Symptoms.

The rapid diffusion of blood throughout the subdural space, and the usual coexistence of extensive injury to bone and brain, seldom permit of the development of such definite symptoms as might accurately define the localization of the hæmorrhage. The most important feature in the diagnosis lies in the fact that compression symptoms are early in onset and progressive in nature. The ‘lucid’ interval, so prominent a feature in middle meningeal extravasations, is either absent or of such short duration as to be difficult of recognition. The rapid development of symptoms pointing to brain compression, and the nature of the injury itself should enable the surgeon, in the majority of cases, to come to the conclusion that the patient is suffering from diffuse subdural hæmorrhage. In all cases of doubt, lumbar puncture should be carried out, the presence of blood-corpuscles in the cerebro-spinal fluid confirming the diagnosis.

Indications for operation.

Whether one considers the case from the point of view of the more immediate prognosis or from the more remote aspect of the case, operation is indicated, if the condition of the patient is compatible with such treatment. In considering the advisability of adopting an active form of treatment, it must be taken into account that, if the patient recovers without operation, the presence of an extensive subdural blood-clot must necessarily interfere, as an after-result, with the functions of the cortex, and that the removal thereof affords considerable hope of permanent cure.

Operation.

Operative measures may be considered as follows:—

The treatment of the fracture and of the dural rent.

The treatment of the subdural extravasation.

The treatment of the fracture and of the dural rent. A scalp-flap is framed, suited to the occasion and formed with due regard to existent scalp laceration. The fracture being fully exposed, depressed or comminuted fragments of bone are elevated or removed. Complete exposure of the sinus-wall, both in front and behind the site of laceration, is required, and for this purpose the craniectomy forceps may be called into requisition. In the event of copious bleeding during these procedures, strips of gauze should be inserted on either side of the sinus rent between the dura and the bone, thus compressing the sinus and stopping the bleeding.

The sinus rent may be treated after one or other of the following methods:—

1. It may be sewn up with mattress sutures of fine catgut, by which means it may be possible to stop the hæmorrhage without interfering with the sinus blood-stream.

2. The open mouth of the sinus may be puckered up by means of a purse-string suture.

3. The needle may be passed right round the sinus on either side of the rent, piercing the falx cerebri in the case of the superior longitudinal sinus and the tentorium cerebelli in wounds of the lateral sinus. The two ligatures are then tightened up and the bleeding controlled.

4. The gauze plugs (see above) may be allowed to remain for twenty-four hours or more, and then carefully withdrawn.

The treatment of the subdural hæmorrhage. Though the complete evacuation of the clot is seldom practicable, much may be done to remedy the condition. The tenseness of the dura mater, the absence of pulsation, and the peculiar plum-colour imparted to that membrane by the presence of underlying blood-clot point to the nature of the trouble.

The dura mater is incised and the presenting clot removed, as far as circumstances permit, with the aid of a spoon and irrigation (hot saline solution at a temperature between 110° and 115° Fahrenheit). Free drainage must be supplied, and it is necessary, therefore, that a counter incision should be made at the most dependent part of the clot. A suitable region may present itself if the bone be extensively comminuted. Under other circumstances, a narrow channel may be cut in the bone, prolonged in the downward direction, till the lower limits of the clot have been reached (see Fig. 56).

A rubber drainage-tube may be inserted in the manner depicted in the same figure. Except at the point of emergence of the tube, the dura mater is sewn up (with fine interrupted catgut sutures).

(B) Localized subdural hæmorrhage (subdural hæmatocele).

We are greatly indebted to Bowen[31] for our knowledge of subdural hæmatomata. That subdural hæmorrhage might take the form of a localized collection was a recognized fact, but the condition was but little understood, the typical clinical symptoms were not recognized, and surgeons hesitated to adopt surgical remedies. All these facts impeded advance in both diagnosis and treatment. Subdural hæmatoceles, even at this date, are often regarded as rarities, but, in the light of present knowledge, it would appear that wider recognition of the hæmorrhage in its clinical aspect will show that such ideas are erroneous.

In the preceding section it was shown that subdural extravasation resulting from sinus-injury tends to become diffused throughout the subdural space. With respect to localized hæmorrhages our data are by no means complete, but all available evidence tends to show that subdural hæmatoceles are dependent on laceration of the pia-arachnoid vessels—a condition practically synonymous with superficial laceration and contusion of the cortex. The blood, derived from small cerebral veins and minute cerebral arteries, exercises primarily but slight pressure effect. Its force is expended on compressing and emptying the subjacent and surrounding cerebral vessels, producing, in other words, a condition of local cerebral anæmia. This pressure is insufficient to lead to the development of general compression, but suffices to produce certain rather indefinite symptoms. We have, therefore, before us a very different picture to that depicted in cases of middle meningeal hæmorrhage. In such extra-dural hæmorrhages some definite period of time must elapse before the dura mater is sufficiently stripped from the bone to allow of the formation of a clot of size sufficing to exercise both local and general compression effects. Pressure effects then become very manifest.

On the other hand, in localized subdural extravasations there is an immediate effect, for the brain is contused or lacerated. On recovering from the immediate effects of the injury—concussion of a greater or lesser degree of intensity—the patient does not regain complete mental and bodily convalescence. He suffers from symptoms suggestive of brain irritation—headaches, photophobia, mental irritability, insomnia, loss of appetite, the pulse accelerated, and the temperature slightly raised. Later on, more definite symptoms arise, but, intervening between the day of the accident and the time at which these more definite localizing symptoms develop, there is an unmistakable latent period—a period to be sharply differentiated from the previously mentioned lucid interval (see p. 139).

