MENINGITIS

Previous to entering into the question of general meningeal infection, some allusion must be made to the rarer forms of meningitis.

Serous meningitis.

Quincke demonstrated in 1895 the existence of a serous form of meningitis, one characterized by a sero-fibrinous exudate. He showed that, just as we have to deal with a serous or purulent pleurisy, so we have to consider the possibility of a serous or purulent form of meningitis.

The exudate appears at first sight to differ but slightly from normal cerebro-spinal fluid, being clear, yielding the normal chemical reactions of that fluid, and occupying the subarachnoid region. Later on it becomes slightly turbid, contains a fair quantity of albumen, and is proportionately rich in cellular elements—lymphocytes and polymorphonuclear leucocytes. The membranes are swollen, the vessels dilated, whilst occasionally many minute hæmorrhages may so allow of the escape of red blood-corpuscles as to impart to the exudate a yellowish-red coloration. At a still later stage the exudate becomes flocculent as a result of the deposition of a fibrinous coagulation, a gum-like material forming over the surface of the brain.

Pachymeningitis externa.

Pachymeningitis externa is almost necessarily dependent on disease of the middle ear, on suppuration in the accessory sinuses of the nose, and on infected fractures of the vault and base. The inflammatory changes primarily involve the external aspect of the dura mater, the external surface of which is injected, roughened with fibrinous exudate, and, in the more chronic cases, covered with granulations. In itself the process seldom gives rise to symptoms, but so soon as the inner surface of the dura shares in the affection (meningitis), or the infection spreads to the venous sinuses (sinus thrombosis), or to the brain (brain abscess), definite symptoms arise pointing to the nature and character of the change.

Pachymeningitis interna and pachymeningitis interna hæmorrhagica.

As the direct result of alcoholic excess, of syphilitic infection, and of trauma, the inner surface of the dura mater loses its shiny appearance, becomes opaque and thickened, especially in the region of the falx cerebri and over the convexity of the brain. The sodden and œdematous condition of the dura gives rise to a fibrinous and membranous exudate, terminating in the formation of false membranes—one of the factors in the formation of so-called ‘arachnoid cysts’ (see p. 203). These membranes are seen to be attached to the dura mater by means of newly-formed vessels, some of which may rupture, giving origin to blood exudate sufficing to impart to the membranes a brownish-red coloration. In the more marked cases, especially in those of a recurrent nature, the membranes partake of a lamellated type. Occasionally, the hæmorrhages are more excessive, giving rise to the formation of subdural hæmatomata from the partial absorption of which the various types of pachymeningitis hæmorrhagica arise.

These rarer forms of meningitis seldom give rise to such definite symptoms as to allow the surgeon to carry out surgical procedures in their earlier stages. Later on, by reason of the development of cystic accumulations of fluid or other complication, operation may be carried out with a reasonable degree of success. The operative technique adapted to the individual case is discussed under appropriate headings—Jacksonian epilepsy, meningeal cysts, &c.

It is possible that some criticism may be aroused with regard to the non-inclusion of tuberculous meningitis. Insomuch, however, as I have operated on a considerable number of cases of tuberculous meningitis—some intentionally from a decompression point of view, others by reason of doubtful diagnosis—and have never brought about more than some temporary alleviation, I have come to regard such cases as beyond the realms of surgery.

Acute lepto-meningitis.

This condition will be considered under the more familiar, though less correct, designation—meningitis.

Attempts have been made to classify the various forms of meningitis on a bacterial basis. When, however, it is realized that almost any known form of organism may be present in the exudate, and that the symptoms dependent on these various infections closely resemble one another, merely differing in their acuteness and intensity, it would appear that some other form of classification is preferable.

The following method of classification will suffice:—

1. Meningitis of traumatic origin.

The organisms either obtain direct entrance to the meningeal space by means of a compound fracture of the vault or base of the skull, or reach their destination along the course of the numerous emissary and diploic veins that bring the extra- and intra-cranial channels into communication.

