On the Relation of Epilepsy to 
Injury of the Head. 
BY 
JAMES J. PUTNAM, M.D., 
BOSTON. 
Reprinted from the Boston Medical and Surgical Journal of 
January 7, 1892. 
BOSTON: 
DAMRELL & UPHAM PUBLISHERS, 
No. 283 Washington Street. 
1892. S. J. PARKHILL & CO., PRINTERS 
BOSTON ON THE RELATION OF EPILEPSY TO INJURY 
OF THE HEAD.1 
BY JAMES J. PUTNAM, M.D. 
At the recent Congress in Washington the import- 
ant subject of traumatic epilepsy from fracture of the 
skull was brought up by Dr. Agnew,2 of Philadelphia, 
in the course of his paper on " The Surgery of the 
Brain." After speaking of the unsatisfactory results 
of operative treatment after the neurosis has once 
established itself, he expressed the opinion that the 
improper surgical treatment of the case at the time of 
the occurrence of the fracture is responsible for much 
of the subsequent mischief, and, went on to say: 
"Whenever, therefore, in my judgment, the profession 
can accept the doctrine that all depressed fractures of 
the cranium, however slight may be the depression, 
and entirely irrespective of pressure symptoms, are 
proper subjects for trephining, then will traumatic epi- 
lepsy largely disappear from the list of surgical dis- 
eases ; indeed, I am sure that he who shall propose to 
tabulate, at the end of the next twenty-five years, the 
cases of epilepsy, will find, as compared with the pres- 
ent time, a meagre supply for his purpose. It is not 
improbable, indeed, in view of the greatly diminished 
risk from trephining, that the operation will be ex- 
tended even to cases of simple fracture or fissure of 
the skull." 
1 Read before the Boston Society for Medical Improvement, No- 
vember 9, 1891. 
2 Published in the University Medical Magazine, Philadelphia, 
October, 1891. 2 
It will be fortunate, indeed, if this optimistic view 
turns out to be well founded. Since, however, it is of 
the highest importance for us to know, in detail, on 
just what principles we ought to proceed, when called 
to a case of fracture, and how much immunity from 
epilepsy or insanity we can promise our patient in re- 
turn for his submitting, though free from symptoms, 
to trephining and perhaps to opening the dura, it 
seems worth while to re-examine the evidence as to 
the frequency and the causes of the unwelcome result 
and the possibility of avoiding them. 
The adoption of this view assumes that the cause of the 
epilepsy is the irritation at the seat of principal injury, 
and especially the irritation due to displaced fragments 
of bone,8 and the failure of late operations for removal 
of the bone to effect a cure is considered as due to 
the epileptic habit having become established. 
It is difficult to test the correctness of this explana- 
tion, but it is not an altogether satisfactory one. It is 
common enough to see cases where trephining, under- 
taken after a certain number of fits have occurred, do 
check their recurrence for several years, long enough, 
one would think, to break up the epileptic habit, if 
there were nothing else besides the irritation starting 
from the depressed bone to maintain it. But not only 
do the fits almost always recur in the end after trephin- 
ing, but they usually recur when, besides the bone, por- 
tions of the cortex, which the symptoms indicated to 
be the centres of origin of the attacks, have been re- 
moved likewise, as Dr. Agnew himself points out. 
Moreover, the recent excisions of motor areas which 
were responsible for outbreaks of ordinary 
epilepsy of the localized type, also seem to be far less 
8 Dr. Agnew (loo. cit.) speaks particularly of the irritation of the 
sensory nerves of the dura by depressed or broken bone, " an irrita- 
tion propagated to the meninges, and, later on, to the cortex and 
brain-ganglia." 3 
effective than was hoped. The attacks are usually 
arrested, sometimes for one or two years, or even 
longer, and in exceptional cases they may never return ; 
but this is hardly more than seems occasionally, 
(though less often) to happen after other operations 
where neither cortex nor diseased bone are removed, 
so that, important as both trephining and cortical ex- 
cision may be as a means of treatment, where we wish 
to gain a temporary respite, or to take every chance 
of cure, they must for the present count rather as ex- 
cellent inhibitory measures, than as proving the nature 
or origin of the disease. 
