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:—
A prize-fighter was knocked out by a blow on the right side of the head, dying a few hours later. The post-mortem revealed no fracture of vault or base, but a linear laceration of the brain on the mesial aspect of the right hemisphere which exactly corresponded to the free margin of the falx cerebri. In this case, therefore, conclusive evidence was obtained that the brain had been driven from right to left against a firm and resisting barrier, corresponding laceration resulting.
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]).
Fig. 57. The Areas concerned in Speech Expression.
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.
Fig. 58. The Cortical Motor and Sensory Areas.
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:—
| 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.
CHAPTER VI
THE REMOTE EFFECTS OF HEAD-INJURY
General considerations.
It is often stated that a patient who has received a severe head-injury is ‘never the same man afterwards’. Before accepting such a sweeping statement—the gravity of which is obvious—it is essential that an extensive survey should be made into the remote effects of head-injury, and, in their consideration, the surgeon must not be biased by those cases that seek hospital relief. It is the unfavourable cases that present themselves for examination, the more favourable are usually lost to view. Furthermore, whether the early results are completely satisfactory or not, but little guide can be obtained into the more remote results unless, as a routine procedure, an attempt be made to trace all such cases in their after-history. The more remote results can then be estimated at their true value.
The difficulties attendant on all attempts at following up hospital cases are considerable, and consequently we are greatly indebted to Crisp English[36] for his tabulation and discussion on the after-history of 300 cases treated at St. George’s Hospital—300 cases personally investigated at periods varying from one to twenty years subsequent to the time of the injury.
English’s conclusions have been compared with those derived from my own personal experience, with the result that they were found to coincide so closely that they may be accepted as affording an accurate guide into the remote results of head-injury in general.
English classified his cases into three series—each 100 in number—according to the severity of the lesion.
Series 1. Fracture cases.
Series 2. Cases of concussion, contusion, and laceration.
Series 3. Miscellaneous cases.
The remote results as observed in the first and second series were as follows:—
| Series 1. | No effects | 31 |
| Slight effects | 50 | |
| Marked effects | 19 | |
| Series 2. | No effects | 48 |
| Slight effects | 42 | |
| Marked effects | 10 |
In the 200 cases, therefore, that come under Series 1 and 2, 79 experienced no ill effects from the injury, 92 developed slight effects, and definite defects were present in 29 cases.
Before alluding further to the mental and bodily condition of the patients subsequent to the accident, including their wage-earning capacity, it is necessary to enlarge on the fact that the depreciation in mental and physical faculties depends, not only on the severity of the injury, but also on the age, disposition, and status of the patient.
The effect of age.
All evidence tends to prove that head-injuries in the young and the old are more serious than when the accident occurs during middle life. In the old, the power of repair is impaired; in the young, the developing faculties are impeded in their progress.
The effect of disposition.
The temperament of the patient must always be taken into consideration, the neurotic type seldom recovering so quickly or so completely as the more plethoric.
The effect of status.
A complete recovery is far more likely to occur when the status of the patient allows of complete rest, bodily and mental, for some considerable time subsequent to the accident. A premature return to work, with possible added family troubles, invariably acts as a deterrent to complete recovery. In the milder cases a few weeks suffice to allow of restoration to health, in other cases an interval of at least one year should be allowed before the patient again takes up his duties. It is obvious, therefore, that family troubles and business emergencies influence to a marked degree the completeness of recovery. It might be anticipated that the financial necessities of the case would cause the various after-results of head-injuries to be more marked amongst the labouring classes. The personal equation, however, enters largely into the question, and due allowance must be made for the greater financial and social losses entailed when the injury involves one who occupies a high social sphere. It must also be borne in mind that those occupying such spheres may not benefit from the Workmen’s Compensation Act.
On referring again to English’s cases, it was found that the wage-earning capacity of the patient afforded a valuable clue in the estimation of the remote results in general. Thus in Series 1 and 2 the following results were obtained:—
Series 1. 86 cases:
| 52 | carried out the same work at the same wages. |
| 13 | carried out lighter work. |
| 7 | could do but little work. |
| 8 | had to take to other work, less dangerous. |
| 6 | were totally disabled. |
Series 2. 78 cases:
| 51 | carried out the same work at the same wages. |
| 12 | worked as before, but without much interest. |
| 6 | were compelled to undertake lighter work. |
| 4 | could do a little work. |
| 2 | gave up their trade for another, less dangerous. |
| 3 | were totally disabled. |
Thus 59 per cent. in Series 1 and 80 per cent. in Series 2 were able to do the same work at the same wages as previous to the accident.
