Tetanus : lecture delivered at the College of Physicians and Surgeons, Chicago

LECTURE DELIVERED AT THE
COLLEGE OF PHYSICIANS
AND SURGEONS,
CHICAGO.

' ^ BY

NT SENINT, M. D.,

Milwaukee, wis.,

Surgeon to Milwaukee Hospital, Proeessor of
Principles and Practice of Surgery and
Clinical Surgery.

✓

1886.

x/ €^arY

TETANUS

LECTURE DELIVERED AT THE
COLLEGE OF PHYSICIANS
AND SURGEONS,
CHICAGO.

V,. BY

N. SENN, M. D.,

Milwaukee, Wis.,

Surgeon to Milwaukee Hospital, Professor of
Principles and Practice of Surgery and
Clinical Surgery.

TETANUS.

Gentlemen: Having finished the sub¬
ject of wound infective disease proper, I shall
call your attention this evening to a more in¬
frequent wound complication, in which the
symptoms point towards the cerebro-spinal
centres as the primary and principal seat of
the disease. This disease constitutes one of
the most terrible in the long list of surgical
affections, and up to the present time is
wrapped in a great deal of obscurity. I
refer to tetanus. Terrible, from the great
mortality attending it, and from the intense
suffering with which it is accompanied; ob¬
scure, because from the present standpoint of
pathology, we are still in ignorance as far as
its essential nature is concerned. Tetanus, I
will define as being a disease of the nervous
system, due to infection of a specific charac¬
ter, combined in many instances with peri¬
pheral irritation of a sensitive nerve; it is
characterized by spasm of definite muscular
groups, and attended by a continued form of
fever. If I include the adjective “infective”
( 3 )

4

in tetanus, it is more on account of reasoning
by analogy than positive pathological or
clinical demonstration; nevertheless analogy
should teach us that the well-marked period
of incubation between the supposed time of
infection and the development of the active
symptoms resemble other forms of infective
diseases very closely. That the direct cause
of tetanus is due to a specific microbe, is
claimed by a number of the most eminent
writers, and further study and research will
undoubtedly substantiate its infectious char¬
acter. This disease is not a new one, inas¬
much as it was well known to and described
by Hippocrates, who recognized both an idio¬
pathic and traumatic form, the latter of
which he referred to wounds, abrasions, and
to various pathological conditions indepen¬
dently of traumatism. Most all of the old
classical works contain lengthy chapters on
this subject, which reflect the most diverse
opinions concerning its nature and etiology,
which have been promulgated by different
authors at various times.

In considering its geographical distribu¬
tion, it has been observed that it is more fre¬
quently met with in the torrid zone, and
more especially in India and South America.
Statistics also show that in these countries
the disease is noted for the gravity of its

5

symptoms and its greater mortality. In
speaking of race influence, it can be stated
that the colored races, as a rule, are more
subject to it, and when suffering from the
disease, it is usually attended by a greater
mortality. Age appears to exert a predis¬
posing influence, as after exclusion of tetanus
neonatorum, at least 40 per cent, have oc¬
curred in patients 10 to 30 years of age. In
order to prepare you for a pathological de¬
scription of this affection, I shall call your
attention to a form of toxic tetanus produced
by the introduction into the circulation of
certain chemical poisons. There is, how'-
ever, this difference between this form of
tetanus and traumatic tetanus ; that in the
former case the active symptoms of the dis¬
ease make their appearance immediately
after the poison has been brought in contact
with the cerebro-spinal centres by the circu¬
lating blood. There is no period of incuba¬
tion ; no premonitory stage. The tetanic
symptoms are well marked and fully devel¬
oped as soon as the toxic effects of the drug
have manifested themselves. The agents in
our materia medica which are known to pro¬
duce certain forms of tetanus, are strych¬
nine, brucin, ergotine, and thebain; the
forms of tetanic convulsions, however, vary
according to the drug which has been ad-