If I)r. Agnew's opinion, which represents that of 
many surgeons, cannot be sustained by evidence, and 
the patient's prospects are not improved by treatment 
of the local injury to anything like the degree indi- 
cated, it is eminently important that we should not let 
ourselves be turned aside by it from the search for 
other influences that may turn out to be equally im- 
portant in the causation of epilepsy. If, on the other 
hand, that opinion can be sustained, and if trephining 
carries with it so little risk of inducing either imme- 
diate or subsequent mischief, then, I think, it should 
be seriously considered whether we ought not to tre- 
phine, also, in cases of healed fracture that come to us 
not too long after injury, but before epileptic symp- 
toms have appeared. 
There is, of course, no question as to the propriety 
of trephining, in many cases of fracture even without 
symptoms, on general surgical grounds. The indica- 
tions for doing this have been clearly laid down by 
various writers, and among others by Wagner, in an 
excellent address published in 1886 as Nos. 271, 272, 
of Volkmann's Klinische Vortrage. The treatment 
there advised is based almost wholly on the import- 
ance of preventing or curing local infection, though 4 
with the secondary aim of getting rid of irritating 
fragments of bone. Simple depression is considered 
as dangerous, not as a cause of intracranial pressure, 
but only in that it is liable to interfere with the union 
of the broken bones and lead to suppuration by dis- 
turbing the circulation in the diploe, and he recom- 
mends that when the fracture is not compound a mod- 
erate depression should be left untreated. Linear 
fracture without symptoms, even when compound, is 
considered as calling for treatment only when hairs or 
other foreign substances are caught in the crack, and 
then he uses the chisel so far as is necessary for re- 
moving them. 
Wagner recognizes at the same time that trephining 
is a relatively trifling operation.4 He urges it for lo- 
calized meningitis, or to secure a more aseptic condi- 
tion of the broken bone and underlying parts, as in 
perforating wounds, and even, in case of doubt, for 
exploring the condition of the tissues beneath the bone, 
especially when suppuration of the dura is suspected. 
Although Wagner considers it important to remove 
broken fragments of the inner table when feasible, he 
calls attention to the fact that they generally heal 
smoothly if left alone, and this opinion gains some 
support from the fact that the osseous plates which so 
often form in the dura usually do no harm, though 
they are considered by some pathologists* as of in- 
flammatory origin. 
Do we know with any approach to accuracy how 
much immunity from epilepsy is secured by early 
trephining,® or in what class of cases immunity is se- 
cured at all ? v 
4 Dr. Manley, of Brooklyn, demurs to the view that trephining 
after injury is so safe, and quotes cases to show the danger of hernia 
cerebri. 
6 See Ziegler's Handbook of Pathological Anatomy. 
6 This term is to be taken, of course, as covering all the measures 
used in exploring the injury of the bone and underlying parts. 5 
The absolute evidence of the character necessary 
for answering these questions is small in amount. No 
systematic attempt has been made by any writer to 
compare, as regards the subsequent occurrence of epi- 
lepsy, any large series of cases in which the skin, bone 
and underlying parts were treated early by the best 
modern methods of surgery, with a similar number 
which were not so treated; and, on the other hand, 
there are plenty of individual cases on record where, 
under such treatment as was adopted, the parts healed 
satisfactorily and showed later no sign of disease, and 
yet epilepsy supervened. 
Among the cases of fracture, especially of gun-shot 
fracture, occurring in our late war,7 this happened re- 
peatedly, though of course the methods then followed 
were not as thorough as those in use to-day. 
An analyses of these cases made for me by Mr. F. Cog- 
geshall, shows that five per cent, of the patients trephined 
at the time of injury subsequently had epilepsy, and 
that thirty-two per cent, of all the patients who became 
epileptic later had been trephined at the time of injury. 
It is not enough to point out that cases of epilepsy 
following properly treated fracture do not present 
themselves in our dispensaries and consulting-rooms, 
for the whole number of cases that would be admitted 
by the best surgeons as having been properly treated 
is extremely small, and the proportion of cases in 
which epilepsy occurs after fracture, treated or not 
treated, is also a small one, though the danger is apt 
to loom up prominently when we are first called to 
such a case. • 
Does the simple persistence of a depression in the 
bone, for example, without detached fragments or 
signs of inflammatory processes, at the end of a num- 
ber of years, prove that the case was not properly 
7 Surgical History of the War of Rebellion. 6 
treated at the outset? From the point of view of 
surgical treatment we should perhaps have to answer 
yes, but, in fact, it is doubtful whether the chances of 
epilepsy are really much increased by such a condi- 
tion, except where the displacement prevents the bone 
from healing properly, as sometimes happens.8 
Not only is it common enough to see depressions in 
the skull without epilepsy, but it is difficult to see why 
epilepsy should result unless the depression is the 
cause or accompaniment of osteitis or meningitis, or 
changes in the nutrition of the brain, and that these re- 
sults usually occur is not shown by the records of subse- 
quent operations or post-mortems, or by the inspection 
of the specimens in our museums. Microscopic investi- 
gations might tell a different story, but at any rate 
there is no reason to think that the simple increase 
in intracranial pressure from a moderate depression 
causes symptoms of cerebral compression, except some- 
times at the outset. If depression in itself is a cause 
of epilepsy it must be because, as Dr. Agnew suggests, 
it sets up an irritation of the dural nerves, and, in 
some way not known to us, possibly by way of neuritis, 
an impairment of the cerebral nutrition. 