This ‘latent’ period lasts for a variable period of time—seldom less than a week or more than three months. At the end of that time the picture changes, and the patient evidences symptoms obviously referable to local brain compression. From a clinical point of view it is fortunate that subdural hæmatoceles tend to involve the fronto-parietal region with the consequent development of motor symptoms, especially paresis or paralysis of the contra-lateral side. Hence the name sometimes applied to the condition—traumatic late apoplexy. The speech areas are implicated if the injury be situated on the left side. Paralysis limited to the lower extremity is exceedingly suggestive, such a palsy occurring only with the greatest rarity in extra-dural hæmorrhages (from the middle meningeal artery).

If the pressure be unrelieved by operation the patient passes from the excitatory to the paralytic stage of brain compression, gradually falling into a condition of coma, the pulse increasing in frequency and the respiration becoming more and more embarrassed.

In the study of this condition, the following are the points to which special attention should be paid:—

1. The comparative want of severity with respect to the injury received.

2. The absence of any ‘lucid’ interval, such as is present, for example, in middle meningeal hæmorrhage.

3. The presence of a definite ‘latent’ period.

4. The late development of symptoms pointing to general and local brain compression.

Finally, it may be stated in general that the more indefinite and the more deferred the pressure symptoms, the greater the probability that we have to deal with a localized subdural hæmorrhage. Lumbar puncture may materially aid in the differential diagnosis between extra-dural and subdural hæmorrhages.

The following case affords a typical example of subdural hæmatocele:—

Operation.

The lesion is usually of so gross a nature that little difficulty will be experienced in determining the site for trephining. The protective gauze and scalp-tourniquet are applied as usual (see p. 14), and a bradawl introduced through the scalp so as to indent the external table and allow of the subsequent accurate application of the trephine. A scalp-flap, suited to the occasion, is framed, the skull trephined, and the disk of bone elevated and removed. The appearance of the dura mater now allows the operator to verify his diagnosis—the membrane is non-pulsatile, it bulges markedly outwards and presents a blue-purple colour. The bone is then nibbled away in the downward direction towards the lower limit of the clot, the scalp incision being prolonged according to requirements.

In the region of the trephine-hole the dura is incised in a crucial manner, and the four flaps held aside by catgut sutures passed through the apex of each flap. A blunt director is introduced beneath the dura, passing towards the lower limit of the clot, and the membrane slit up to within a short distance of the lower margin of the gap. All meningeal vessels that cross the line proposed for dural section must first be underrun on either side of that line. Retraction of the dura will now allow of adequate exposure of the underlying hæmatoma. Its removal can be carried out with the aid of a spoon, and by means of gentle irrigation (hot saline at a temperature between 110° and 115° Fahrenheit). It is usually impossible to remove the whole of the coagulum, but the greater portion can be got rid of in the manner described.

The dura mater is approximated above by the cross-union of the four apical sutures, whilst the downward prolongation is also sutured except at the most dependent point, where a rubber drainage-tube is inserted beneath the dura mater and brought out through the scalp-flap (see Fig. 56). This tube should be anchored to the dura mater with a single fine catgut suture.

The tube should be allowed to remain in position for at least thirty-six hours. In this the surgeon must be guided by the amount of discharge and the general progress of the case.

Results.

The most complete results obtained by operative treatment are supplied by Bowen, who classifies a series of 72 cases as follows:—

Class A. Subdural hæmorrhage, apparently without other serious injury to bone or brain.

Class B. With serious brain-injury.

In other words, every case died in which no operative measures were adopted, whilst after operation 28 recovered and 23 died. My own experience is limited to 4 cases, 3 of which recovered.

Pia-arachnoid hæmorrhage.

From evidence obtained at post-mortem examinations, it may be concluded that the great majority of cases of severe head-injury—especially those in which ‘irritation’ of the brain is a prominent feature—are associated with pia-arachnoid hæmorrhage. This is evidenced by the presence of a film of blood and serum over certain regions of the brain, not confined to the region subjacent to the skull area primarily involved, but also present over the opposite pole of the brain (injury by contre-coup).

Subpial hæmorrhage differs from the subarachnoid variety in that the blood follows the invaginations of the pia mater, lining, therefore, both major and minor cerebral sulci. Subpial and subarachnoid hæmorrhages are, however, generally co-existent, and the term—pia-arachnoid hæmorrhage—aptly describes the conditions commonly found.

The symptoms resulting from such blood extravasations are such as are described in the sections dealing with concussion and irritation of the brain (see p. 166).

INJURY TO THE BRAIN

Injury to the brain must always be regarded as by far the most important of the many complications associated with fracture of the skull. A fracture is not necessarily accompanied by brain-injury, and laceration of the brain may exist without a fracture. There can, however, be no question that the more severe cases of head-injury are almost invariably associated with some degree of brain-injury—varying from contusion to extensive laceration, cortical or central.

No part of the brain is exempt from injury, but two regions, the antero-inferior aspect of the frontal lobe and the antero-external aspect of the temporo-sphenoidal lobe, show a special liability to contusion and laceration.

The brain may be injured immediately subjacent to the site at which the blow is delivered (direct injury), or at the pole directly opposite that at which the blow was applied (indirect injury).

Direct injury results from the in-driving of comminuted and depressed fragments of bone, from the passage of a foreign body, and from the direct transmission and diffusion of forces through the subjacent cerebral substance.

The indirect forms of injury are less readily explained. Their frequency cannot be disputed. I drew attention to the subject in my Hunterian Lectures in 1904, there stating that indirect injury to the brain was more common than the direct form. My opinion is confirmed by Phelps,[32] who states that injury by indirect violence is of almost constant occurrence.

Three theories have been advanced in explanation:—

1. ‘Their production has been ascribed to the change in form that is suffered by a skull in virtue of its elasticity when subjected to violence which causes distortion of the brain to the point of bursting.’