6

ministered. Taking strychnine poisoning as
a type of toxic tetanus, we find that the
pathological conditions are always referable
to vascular changes in the brain and spinal
cord—changes marked by an increased af¬
flux of blood, by an active hvpenemia or
congestion, which later result in morpholog¬
ical changes indicative of the first symptoms
of inflammation. Experiment has estab¬
lished the fact that the reflex action attend¬
ing toxic tetanus is the result of excessive
innervation from the spinal cord. If the
spinal cord in an animal is crushed at a cer¬
tain point, tetanic convulsions will only take
place in the muscles supplied by the nerves
from the intact portion of the cord. If,
again, you should divide the posterior roots
of the spinal cord near their exit from the
spinal canal, or the posterior columns of the
cord, there will be no response to the toxic
irritation in the muscles supplied by the
nerves which have been divided, or below
the section of the cord. Furthermore, if
previous to the intoxication you should re¬
move the brain, the pons, or even the me¬
dulla oblongata, the toxic effect of the drug
will not be impaired, showing conclusively
that 'the tetanic convulsions or spasms are
the direct result from the toxic effect of the
drug upon the spinal cord.

7

In considering tetanus as it presents itselt
to the physician and surgeon, we still recog¬
nize an idiopathic and traumatic form. By
the term “ idiopathic,” I mean a tetanus un¬
attended or preceded by an appreciable
traumatism. Traumatic tetanus, on the
other hand, as its name indicates, is that
which follows an injury. We place great
stress upon the fact that there must have
been somewhere a loss of continuity of sur¬
face, an infection atrium, as we term it,
through which the specific germs gained en¬
trance into the circulation. In many cases
of so-called idiopathic tetanus, the traumatic
lesion may have been so slight as to elude
detection at the time when the disease made
its appearance, and yet the traumatism may
have been the direct and only cause of the
disease. Of the seven hundred cases col¬
lected by Thamhayn, the disease had a well-
defined traumatic origin in six hundred
cases, while in the remaining one hundred
cases there was no apparent evidence of pre¬
vious injury found, and they were conse¬
quently classified as belonging to the spon¬
taneous variety. To impress upon you the
necessity of looking carefully for the source
of infection in doubtful cases, I will briefly
refer to a case that recently came under my
observation, where from the history of the

8

case I thought I was dealing with a genuine
case of idiopathic tetanus. The patient was
a child five or six years of age, who had
been ill for several days when it came under
my care. The case presented all the symp¬
toms of a mild type of tetanus, and in the
absence of traumatism as a cause, I consid¬
ered it as a typical case of so-called idio¬
pathic tetanus. I had trismus, opisthotonos,
and a mild form of continued fever with
considerable disturbance in the function of
the vascular system. After treating the
case for a week or so, I accidentally one day
found an exceedingly tender point in the
sole of the right foot, which corresponded to
a small cicatrix. On questioning more
closely, the patient finally admitted having
stepped upon a nail some time before, an
accident which had been entirely overlooked
by the parents and forgotten by the patient.
Unless by accident the primary cause had
been detected, this case would have been
considered as belonging to the idiopathic
variety, when in fact it was a well marked
but mild case of traumatic tetanus. I sim¬
ply make this allusion to put you on your
guard in cases of so-called idiopathic tetanus,
to search diligently and unceasingly for a
tangible primary cause, as a slight injury or
obscure cause of peripheral irritation might

9

be easily overlooked, which would lead to an
incorrect interpretation of the etiology of
the disease. There may be such a thing as
idiopathic tetanus, without any apparent
breach of surface, as specific germs may pos¬
sibly gain entrance into the circulation
through an intact mucous membrane in the
same manner as in other instances of wound
infective diseases, the microbes finding in
the cerebro-spinal centres a favorable place
of localization and reproduction. Future
research, however, will have to verify or
contradict this supposition.