It will be of interest to compare English’s results with those obtained by other investigators. Thus, in 48 cases examined by Graf, the following results were obtained:—
| In | 9 | cases, no bad results. |
| 10 | cases, slight troubles or impaired work-power. | |
| 12 | cases, limited power of work. | |
| 17 | cases, complete incapacitation from work. |
Thus 35 per cent. of cases were completely incapacitated from work, results far more serious than according to English’s investigations.
Again, Crandon and Wilson made inquiries into the after-effects in 38 cases, with the following results:—
| Yes. | No. | |
|---|---|---|
| Headache | 13 | 25 |
| Eye troubles | 17 | 21 |
| Dizziness | 15 | 23 |
| Deafness | 16 | 22 |
| Paralysis | 1 | 37 |
| Faints | 4 | 34 |
| Fits | 2 | 36 |
| Loss of memory | 4 | 34 |
| Troubled by the sun | 13 | 25 |
| Troubled by alcohol | 6 | 32 |
On investigating those cases reported by English, in which the patient was compelled to take on lighter work or change his vocation, one at once encounters a diversity of symptoms, some so indefinite as to be included under the term traumatic neurasthenia, others so distinct as to fall naturally under certain well-recognized groups, such as traumatic cephalalgia, epilepsy, &c.
Traumatic neurasthenia.
All those cases characterized by the indefinite nature of their complaint require the most careful sifting—to separate the wheat from the chaff—for there is always a certain proportion of malingerers, such as realize the pecuniary advantages of their position. When these are excluded, a large class remains in whom the injury must undoubtedly be regarded as the fons et origo mali. A curious and interesting train of symptoms supervene after the accident, indefinite from a localizing point of view, but quite definite from the standpoint of the patient himself. Mental irritability, with a ready tendency to fly into a passion—Kaplan’s explosive diathesis—may be regarded as an almost constant symptom. The patient is changed in his manner towards those near and dear to him, restless, irritable, and intolerant of noises, morose, and incapable of managing his financial affairs.
The change may be insidious in origin, but, in the absence of appropriate treatment, steadily progressive. The mental changes, unless checked in time, tend to merge into definite insanity, not infrequently of a homicidal or suicidal character.
Insomnia, with terrifying dreams, loss of appetite, emaciation, headache, vertigo, nervousness, amnesia, lack of power of mental concentration, and mental depression are all noticeable features. All such symptoms are aggravated by indulgence in alcohol, exposure to the sun, &c.
From a localizing point of view the symptoms are obscure, but they are probably none the less dependent on pathological changes—thickening of the meninges, effusion into the subdural and subarachnoid spaces, œdema of the cortex, &c. Furthermore, it will usually be found that, during the height of the attacks, the pulse-rate is slowed, the temperature raised, and the respiration embarrassed—symptoms suggestive of cerebritis and alterations in the intracranial pressure.
In exploratory operations conducted in cases of this nature, I have been particularly struck by the fact that in a large proportion of cases one finds what appears to be a condition of local œdema—some fluid beneath the dura mater, and a greater excess of the same in the pia-arachnoid meshwork. This œdema is a manifest condition readily demonstrated to onlookers. I am not an advocate of ventricular puncture in these cases, mainly on the ground that it complicates the operation and brings no added benefit in its train, but in such cases as it has been carried out the jet of cerebro-spinal fluid proves the added existence of an increased intraventricular pressure. From Leonard Hill’s experiments it would appear that this œdema is dependent on chronic vascular changes—arterial anæmia, venous congestion, and cerebro-spinal and serous accumulation.
At a later date the meninges may become thickened and adherent to one another and to the surface of the brain, whilst false membranes and arachnoid cysts may develop.
Treatment.
For these more general and indefinite remote results of head-injury the treatment comprises REST, bodily and mental, light diet, fresh air, cheerful but quiet surroundings, and encouragement. Potassium iodide and mercury (preferably by inunction) often do good, whilst phenacetin and antipyrin are perhaps the best drugs for relief of headache. For sleeplessness potassium bromide is perhaps the best remedy.