It must, I think, be admitted, with regret, that the 
view which looks for so much security in the treat- 
ment of the fractured and depressed bone is not based 
upon a sufficient recognition of the obscurity which 
still surrounds the origin of epilepsy, and of the variety 
of the possible causes liable to be set in action by 
severe injuries to the head, some of which are amen- 
able to early treatment, while others are not. 
The study of epilepsy as it occurred among the Ger- 
man troops in the late Franco-German war is full of 
interest in this connection.9 
8 Compare Wagner (loo. cit.). 
0 Vol. vii, Erkrankungen des Nervensystems, Berlin, 1886. 7 
It is, in the first place, worthy of note, that by far 
the greater number of cases occurring in the German 
army and due to army life were of other than trau- 
matic origin,10 because it reinforces the view that epi- 
lepsy is usually a general cerebral neurosis. 
That it may arise from purely local cerebral disease 
seems unquestionable, especially when we consider that 
it may be excited in animals by localized faradization 
of the cortex. But in many of the traumatic cases, 
and especially where the outbreaks do not occur until 
years after the injury, influences are present affecting 
the nutrition of large areas of the brain, and these 
certainly constitute possible causes of the disease. 
Of the sixty-three traumatic cases (omitting a large 
number of epileptiform vertigos, etc., and a few un- 
classified cases) forty-six followed injuries of the head, 
seventeen, injuries of the body and limbs. 
Again, epilepsy occurred out of 
8,985 injuries of the head . , . . . 28 times = 0.31 % 
11,091 " " neck and trunk. 5 " =0.04% 
30,700 " " arms5 " = 0.016% 
35,670 •* " legs7 " = 0.02 % 
The greater number of the epilepsies from head in- 
jury appeared to be from sensitive scars of the scalp, 
combined with the effects - difficult to estimate - of 
cerebral contusion and concussion ; but that these latter 
were of themselves sufficient causes (and causes which 
are present in almost all cases of fracture) was shown 
by the history of seven cases where the head sustained 
no local injury, but only suffered from general concus- 
sion. 
The sensitiveness of the scars of the scalp seems to 
have been due to the bruising of the skin against the 
hard underlying surface by bullets or fragments of 
10 Fatigue, acute disease, excitement, over-exertion, fright, cold, 
general conditions. 8 
shell; and the scars following sabre-cuts were gen- 
erally non-sensitive. The avoidance and removal of 
such scars would, of course, be eminently in place, and 
the same may be said of irritations of the dura. 
It may be easily conceived that, besides fractures 
with displacement, cases of healed fracture would oc- 
casionally present themselves where - as a protection 
against epilepsy - trephining for the removal of sus- 
pected irritation of the dura would be justifiable. 
Local injuries of the brain are recognized in these 
reports, as well as by all surgeons, as a possible cause 
of epilepsy, and these local lesions are liable to be 
beyond the reach of such surgical treatment as will 
remove the danger of epilepsy. 
Dr. Keen11 has, to be sure, suggested the impor- 
tance of the systematic removal of disorganized brain 
tissue, and this may mark a decided advance over 
Wagner's method,12 which consisted in removing only 
such parts of the brain as protruded beyond the dura, 
but it is too early to tell how thoroughly this plan can 
be carried out or with what results. 
It is quite possible that we attribute too much im- 
portance to the irritation at the seat of fracture as 
the cause of the subsequent epilepsy, instead of con- 
sidering it as only one, though usually the chief of 
several contributive causes. At any rate the following 
facts should be borne in mind before we commit our- 
selves to a definite conclusion. 
