The Surgery of the Skull and Brain

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:—

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:

Series 2. 78 cases:

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:—

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:—

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.

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.

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.

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.

MENINGEAL CYSTS

Amongst the pathological conditions responsible for the development of epilepsy, chronic cephalalgia, &c., meningeal cysts must be regarded as of frequent occurrence.

Traumatic meningeal cysts are varied in size, site, and structure. They may be classified as follows:—

Cysts within the calvarium.

Traumatic cysts within the calvarium, whatever their situation, may be divided into two definite groups:—

1. Where the cyst possesses fibrinous walls (in which hæmatoidin cysts may be deposited) and contains a grumous material. These cysts are usually subdural in position, are dependent on the previous existence of a hæmatoma, and are known as ‘blood-cysts’.

2. Where the cyst—often of considerable size—is lined by a thin, shiny, membranous wall. The contained fluid is almost colourless, closely resembling cerebro-spinal fluid, but albuminous and having no sugar-reducing reaction. The fluid is at high tension, spurting out when the cyst is punctured. The cyst usually lies in relation to the arachnoid membrane. Hence the name, ‘arachnoid cyst’.

To account for the development of these ‘arachnoid cysts’ two theories have been advanced. Firstly, that they arise as the ultimate result of a long-continued circulatory disturbance of the vessels of the membranes or of the cortex, with consequent local cystic accumulation of cerebro-spinal fluid or serum; and secondly, that shrinking of the brain occurs in the region of an injury as the result of sclerotic changes in the cerebral substance, any contraction tending to lead to the formation of a vacuum which becomes filled with fluid derived from the surrounding membranes. According to this latter theory, arachnoid cysts are in reality ‘cysts ex vacuo’.

As regards symptomatology, little need be said. Occasionally ‘arachnoid cysts’ of considerable size have been discovered at post-mortem examinations which appeared to have exercised no local or general pressure effects during life. More often the cysts, whether ‘blood-cyst’ or ‘arachnoid cyst’, lead to the development of Jacksonian epilepsy, chronic headache, and the like, and are discovered during the exploratory operation carried out for such conditions. Occasionally they may be shelled out entire, but it is more usual for the surgeon to remain content with the removal of the parietal wall (see p. 195). The results obtained by surgical treatment are sufficiently gratifying.

TRAUMATIC ORBITAL ANEURYSM
(Pulsating Exophthalmos)

This condition was first investigated by Rivington in 1875. Since that date many other cases have been reported, and the following remarks are based on the examination of the records of 26 cases, 2 of which have come under my own care.

The nature of the trouble, the results obtained by operative treatment, and the direct evidence supplied by post-mortem examination furnish sufficient proof to justify the statement that the symptoms are dependent on the formation of an arterio-venous aneurysm, the internal carotid artery and the cavernous sinus intercommunicating by means of one or more fistulous channels. That such a lesion may arise from direct violence—the introduction of some sharp weapon along the upper and inner portion of the orbital cavity—-is readily comprehensible. Such injuries are, however, of rare occurrence, and the formation of the aneurysmal communication is usually the result of indirect violence—the application of severe blows to the antero-lateral and lateral aspects of the head.

In explanation, the following preliminary facts may be accepted:—

In the great majority of cases the blow was applied to the temporal region, the patient was rendered unconscious, bleeding freely from the ear, nose, and mouth, and remained under treatment for some considerable time. From these facts it may be assumed that the patient suffered from a fracture of the base of the skull—anterior or middle fossa, or both fossæ. Evidence has already been brought forward to show (1) that the majority of fractures involving both anterior and middle fossæ traverse the body of the sphenoid, and (2) that the cavernous sinus is very susceptible to injury. It was also demonstrated that the internal carotid artery is only liable to injury in that part of its intracranial course where it is embedded in the outer wall of the cavernous sinus. Two instances of such a lesion have been described in the section dealing with injuries to intracranial vessels (see p. 148, and Figs. 53 and 54).

From these facts and from the post-mortem evidence supplied by the few cases that have come to autopsy, it may, I think, be concluded (1) that traumatic orbital aneurysm implies a condition of arterio-venous aneurysm with direct communication between the internal carotid artery and the cavernous venous sinus, and (2) that the aneurysmal formation is dependent on a basic fracture which traverses the region of the body of the sphenoid bone.

The exact nature of the communication between the two vascular channels may be estimated from the fact that proptosis—usually the first symptom to make its appearance—seldom becomes apparent till one or two months have elapsed after the accident. It would appear, therefore, probable, that the artery is not ruptured but merely weakened at the time of the injury, the weakened arterial wall gradually giving way before the force of the blood-stream till a definite communication is formed between the two channels.

The male sex, by reason of its greater liability to severe injuries, is generally the one involved, especially between the ages of 20 and 30.

Symptomatology.

1. Proptosis

—usually the first symptom to develop—seldom makes its appearance till after the lapse of one to two months. The eyeball is protruded in the downward and outward direction, the main pulsating tumour presenting at the upper and inner quadrant of the orbit. Proptosis is generally steadily progressive, and, in the most marked cases, the globe may be almost pushed out of its socket. In any case the ‘whites’ of the eye are unduly prominent.

2. Aneurysmal symptoms.

The tumour pulsates synchronously with the heart’s beat, whilst compression of the common carotid of the same side results in cessation of pulsation and great diminution in the size of the aneurysmal swelling. On releasing the compression force the tumour regains its original size in two or three beats of the heart, and, for a short time, pulsates more forcibly than before. A definite thrill is imparted to the examining finger, and, on auscultation, a loud murmur is heard, not only over the tumour itself, but also widely conducted over the bones of the vault, especially along the line of the superior longitudinal sinus. The free collateral circulation between the angular and ophthalmic arteries permits of the involvement of vessels in the inner orbital and upper nasal regions. This is well shown in the case depicted in Fig. 61.