I have found in some cases that Turkish baths and massage have brought about considerable improvement. In advising such energetic treatment the surgeon must be guided by the case before him, these measures being more or less restricted to the less serious and more chronic cases.
In the more serious cases, especially when slowing of the pulse during the height of the attacks and some blurring of the disks point to a probable increase of intracranial pressure, operative measures must be considered. The greatest circumspection is required in determining the class of cases in which operation may be proposed, and the surgeon must be most guarded in his prognosis. So far as my personal experience goes, the operation has invariably brought about some amelioration in the condition of the patient, whilst now and again a complete cure may be anticipated. Those cases which on exploration evidence an œdema of the brain are the least favourable; those in which the surgeon finds a subdural cyst or hæmatoma offer the best prognosis.
With respect to the details of the operation, two courses are available: (1) examination of the meninges and brain at the seat of injury, and (2) a ‘decompression’ operation. The former course should be adopted whenever the local conditions are favourable, that is to say, whenever depression or absence of bone, localized headache, &c., suggest a localized lesion. Under other circumstances Cushing’s intermusculo-temporal method of decompression should be carried out. This operation should be conducted first over the right temporal region, thus avoiding all possibility of inclusion of Broca’s area, a similar operation being done on the left side at a later date in the event of incomplete success.
Traumatic cephalalgia.
Of all the after-results of head-injuries, headache is the most constant symptom, either localized to the region primarily involved or diffuse. Even when diffuse, however, the aching is frequently referred to the frontal region. Localized headaches are the more acute. The patient can place his finger over the site of the trouble with accuracy and constancy. Examination on the part of the surgeon causes him to wince or cry out. Percussion with the tip of the finger not only leads to marked exacerbation but also induces a dull aching sensation, which lasts for some time afterwards. Whether acute or dull, exacerbations are of frequent occurrence, and during these attacks the patient is entirely incapacitated, desiring nothing more than to be left alone.
In some cases the pain is referred along the course of one of the superficial nerves, in which case it is probable that the affected nerve is caught up in the scar.
Headache, of whatever nature, is increased by exertion, indulgence in alcohol, exposure to the sun, &c.
Crisp English considers that many cases of localized headache are dependent on a localized chronic osteitis, and recommends trephining and removal of the affected bone. There can be no doubt that the mere removal of a disk of bone will occasionally bring about a cure, but, from my own experience, I take a different view with respect to the pathological lesions present. I have operated on over a dozen cases of chronic cephalalgia, and I have found in nearly every case definite pathological lesions—depression of internal table, thickening of the meninges, subdural cysts and subdural hæmatomata. The mere removal of a disk of bone may relieve the symptoms by reducing the local pressure or by removing a source of meningeal irritation, but such treatment seldom brings about permanent relief. The dura mater should be opened in nearly every case, the frequent discovery of a subdural complication—cyst or hæmatoma—showing that such a course is necessary.
These patients suffering from chronic headache are often pitiable subjects, spending their time in wandering from doctor to doctor, from hospital to hospital, seeking relief. They are only too eager to obtain benefit from surgical intervention. The greatest care is required in deciding as to operative procedures. Injudicious surgical measures are not only disappointing to both surgeon and patient, but also discreditable to this branch of surgery. On the other hand, it must be acknowledged that remedies other than surgical are generally inefficacious. The surgeon, therefore, takes considerable responsibility on his shoulders when he states that an operation is inadvisable. Though guarded in my prognosis, I generally advise operation on the ground that it is impossible to foretell the cause of the headache, and brilliant results may be obtained.
Treatment.
When the headache is diffuse, REST, aided by the administration of phenacetin, &c., may exercise some effect. Operative treatment should not be recommended unless the intensity of the attack, blurring of the disks, and slowing of the pulse suggest that there is some increase in the general intracranial pressure. Under such circumstances, exploration should be carried out over the region at which the injury was received. In the absence of evidence with respect to external injury, a subtemporal decompression operation is the operation of election.
When the pain is localized to some special region, the outlook is more favourable. Operative measures should then always be carried out over the painful spot. A scalp-flap is framed according to the region which it is desired to expose, the disk of bone removed, and the meningeal territory examined. For detailed operative technique, see [p. 20].
When the pain is referred along the course of one of the scalp nerves, it may be relieved by alcohol injections (see [p. 314]), or by exposure of the nerve, followed by removal of at least 1 inch of its trunk.
Traumatic epilepsy.
