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treatment. Every scalp wound, however, should be carefully
examined, lest it lead down to a fracture of the subjacent

(b) Fractures of the cranium are generally, but not invariably,
compound. We may meet with fissured fracture of both tables,
often radiating for long distances from the site of the blow, and
frequently associated with extra-dural haemorrhage. The extent
of a fissured fracture is best determined by radiography. Fissured
fractures often extend to the base of the skull, where they
may implicate various foramina, producing cranial-nerve palsies.
Punctured fracture, in which, at the floor of a scalp wound, there is
a small localised aperture in the cranium, is less common than a
fissured fracture, but is highly dangerous if overlooked, since it is
frequently associated with laceration of the dura and with infec-
tion of the meninges and brain-substance. Gutter fracture is very
common, running either sagitally, transversely, or obliquely, and


grooving either the outer table alone, exposing the diploe, or, more
commonly, affecting both tables of the skull.

Each of the foregoing fractures is Hable to be associated with
defressed fracture of the inner table, always more extensive than
the fracture of the outer table, indenting and often lacerating the
dura mater.

In all these fractures the subjacent brain-tissue may be pulped
by the impact, or there may be a superficial cortical haemorrhage
from laceration of the thin- walled surface-veins or from penetration
of a tough-walled venous sinus.

In every compound fracture the cardinal point to determine
is whether or not the dura — ^the great barrier against intra-cranial
infection — has been lacerated. This is determined by careful in-
spection and palpation of the wound, often greatly assisted by an
X-ray photograph. A probe should never be used to search for a
gap in the dura, for not only does it tend to make a false track, but
it may push infective material inwards towards deeper structures.
So long as the dura is untorn, sub-dural lesions usually
remain free from infection and run an aseptic course. If, how-
ever, the dura be lacerated, the brain-substance is now in
direct continuity with the septic outer world.

2. Penetrating Wounds of the Cranial Cavity. — These are
wounds in which bullets, metallic fragments, bony fragments,
and sometimes portions of the patient's headgear become lodged
within the dura at varying depths beneath the surface. Some-
times a spray of bony splinters becomes projected deeply into
the brain substance (see Figs. 233 and 234), whilst the bullet itseK
glances off or merely indents the cranium. Sometimes the bullet,
after traversing the brain, impinges on the opposite side of the
skull, where it either produces an elevated fracture or rebounds
to some other part of the brain. Metalhc or bony fragments
within the brain are often multiple. X-rays are of the greatest
value in locahsing them. Here again a probe should not be used
for their detection. Gentle palpation with the finger-tip is some-
times permissible, but the area of cortical destruction should not
be increased by the crude method of introducing the finger into
the brain- sub stance.

3. Perforating, or Through-and-through, Wounds are those in
which the missile has traversed the cranial cavity, entering
through one and coming out through another, generally a larger,


opening. The edges of the bony apertures are usually extensively
comminuted, and from them fissured fractures radiate in various
directions. Haemorrhage in the bullet-track is most abundant near
the point of entry, and tends to diminish in amount in the deeper
parts. (See Figs. 235 and 236.) Many of these cases are rapidly
fatal from shock to the vital centres in the brain-stem, associated
with intra-cranial haemorrhage. Wounds which traverse the
cerebral ventricles, or which pass through the brain-substance
beneath the ventricles, are always fatal. A few through-and-

Fict. 233. Vi„. 234.

Figs. 233 and 234. — Brain sections from the case of a patient who was admitted
moribund with total left-sided hemiplegia and a cranial gap in the right
parietal region. An area of softening extends through the centrum ovale
from the site of the tangential wound to jnst outside the posterior horn
of the lateral ventricle. No bullet or metallic fragment was found
within the brain. The haamorrhagic area was most marked near the sur-
■ face (Fig. 233), the deeper part of the softened area being free from
haemorrhage. Numerous bony splinters were driven deep into the brain,
being most numerous immediately outside the lateral ventricle (Fig. 234),
which was not penetrated.

through wounds, however, are compatible with survival, e.g.
wounds through the pre-frontal lobes or through the upper region
of the cerebral hemisphere above the level of the ventricles.

4. Large Cranial Gaps, with. Extensive Comminution, may be
produced either by glancing blows from a large missile, or as
exit-openings of through-and-through wounds. Most of them are
fatal. A few patients survive, if adequate drainage can be pro-
vided and general intra-cranial infection prevented — a rare and
lucky occurrence.