In considering the exciting causes of tet¬
anus, I will allude first to peripheral irrita¬
tion. Before the infective nature of tetanus
was recognized, it was generally considered
that the disease was invariably the direct
result of peripheral irritation. Clinical ex¬
perience has demonstrated the important
bearing of irritation of sensitive nerves, at
least as a determining cause, inasmuch as
in 380 cases reported by Thamhavn, it was
found that 75 per cent, of them were the
result of injury to the fingers, toes, hands,
and feet—localities where we have an abun¬
dant supply of sensitive nerve filaments,
so that it may be accepted as a well
known and established fact that injuries of
the hands and feet are more prone to be fol-

10

lowed by tetanus than wounds in any other
locality.

Another form of peripheral irritation,
aside from the traumatic, are pathological
conditions due to inflammation, which affect
the sensitive nerves the same as when the
irritation is produced by an injury. Tetanus
produced in this manner has been observed
as a complication in pleuritis, pneumonia,
metritis; in fact, as a result of pathological
conditions which involve in the same manner
an extensive area of sensitive nerves as the
effects of traumatism. In the idiopathic form
of tetanus, authors still recognize a central
lesion or point of irritation independently of
any peripheral or eccentric pathological irri¬
tation. By this I mean central irritation by
pathological conditions involving directly the
brain or spinal cord, independent of trau¬
matism. Cases have been observed in the
post-mortem room where well marked patho¬
logical conditions existed in the brain and
spinal cord, independent of either traumatic
pathological peripheral irritation, where dur¬
ing life the characteristic symptoms were
well marked. These cases may serve to ex¬
plain the theory that the specific germs of
tetanus once introduced into the system may
have a special elective affinity for the nerve
centres, and may there manifest their toxic

11

influence by producing pathological condi¬
tions which induce tetanic spasms. Specific
infection, then, must be recognized as the
most important and essential factor in the
etiology of tetanus. Recent literature on
this subject seems to have established the
fact, that like wound infective diseases,
tetanus is simply an expression of a specific
form of intoxication, which implicates, prin¬
cipally, the cerebro-spinal centres, the result
of the introduction of specific microbes.
This hypothesis does not lack analogy in dis¬
eases which are marked by a well-defined
period of incubation, where a certain time
elapses between the introduction of the virus
and the active development of the symptoms;
in other words, diseases preceded by a period
of incubation, in contradistinction to diseases
which are caused by the introduction of a
formed chemical poison, means simply that
the germs introduced at the time when the
injury was inflicted keep on multiplying
until a sufficient number of them have been
generated in the system, when the toxic ef¬
fects are announced by the active develop¬
ment of symptoms. If tetanus were the re¬
sult of the introduction into the system of a
pre-formed or chemical poison, the active
stage of the disease would commence as soon
as the poison had entered the circulation,

12

which evidently has never been the case. If,
however, a certain period elapses from the
time of supposed infection until the active
development of the disease, we recognize the
fact by well demonstrated analogy that these
specific germs have been introduced into the
system, and have found a favorable soil for
their growth and multiplication in the cen¬
tral nervous system until their direct toxic
effects are manifested by tetanic convulsions.
The period of incubation in tetanus is not as
well marked and definite sis in some other
infectious diseases, but the same can be said
of other affections where there can be no
doubt concerning their microbic origin, hy¬
drophobia, for instance. The most charac¬
teristic symptom of tetanus consists in tonic
spasm of certain well-defined muscular
groups, as a rule, the affection following in a
descending direction. We will, for the sake
of convenience, assume that tetanus has fol¬
lowed a compound comminuted fracture of
the leg, and will describe the symptoms in
their proper order. About the fifth or sixth
day (the earliest period of incubation) our
patient will probably complain of a certain
ill-feeling in the broken limb, marked by
irregular jerking; if, at the same time, he
complains of general malaise, loss of appe¬
tite, of symptoms indicative of infection, we