2. Meningitis secondary to disease of neighbouring regions.

(1) The accessory sinuses of the nose and ear.

(2) The bones of the skull.

(3) The soft parts—scalp, orbit, nose, and face.

3. Meningitis secondary to disease of more distant regions.

Through the medium of the blood-stream bacteria may be carried to the meningeal region in many acute infections—more especially in diseases of the lung.

Some anatomical considerations of meningitis.

The pia is closely applied to the surface of the brain, dipping down into all the fissures, both major and minor. The arachnoid is only reflected into the greater fissures—the mesial longitudinal fissure, the fissure of Sylvius, Rolando, &c. The pia and arachnoid are therefore separated from one another by a potential space over the convolutions themselves, and by an actual space in the region of many of the cortical fissures.

On the under aspect of the brain the two membranes are so disposed and so separated from one another as to form three great basins or cisternæ, three great spaces acting as a water-bed for the brain. These are the cisterna magna, the arachnoid bridging over the wide interval between the back part of the under surface of the cerebellum and the medulla, the cisterna pontis, the angular space between the pons, medulla, and cerebellum, and the cisterna basalis, the arachnoid there covering in the structure situated in the interpeduncular space, including the Circle of Willis.

The subarachnoid space, both cortical and basal, is traversed by numerous trabeculæ which, passing from one membrane to the other, break up the space into innumerable small compartments, all containing cerebro-spinal fluid and all intercommunicating. The cerebral vessels ramify in the space, the tributaries being supported by the framework and bathed in the fluid.

All cranial nerves carry with them in their emergence from the skull a process of both pia and arachnoid, variable in extent, but so arranged that the nerve trunk is surrounded for some distance by a funnel-shaped process of membrane, the cerebral cerebro-spinal fluid being thus brought into connexion with the cervical lymphatic spaces.

With respect to the origin of the cerebro-spinal fluid and its wave of flow, the researches of Leonard Hill tend to prove that it is formed from the lining ependyma and choroid plexuses of the three main ventricles of the brain, passing thence into the spinal cerebro-spinal region and, by means of the foramina of Majendie, Key, and Retzius—apertures in the roof of the fourth ventricle—on to the surface of the brain. From this latter region there appears to be a general tendency for the fluid to pass upwards from the basal aspect of the brain towards the superior longitudinal sinus where it is again absorbed, probably through the medium of the Pacchionian bodies and lacunæ laterales of the venous sinus.

From these few anatomical facts it is manifest (1) that a subarachnoid purulent effusion has every opportunity of spreading widely over the surface of the brain, and (2) that inflammation and its results in the immediate neighbourhood of the roof of the fourth ventricle will tend to impede the normal flow of cerebro-spinal fluid through the foramina in that region, thus inducing a degree of internal hydrocephalus directly proportionate to the degree of obstruction.

Furthermore, it is obvious that the anatomical arrangements are entirely opposed to the possibility of providing adequate drainage in cases of general meningeal infection. It has been suggested that trephine holes should be made on either side of the skull, and that the intervening meningeal space should be washed out between the two apertures. It is, however, impossible to attain such a result, not only because of the futility of attempting to wash through the subarachnoid meshwork, but also on account of the outward bulging of the brain substance through the trephine holes and the corking up of those apertures.

The pus rapidly spreads over the surface of the cerebrum and over the base of the brain, along the sheaths of the emerging cranial nerves, and down the spinal canal. Associated with vascular dilatation there is extensive leucocyte extravasation into the perivascular spaces, the course of the line of the attack being mapped out by white and yellow lines and areas of exudation. Insomuch, also, as the meningeal vessels are in direct continuity with those of the cortex itself, it follows that a well-developed case of meningitis implies a corresponding degree of cerebritis, with red or white softening of the brain substance according to the degree of hæmorrhagic extravasation.

Symptomatology.