Morbid Anatomy of Brain Wounds. — Except in the case of
injuries at close range, or by large fragments of shell, as a result
of which portions of the skull and brain may be blown away, sutures
torn apart and the cranial base burst open, the amount of actual
destruction of nerve-cells and nerve-fibres produced directly, by
the bullet itself, is relatively small. Most of the structural
damage which results is caused by hsemorrhage, septic infection,
or other secondary event. Moreover, the severity of a cerebral

Fig. 235.

Fig. 236.

Figs. 235 and 236. — Perforating wound of brain. The point of entry is at the
posterior end of the left occipital lobe, one inch from the middle line. The
bullet-track crosses the middle line above the level of the corpus callosum,
and emerges through the posterior end of the second frontal gyrus on the
right side.

The heemorrhage in the bullet-track is most abundant in the left occi-
pital lobe, diminishing in amount as the track traverses the right cerebral
hemisphere. The anterior end of the track consists of disintegrated brain-
tissue, free from hemorrhage, except immediately around the aperture of
exit, where there are a few petechial points in the cortex and sub-cortex.

lesion is not necessarily proportional to that of the cranial injury.
War injuries are usually in young and healthy brains, free from
vascular or degenerative disease. Rarely is a cortical centre com-
pletely destroyed, so that in almost every case of survival, a cer-
tain amount of recovery may be expected. Cerebral concussion
at the time of the injury is common, with its frequent, feeble
pulse, low blood-pressure, and shallow, irregular respiration, fol-
lowed, if the patient survives, by a stage of reaction, with headache,


flushed face, high blood-pressure, and powerfully-beating heart
(see p. 62). Concussion varies in degree in different cases, and is
not always proportional to the apparent severity of the Vjlow.
Thus in one case a comparatively slight head-injury, without
fracture of the skull, may produce severe concussion or other intra-
cranial Eymptoms, whereas another patient may sustain a severe
cranial lesion, or even a perforating wound, and yet concussion
symptoms may be shght or transient. Cerebral compression, from
intra-cranial haemorrhage, produces a characteristic and easily-
recognised syndrome (see p. 65), which is often preceded by a
stage of cerebral irritation, during which the patient lies curled up
in bed, with all his limbs flexed, burying his head under the bed-
clothes owing to photophobia, and resenting any examination,
noise, or conversation. Meantime he suffers from violent headache,
whilst the temperature is raised to 101° or 102° F.

Meningeal adhesions usually develop within a few hours around
any wound in the dura mater. These adhesions are nature's effort
to shut off the infected area from the cerebro -spinal lymph system
and thus to prevent a diffused meningeal infection. Meningeal
adhesions of this sort constitute a barrier which should be treated
with the greatest respect, and should not be broken down by the

Structural damage of brain tissue is mainly due to the following
secondary processes :

1. Contusion or laceration by hcemorrhage, which may be
superficial or deep. A superficial haemorrhage, sub-dural or sub-
pial, is not necessarily arterial. It is often due to tearing of cortical
veins by a depressed fragment of bone, or to rupture of thin-walled
surface-veins near their point of entry into the rigid superior
longitudinal sinus. Superficial haemorrhage, whether arterial or
venous, produces signs of cortical lesion, varying with the particular
region affected. Thus in the motor cortex we have localised
paralysis with muscular rigidity and sometimes Jacksonian fits ;
in the sensory cortex, anaesthesia of cortical type ; in the visual
cortex, impairment of vision, sometimes preceded by subjective
luminous sensations, and so on. There are also various " silent
areas " of the brain which may be severely damaged without
producing any obvious focal signs whatever.

Deeper-seated haemorrhage within a bullet-track is generally
more marked near the surface of the brain. It may sometimes



extend througliout tlie track of disintegrated brain-substance, but
often the deepest part of the wound is practically free from

Severe contusions of the brain- sub stance may occur from a
bullet-wound of the head apart from traversing the cranial cavity
or laceration of the dura mater, as in the case shov/n in Fig. 237.

In this case the bullet entered the head in the mid-frontal region,
half an inch above the nasion. It then traversed the right orbit,

Fig. 237. — Contusion of right temporal lobe, wiih fracture of cranial
base, from extra-dural bullet-wouud.

producing paralysis of the ocular muscles, and emerged below the right
mastoid process, fracturing the lower jaw and paralysing the right
facial nerve en route.