2. ‘In the displacement of the cerebro-spinal fluid by the consecutive depression and bulging that is believed to follow a blow on the head; a momentary vacuum is formed at either axis of force, and the vessels of the brain and meninges rupture from lack of support.’

Neither of these theories are tenable, insomuch as they are based on an acceptance of the ‘bursting and compression’ theories (see p. 74)—theories which, in my opinion, it is impossible to accept.

3. The ‘contre-coup’ theory. According to this theory the injury is due to sudden and violent displacement of the brain against the opposing osseous barrier. This theory has been opposed by many—notably by Helferich—on the ground that the brain is said to completely fill the cranial cavity, and that ‘shaking’ from side to side is impossible.

This theory affords, however, the most satisfactory explanation of contralateral laceration. The following points may be advanced in its favour:—

(a) The frontal and temporo-sphenoidal lobes are more liable to contusion and laceration than any other parts of the brain, both regions possessing certain anatomical relations accounting for their ready injury. The frontal pole is related to the angle of junction between the horizontal and vertical plates of the frontal bone, the temporo-sphenoidal lobe to the cul-de-sac, at the anterior part of the middle fossa, that is overhung by the wings of the sphenoid bone.

(b) The lacerated area is almost invariably situated at that part of the brain which lies opposite to the region struck in the line of the transmitted force. Furthermore, brain lesions are most prevalent when the accident results from a fall from a height, a class of accident in which ‘shaking’ of the brain is most likely to occur, and least common when the basal fracture is dependent on a bilateral compression force.

(c) The statements that ‘shaking’ cannot take place, and that the soft cerebral substance cannot be driven forcibly and violently against the opposing bony barrier, so as to be locally bruised and torn, are incorrect.

That such violent displacement of the brain can and does occur is proved by the following case:—

The lacerated area is usually cone-shaped, the base corresponding to the surface of the brain, the apex facing towards the lateral ventricles. In the most severe cases the anterior or lateral horns of the lateral ventricles may be involved at the apex of the cone, and, in the event of further cerebral softening, the horns of the ventricles may, as it were, bulge outwards, thus assisting in the formation of those traumatic cephaloceles that communicate between the lateral ventricle and the surface of the brain.

On the other hand, if the degree of laceration be slight and the injury compatible with life, organization and partial resolution takes place, with the formation, in nearly all cases, of adhesions between the cortex and the membranes, of false membranes, arachnoid cysts, and of blood cysts. In the more serious cases cerebral fibrosis results, in direct proportion to the degree of cerebral destruction, with corresponding degeneration, both of the cerebral cortex and of the tracts that evolve therefrom.

Symptoms.

Certain regions of the brain may, when injured, give rise to localizing symptoms. More generally, however, all localizing features are obscured by an overpowering element—the presence of concussion, irritation, or compression of the brain.

Still, in some cases, the localizing features are sufficiently marked, at some period of the case, to allow of a more definite diagnosis. The symptoms, therefore, must be considered under the two heads, (A) localizing, and (B) general.

A. Localizing symptoms.

Localizing to the frontal lobes.

Phelps,[33] from a series of 130 cases, arrived at the following conclusions—that, ‘in nearly every case in which consciousness was retained or regained, and the mental faculties not perverted by general delirium, laceration of the left frontal lobe was attended by default in intellectual control, and that the lesion was usually of the anterior region and implicated its inferior surface.’ ‘Subcortical disintegration was characterized by abrogation of mental power, and superficial laceration by aberration in its manifestations.’ And secondly, that, ‘in nearly every instance in which laceration was confined to the right side, the mental faculties remained unaffected, except as they were obscured by delirium and stupor occasioned by coincident general lesion.’

Although the above statements have not altogether been confirmed by cases that have come under my observation, yet, coming from such a source, they must be accepted unless refuted.

Bianchi states that, after extirpation of the frontal lobe of the ape, the whole intellectual life of the animal is changed. Perception, attention, inhibition, and in particular memory and association are enfeebled. The psychical tone is lowered; the ape lacks initiative, courage, and spirit.

Laceration of the under aspect of the lobe may, by direct involvement of the olfactory region, interfere with the faculties of smell and taste.

Localizing to those parts that minister to the function of speech.

The condition of the patient usually prevents one from obtaining early information as to the power of speech. Isolated lesions of the posterior part of the third left frontal convolution result in motor aphasia, a condition characterized by the inability on the part of the patient to speak, in spite of the fact that comprehension is unimpaired. The brain-injury is, however, seldom so defined as to be characterized by loss of speech without other phenomena. In very close relation to the area responsible for speech is the writing centre, situated at the posterior end of the middle frontal gyrus, near the centre for the movements of the hands and fingers. Injury to this centre results in agraphia and alexia.

Word-deafness

results from lesions implicating the upper temporo-sphenoidal lobe, and word-blindness from injuries to the supramarginal and angular gyri (see Fig. 57).

Phelps pointed out that the lesion must be an extensive one if the symptoms included under the term sensory aphasia (word-blindness, word-deafness) are to be evolved. No localized injury to any small area suffices, and the cortex must be deeply involved. Lacerations of the brain are usually of so gross a nature that further differentiation is seldom to be obtained. Here it might be noted that the cortical centres responsible for speech and its accessories, word-seeing, word-writing, and possibly word-hearing, are all situated on the left side in normal right-handed individuals. The corresponding areas on the right side may be regarded as ‘silent’ areas, and may be utilized, if desired, for decompression purposes. No operation, with that purpose in view, should be carried out, however, unless the surgeon is assured that the patient is right-handed in his actions. A case has recently come to my knowledge where a right-parietal decompression operation was carried out with disastrous results.

Localizing to the temporo-sphenoidal lobe.