13

should realize that these premonitory symp¬
toms are but the precursors of the gravest of
all wound complications—tetanus. If these
early symptoms are followed a little later by
the appearance of trismus, there can be no
further doubt as to the nature of the disease.
By trismus, I mean a contraction of the mus¬
cles of mastication, as evidenced bv difficulty
in opening the mouth. Going still further
down, other muscular groups are implicated,
and we have what is known as opisthotonos,
a bending backwards of the body in contra¬
distinction to emprosthotonos, a bending of
the body in the opposite direction. If the
muscles on one side of the chest are
affected, we have pleurosthotonos; if still
further, all the muscles in the body (usually
the extensors, however,) are affected, and the
entire body becomes rigid, we have ortho-
totonos. If the muscular spasms have be¬
come well developed, involving the area of
the respiratory muscles, we expect an impair¬
ment of the function of respiration. By
spasmodic contraction of the muscles con¬
cerned in that function, respiration becomes
imperfect on account of the constant rigidity
of the muscles which are active in producing
the respiratory movements.

The temperature is increased in almost
every case, the rise depending upon the in-

14

tensity of* the infection, the acuity of the
attack, and especially the rapidity with
which the disease progresses. A limited area
of muscular rigidity and a slight rise in tem¬
perature, are favorable prognostic indications.
In some instances the temperature has been
found unusually high. A temperature of
108°, even 110°, as observed by Wunderlich
and Billroth, denotes great danger, and is
almost without exception followed by a fatal
termination. These authors have placed
stress upon the importance of temperature
in tetanus, watching its rise in the axilla at
different times of the day, and observing that
an increase of temperature beyond 104° or
105° is usually followed by death. Another
curious fact has been noticed, and that is an
increase in temperature after death. Wun¬
derlich explains the high temperature in tet¬
anus by assuming a loss of function, or a loss
of control of the heat moderators in the
brain, the heat centres being impaired by the
direct action of the poison upon this particu¬
lar portion of the cerebral mass. The post-
mortal rise in temperature has been attributed
by Fick and Huppert to evolution of heat
during the coagulation of the myosin. The
sensorium usually remains unimpaired to the
last, showing distinctly that that portion of the
brain concerned in that function remains un-

15

impaired, that the disease for some unknown
reason expends itself upon the motor tracts,
and especially upon that portion of the cere-
bro-spinal system connecting the brain and
spinal cord, the medulla oblongata. When
the spasms are severe and prolonged, the
respiration becomes impaired, the pulse small
and rapid, and the surface of the body is
bathed with a profuse perspiration. As the
disease progresses, evidences of capillary
stasis become more and more apparent, the
eyes are suffused, and the visible mucous mem¬
branes livid; the tongue is coated, appetite
diminished, and the bow T els are obstinately
constipated; all causes of peripheral irritation,
as a draft of air, loud noises, etc., will pro¬
voke easily a repetition of spasmodic attacks.

The first attempt at an intelligent explan¬
ation of the morbid anatomy af tetanus w 7 as
offered by Rokitansky, who found on exam¬
ining the nerves supplying the injured part
evidences of inflammation in the nerve it¬
self, and hence described the disease as a
form of neuritis, a neuritis ascendens. As
proof of this view of the disease he de¬
scribed the pathological conditions found in
the affected nerves as consisting in an exuda¬
tion between the nerve fibres, granular de¬
generation and hyaline changes in the nerve
fibres themselves, finally resulting in com

16

plete disorganization and disintegration. He
regarded the disease essentially as a “ neuritis
ascendens,” the morbid process commencing
in the nerve at the point of injury, and ex¬
tending by continuity to the cerebro-spinal
centres. All pathologists agree that the
brain and spinal cord are always found in a
state of congestion, but some go still further
—Lockhart, Clarke, and Dickinson, for in¬
stance, asserted that the brain was not only
hvpersemic, but that there was an actual in¬
flammation of the cortex of the brain itself,
resulting in granular disintegration. Others
have found, on examining the spinal cord,
pathological changes well marked in that
portion of the nervous system, consisting of
hypersemia, extravasation, softening, in¬
creased proliferation of connective tissue, de¬
generation of the anterior and posterior col¬
umns. Tyson, on the other hand, found in
two cases well marked degeneration of the
central canal and disintegration of the pos¬
terior columns of the cord. Aufrecht found
cellular atrophy in the anterior and posterior
cornua of the cord and granular degenera¬
tion of the gray substance of the cord.
From all that I have stated it appears evi¬
dent that so far no unanimity exists among
pathologists in localizing the central lesion,
but from what we have learned it becomes

17

apparent that the most constant pathological
changes are found in the upper portion of
the spinal cord.