Meningitis is generally sudden in onset and ushered in by a rigor, frequently of a most intense character. Headache is always a marked feature, commonly diffuse, but sometimes localized to the region primarily and mainly affected. The headache is intense and exacerbations are marked, the patient crying out in his agony. There is great mental irritability and all attempts at clinical examination are strenuously resisted.

After the initial rigor the temperature remains high, with occasional remissions during the early hours of the morning. Vomiting may be frequent and violent, but, according to my observations, this has not been a conspicuous feature.

The pulse-rate is increased, whilst, in the early stages, the volume is full and the tension high. The skin is burning hot and dry, except during the post-rigor periods when sweating predominates.

The face is flushed, often turgid, and the eyes are bright. General restlessness is a marked feature.

The more localizing features may be arranged in three groups: intellectual, motor, and sensory.

Intellectual symptoms.

The condition of the patient is one of great restlessness, increasing sometimes to actual violence and mania. Attendants are usually required to restrain his movements, and, tossing about in bed, crying out in his pain, muttering and wandering in his delirium, he offers a typical clinical picture of cerebral irritation.

Motor symptoms.

The motor symptoms vary according to the region mainly involved, cortex or base. In the former case, excitation results in twitchings and convulsions of the regions supplied by the cortical areas involved. Convulsions may be general or confined to a certain group of muscles, the former condition usually present in children, the latter more often observed in adults and occasionally partaking of the Jacksonian type. Convulsions may be associated with contractures of the limbs, the flexors mainly affected in such a manner that an attitude of general flexion may be assumed. The patient appears to suffer pain when attempts are made to straighten the limbs. In any case, such attempts are resisted.

Implication of the base of the brain. This is evidenced by symptoms sufficiently definite. Thus, the following symptoms may be observed:—

Optic neuritis.

Myosis and squints, from involvement of the third, fourth, and sixth nerves.

Trismus, from implication of the third division of the fifth nerve.

Facial paralysis, from implication of the seventh nerve.

Deafness, from involvement of the eighth nerve.

Dysphagia and dyspnœa, from involvement of the ninth and tenth nerves.

Rigidity of the neck and torticollis, from involvement of the eleventh nerve.

Retraction of the head and neck, from involvement of the posterior divisions of the upper cervical nerves.

Opisthotonos, from the involvement of the posterior divisions of the upper cervical nerves, sometimes of so excessive a nature that the body is bent backwards to such a degree that the head and heels are almost brought into contact. More rarely, pleurosthotonos or lateral flexion is observed.

Sensory and other phenomena.

Amongst such symptoms may be mentioned cutaneous hyperæsthesis, photophobia, and vaso-motor changes—the last-named evidenced by flushings, sweats, and tâche cérébrale.

Rapid emaciation, anorexia, and distaste for all nourishment are the rule, whilst retention of urine, albuminuria, and glycosuria have been observed.

The reflexes, both deep and superficial, are often increased. Kernig’s sign is generally present.

The period of depression.

The acute stage seldom persists more than two or three days, the period of excitation giving place to that of depression. The transition is usually of a rapid nature. The depression stage is dependent on exhaustion of the cortical and basal centres.

The temperature remains high, rising towards the evening and falling a degree or more in the early hours of the morn. Death usually takes place when the temperature is at its highest.

The pulse may become slower as the intracranial pressure increases, but, more commonly, as the result of toxic poisoning, the rate increases whilst the rhythm becomes irregular and the tension lowered.

Respiration may partake of the Cheyne-Stokes type, whilst the impaired æration of the blood and the weak action of the heart are evidenced by cyanosis of the face, œdema of the lower extremities, &c.

Death, primarily due to respiratory failure, is often preceded by general twitchings or convulsions.

The whole course of the illness seldom lasts more than a week, the more acute cases terminating within two or three days.

Treatment.

Whether threatening, developing, or obviously present, the patient should be treated with urotropin (see p. 116). In its early stages of development immediate operation affords some hope of cure, such treatment having as its basis the supply of adequate drainage. The source of the infection must be removed—so far as circumstances permit—the dura mater freely incised, and the pia-arachnoid region so opened up as to allow of the escape of some of the purulent or semi-purulent fluid. The wound is largely allowed to remain open, packed with gauze. The predominant organism may be isolated and, if time allows, suitable vaccine treatment instituted. In the meantime, 20 to 40 cc. of pyogenes serum should be administered.