The relation of sensory aphasia to lesions of the temporo-sphenoidal lobe has already been mentioned. The anterior poles of this portion of the brain, a region frequently involved in head injuries, may lead to the development of impaired smell and taste, especially if the lesion includes the uncinate lobe and be situated on the left side. In other respects, the temporo-sphenoidal lobe may be regarded as a ‘silent’ area of the brain.

Localizing to the pre- and post-central convolutions.

Injury to the pre-central or motor area usually leads to the development of definite symptoms—twitchings, convulsions, or paralysis of the face and extremities on the contra-lateral side. In the earlier stages reflexes are abolished. Later on, as the result of degenerative changes in the pyramidal tracts, spasticity, contractures, and rigidity, with increased reflexes will be observed in the affected limbs. On the other hand, the muscles do not show any reaction of degeneration. Babinski’s sign is generally present.

Injury to the post-central convolutions might be expected to lead to various alterations in tactile and muscle sense, in stereognosis, and in sense of pain and temperature, but the general condition of the patient seldom permits accurate demonstration. Such sensory disturbances are more frequently observed as late results of head-injury.

Localizing of the occipital lobes.

Laceration of the occipital lobes may lead to homonymous hemianopia, for which defect it is probable that the degree of laceration must be considerable, involving mainly the mesial aspect of the occipital lobe (see Fig. 69). Schäfer has shown that the greater portion of the occipital lobe may be removed in monkeys without producing loss of vision, and it is only when the lesion involves the parieto-occipital fissure and passes into the occipito-temporal convolutions that loss of vision is permanent.

Slighter degrees of occipital injury may lead to subjective symptoms, such as flashes of light, colour changes, &c.

Localizing to the cerebellum.

Lesions of the cerebellum rarely permit of the development of such localizing symptoms as are observed in cerebellar tumours. Inco-ordination of movement, ataxia, and other symptoms observed in cerebellar tumour formation are, from the general condition of the patient, incapable of demonstration in cerebellar laceration. It is necessary, however, to draw attention to the significance of yawning and gaping. This symptom has been observed in several recent cases, and, as far as my observation goes, is only present in cerebellar lesions.

In the consideration of these localizing symptoms, it must be borne in mind that brain lacerations are of an exceedingly gross nature, and that there may be—as the late Professor von Bergmann[34] pointed out—‘notwithstanding the severest brain symptoms, not the slightest discoverable anatomical alteration in the brain. On the other hand, notwithstanding the absence of all brain symptoms, extensive and striking destruction of the brain substance.’

B. General symptoms.

Concussion or cerebral shock.

Its pathology. Concussion used to be regarded as implying a ‘molecular disturbance’ of the brain—a definition so unsatisfactory that it may be relegated to a desired obscurity. At the present day, though some difference of opinion exists as to whether the condition is or is not necessarily dependent in its development on associated cortical or subcortical lesions, macroscopical or microscopical, concussion is regarded as implying a condition of acute cerebral anæmia through sudden inhibition or paralysis of the vaso-motor centre.

With respect to the existence of visible lesions of the brain, Kocher maintains that such lesions—hæmorrhages and the like—are necessarily present, proposing that the term ‘brain concussion’ should be eliminated in favour of ‘brain contusion’. On the other hand, the late Professor von Bergmann pointed out that such a course was not possible, instancing the many cases of concussion where contusion could not possibly have existed.

There cannot, in my opinion, be any question as to which is the correct view. It is unreasonable to ask one to believe that the milder cases of concussion, cases in which the patient merely suffers from loss of consciousness for a few minutes, from which he rapidly recovers and is discharged from treatment within a few days, and from which he suffers in the future from no remote ill effects whatsoever, it is unreasonable to ask one to believe that such cases have experienced so severe a lesion as brain contusion or laceration. Both these conditions would require a long period of convalescence, and would tend to leave in their train very serious after-results.

It is obvious, therefore, that there exists a degree of concussion from which the patient can quickly and entirely recover. It is also clear that in many cases the patient passes through a long and serious illness, whilst, in some cases, a fatal termination may ensue—and that too within a few hours. It is consequently clear that we have to deal with varying grades of concussion, some of which are of so mild a nature as to be clearly unassociated with definite cerebral lesion, whilst others are of so serious a nature that death may take place within a few hours, and in such cases the gravest cerebral lesions may be found at the autopsy.

In other words, it would appear that concussion is more or less dependent in its severity on the degree of associated cerebral change.

It is, however, to the milder type of case that we should turn in order to determine what is exactly meant by concussion. In such cases the patient merely suffers from a mild degree of cerebral shock, a condition closely resembling shock in general. ‘Shock’ is defined as a ‘condition resulting from fall in blood-pressure, due to inhibition or paralysis of the vaso-motor centre’. The afferent impulses that pass up the various sensory paths inhibit or paralyse the vaso-motor centre, a centre that has for its main function a tonic constricting influence on the peripheral arteries. Hence, these vessels dilate atonically, the blood collects in the great splanchnic area, and, insomuch as the cerebral arteries possess no separate vaso-motor apparatus, they passively follow the changes in the general circulation. The brain is consequently in a state of arterial anæmia, the arteries relatively emptied, the veins passively engorged.

Clinically, concussion or cerebral shock differs from ordinary shock in one manifestation only—sudden loss of consciousness. This development is readily explained on the ground that concussion results from a violent blow applied in the near neighbourhood of the vaso-motor centre, with consequent sudden vaso-motor depression and acute anæmia of the cerebral cortex. This leads to immediate great fall of blood-pressure, loss of consciousness, and lack of muscular control.

Statements have recently been brought forward to the effect that concussion is in reality a mild type of compression. This view received at first sight some confirmation from the experiments of Koch and Filehne, who, from the application of consecutive slight blows to the heads of dogs, showed that each blow resulted in bulbar stimulation followed by bulbar depression. The blows being continued, the degree of stimulation decreased and that of depression increased until exhaustion and death resulted. During the periods of stimulation the pulse-rate slowed, during those of depression it increased.