In considering the diagnosis, particular
attention should be paid to the history of
the case, fully eliciting the possibility of any
previous traumatism or infection serving as
a tangible cause. In cases of spasm of
definite groups of muscles, we should ascer¬
tain the existence or absence of fever by the
use of the thermometer.

Although no uniform pathological condi¬
tion appears to have been found character¬
istic of tetanus, the weight of evidence points
towards the spinal cord as the central seat of
the lesion, in this respect showing a resem¬
blance to hydrophobia, an affection which it
simulates in many respects.

Muscular spasm resulting from a neurotic
source and limited to a group of muscles
unattended by general infection, is not
marked by rise in temperature. If, on the
other hand, we have muscular spasm at¬
tended by an increase of temperature (par¬
ticularly if we have reason to believe that it
is the result of previous traumatism or infec¬
tion), the case becomes suspicious, and merits
a scrutinizing examination. In tetanus, as
a rule, the muscles on the extensor side are
affected, while in cases of inflammatory dis-

18

ease in bones and joints, the contractions oc¬
cur on the flexor side.

In the differential diagnosis, consider the
possibility of toxic tetanus from poisoning
with strychnine or any of that class of rem¬
edies which are known to produce tetanic
spasms. The mental condition of the pa¬
tient and the surrounding circumstances of
the case will aid you greatly in eliminating
uch a cause. In strychnine poisoning,
orthotonos is produced as soon as the drug
has been absorbed, and tetanic spasms of
muscular groups pass in a descending direc¬
tion.

Hysteria may simulate tetanus, but you
must remember that your hysterical patient
cannot, for any length of time, maintain
muscular spasm limited to definite muscular
groups. The pupils of the eyes in tetanus
are generally contracted, and the tempera¬
ture is increased, while in hysteria both of
these symptoms are absent.

The next disease which may be mistaken
for tetanus is cerebro-spinal meningitis. If
an epidemic of this disease prevails in your
locality, carefully consider the differential
diagnosis. In cerebro-spinal meningitis the
symptoms point equally to an affection of the
base of the brain, while brain symptoms
proper do not belong to the clinical history

19

of tetanus; hence, you will encounter symp¬
toms in the former which point towards an
active inflammation of the meninges of the
brain, as well as of the spinal cord. If the
disease has lasted for a sufficient length of
time, you will look for the symptoms aside of
muscular spasm which characterize cerebro¬
spinal meningitis. Basilar meningitis is at¬
tended by symptoms indicating irritation at
the base of the brain; and as it is almost al¬
ways of a tubercular nature, you will care¬
fully inquire into the history of the case, and
concomitant tubercular lesions.

The last disease which it might be mistaken
for is hydrophobia. The muscular spasms
in hydrophobia are more of a clonic charac¬
ter, and remain limited to the muscles of
deglutition and respiration. In the progno¬
sis you must be guided, in the first place, by
the extent of the central lesion, as evidenced
by the number of muscular groups affected.
If the central irritation is circumscribed,
only a limited number of muscular groups
are affected, and when this is the case, we
are usually dealing with a mild form, of the
disease. If, on the other hand, in the early
history of the disease there is rigidity of an
-extensive muscular area, the disease is a
grave one ; and more particularly if at the
same time, as will likely be the case, there is
a high temperature. Time is one of your

20

most important elements in rendering a prog¬
nosis. Hippocrates always considered the
prognosis dubious the first four days. Severe
cases may terminate fatally from the second
to the sixth day, usually, so that time gained
after the sixth day, with the symptoms re¬
maining stationary, the prognosis becomes
more favorable as time increases. In the
mild cases of tetanus, terminating in recov¬
ery, it may take weeks and sometimes months
before all muscular rigidity has disappeared.
I have observed several severe and acute
cases where within forty-eight hours after the
commencement of the first symptoms, death
occurred; but after the sixth day, with symp¬
toms remaining stationary, the surgeon’s hope
increases as time elapses.