(1) Traumatic epilepsy is by no means always of the 
localized, so-called "Jacksonian" type. In many cases 
the loss of consciousness is as early and as sudden, and 
the first convulsive symptoms as widespread, as in or- 
dinary epilepsy, and although the irritation of the dura 
at the seat of fracture might account for such attacks, 
11 American Journal Medical Sciences, September, 1891. 
12 Compare Wagner, Volkmann's Klinsche Vortrage, Nos. 271, 272. 9 
we have no right to consider that it is the only or even 
the principal cause, so long as other possible causes 
are present, and this, in severe head injuries, is usually 
the case. As a rule, whether the skull be fractured or 
not, the brain is injured in a number of different parts, 
and the lesions of the-brain near the seat of injury to 
the bone are liable to be much more extensive than 
the osseous fracture, and more or less independent 
of it,.18 
Either one of these various lesions, as well as the 
general injury which the brain sustains from concus- 
sion, are adequate causes of epilepsy, and it is not 
improbable that they may work together as con- 
tributive causes. Of course, even if this be true, we 
are not relieved from the duty of treating the original 
wound so as to secure a healthy and rapid repair of all 
the injured tissues, including the brain, so far as this 
is possible, but even after doing this we should be 
guarded in our prognosis. I shall refer again below 
to the important subject of the contributive action of 
several partial causes in inducing epilepsy even of the 
Jacksonian type. 
(2) In many cases there is a considerable interval, 
often years in length, after the injury and before the 
epilepsy appears. Are we to assume that, during this 
period of latency, the hidden danger is silently draw- 
ing nearer, or is it more probable that while the irrita- 
tion remains the same some new cause comes in to 
precipitate the outbreak ? If the former is probably 
true, have we a right to assume that the series of 
nerve and brain changes resulting in the epilepsy are 
alone those which have the injury at the seat of frac- 
13 Widespread haemorrhagesand softening often ending in adhesive 
meningitis, are extremely common. See Byrant, Hunterian Lec- 
ture, Lancet, June, 1888 ; also Duret, Traumatismes ; and 
an interesting case reported by Walter Channing in this Journal, 
July 8, 1886. 10 
ture as a focus? Is it improbable that the inflamma- 
tions and irritations starting from other foci of injury 
to the bone, membranes or brain, play their part in 
inducing the result? The answer to this question 
must depend upon the evidence with regard to the 
contributive influence of partial causes. 
The immediate causes of epilepsy in these traumatic 
cases are so obscure and baffling that we ought to keep 
ourselves in a very catholic spirit during our search 
for them. 
The only way to answer the question as to what 
are the significant alterations that occur before the 
attacks appear would be to tabulate all the morbid 
changes which do take place during this interval and 
that could possibly be causes of epilepsy, and then try 
to discriminate between their effects. 
The physiological characteristic of the epileptic 
brain is generally believed to be that a greater or less 
portion of its ganglionic matter has acquired the habit 
of discharge under less than the normal stimulus; and 
from what we know of the physiology of the nervous 
system it is fair to assume as probable that this liabil- 
ity to premature discharge might be brought about in 
three general ways: (a) by modifications of the nutri- 
tion of some particular centre or area of the brain ; 
(6) by impairment of the inhibitory relations between 
different parts of the brain ;M (c) by an unnatural in- 
crease in the number or force of the stimuli tending 
to provoke the discharge of a given part of the brain. 
It is in this latter way that we may suppose "reflex" 
epilepsy to be caused, and we might class as " reflex " 
- at least for purposes of investigation - those epi- 
leptic attacks which are produced by the action of one 
part of the brain upon another. 
In seeking the cause of epilepsy from injuries of the 
11 See Hare's recent monograph on epilepsy. 11 
head, such as fracture with depression, we are too 
prone to look only at the lesion indicated under a, 
and fail to recognize sufficiently the more distant and 
obscurer lesions falling under b and c. 
I think there is reason to suspect that even when 
the " signal symptom " of an epileptic attack, in a case 
of head injury or cerebral disease is sharply localized, 
the responsibility for the outbreak should not always 
be laid exclusively at the door of the centre especially 
correlated with this " signal symptom," but that it 
often implies an abnormal condition of other parts 
of the brain, or of the brain at large. Certainly a 
number of cases have been reported 15 of epilepsy of 
the Jacksonian type where careful examination has 
failed to reveal any lesion of the corresponding cen- 
tres in the cortex. 
We do not yet know the anatomical correlates of 
the epileptic state with enough exactness to make it 
worth while to describe them, but we may hope to 
arrive at them eventually by a conscientious study, 
macroscopic and microscopic, of the changes occurring 
in epileptic brains, especially during the pre-epileptic 
stage. 