It should be noted, however, that concussion, as observed in the human being, results from one sudden and violent blow. It may, I think, safely be assumed that, in such cases, the stimulating effect of the blow is entirely abolished in favour of an acute depression. And, as Archibald[35] says, ‘their records of respiration, pulse, and blood-pressure resemble far more closely the course of an increasing compression, with its gradual slowing of pulse and respiration and steady rise of blood-pressure, than that of concussion with its sudden standstill of pulse and respiration and fall of blood-pressure.’

In favourable cases the injury being of a comparatively mild nature, the vaso-motor centre soon recovers tone, and, as the result of previous depression, the vascular conditions are now reversed—the stage of depression giving place to the stage of reaction. The blood-pressure rises, the carotids pulsate forcibly, the face is turgid and flushed, the skin hot and moist, whilst the temperature rises, and the general cerebral hyperæmia is evidenced by headache, restlessness, and perhaps by delirium.

In the more severe cases the vaso-motor depression is unduly prolonged, or persists till death, the patient remaining concussed for a considerable period of time, or dying in that condition. In these fatal cases the post-mortem examination usually reveals brain laceration, but always evidences considerable engorgement of superficial cerebral veins, increase of cerebro-spinal fluid and œdema, both of the pia-arachnoid region and of the brain substance itself. These latter phenomena are accounted for by the fact that, insomuch as the venous pressure and cerebro-spinal tension are equal, the greater the engorgement of the cerebral veins the more extensive is the transudation of fluid into the pia-arachnoid and cerebral systems. In a fatal case of concussion—recently under my care—the surface of the cortex, when exposed by operation, was obscured by a layer of œdematous pia-arachnoid ¹⁄₄ inch in depth.

Arguing from the presence of the very definite pathological changes observed in all fatal cases—contusions, lacerations, hæmorrhages, and œdema—one may arrive at the conclusions (1) that lesions of a similar but less serious nature are existent in the serious but non-fatal cases, and (2) that the prolongation of the stage of depression is directly dependent on the presence of such lesions.

On investigating the numerous cases that come under the care of the surgeon, certain features present themselves which are not always readily explained on the definition of concussion as given above. Thus, the variability of the symptoms evinced in cases of concussion admitted into hospital are well exemplified by the following table, compiled from a consecutive series of 50 cases admitted into St. Bartholomew’s, diagnosed and treated as concussion:—

Still, when all is considered, concussion and compression are but ill-defined from one another, both in their clinical and pathological aspects. The more indefinite cases of concussion are probably such as border on compression, the increasing œdema gradually carrying the patient across the border line between the two conditions.

In the present state of our knowledge respecting concussion or cerebral shock it may, I think, be accepted (1) that concussion is dependent on an acute inhibition or paralysis of the vaso-motor centre; (2) that the milder cases are unassociated with any pathological visible changes; (3) that the prolongation and severity of the depression stage are directly proportionate to the extent of the brain lesion, such lesions varying from œdema and contusion to extensive hæmorrhages and lacerations.

Its symptomatology.

The stage of depression. The symptoms are evoked immediately on the receipt of the blow, the patient falling to the ground from lack of muscular control and loss of consciousness. The muscular system is completely relaxed, the limbs, when raised, falling helplessly to the ground. The face is deathly pale, the eyes usually open, fixed, and expressionless, the pupils equal, commonly dilated and responsive to light. The patient may be aroused by strong stimuli—pinching, shouting in the ear, pressure over the supra-orbital nerves, &c.

The pulse is small, slightly accelerated, and occasionally intermittent. The respiration is weak, shallow, and often irregular. The temperature is lowered, sometimes to such an extent that it cannot be registered on the thermometer. The surface of the body is cold and clammy, beads of sweat standing out on the brow. The deep reflexes are abolished. Some attempts may be made at swallowing when fluids are placed in the mouth.

Urine is often expelled at the time of the accident, and, more rarely, fæces may also be passed involuntarily.

The condition either gives place to that of reaction or the state of unconsciousness and collapse becomes more profound, in which case the prognosis is most unfavourable.

The stage of reaction. Weak, purposeless movements are observed and the patient may sigh heavily, mutter, or groan. This is followed by profuse vomiting, after which the temperature begins to rise, the body becomes warmer, and the patient recovers his senses either entirely or in part. The heart beats strongly, the pulse being full and slightly accelerated in rate. The carotid arteries are seen to pulsate forcibly, the face is flushed and moist. The patient is restless, and complains of severe headache, due in all probability to intradural hypertension. Under efficient treatment these symptoms of cerebral hyperæmia abate, the patient recovering quickly or slowly, according to the severity of the blow. Retrograde amnesia is often a conspicuous feature in the more severe cases, varying greatly in depth and character, seldom permanent.

In the more serious cases—those associated with severe cerebral injury—the pupils dilate fully and do not react to light. Corneal reflex is absent. The medullary centres gradually become exhausted, the pulse becoming smaller, increasing in rapidity, and finally unrecognizable. Respiration becomes weaker and often Cheyne-Stokes in character. Respiration ceases before the heart gives out.

Cerebral Irritation.

Its pathology. Sufficient evidence is supplied, both by clinical symptoms and by post-mortem examination, to show that brain irritation is dependent on definite brain lesions, these varying from ‘bruising’ to minor degrees of laceration. Bruising or contusion of the brain—evidenced by pia-arachnoid hæmorrhages and by cortical and subcortical hæmorrhages—is most prevalent in the frontal and temporo-sphenoidal regions. The same may be said with respect to laceration.

Its symptomatology. From the initial stage of concussion the patient passes into that of irritation, the reaction being of a rather violent type and accompanied by considerable rise of blood-pressure.