Another important point is the probable
eause of the disease. If the injury has been
slight, infection limited, the disease assuming
a mild type, your prognosis may be favor¬
able ; but should the symptoms develop them¬
selves incidental to injuries grave in them¬
selves, the prognosis becomes correspondingly
serious, so that in tetanus attending severe
lesions, followed by traumatic infection of
other types, attended, perhaps, by septicaemia
or pyaemia, our prognosis always must be un¬
favorable ; in other words, if there is no pos¬
sibility of removing the primary cause or

21

source of infection or irritation, the prognosis
increases in gravity.

Like in all other forms of wound infective
diseases, the prophylactic treatment is the
most important. Practically, it is important
to recognize the microbic origin, and insti¬
tute early and efficient treatment in accord¬
ance with this supposition. I therefore,
again, emphasize the necessity of adopting
aseptic measures in the treatment of wounds,
with a view not only of preventing suppur¬
ation, but also other forms of infection.
There can be no question but that since the
introduction of antiseptic surgery tetanus
has been uncommon. The clinical fact is
patent that it is prone to follow injuries
where a foreign body has remained in the
wound, and where subsequently from this
cause there is greater danger of infection on
the one hand, and peripheral irritation on
the other ; this is especially true of injuries
about the hand. It is therefore of para¬
mount importance to treat slight injuries of
the hand, and more especially 4th of July
injuries, which so frequently end in tetanus,
with the greatest care. No matter how
trifling the injury may be, disregard in this
direction has only too often been followed by
the most serious consequences. A small
Wound of the hand when neglected may serve

22

as aii avenue for the ingress of germs, which
according to their action may destroy life in
a variety of ways. If necessary, enlarge
the wound, search carefully for foreign
bodies, if there is reason to believe that they
are present; take plenty of time to secure
an aseptic condition for the wound, and con¬
duct the subsequent treatment on strictlj
antiseptic principles. If- suppuration should
take place, be sure to secure efficient drain¬
age, and resort to frequent antiseptic irriga¬
tions. By following these directions you
will not only have the satisfaction of secur*
ing the most favorable condition for the heal¬
ing of the wound, but you will have, at the
same time, carried out the most efficient pro¬
phylactic treatment against tetanus.

In the curative treatment, we consider
first the importance of removing the source
of infection and irritation. If a foreign
body remains in the wound, search diligently
for it, and if possible remove it. If the in¬
jury is attended by inflammation, burrowing
of pus, destruction of tissue underneath the
skin, secure ample and efficient drainage;
in other words, convert the wound, as near
as you can, from a septic into an aseptic
condition. If we are dealing with a painful
or tender cicatrix, which by producing
peripheral irritation may determine tetanic

23

spasms, it is proper to excise it. We can
readily conceive that the infection may have
been so mild as to produce only slight
changes in the spinal cord, which but for
some peripheral irritation would not have
resulted in muscular spasms, and these are
the cases where the removal of the exciting
cause of’the spasms is followed by a cure.
I recollect a case of a mild form of tetanus,
the result of a slight injury at the distal ex¬
tremity of the index finger, which left a
painful, tender scar, where the trismus was
always increased by pressure, and which
yielded promptly to removal of the exciting
cause.