When epilepsy arises after a head-injury, it is almost the invariable rule that the attacks should partake at first of the focal or Jacksonian type. A case of traumatic epilepsy should, therefore, possess the following characteristics:—
1. The fit should be preceded by some sensory or motor aura—the aura corresponding to the region of the brain primarily involved.
2. The fit should always start by twitchings of the parts supplied by the motor area which is in direct relation, or in close proximity, to the site of dural or osseous lesion.
3. The fit may remain localized to the region first affected, or, as is more commonly the case, may spread to other regions. In the latter case the various motor areas are affected in a certain definite order, according to their cortical arrangement. Thus, a fit arising from irritation of the right cortical face-area leads first to twitchings, then to convulsions, and perhaps finally to paralysis on the contralateral face-muscles, the movements then spreading from the face to the upper extremity, and from the arm through the trunk to the lower extremity. When the fits become generalized, spreading to the opposite side of the brain, the cortical areas are affected in the reverse order.
4. The patient should retain consciousness throughout the attack.
5. The fits should not be succeeded by any paresis or paralysis.
Later on, when the fits become more frequent and severe, they lose their typical Jacksonian characters, the various regions being affected so rapidly one after the other that all focal symptoms tend to be obscured. The fits are then often associated with definite loss of consciousness, and succeeded by paresis or paralysis of the parts primarily affected. The patient also usually complains of lassitude or headache, this lasting some hours after the termination of the fit.
Traumatic epilepsy does not always partake of the typical Jacksonian type. Sometimes the fits are so sudden in onset and violent in character that, from the first, the more typical features are absent. Again, fits of the focal or Jacksonian type do not necessarily imply that some pathological causative agent will be found on exploration. Ordinary epilepsy sometimes partakes of the focal type. I have myself operated on three cases of focal epilepsy, deceived by their Jacksonian characteristics, and found nothing abnormal. On the other hand, in all these cases definite and permanent improvement was observed subsequent to the surgical procedures.
It might also be added that encouraging reports are to hand, not only in cases of idiopathic epilepsy with focal symptoms, but also in cases without focal symptoms. A decompression operation is carried out on the basis of Kocher’s statement to the effect that the fit is immediately preceded by a rise of intracranial pressure, for which a safety-valve must be supplied—such as is afforded by an intermusculo-temporal operation of decompression. Whether Kocher’s statement is correct or not, the fact remains that some cases of idiopathic epilepsy, without focal symptoms, benefit considerably from operation.
The localizing symptoms of traumatic epilepsy.
When the cause of the trouble is situated over the motor area—the pre-Rolandic cortical strip—the fits should commence by twitchings of the fingers, toes, corners of the mouth, &c., according to the site of the lesion. The fits are seldom preceded by any sensory auræ, though occasionally such may be the case, for even at the present day some doubt exists as to whether the precentral area should be regarded as purely motor or sensori-motor. In other cases, the patient, without being able to state definitely his sensations previous to the onset of the fit, may be able to foretell its immediate development, and still more rarely he may be capable of aborting the fit or diminishing its intensity by grasping firmly or massaging the region of the body in which the fit first develops.
When Broca’s motor speech-area is primarily involved, the fits are preceded by difficulty in phonation, mumbling of words and incoherence, grinding of the teeth, &c., the fits then rapidly spreading to the parts responsible for the movements of the muscles of face and upper extremity.
When the fits arise from a post-central source of irritation, they are usually preceded by well-marked sensory auræ—tinglings, burning and painful sensations—again according to the region affected.
When preceded by sensations of taste and smell, the lesion is probably situated over the anterior part of the temporo-sphenoidal lobe.
When by visual impressions—flashes of light, &c.—the lesion is probably situated over the occipital lobe of the brain.
Pathology.
The pathological conditions responsible for the development of fits are various, resolving themselves, when fully investigated, into two main groups: those associated with meningeal changes only, and those accompanied by definite cortical scarring and tract degeneration.
In the event of osseous deficiency the scalp is usually more or less adherent to underlying structures, and the gap in the skull filled with dense fibrous tissue, which is itself adherent to the membranes of the brain and perhaps to the brain itself.
In the absence of osseous deficiency, the cerebral irritation is usually dependent on depressed fragments of bone, on subdural hæmatomata and cysts, and on meningeal thickening.