The patient lies curled up in bed, the lower extremities flexed at the hip and knee, the upper limbs bent across and partially covering the forwardly flexed head. He is exceedingly restless. Restraint is usually required. The eyes are tightly closed, and all attempts at pupillary examination are strenuously resisted. The patient groans, mutters, and uses language, perhaps suited to the occasion but not adaptable to polite society. Headache is severe, often referred to the frontal region. The skin is hot and dry—burning—the body temperature is raised whilst the pulse is accelerated and its tension increased. Both urine and fæces may be passed into the bed, not so much from loss of bladder and rectal control as from transitory moral perversion.

The state of irritation subsides or merges into that of cerebral compression.

Compression.

Its pathology. A compression force—whether foreign body, blood extravasation, abscess or tumour—must act on the brain substance or on the fluid constituents of the skull. The brain, however, is itself incompressible. It may be squeezed like a sponge, but its actual structure is unalterable. Consequently, the compressing force exercises its main influence on the fluid contents, driving out the cerebro-spinal fluid, depleting the cerebral veins and emptying the arterioles, producing in other words a state of brain anæmia.

Experimentally, it has been ascertained that from 3 to 6 per cent. of the cranial capacity can be taken up by a foreign body without producing compression symptoms—probably owing to the escape of cerebro-spinal fluid into the spinal canal, and the recession of the medulla and cerebellum into the foramen magnum. Furthermore, it would appear that the incidence of compression symptoms is associated with depletion of those cerebral veins which are in closest relation to the compression force. As this force increases—for example, in middle meningeal hæmorrhage—the pressure exercised on the surrounding regions increases proportionately, to the level of the capillary pressure, and even to that of the smaller arteries. A state of cerebral anæmia results, first localized to the region primarily involved, then invading more widely and finally affecting both supra- and infra-tentorial spaces.

With regard to the continuity of pressure between these three spaces, there is but little pressure discontinuity between the two supra-tentorial spaces, whilst, between the supra- and infra-tentorial regions, there is less ready communication.

A slight degree of compression in the supra-tentorial space will act on the corresponding space only, greater degrees will involve all three. On the other hand, a rise of infra-tentorial pressure is not of necessity associated with a corresponding elevation in the other two regions. For example, a cerebellar tumour readily affects the medullary centres, whilst the higher cortical regions are for the time being totally unaffected. Again, a tumour situated in the frontal pole does not necessarily produce any of those symptoms of cerebral compression which are regarded as referable to an increase of subtentorial pressure—slow pulse, vaso-motor disturbances, subnormal pressure, and deep rhythmical respiration.

Returning once more to the vascular effects of a localized compression, it is obvious that whilst the compressing force is producing a surrounding anæmia—depleted veins and arterioles—yet that the neighbouring but more distant brain is venously engorged—from venous retardation. Insomuch, moreover, as the venous tension and cerebro-spinal pressure are equal, it is obvious that, as the result of venous engorgement, there is some surrounding serous transudation into the perivascular, pia-arachnoid, and cerebral regions. The brain bordering on the anæmic area is therefore œdematous, the œdema diminishing and fading away in direct proportion to the distance of the area involved from the primary focus of compression.

If the compression force is of a progressive nature, the engorged area becomes in turn anæmic, and still more distant regions become engorged and œdematous. This state is known as that of progressive œdema. Its complete development is largely dependent on brain infection—abscess of the brain, &c.

The rapidity with which the symptoms of compression develop are largely dependent on the producing cause. Thus, three examples may be cited:—

(1) Compression of slow development, requiring weeks or months before typical symptoms are observable—e. g. tumour formation.

(2) Compression of medium development, requiring days only: e. g. abscess, subdural hæmatocele, and some forms of middle meningeal hæmorrhage.

(3) Compression of acute development, almost immediate: e. g. diffuse subdural hæmorrhage, some cases of middle meningeal hæmorrhage, depressed fractures, and intracranial foreign bodies.

The special symptoms of compression are, as Leonard Hill pointed out, referable to the effects produced on the bulbar centres. That such is the case is suggested by the following facts:—

(1) The same compression symptoms result wherever the compressing force acts.

(2) Experimentally, an increased pressure in the posterior fossa produces compression symptoms earlier than when the compressing force is exercised in some more distant region of the brain.

(3) A fracture involving the posterior fossa gives rise to compression symptoms earlier than a fracture in some more distant region.

(4) A far smaller body kills in the bulbar region than in the cerebral chamber.

(5) The general pressure effects are in no way due to excitation of the part of the brain pressed on, for, after division of the mesencephalon, the pressure was just as active in calling forth changes in respiration and circulation (Sir Victor Horsley).

Leonard Hill also pointed out that the first effect of anæmia of the bulbar region was in the nature of stimulation, the vaso-motor centre being influenced in such a manner as to produce a general rise of blood-pressure. A further degree of compression may again produce the same result, the arterial pressure rising considerably above the normal. Later on, the medullary centres—and more especially the vaso-motor—become exhausted, with consequent grave fall in blood-pressure. The pulse, previously slow and full, becomes rapid, small, readily compressible, and irregular in rhythm, whilst the respiration, previously deep and regular, becomes gasping, irregular, and Cheyne-Stokes in character.

The sequence of events may be depicted in another manner. In cerebral compression, the battle—as pointed out by Schüster—largely resolves itself into a life and death struggle between the attacking compression force on the one hand and the defending vaso-motor centre on the other.