Another practical point in the treatment
is the consideration of the propriety of am¬
putation. If we are dealing with a com¬
pound comminuted fracture of the leg or
a rra, attended by all the symptoms of wound
infection, and if present indications point
towards the fact that the limb, independently
of the existence of this complication, could
not be saved, it is only rational to resort to
amputation. It is, however, proper to state
that in the great majority of the cases thus
treated the tetanus continued unabated after
the operation, and only in exceptional cases
has life been saved by this procedure. Rec¬
ognizing the fact that according to Rokitan-

24

sky’s theory, tetanus simply means “ an as¬
cending neuritis from the point of injury to
the spinal cord,” attempts have been made to
arrest the progress of the disease by inter¬
rupting the nerve above the disease by nerve
section, but results have shown that this op¬
eration had no effect in modifying the ter¬
mination of the disease. You will readily
understand why, if you assume its central
location and its infective character. If tet¬
anus were simply a “ neuritis ascendens,”
we might reasonably expect to arrest the
progress of the disease by division of the
nerve trunk, by making the section through
healthy tissue on the proximal side of tbe
inflamed portion of the nerve. Granted
that this operation would be efficient in pre¬
venting extension of the inflammatory pro¬
cess, it would not be applicable in all in¬
stances, from the inability of the surgeon to
locate the disease with sufficient accuracy.
Imagine an injury involving the palm of the
hand, where we have filaments of different
nerves implicated; it would be difficult if not
impossible to ascertain in every case which
nerve trunk was the seat of irritation. Tak¬
ing it for granted that the neuritis is simply
a local expression of the nerve injury, and
that the real cause of tetanus consists in a
specific infection, expending itself upon the

25

brain and spinal cord, all efforts at correct¬
ing or curing the disease by submitting
nerve trunks to operative measures are in
discord with the true pathology of the dis¬
ease. A somewhat similar and more recent
operation for the same object as nerve section,
we find in nerve stretching. For the last
few years it has become the operation for all
obscure nervous diseases, such as locomotor
ataxia and central irritation of various
kinds; consequently it is not surprising that
it has been resorted to in the treatment of
tetanus.

Benedict collected twenty-four cases of
traumatic tetanus treated by nerve-stretch¬
ing, of which number four recovered. I have
stated that the disease in the milder form
shows a tendency to cure itself; consequently,
all operative measures which have been re¬
sorted to for the purpose of arresting its pro¬
gress must be accepted with a great deal of
caution, inasmuch as statistics have shown,
on the whole, that twenty-five per cent, have
recovered without operative interference by
the ordinary treatment; consequently, we
have no proof that these four cases would
not have recovered without nerve-stretching.
All the possible good that can accrue from
operations on nerve-trunks is simply to in¬
terrupt the nerve-current between the central

26

disease and the peripheral irritation, and in
many instances it is impossible to decide
which of the larger trunks connects the two.

The medical treatment consists in the ad¬
ministration of drugs which are known to
relieve muscular spasm. In animals tetan-
ized with strychnine the spasms are promptly
relieved by injecting hydrate of chloral into
the veins. Woorara has been given with a
view of relieving muscular spasm. On ac¬
count of the potency of this remedy, its ef¬
fects must be carefully watched and its use
promptly suspended as soon as its physio¬
logical action becomes apparent. It is best
administered hypodermatically. Bromide of
potassium in large doses is well known to
cause cerebral anaemia, and on this account
it should be given to relieve the hvperaemia
which is always present in the cerebro-spinal
centres. A combination best adapted to ful¬
fil the two most urgent indications, to relieve
cerebral and spinal congestion and to over¬
come muscular spasm, are chloral and bro¬
mide of potassium. The remedies should be
given in large doses, frequently repeated, un¬
til the desired result has been obtained. In
severe cases, chloroform should be adminis¬
tered by inhalation with a view of relieving
urgent symptoms; cold drafts of air, noise,
and all forms of peripheral irritation, should

27

be carefully excluded from the patient’s
room, for the purpose of securing rest, and
with a view of not aggravating reflex spasm.
Alcoholic stimulants and external heat are
indicated when the heart’s action has become
feeble from general capillary stasis.