness of movements of the hand and fingers, owing probably to 
the simultaneous pressure upon the hand and finger centres. As usual, 
there was, in addition to motor aphasia, paraphasia and pai’agraphia. 
It is rather singular, that, after the patient had tried to pronounce a BREMER, CARSON, APHASIA. 
13 
number of simple and short words, he all at once was able to say 
“ pocket-knife.” The tendency to call everything “ pocket” after he had 
succeeded in pronouncing this word finds its analogue in other reported 
cases of motor aphasia. A beaten path for certain words and syllables 
remains intact amidst many others that are destroyed or obstructed, and 
every effort at speech is bound to travel this path. 
The meaningless monosyllables of “ zer,” “ sem,” and “ shay” must 
also be looked upon in this light. In prefixing these easily pronounce- 
able syllables to other words he “ oils,” so to speak, the machinery of 
speech. With some people such meaningless and nonsenical prefixes 
are physiological; they not only fill out a gap in the thinking process, 
but they act as starters in the speech-mechanism. 
In bis efforts at writing he succeeds best, as is also usual in these 
cases, with bis own name and with figures: 
At the last (fifth) French Congress of Surgery, held in Paris (April, 
1891), Dr. Michaux presented a case of non-traumatic meningeal 
hemorrhage cured by trephining. The topical diagnosis was made 
from focal symptoms. The clot was under the dura over the Rolandic 
region. It occurred in an alcoholic, and Dr. Michaux thinks the rup- 
ture due to alcoholism and uraemia. 
In the case under discussion the alcohol certainly played, pathologi- 
cally, a very subordinate part, and it is, to my mind, very doubtful 
whether there ever has been a well-authenticated case of idiopathic 
meningeal hemorrhage of the type exemplified by our case. If such is 
said to occur in an alcoholic, it must be remembered that a toper is 
more liable to accidents which are forgotten than anyone else. 
This is not the place to discuss the necessity or justifiability of trepana- 
tion for blood-clot. In our case there was a vital indication for operative 
interference. Whether in a number of other cases it would be safer to 
trust to the healing and absorbing powers of the membrane and adopt 
the expectant plan, is a question as difficult to solve as the propriety of 
operating in given cases of appendicitis and ileus. But the concurrent 
testimony of the surgeons of to-day is in favor of operation, even where 
less urgent symptoms are present. Even with much less extensive 
hemorrhage than in our case the outlook as to complete absorption is far 
from favorable. Epilepsy and mental impairment are the usual sequels 
of neglected blood-clot in the brain, and it is certainly much more in 
keeping with the principles of conservative surgery to operate early and 
remove the possible and even probable cause of epilepsy, than to wait 
until the latter has declared itself, and the epileptic change has taken 
place in the brain. 
A case of undoubted meningeal hemorrhage in which an operation 
was desisted from is the following : 14 
BREMER, CARSON, APHASIA. 
On June 23, 1891, Mrs. L. fell, with her two-and-one-half-year-old 
child, down a flight of stairs and landed on a pile of bricks. She had 
managed to hold the child in her arms and believed that it had escaped 
injury. After her arrival home the child went to sleep. When it 
woke up, it vomited, lost consciousness, and passed into general convul- 
sions. It remained unconscious for six hours, during which time it had 
a number of general convulsions, while it jerked continually with the 
right side in the intervals. 
After the spasms had ceased, it remained unconscious for four hours. 
On waking up, it was paralyzed on the right side. After a few hours, 
however, the right leg moved slightly, whereas the arm remained per- 
fectly motionless. At the same time the child had lost its speech. 
An examination, on June 25th, revealed a slight depressed fracture 
large enough to hold the tip of the forefinger, and situated about three 
inches above the meatus auditorius externus. The child was aphasic, 
right leg somewhat paretic; knee-jerks absent on the right, normal on 
the left. Right arm paralyzed. Pupillary reaction normal. Pulse 70 
and 65. Diagnosis : Depressed fracture of the parietal bone on the right 
side ; meningeal hemorrhage by contre-coup on the left, involving the 
arm and motor speech centres. No paralysis of facial muscles could be 
made out. 
On the 26th, she spoke a few words; an occasional slight voluntary 
movement of the right arm had been observed. June 30th, the child was 
able to stand on the leg and moved the arm much better. She had been 
able to walk a few steps. From this on the improvement was steady 
and rapid. July 10th, all paralytic symptoms had disappeared. The 
mother claims that the child talks much better than before the accident. 
The question in this case would arise, whether it would not be a safe 
plan to at least elevate the bones of the depressed fracture, and, Is not 
this fracture, situated in the binauricular line, apt to lead to epilepsy 
later in life ? 
That such is not always the case I can prove in a young man 
twenty-two years of age, who, when five years old, had meningeal 
hemorrhage, from the effects of which (left-sided hemiplegia) he recovered 
in the course of six weeks. There is now a very perceptible depression 
about two inches above and a little anteriorly to the right auditory 
meatus. He has never shown any sign of epilepsy. 
October 15, 1891.—The patient H. T. K. has been hard at work in 
a brick-yard for a couple of months. He is in his usual health with all 
his faculties intact, and a steady worker. :Irl)e Jotirijal 
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