Up to a certain point the vaso-motor centre holds the whip-hand. The capillary anæmia as produced by the compression force—cerebro-spinal tension, &c.—brings about a condition which not only acts as a stimulus to the vaso-motor centre but also exercises a marked effect on the vagus and respiratory centres. The blood-pressure rises, the pulse is slowed in rate, and its tension markedly increased, whilst the respiration is slightly irregular both in depth and rhythm. The vaso-motor centre thus attacked sends out further impulses so as to raise the blood-pressure to slightly above requirements. The bulbar centres are again flushed with blood, the vaso-motor centre ‘slacks off’, and the blood-pressure falls again.

The compressing force is, however, still active and full of fight. A further capillary anæmia results. The vaso-motor centre again responds and the blood-pressure rises higher than ever, the pulse-rate is further slowed, and the respiration is deeper, less regular, and even stertorous.

This combat continues, and, in the presence of an active compression force, there is that rhythmic activity of the vaso-motor centre which is represented by the well-known Traube-Herring curves; again, the height to which the vaso-motor centre drives the blood-pressure may be taken as representing the activity of the compression force.

When the compressing force rises above a certain limit the débâcle occurs—the vaso-motor centre retires from the fight, there is a rapid fall in blood-pressure, the medulla is emptied of blood, and both cardiac and respiratory centres share in the defeat (rapid pulse of poor volume and Cheyne-Stokes respiration).

These being the effects as exercised by compression on the bulbar centres, one must not omit to consider the results produced on the higher cortical centres. Anæmia is the feature and unconsciousness is the ultimate result, preceded by headache and drowsiness progressing on to stupor and coma. Intermediate between the stages of sleepiness and coma, one observes occasionally a stage of irritation—such as is pictured in many cases of typical middle meningeal hæmorrhage.

In fatal cases the respiratory centre gives out first, the heart often beating for some time after all attempts at respiration have ceased. In a case recently under my care, respiration ceased during the process of trephining. The patient was kept ‘alive’ for three hours by means of artificial respiration, and under such mechanical breathing the patient retained a good colour and the heart worked well. So soon, however, as efforts were relaxed, the pulse became weaker and weaker until further artificial respiration again restored the balance. This process was kept up till it was realized that the respiratory centre was ‘dead’.

From these facts, it may be assumed that the special symptoms of compression are dependent (a) on anæmia of the bulb—with corresponding cardiac, respiratory, and vaso-motor changes; and (b) on anæmia of the cortex—with unconsciousness.

Its symptomatology. According to Kocher, the following are the four stages of compression:—

1. The stage of compensation. A mild degree insufficient to seriously compromise the circulation. Cerebro-spinal fluid escapes into the spinal canal and some of the venous radicles are compressed. Some venous engorgement. Some headache, possibly some focal symptoms. Some mental dullness.

2. Stage of beginning compression. Beginning failure of the circulatory compensation. Headache pronounced, vertigo, restlessness, excitement or delirium. Objective symptoms of venous stasis—dilatation of the veins of the eye, both external and internal, œdema of the disk. Affection of the medullary centres, shown by a slowed pulse and a slight rise in temperature.

3. Stage of fully-developed compression. Widespread capillary anæmia. Medulla affected markedly. The period of vaso-motor regulation has set in with its high blood-pressure, and this, with its vagal quality, gives the pulse its bounding character. The rise in blood-pressure shows a definite rhythm. Also rhythmicities in respiration which may acquire the Cheyne-Stokes character. Rhythmic alterations in the size of the pupils, with alternate increase and decrease in the depth of stupor, so that the ‘up-wave’ causes the patient to moan, become irritable, and thrash about, whilst the ‘down-wave’ sees him completely comatose. Pulse is markedly slowed and the disks evidence pronounced ‘choking’. Reflexes are abolished, cyanosis extreme, respiration snoring.

4. Stage of paralysis. Irregular cardiac and respiratory efforts, pulse grows rapid, coma deepening, muscular relaxation, pupils widely dilated, and permanent fall in blood-pressure. Respiratory paralysis.

Treatment.

(a) Of concussion. In considering the treatment of concussion, it has to be remembered that we are treating a condition dependent on vaso-motor depression, and that we are ignorant—at any rate for the time being—as to the nature and extent of a possible cerebral lesion. It is obvious, therefore, that although we are clear as to the general lines on which treatment is to be carried out, yet that our earlier methods must be expectant and our subsequent methods symptomatic. In other words, we must be prepared, at any moment, to change the method of treatment according as symptoms demand.

The more general treatment—applicable to all cases, of whatever severity—consists in putting the patient to bed with the head low, in the application of warmth to the body and extremities, and in the administration of hypodermic injections of morphia, a drug of great value in the more severe cases of concussion. It must, however, be administered with caution, lest important symptoms be masked.

Strychnine and brandy are practically useless. They merely whip the willing horse—the heart is doing full duty and cannot be further stimulated by such measures.

In mild and moderately severe cases this form of treatment will suffice to tide the patient over the collapse stage and induce the stage of reaction. So soon as this commences, the rising temperature and vomiting heralding the change, the head of the bed should be lowered, hot bottles and blankets removed—the patient being covered with a linen sheet only—and all forms of stimulant avoided.

Calomel should be given by the mouth, 1 to 5 grains, according to the age of the patient. Headache may be relieved by applying ice-bags to the head, by tying round the forehead a handkerchief soaked in a weak solution of eau-de-Cologne, and by the administration of various drugs, more especially aspirin (10 grs.), antipyrin (10 grs.), and hyoscin (gr. ¹⁄₁₀₀).

In more severe cases more radical measures must be adopted to combat the severe vaso-motor depression, with its consequent splanchnic congestion and cerebral anæmia. No method is more desirable than infusion. This method, with its attendant advantages and disadvantages, has been detailed on p. 118. It is merely necessary to add that infusion must not be carried out in a haphazard manner. Its application is based on scientific principles, and its results must be noted with the greatest care. The surgeon must keep a watchful eye on the temperature and blood-pressure, and he must be prepared at any moment to change his plan of campaign.