We do know already that during the latent stage of 
traumatic epilepsy the morbid changes developed by 
the injury (which may have several centres) are liable 
to spread laterally (Ziegler) as well as to become locally 
more intense ; and we know further that localized epi- 
lepsy is liable to occur in brains which have been for a 
long time the seat of extensive and progressive morbid 
processes, as in the case of the post-hemiplegic epilepsy 
of children, and the epilepsy in paretic dementia. 
Again, we know that influences acting on sensory cen- 
16 Charcot and Pitres : Rev. Mensuelle, 1878, xi. See also Lbwen- 
feld : Arch fiir Psych., etc., vol. xxi; and Kramer : Jahrbuch fur 
Psych., 1891, 1. 12 
tres in the brain, such as fright, or fatigue, or toxic 
substances in the blood, may precipitate an attack, or 
even cause the disease. Lbwenfeld 16 calls especial at- 
tention to the fact that epilepsy having its starting 
point in the irritation produced by a tumor or other 
gross lesion, may remain latent until some other gen- 
eral cause comes in to increase the effectiveness of the 
local cause. 
It is reasonable provisionally to suspect, therefore, 
that in the traumatic cases, multiple and spreading 
lesions which often exist, may contribute to increase 
the injurious effect of a predominant local injury. 
It is undoubtedly true that purely local irritations of 
the cortex may excite epileptic attacks, just as these 
may be excited by localized electrical stimulation ; but 
there is a body of facts, to which I think too little at- 
tention has been paid, which indicate that both in so- 
called idiopathic epilepsy and in some forms of trau- 
matic epilepsy, the special and "localized " auras and 
convulsions are sometimes only the expression of a 
morbid condition involving a large cerebral area, or a 
whole hemisphere, or the whole brain, just as the 
feeling of anger may cause habitually, in one per- 
son a clenching of the fists, in another a frown or a 
paleness of the face, in another a sense of intellectual 
inhibition. 
The character of the first, and, through the estab- 
lishment of habit, of the subsequent outbreaks, would 
then be referable to a greater physiological excitability 
of one or another part of the brain, either native as 
in the case of the hand and face centres, which, as 
Hughlings-Jackson long ago pointed out, are so prone 
to be the first to discharge in ordinary epilepsy, or 
due to local disease or irritation of the brain or of the 
peripheral nerves as in traumatic and reflex epilepsy. 
16 Ldwenfeld : Arch, fUr Psych., etc., vol. xxi. 13 
This principle has been abundantly established by 
both physiological experiment and clinical observa- 
tions,17 but its practical significance as necessitating a 
modification in the application of the doctrine of the 
localization of functions in the brain,18 has not been 
sufficiently dwelt upon. The character of the most 
important pieces of evidence may be briefly indicated 
as follows : 
(1) The experiments of Ferrier,19 of Paueth,20 of 
Bubnoff and Heidenhain,21 and other physiologists 
have shown that the movements of certain parts, such 
as the face, may often be excited by minimal stimula- 
tions of the cortex which are ineffective as regards 
other movements. 
(2) It is asserted by Bubnoff that if an animal, in 
the course of an experiment, makes an accidental 
movement of a limb, the same movement is especially 
likely to be called out by the subsequent electrical 
stimulations of the cortex ; or that if one limb is 
stroked or moved, movement is more likely to occur 
there than in other parts under a stimulation of given 
strength applied successively to all parts of the motor 
area. 
(3) It is a remarkable fact, noted by Dr. Hughlings- 
Jackson, that the primary or " signal " (sensory or 
motor) symptoms of an epileptic attack in man occurs 
far oftener in the hand or face than in other parts, 
evidently because of the great physiological mobility 
and sensitiveness of these parts, so much so that I 
think such symptoms are of less value as indicating 
a localized irritation of the brain than the similar 
symptoms when affecting other less mobile parts, such 
17 Hughlings-Jackson and others. 
181 have called attention to some of its relations in a paper pub- 
lished in the Transactions of the New York State Medical Associa- 
tion in 1890. 
19 Localization of Functions in the Brain. 
99 Pfluger's Arch., 1888. 21 ibid., 1889. 14 
as the leg or shoulder ; that is, the hand or face may be 
thrown into convulsion alone, or primarily alone, by 
an inflammatory process covering a large area. This 
principle applies both to traumatic and inflammatory, 
and to so-called idiopathic cases. I say so-called, be- 
cause I believe that, pathologically considered, the 
traumatic and nou-traumatic cases are often closely 
analogous. 
