Chapter V (2)

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:--

=12= _cases in the hospital for 7 days or less_ (_cerebral shock
only_).

_Temperature_ on admission: 8 subnormal.
2 normal.
2 slightly raised.

_Pulse_ on admission: 3 subnormal.
3 normal.
6 accelerated.

=26= _cases detained for 7 to 10 days_ (_probably cerebral shock
only_).

_Temperature_ on admission: 6 subnormal.
9 normal.
11 slightly raised.

_Pulse_ on admission: 4 subnormal.
12 normal.
10 accelerated.

=9= _cases detained for 14 to 21 days_ (_probably cerebral
contusion_).

_Temperature_ on admission: 2 subnormal.
3 normal.
4 slightly raised.

_Pulse_ on admission: 6 subnormal.
1 normal.
2 accelerated.

=3= _cases detained for 21 to 30 days_ (_certainly cerebral
contusion_).

_Temperature_ on admission: 1 normal.
2 slightly raised.

_Pulse_ on admission: 1 subnormal.
1 normal.
1 accelerated.

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,

A stands for Alcohol and Apoplexy.
E „ „ Epilepsy (post-epileptic coma).
I „ „ Injury.
O „ „ Opium poisoning.
U „ „ Uræmia.

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.

[26] _Syst. of Pract. Surg._, vol. ii.

[27] _Deutsche Zeit. für Chir._, Bd. 4, vols. i and iii.

[28] _Guy’s Hosp. Reports_, 1885-6.

[29] Bergmann’s _System of Surgery_, vol. i.

[30] _Ruptures de l’Artère méningée moyenne._

[31] _Guy’s Hospital Reports_, vol. lix.

[32] _Traumatic Injuries of the Brain._

[33] _Traumatic Injuries of the Brain_, p. 138.

[34] _System of Surgery_, vol. i, p. 179.

[35] _American Practice of Surgery_, Bryant and Buck.