(b) Of irritation. The patient should be kept in a darkened room and should not be worried more than is absolutely necessary for diagnostic purposes. An attendant is usually required, whose methods should be persuasive rather than forcible. Great tact is required.

Morphia is of the greatest value in the treatment of this condition. It relieves the headache, acts as a damper on the hyperæmic brain, and keeps the patient from threshing about in bed and injuring himself. Sleep is essential for an early recovery and cure.

In the more severe cases venesection should be carried out, and operative measures will be required if the rising temperature and slowed high-tension pulse herald the advent or indicate the presence of compression of the brain.

(c) Of compression. The various operations carried out for the relief of compression of the brain are discussed elsewhere. They include such operations as are conducted for localized hæmorrhages, whether subdural or extra-dural (see Chap. V), and such also as are described as ‘decompression’ operations (see p. 121).

With regard to the general indications for adopting active surgical measures, the surgeon is, of course, guided in his estimation of the case by the general condition of the patient—depth of unconsciousness, &c.—but more especially by the temperature changes and alterations in blood-pressure. In my own practice I am guided very largely by the temperature changes—as described on p. 114. On the other hand, some surgeons pin their faith more especially on the blood-pressure changes. Thus Archibald writes: ‘If the blood-pressure be 130 mm. Hg. on admission, an hour later 150, still later 200 or 250, we are immediately in possession of the fact that the available intracranial space is being steadily, dangerously reduced, and that the vaso-motor centre is straining every nerve to stave off defeat.’

I am, of course, ready to concede the great value of blood-pressure tracings, but, in my experience, the temperature changes have been even more consistent, so much so that I base my treatment of a case very largely on such changes. One word of warning—the temperature must be taken every half-hour, and active surgical measures adopted so soon as the rising temperature, slowing high-tension pulse, and deepening unconsciousness point to advancing compression.

There is undoubtedly a growing tendency amongst those who have carefully studied the effects of trauma on the skull and brain to carry out exploratory and decompression operations at an early period, even in cases which present no symptoms of special localizing significance. The pathological conditions so commonly found and the excellent results that have been obtained prove that the adoption of early surgical treatment is founded on a very sound basis.

Points in the differential diagnosis between traumatic and other forms of coma.

The previous history of the case, the nature of the accident, and the lesions found may enable the surgeon to arrive at ready diagnosis. Often, however, it is impossible to exclude non-traumatic forms of coma without an exhaustive examination of the patient. In the process of examination, it is convenient to have in one’s mind a simple memoria-technica. Thus,

To this list must be added Diabetic Coma.

Having these conditions in mind, the patient is examined from head to foot in the following manner:—

The vault of the skull is first examined and all evidence obtained as to the presence and extent of external injury.

The ears and nose are investigated for escaping blood or cerebro-spinal fluid, important symptoms in the diagnosis of fracture of the base.

The eyes are next examined. Ocular palsies suggest injury or apoplexy; hæmorrhages—subconjunctival or palpebral—point to injury; whilst the condition of the pupils and disks may offer valuable information. Thus:

In concussion, the pupils are equal, dilated, but responsive to light.

In irritation, they are equal but contracted.

In compression, they are either equal, dilated and fixed, or unequal.

In alcohol, they are more or less normal, except in the deeper stages of intoxication, when they are dilated and irresponsive to light.

In apoplexy, dilated and fixed, or unequal. Pin-point in pontine hæmorrhage.

In epilepsy, usually equal and responsive.

In opium, immovably and symmetrically contracted.

In uræmia, dilated and sluggish.

In diabetes, equal but dilated. React to light.

In doubtful cases an examination of the disks may clear up the diagnosis. The presence of albuminuric retinitis, optic neuritis and atrophy (diabetes and uræmia), retinal hæmorrhages (injury), offer material diagnostic aid.

The tongue should be examined for such biting as is observed in epilepsy. The odour of the breath is investigated—the sickly smell of alcohol, the sweetish odour of uræmia, the peculiar smell of opium, the chloroform-like smell of diabetes.

The appearance of the face may be suggestive. The unilateral facial palsy of trauma and apoplexy; the stertorous respiration, puffing out of the cheeks, and general turgidity of compression, uræmia, apoplexy and deep alcoholism; the quiet breathing and pale face of concussion, opium poisoning, and of post-epileptic and diabetic coma.

The urine should be examined for albumen and sugar, and the body and lower extremities for œdema.

The extremities are investigated with respect to unilateral palsy, a condition only present in trauma and apoplexy. General convulsions point to injury, uræmia, and epilepsy. Resistance to manipulation is suggestive of alcoholic excess. Unilateral palsy may be associated with corresponding alteration in the deep reflexes.

The pulse-rate and the condition of the arteries supply valuable evidence. The coats may be atheromatous, whilst the slow, full pulse is strongly suggestive of compression, apoplexy, and alcoholism.

The temperature should be taken on both sides of the body. A rise of temperature is usually dependent on brain injury, apoplexy, and alcoholism. In opium poisoning, uræmia, and epilepsy the temperature is more likely to be normal or subnormal. In pontine hæmorrhage, hyperpyrexia is commonly observed.

Some difference in the temperature on the two sides of the body points to injury or apoplexy.

The depth of the coma is often of the greatest assistance in the differential diagnosis. Thus, in concussion, alcohol poisoning, and in the minor grades of epilepsy and uræmia, the patient may often be sufficiently aroused by shouting in the ear, digital pressure over the supra-orbital nerves, or by the application of the battery, as to give some account of the accident, &c. In compression, in the deeper states of uræmic and diabetic poisoning, and in the status epilepticus, the patient can seldom be aroused from the deep coma into which he is sunk.

In all cases of doubt the patient must be kept under careful observation.