Thus, to take one case out of many that could be 
cited, Dr. J. C. Warren operated recently, at my re- 
quest, on a patient who, in consequence of a meningeal 
haemorrhage or meningitis which had occurred during 
a typhoid fever eight or ten years before, had had a 
transient hemiplegia followed by epilepsy. 
He had distinct auras, both sensory and motor, in 
the left hand, frequently without loss of conscious- 
ness, but at the operation the lesion was found to 
cover a good part, if not the whole, of the arm and 
face area. We snipped out a bit of the cortex, simply 
guessing at the hand centre, since no electrical re- 
sponses could be obtained, and for the next week the 
hand was paralyzed, obviously because its cortical 
arrangements were especially sensitive to damage, as 
they had previously been to irritation. 
(4) Localized convulsions are liable to be set up by 
irritations at a distance from the corresponding centre. 
CONCLUSIONS. 
(1) The causes of epilepsy are numerous ; and we 
cannot hope in most cases to remove them all by early 
trephining and care of the wound, though these meas- 
ures, and especially the removal of fragments, are prob- 
ably very important. 
(2) The local and the general injury of the brain 
are probably of prime importance, as causes of epi- 
lepsy, and are to some extent independent of fracture. 15 
The former may perhaps sometimes be treated as sug- 
gested by Keen, but the latter can only be reached by 
general treatment. 
(3) The treatment of the general conditions of the 
brain, by cold and by prolonged, absolute mental rest 
is probably of great importance, and might perhaps be 
reinforced by other measures directed to the same end. 
(4) The occurrence of localized convulsions or 
auras does not necessarily indicate limited local disease, 
to be removed by operation; since, on the theory that 
the disease is a general one, it would have to find some 
local expression. It is especially true that convulsions 
or sensory auras beginning in the hand or face are un- 
trustworthy indications of the extent of the cerebral 
lesion, because the cortex corresponding to these parts 
has a high degree of irritability. 
(5) Considering the long period that usually elapses 
after an injury to the head, before epilepsy declares 
itself, a period during which the patient may be per- 
fectly well, it is reasonable to seek for some better 
term than " local irritation " to express the connection 
between the two events. We may fairly suspect that 
in most such cases a degenerative process goes on, 
which increases in extension and perhaps in intensity. 
Sometimes a neuritis, starting from the seat of injury 
seems the important link [" History of Franco-German 
War "; NothnagelJ. 
We know that such a progressive degenerative 
process as this is capable of giving rise to epilepsy of 
the localized type, independently of any gross local 
irritation, as in the case of epilepsy complicating gen- 
eral paresis, of ordinary epilepsy of certain types, 
and perhaps of epilepsy in cases of head injury with- 
out fracture, and of diffuse cerebral sclerpsis. We 
know, further, that the removal of gross irritations in 
case of an already existing epilepsy of traumatic origin 16 
usually gives only a temporary relief. It is, therefore, 
reasonable to suspect that the state of impaired storage 
power on the part of the ganglion cells, which we call 
the epileptic state, is liable to be more widespread than 
the signal symptoms of the fit would suggest; that 
we have as often to deal with impaired inhibition or 
impaired mutual support between different cerebral 
centres as with locally impaired storage power; that 
the fit may be local in its first expression because the 
centre corresponding to the initial symptom was au 
especially irritable centre (for physiological or patho- 
logical reasons), and that the impulse to its discharge 
may originate elsewhere, or be inoperative unless rein- 
forced by other influences. 
How near the epileptic condition may be to apparent 
health, that is, the possibility that the epileptic state 
may exist in a latent form, is shown by the fact that 
epilepsy interchanges with other neuroses, and that 
the attacks may be brought on by slight causes. 
This, of course, is a reason for trying, first, to inhibit 
attacks for a time so as to check the habit, and, next, 
to keep away all possible exciting causes. This may 
constitute a sufficient reason for trephining even when 
we cannot believe that we can remove the whole cause 
of the disease. 
(6) May not operation by trephining, for the sake of 
exploring the parts, be occasionally called for in the 
case of patients presenting themselves for the first time 
after a fracture has healed, but before the outbreak of 
epilepsy - say within six months or a year? In some 
respects the tissues are perhaps in better condition for 
exploration, with the prospect of finding a delimited 
and removable lesion, a short time after the injury, 
though it is also true that degenerative processes may 
already hive been initiated. This is a matter for 
further study. THE BOSTON 
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