At the autopsy the dura mater was found intact, but there was a
fracture of the cranial base, implicating the cribriform plate and floor
of the right middle fossa of the skull. The anterior part of the right
temporal lobe was severely contused, and also slightly the orbital
surface of the right frontal lobe.

In rare cases a second cerebral haemorrhage may occur inde-
pendently of the bullet wound, thereby compUcating the diagnosis,
as in the following case (Figs. 238 and 239) : —

A patient who had sustained a perforating trans-frontal wound,
entering, through one temporal fossa and emerging at the other, was



admitted witli complete left-sided flaccid heniijjlegia. The trans-
frontal wound was insufHcient to accoimt for his symptoms. These

Fig. 238. — Transfrontal wound. Entry through right Sylvian point.
Exit through left frontal lobe, at posterior end of F3 gyrus.

were explained, however, at the autopsy, which showed an independent
haemorrhage, the size of a walnut, above and behind the right internal

Fig. 239. — -HEemorrhage in right centrum ovale, from the case
of transfrontal wound shown in Fig. 238.

capsule, at a considerable distance from the bullet track through the
frontal lobes.


2. Acute cerebral softening or necrosis of brain-tissue occurs along
the track of a bullet wound. It also occurs tbrougbout tbe area
of brain destruction produced by the sudden impact of a projectile,
whether the superjacent cranium and dura be lacerated or not.
The superficial part of the softened area then becomes infiltrated,
to a varying extent, by effused blood, forming a hsemorrhagic
softening, whilst the rest of it, especially at the deepest part from
the surface, may remain as a pale area of simple disintegration,

Fig. 240. — Transverse wound of frontal bone, causing deep-spread abscess
of right frontal lobe, with a second commencing abscess at tip of left
prefrontal region.

free from haemorrhage. Such a softened area, if infective organisms
gain access to it, readily develops into an abscess.

3. CEdema of the brain-tissue, around the contused or lacerated
area, is a common occurrence. It is due to local obstruction of
the venous circulation. This oedema throws out of action, for a
time, a wider area of brain-tissue, with a corresponding increase
in the extent of the focal signs and symptoms. Fortunately it
tends to subside gradually, and with it the brain symptoms corre-
spondingly recede.

4. Abscess (or suppurative encephahtis) may form around
the infected track within the brain. Unless successfully evacuated
and drained externally, the suppurative process tends to spread



inwards, and ultimately, after weeks or even months (even
after the original wound may have healed on the surface),
may reach one of the ventricles of the brain (see Fig. 240). Death
is then inevitable within a few days, from infection of the cerebro-
spinal fluid. There is sometimes a premonitory stage of shght
pyrexia with reappearance of traces of the former focal signs. The
infection passes outwards from the ventricles, through the great
transverse fissure, to the base of the brain, and thence all over the
meninges, from base to vertex. Retained foreign bodies, whether
fragments of bone or bullets, which have carried infection inwards,
are frequent causes of brain abscess, but
abscess may also occur even when no foreign
body is present. Suppuration is specially
common within or near a cerebral hernia.

5. Diffuse purulent meningitis is the cause
of death in three-fourths of the fatal cases
(apart from immediate fataKties on the field).
It is generally more severe at the base of the
brain than on the convexity. Sometimes the
meningeal infection spreads directly from the
neighbourhood of the wound in the dura,
before there has been time for defensive
adhesions to fence off the sub -arachnoid
space. In other cases infection of the
cerebro-spinal fluid and meninges occurs from
subsequent operative procedures, which break
down protective adhesions, e.g. during an
attempt to reach a foreign body within. In
other cases, again, meningitis is secondary
to infection of the cerebral ventricles, and it is in this way that
a large proportion of cerebral abscesses cause death.