From the point of view of diagnosis, lumbar puncture should never be omitted. The fluid escapes at high tension, is turbid and contains many polymorphonuclear leucocytes and organisms, the latter verified with the greatest advantage after centrifugalization. Repeated lumbar punctures are also said to be of some benefit with respect to treatment.

SINUS THROMBOSIS

Lateral sinus thrombosis.

Soon after entering on its course across the mastoid process the lateral sinus presents a well-marked S-shaped curve. This sigmoid sinus bulges markedly forwards—especially on the right side—towards the region of the mastoid cells and antrum, so much so that a mere shell of bone intervenes between the sinus on the one hand and the antral region on the other. Indeed, the relations are so intimate that one would expect a more frequent occurrence of lateral sinus thrombosis. Furthermore, the sinus receives numerous venous communications from the mastoid cells, antrum, and other parts of the temporal bone, conspicuous amongst the last-named group of vessels being the mastoid emissary vein which, passing inwards at the upper and posterior border of the mastoid process, connects the posterior auricular and occipital veins with the lateral sinus.

From these considerations it is obvious that any acute or chronic infective process originating either in the aural region or in the neighbourhood can readily infect the sinus by direct propagation of organisms along one or more of these inter-communicating vessels (thrombo-phlebitis).

The sinus may also become infected in middle-ear disease by the more gradual process of mining and sapping, the osseous barrier between the antrum and sinus being progressively destroyed by the backward progress of the aural disease. The sinus may erect an additional barrier by throwing out granulations (external pachymeningitis) against the invading host, but, in the event of the attack overcoming the defence, sinus thrombosis may result, at first perhaps of a non-infective type but soon becoming definitely septic, the clot softening and disintegrating (osteo-phlebitis).

There can be no question that middle-ear disease is responsible for the very great majority of cases of lateral sinus thrombosis, and whether the infection takes place by extension of thrombus along the connecting veins (thrombo-phlebitis), or after destruction of the osseous barrier (osteo-thrombosis), the results are more or less identical.

Thrombosis first occurs in that part of the sinus which is in closest relation to the primary cause of the infection, the clot rapidly increasing in size until the lumen of the sinus is entirely obliterated. In its early stages the thrombus is of a chocolate colour, softening at a later date and breaking down into a purulent material. Many varieties of bacteria may be present though the infection is mainly dependent on the presence of the streptococcus pyogenes.

Two changes may now occur:—(1) the central portion of the thrombus, having softened into a purulent material, may be limited by the firmer thrombus in front and behind; and (2) the thrombus may extend into the neighbouring and connecting venous channels downwards along the course of the internal jugular vein, backwards along the course of the lateral sinus, inwards along the course of the superior petrosal sinus, outwards along the line of the mastoid emissary vein, downwards through the posterior condyloid foramen, and inwards along meningeal veins.

The symptomatology may be considered as follows:—

(1) Symptoms dependent on the extension of the thrombus to neighbouring venous and lymphatic channels.

(2) Symptoms resulting from toxic absorption or dependent on the transmission of infected material to other parts of the body.

1. Symptoms dependent on the extension of the thrombus to neighbouring venous and lymphatic channels. When the thrombus spreads downwards along the course of the internal jugular vein, there is swelling and tenderness along the line of the vein. The vessel, though thrombosed in its upper part—perhaps throughout its whole extent—is itself seldom palpable, the cervical swelling usually being dependent on associated lymphadenitis and lymphangitis. In those few cases where the thrombosed vein can be felt, resembling a ‘buried lead pencil’, the thrombus is sometimes of the non-infective type.