In the event of cerebral degenerative changes it may be presumed, whether there is a deficiency in the bone or not, that considerable matting of meninges and cortex is existent with pyramidal degeneration.
In the absence of evident signs of external injury, cases of focal epilepsy in the young require careful investigation, inquiry being made as to difficult labour, for, as Harvey Cushing points out, ‘When we consider the widespread lesions associated with those cases that later on are recognizable as Little’s disease, and that presumably an enormous number of children receive at birth some trifling injury which, from lack of symptoms, is overlooked, may it not be that many cases of so-called idiopathic epilepsy dating from childhood can be safely attributed to the effects of early traumatism?’
In all these, and in other doubtful cases, before undertaking surgical procedures, the surgeon should obtain the services of a skilled neurologist.
The clinical course of the case.
If a typical case of Jacksonian epilepsy can be observed from beginning to end, many curious and interesting features will be observed. The fits, at first typically Jacksonian, gradually lose their typical character, becoming more frequent and less focal in nature, the patient losing consciousness during the fit, and the fits succeeded by weakness or paralysis of the parts primarily involved. The general mental state of the patient suffers proportionately—he becomes morose, despondent, irritable, homicidal, or suicidal in tendency. How far these retrograde symptoms are dependent on degenerative processes in the brain, and how much they result from the moral effect of the frequent epileptiform seizures, are questions that can only be determined by observing the effect of treatment, surgical or otherwise. Some cases respond readily to treatment, others are too far advanced to experience any material benefit, some end their days in the lunatic asylum.
In any case, surgical treatment, if adopted at all, must be carried out before definite brain-degeneration arises—such changes being evidenced by spasticity of the limbs, exaggerated knee-jerks, &c. When such pathological changes are existent, there can be but little hope of benefiting the patient.
Further points in the clinical course of the case, and such also as throw further light on the pathological conditions present, will be obtained by a survey of 21 cases that have come under my own care or close observation.
| Time elapsing between the date of the accident and the first fit. | ||||
| Between 1 and 19 years | 9 cases | |||
| Within 8 months | 9 cases | |||
| After a few days | 1 case | |||
| Uncertain | 2 cases | |||
| Age at time of accident. | ||||
| Before 15, 12 cases. Youngest, 3 years. | ||||
| After 15, 9 cases. Oldest, 55 years. | ||||
| Sex. | ||||
| Males 20. Females 1. | ||||
| Conditions found on external examination and on operation. | ||||
| External examination: | Depression of bone and scar, 6 cases. | |||
| Deficiency of bone, 3 cases. | ||||
| Scar only, 5 cases. | ||||
| Nil, 7 cases. | ||||
| At operation: | Sclerosis of bone, 1 case. | |||
| Tuberculous mass, 1 case. | ||||
| Subdural cyst or hæmatoma, 8 cases. | ||||
| Scalp adherent to dura, 3 cases. | ||||
| Scar in brain, 1 case. | ||||
| Œdema of brain, 3 cases. | ||||
| Nil found, 1 case. | ||||
Some lesion, such as might be accepted as responsible for the development of the fits, was discovered in 17 out of 18 cases. Duret’s experience tends to bear out the view that some pathological lesion will be found in almost every case. In 67 cases reported the following conditions were found:—
Depression of bone, 27 cases.
Splinters of the internal table, 15 cases.
Cysts, subdural, 4 cases.
Thickening of membranes, 7 cases.
Operation.
When the localization of the trouble is suggested by the presence of focal symptoms, and by a corresponding scalp- or bone-injury, no difficulty need be experienced in determining the site of exploration. When the fits are associated with definite focal symptoms, but without the supplementary evidence obtained by visible signs of external injury, exploration should be conducted over that region of the brain from which the fits appear to emanate. In the absence of all localizing brain symptoms, operative measures should be carried out over the site of scalp or bone lesion.
Whatever the circumstances of the case, the preliminary details are identical. The scalp is shaved, cleansed, the head enveloped in gauze, and the scalp-tourniquet applied.
The formation of the scalp-flap.
When the scalp is adherent to the bone, the incision, carried throughout down to the bone, is made in such a manner that the flap will not only allow of the detachment of the scar, but will also permit of the complete exposure of the neighbouring portion of the skull.
When the scalp is adherent to dura or brain, as the result of osseous deficiency, the edge of the knife should be directed towards the under aspect of the flap, and the flap carefully peeled away from the region of the gap.