Hernia cerebri is a condition in which a bulging mass of
brain tissue is prolapsed through a cranial opening (see Figs. 241
and 242). The contents of the hernial swelling are cerebro-
spinal fluid and brain-tissue, in varying proportions in different
hernise. The swelling usually pulsates, synchronously with the

Hernia cerebri is caused by increased intra-cranial pressure,
whether from meningitic changes following a brain-wound or from
the continued growth of an inoperable intra-cranial growth. Some-

2 1

Fia. 2-il.— Bullet-wound
of right frontal lobe.
The only abnormal
sign, on examination
of the nervous system,
was absence of the
left abdominal reflex.
Together with this
there was incontin-
ence of urine. There
was no paralysis, sen-
sory or motor, and the
mental functions were



times a hernia cerebri occurs after a decompressive craniectomy
for the reUef of intra-cranial pressure, e.g. from brain tumour. The
mere presence of a gap in the cranium does not cause a healthy brain
to prolapse through the gap (see Eig. 243). Hernia cerebri following
a brain wound is therefore always a sign of sepsis. In cases that
are getting worse, from increasing intra-cranial pressure, the
herniated tissues often become oedematous owing to strangulation
of the neck of the hernia by the rigid dura and bone. Pulsation
then diminishes and disappears, and the hernia forms a fungus-
like mushroom- shaped mass, which may subsequently slough away.

Fig. 242. — Hernia cerebri of right pre- and post-central region,
associated witli progressive left hemiplegia.

It is remarkable how large an area of cerebral tissue may be in
some cases prolapsed into a hernia without producing paralysis
or other symptoms. Subsidence of a hernia is a favourable sign,
and indicates that the intra-cranial pressure is subsiding.

Transient opic neuritis develops with a large proportion of the
more severe brain-wounds. It does not necessarily foreshadow a
cerebral abscess or a septic meningitis. It comes on within a day
or two of the original injury, and is probably caused by serous
meningitis or meningo- encephalitis, secondary to the local haemor-
rhage or other lesion.



Focal Signs of Brain Injuries
(1) Lesions of the cortical motor areas of the pre-central region

and of the adjacent posterior end of the second frontal gyrus
(Fig. 3, p. 5) are the easiest of all to recognise, since destmction
of these centres produces monoplegia, facial, brachial, or crural,
as the case may be — or, in more extensive lesions, hemiplegia of
the contra-lateral side. Superficial lesions such as sub-pial
haemorrhage, or localised meningitis, or a depressed fracture
pressing on the cortex, may also cause Jacksonian fits, which

Fkj. 243. —Bullet-wound of right frontal lobe, without hernia
cerebri. No mental affection. No incontinence of urine.
No abnormalitj^ of cranial nerves, nor of sensory or motor
functions, save for absence of both abdominal reflexes.

commence in the corresponding muscular group. These Jack-
sonian fits are usually followed by a temporary increase of
paralysis in the previously convulsed limb. A localised fit of this
sort may either remain limited to one limb, or segment of a limb,
or it may spread so as to affect the muscles of the whole of that
side of the body. It may then cross the middle line, becoming
bilateral, with unconsciousness and tongue-biting. Even without
Jacksonian fits, it is not uncommon to have marked tonic rigidity
of the paralysed or paretic limb. This is always suggestive of a
superficial lesion such as a sub-dural haemorrhage.

Lesions confined to the upper end of the pre-central gyrus
(Fig. 244, p. 500) produce crural monoplegia, those at the lower
end cause facial (Fig. 245) or f acio-lingual monoplegia (Figs. 246 and
247), whilst lesions half-way down the pre-central gyrus cause



brachial monoplegia. A purely cortical lesion, in order to produce a

complete hemiplegia, must extend
from the upper to the lower end of
the pre-central gyrus. If, however,
the lesion is sub -cortical, the more
deeply it penetrates through the
centrum ovale towards the internal
capsule, the more completely are
the converging fibres of the pyra-
midal tract involved, so that quite
a small lesion, if deeply situated
in the white matter of the internal
capsule, may produce complete
hemiplegia. In other words, the
more superficial the lesion, the
greater the tendency to mono-

FiG. 244.— Bullet-wound immediately plegia ; the deeper the lesion, the
to left side of middle line, exactly ^^^^ ^-j^^^ ^^^^ ^^ ^^ ^^^ j^g^^-.
over upper end or pre-central _ ■'

gyrus. Horse-shoe flap, crossing plegia, often accompanied by
"S. 'Sem1dSL33! temianaesthesia and even by hemi-

Kolandic fissure are also marked anopia (see pp. 9 and 10).

on the scalp. Tangential wounds of the vertex

often cause a bilateral lesion of the upper ends of both pre-

FiG. 245.— Shell wound at right Rolandic fissure, causing left
facial monoplegia.

central gyri, producing bilateral monoplegia of both legs-
crural diplegia.



Left-sided lesions of the pre-central region, when they imphcate
the motor speech-centre in Broca's convolution, or the sub-cortical

Fig. 246. — Bullet- wound of head, producing pre- and post-Kolandic
lesion, with left-sided facio-liDgual monoplegia, also loss
of.J joint-sense [in left hand, with astereognosis, but without
motor weakness of limbs.

Figs. 247 and 247a. — Left-sided facio-lingual monoplegia from the cortical wound
shown in Fig. 246; Fig. 247 shows the condition at rest, Fig. 247a the
appearances on protruding the tongue.


fibres connecting it witli the other speech-centres, produce motor
aphasia, in addition to monoplegia or hemiplegia, as in the fol-
lowing case : —

The patient was admitted to hospital unable to furnish any account
of his previous history. He had a small bullet hole in the scalp, two
inches to the left of the middle line and one inch in front of the middle
of the Rolandic fissure. The patient was unable to utter any sounds,
not even "yes" or "no." He was able, however, to understand and
execute with ease both written and verbal requests. On trying to
write with his left hand, he made such gross spelling mistakes as to
be unintelligible — e.g. for "doctor" he wrote " dorocks." There was
marked right-sided facio-brachial monoplegia, the upper limb being
totally paralysed and flaccid at all joints. The right lower limb was
only slightly feeble and dragged a little in walking. The right
supinator-] erk was absent, the left present ; the knee-jerks and ankle-
jerks were normal and equal ; the plantar reflexes were both flexor in
type ; the left abdominal reflex was absent, the right present.

On exploring the bullet wound, which was apparently about four
or five days old, a few fragments of metal were found in the outer
table, but there was no depression. A trephine-disc of bone was re-
moved, and on incising the uninjured dura, immediately subjacent, a
mass of blood-clot was at once extruded from the sub-cortical brain-
tissue at that point. Next day, at the first dressing, a further amount
of blood-clot also came away.

Ten days after operation, although still unable to speak, the patient
could write simple words to dictation, and could also copy accurately and
add up columns of figures, using his left hand. The right upper limb
was beginning to regain some power. A month after his operation
he began to recover motor speech, the first word he said being
" Thursday." Next day he could form short sentences, and within a
week was able to speak in normal fashion, although with great delibera-
tion. The monoplegia of the face and arm completely cleared up.

(2) Lesions of the post-central gyrus form a most interesting
group. Their symptoms are essentially sensory. If the lesion
implicates the uppermost or mesial end of the post-central gyrus the
symptoms are confined to the contra-lateral toes and ankle. Pro-
ceeding along this gyrus from above downwards, the cortical
sensory centres correspond in level with the pre-Rolandic motoT
centres for the knee, hip, shoulder, elbow, hand, &c., on the
other side of the central fissure.

The clinical signs of a post-central lesion consist in the presence
of one or more varieties of sensory loss in the contra-lateral limb.
In some cases we observe a degree of blunting of cutaneous
sensation to light touches, most marked at the periphery of the



limb and fading as we ascend towards its proximal end. One
of the chief characteristics of this cortical type of cutaneous
deficiency is its untrustworthiness of response and its excessive
tendency to fatigue, so that responses to touches tend to disappear.
The compass-test in these cases shows definite widening of the
distance at which a pair of blunt compass-points are recognised
as separate. Still more striking is the loss of joint-sense in the
affected limb or segment of a limb, so that, with the eyes shut,
when the patient's joint is
passively moved from the
flexed to the extended posi-
tion, or vice versa, he fails to
recognise its posture. This
loss of joint-sense often pro-
duces marked clumsiness of the
affected hand or foot, which
is aggravated if the patient
closes his eyes. Astereognosis
is another characteristic feat-
ure of post-central lesions,
and is generally, but not
always, proportional to the
loss of joint-sense. Stereo-
gnosis is tested by closing the
patient's eyes and then placing
some familiar object, e.g. a
coin, a key, a pair of scissors,
or a watch, in his hand. In
the case of the foot, we may

Fig. 248. — Left-sided post - Rolandic
wound of braiu, producing profound
loss of joint-sense in right fingers

Online LibraryPurves StewartThe diagnosis of nervous diseases → online text (page 40 of 48)