The examination of the bone.
When no fracture is found, the operator should trephine over the cortical area from which the trouble appears to emanate.
When a fissured fracture is found, trephining is carried out where the line of fracture cuts across that region of the brain which appears to be involved.
When a depressed fracture is found, the trephine is applied in such a manner that the circle just includes the outer segment of the depression. After removal of the disk, the dura mater should be peeled away from the under surface of the bone, and the whole of the depressed area cut away with the craniectomy forceps.
When there is osseous deficiency and when the gap is filled in with fibrous tissue, adherent to the margins of the gap and probably to the dura or brain as well, it is essential that this fibrous tissue should be freely removed. All evidence goes to substantiate the statement that meningeal irritation is the main cause of the fits, &c.
The removal of this tissue is best carried out by beginning at the most promising part of the gap, detaching the tissue adherent to the most prominent portion of the bone, and exposing the underlying dura mater. The central mass of scar tissue should then be seized with forceps, lifted up and detached as completely as possible, both from the margins of the gap and from the underlying dura or brain. In the more complicated cases, where the scar tissue is adherent to dura and brain, the most careful dissection is required, and in many instances it is necessary to include that part of the dura mater which is incorporated with the scar. The cerebral substance should be carefully protected (see below).
The treatment of the dura mater.
When the dura has not been injured during the process of exposure, pulsating freely, and presenting a normal appearance, preparations can be made to close in or protect the gap in the skull.
When the membrane bulges outwards, and when, in other respects, the indications point to an increase of intradural pressure, the dura must be incised in a crucial manner, and further investigation carried out in the search for a subdural hæmatoma, arachnoid cyst, or other lesion. A hæmatoma is washed out and drained, an arachnoid cyst shelled out or treated by excision of the parietal wall (see [p. 204]).
When the dura is thickened, matted, and adherent to the brain, it is picked up at the least adherent part and carefully dissected away, exposing the pia-arachnoid region. The surface of the brain being so brought into view, the scalpel and dissecting forceps may be required to remove all tags and shreds of matted tissues, this process being continued till a reasonably healthy region has been brought into view.
The treatment of a cortical scar.
There is no reason why a superficial scar should not be freely removed, but, unfortunately, this procedure is necessarily followed by the formation of another scar, at least as extensive as the original fibroid condition. The removal of cortical scars has therefore justifiably fallen into disrepute, and most surgeons content themselves with an exposure of the pia-arachnoid region, the actual cerebral substance being left intact. All bleeding must be arrested, blood extravasation merely favouring the formation of fresh adhesions.
The prevention of fresh adhesions between the dura and the brain and between the scalp and the dura or brain.
‘It is useless to talk about the prevention of fresh adhesions; they form in spite of anything that may be done’ (English). With this statement, I am in complete accord. It has been recommended that fresh egg-albumen, gutta-percha tissue, silver foil, &c., should be inserted beneath the dura or between the scalp and the brain. Experience shows, however, that all these substances are useless, being invaded or surrounded by granulation tissue, and, later on, absorbed by or enclosed in dense fibrous tissue.
The formation of adhesions between the scalp and the dura or brain can, however, be effectually prevented by the insertion of plates, &c. (see [below]).
The closure or protection of gaps in the skull.
Indications for operative treatment. Large defects, post-operative or traumatic.
Small defects situated over exposed portions of the skull or over the more important regional areas.
Both large and small defects associated with chronic headache, insanity, Jacksonian epilepsy, &c.
Certain congenital defects in the vault.
Small defects, unless situated in exposed regions or associated with symptoms, seldom demand protection.
Methods.
(a) The formation of bone-flaps, derived from neighbouring parts of the skull, from some other bone of the patient, or from the bones of a freshly-killed animal.
(b) The interposition of plates of some foreign material between the scalp and the bone, or the insertion thereof into the osseous deficiency.
(a) Bone-flaps. The osteoplastic method of König and Müller. Two flaps are framed in the manner described below, and the two interchanged in position. A ⋂-shaped flap, comprising the whole thickness of the scalp, is turned down so as to expose the region of the deficiency, the margins of the incision lying about 1⁄2 inch outside the margin of the gap. The flap is dissected from underlying structures to which it may be adherent, care being taken to avoid injury to the blood-vessels entering at the base of the flap.
A second flap is framed from the scalp immediately to one side of the first flap. This second flap corresponds in size and shape to the one already framed, but differs in that its base points in the opposite direction. It is also peculiar in that it consists of the whole thickness of the scalp plus the external table of the skull. The scalpel is carried down to the bone, and the margins of the incision retracted in such a manner as to allow of the application of the hammer and chisel. The external table is cut through along the line of the scalp incision and split away from the rest of the bone. The two flaps are now interchanged in position and sewn down with a few salmon-gut sutures.
Fig. 59. The König-Müller Osteoplastic Flap. a., The scalp-flap; b., The osteoplastic flap; g., The gap in the skull.
The osteoplastic flap is by no means easy to frame, the external table tending to split up during the process of separation; moreover, its formation is confined to the upper-occipital and parietal regions of the skull, regions where the two tables are separated by diploic tissue. In the temporal and cerebellar regions this method cannot be adopted, and in the frontal region the deformity and scarring act as a bar to such operative procedures.
In suitable cases, however, good results may be obtained by this method. Asepsis is essential to success.
Bone-flaps derived from some other bone of the patient (e. g. the tibia), or from the bones of a freshly-killed animal (e. g. the scapula of a dog), seldom yield satisfactory results. The gap in the skull is first exposed, the margins refreshed, and the size and shape estimated. The bone-graft is then cut from the other bone, suited in every respect to the deficiency, inserted in the gap and sewn into position. The graft, however, seldom retains its vitality, being invaded by granulation tissue, and converted, in the course of time, into dense fibrous tissue. Furthermore, in the event of the slightest failure of aseptic technique, it acts as foreign body and must be removed.
The attendant difficulties and the frequent failures of these auto- and hetero-transplantations of normal bone lead to the utilization of decalcified, calcined, and boiled bone-plates. Between these there is very little to choose, for, whether due to the absence of calcium salts or the destruction of bone-cells, they merely act as scaffolding media for the formation of fibrous tissue and are more or less completely absorbed.
(b) Plates of some foreign material. The following method has been found to give the most satisfactory results. Plates of pure annealed silver are utilized, 9⁄1000 inch in thickness (No. 2 Birmingham metal gauge). The plates are light and of fair malleability. Supposing now that it is required to protect a deficiency in the vault—irregular in shape, round or oval, it matters not—the maximum antero-posterior and vertical diameters are measured and a piece of silver cut out, which is about 1⁄2 inch greater in both diameters. The convexity of the skull in the region of the gap is estimated and the plate hammered into corresponding shape. This is readily carried out by placing the plate on a heavy leaden base and hammering to the required convexity. The convexity is regulated by the site of application of the blows, the heavier being applied to the central or apical portion of the plate, the weaker to the periphery. A rough general convexity is so produced. The edges of the plate are smoothed with the file, and a few holes bored to allow of the escape of any blood or cerebro-spinal fluid that might tend to collect beneath.
Fig. 60. The Author’s Method of covering in a Gap in the Skull. s., The scalp; pc., The pericranium; p., The plate; g., The gap in the skull (inside the irregular dotted line); sc., The scalp-flap.
The plate is then boiled and applied as follows. The osseous defect is exposed by a scalp-flap—not including pericranium—the margin of the scalp-flap lying at least 1 inch external to the margin of the gap.[37] The flap is dissected down so that its base is situated not more than 1⁄2 inch below the lower limit of the gap. The pericranium is then stripped away towards the periphery. The plate is applied so that it rests below against the base of the scalp-flap, lies throughout between the scalp and bone, and overlaps the margins of the gap by about 1⁄2 inch. The pericranium is heaped up around and over the margins of the plate, and the scalp-flap replaced. The plate is maintained in position by the support received from the base of the flap, marginally by the pericranium, and generally by the reposition of the scalp-flap.[38] In the process of time, new bone is formed by the pericranium, this and fibrous tissue developing along the line of the scalp incision fixing the plate accurately and firmly in position.
Needless to say, absolute sterility of the field of operation and of all media is essential. In the event of failure in cleanliness, however slight, it will become necessary to reopen the wound and remove the plate. In such cases a second attempt may be made at a later date.
Results.
The results attained by operative treatment must always be considered under two headings: the immediate and the more remote.
The immediate results are almost always of a satisfactory nature, the fits being more or less completely controlled, or so diminished in quantity and quality as to satisfy both surgeon and patient. Such early results may be regarded as the general rule, and some enthusiasts believe that the ultimate results are equally satisfactory. However, in following up these cases, it will be found that, in a considerable proportion of cases, the more remote results are by no means so satisfactory. A complete and permanent cure is seldom obtained, though the great majority of cases evidence considerable improvement, the fits recurring, though less frequent and less intense than previous to the operation.
The results which may be obtained should therefore be considered as follows:—
Cases of complete and permanent cure.
Cases of definite amelioration.
Cases in which no benefit is derived.
In 20 cases that have come under my own care, the following results were obtained:—
Complete cure in 2.
Marked improvement in 14.
No change in 4.
Cushing reports on 128 cases of traumatic epilepsy, operative measures being adopted in 58, 40 cases of focal epilepsy and 18 exhibiting no localizing feature. The results were as follows:—
12 cases were free from attacks for from 1 to 5 years.
30 were greatly improved or showed some improvement.
17 exhibited no change.
2 died in status epilepticus.
Traumatic insanity.
Traumatic insanity is closely allied to traumatic epilepsy, occurring, as a general rule, late in the history of the case, when the frequency of the fits and the associated disturbance of the higher faculties breaks down the mental and moral control of the patient.
The particular form of insanity varies according to the circumstances of the case. Kraft Ebbing reported on 42 cases, the disease partaking of the following types:—
18 cases of mania.
13 cases of dementia.
5 cases of dementia with epilepsy.
3 cases of general paralysis.
3 cases of melancholia.
Of 104 cases reported by Christian,
16 were of dementia.
29 of mania.
47 of general paralysis.
12 were of epilepsy.
Mania—of a violent type—usually develops within a short time of the accident—a few hours or days. Its development is probably dependent on an acute cerebral œdema—the result of a most severe grade of vaso-motor depression—and it is often, though not necessarily, associated with extensive cerebral injury. There is marked engorgement of the cerebral venous system, and considerable increase of cerebro-spinal fluid, both on the surface of the brain and in the ventricular spaces.
When insanity develops at a later date, of whatever variety, it is probably dependent on definite pathological changes. Ll. Powell, Duret, and others, after investigating the conditions, came to the conclusion that the injury was comparatively superficial—subdural cysts and hæmatomata, pachymeningitis, osteosclerosis, ossification of the dura mater, &c. They also maintain—an opinion that I also hold—that the nervous phenomena are, in most cases, due to reflex meningeal irritation.
Ll. Powell reports on 67 cases submitted to operation, with the following results:—
In 41 there was mental recovery.
In 12 there was marked mental improvement.
In 5 there was slight mental improvement.
In 4 there was no change.
Death resulted in 5 cases.
The results obtained by surgical treatment are largely dependent on the time that has elapsed since the accident. Lapse of time is no bar to operation, but the sooner this procedure is carried out the better for the patient.
Treatment.
I think that it must be accepted that, without surgical interference, the prognosis is of the most unfavourable type. These cases, if left to themselves, drift into the public and private lunatic asylums, there remaining to the end, hopeless wrecks.
If such is the case—and I think that refutation is impossible—and if it be accepted that definite pathological changes are usually present, then it is obvious that surgical interference offers the only hope of cure or alleviation. The surgeon must be guided by the case before him, but, in the absence of hereditary taint, exploration should be carried out, preferably at the site of the original injury, and as early as possible before the advent of definite cerebral and pyramidal degenerations.
The operative details vary according to the necessities of the case. Thus, in acute mania, acting on the supposition that the development is dependent on an acute cerebral œdema, the surgeon should carry out a decompression operation. Personally, I hold the view that Cushing’s subtemporal decompression operation (see [p. 121]) should be carried out on both sides of the skull, with or without lumbar puncture.
In the more chronic cases, operative procedures are conducted over the region injured in the anticipation of discovering depressed bone, subdural cysts, hæmatomata, &c. The operative details peculiar to all of these conditions are discussed in other sections.
With special reference to general paralysis of the insane, Dr. Claye Shaw holds the opinion that a general increase of intracranial pressure is commonly present. At his instigation, and on other occasions, I have carried out decompression operations, but I have not been able to satisfy myself that the patients have experienced any benefit other than temporary. There was on each occasion a considerable excess of cerebro-spinal fluid with surface œdema of the brain, but the ultimate results were certainly disappointing.