The combined venous and lymphatic involvement causes œdema of the tissues, pain, and rigidity on attempted movement. The anterior and external jugular veins may become engorged from the extra strain thrown upon them. Subsequently, the inflamed parts may break down and extensive cervical suppuration result.

When the thrombus spreads backwards along the course of the lateral sinus, the coagulation process may extend as far as the torcula and even further. Evidence as to the nature and extent of the process is not always apparent, though one expects to find some œdema of the overlying scalp tissues.

When the process spreads inwards along the course of the superior petrosal sinus there is considerable risk of involvement of the corresponding cavernous sinus, possibly of the opposite sinus also (see p. 288).

When the process spreads outwards along the course of the mastoid emissary vein, œdema, and dilatation of veins in the post-auricular region are observed, associated with tenderness on palpation. This is most apparent at the upper and posterior border of the mastoid process.

When the thrombus spreads downwards along the course of the posterior condyloid vein, there may be some œdema and pain on pressure in the upper part of the posterior triangle of the neck, associated with glandular enlargement in the region. These symptoms are dependent on the connexion established by the posterior condyloid vein between the sigmoid sinus and the deep veins of the neck.

When the thrombus extends inwards along the meningeal veins, meningitis, meningo-cerebritis, and cerebral abscess result.

2. Symptoms resulting from toxic absorption or dependent on the transmission of infected material to other parts of the body.

Optic neuritis is present, according to Hunter Tod, in about 50 per cent. cases. It develops rapidly and attains a high degree of intensity.

Headache is usually intense in character, persistent, but little remedied by drugs and presenting marked exacerbations. It is often most acute over the affected region.

The mental condition of the patient is subject to variation. In the average case mental symptoms are quite disproportionate to the severity of the disease. Sometimes the patient is cheerful, perhaps rather excited, retaining his faculties to the last, in other cases—as the result of excessive toxic poisoning—he lies in a stuporose, typhoid-like state. When the thrombus is associated with meningitis, meningeal symptoms predominate.

Vomiting is often a conspicuous feature, generally of the so-called ‘cerebral’ type, a regurgitation without nausea and retching.

The pulse is rapid, the rhythm irregular, and the tension lowered.

The temperature. The formation of the thrombus is usually notified by the advent of one or more severe rigors, the temperature rising to 103° or more. During the height of the illness the temperature is high but remittent, and rigors are frequent. The occurrence of a series of rigors is almost certainly indicative of sinus thrombosis. Any marked remission of temperature is succeeded by profuse sweating, but, with this exception, the skin remains dry and burning.

Each rigor implies the extension of the thrombus to other venous channels or the transference of infected particles, by means of the blood-stream, to other parts of the body. In the young general convulsions are often observed.

The tongue is brown and dry, the breath foul and diarrhœa of common occurrence. The skin may be jaundiced, and septic rashes are prone to develop. The liver and spleen may be enlarged and tender. Cough and foul sputum point to pulmonary infarction.

Treatment.

The mastoid antrum is rapidly exposed and the conditions investigated. The bone is then chiselled away in the backward direction, with the hammer and gouge, so as to expose the lateral sinus. The question then arises as to the condition of the sinus. This is a matter that may require considerable experience. The surgeon should be guided, not so much by exploratory puncture as by the surroundings and general appearance of the sinus. Thus, the absence of bleeding from the mastoid emissary vein during the process of exposure is very significant of sinus thrombosis. Again, whilst the normal sinus pulsates, is of dark blue colour and presents a shining surface, the thrombosed channel may be covered with pale granulations or obscured by fibrinous deposit, it does not pulsate, and appears of a yellow or deep purple colour. Between it and the bone there may be a collection of purulent matter. In the event of doubt, the surrounding regions should be carefully protected with gauze, after which the sinus may be punctured with a needle. The absence of fluid blood is conclusive of thrombosis.

In the event of the surgeon concluding that thrombosis is present, subsequent procedures vary according to the extent of the thrombus. Thus, when the clot appears to terminate above the jugular bulb, a strip of gauze is inserted between the bone and the parietal wall of the sinus so as to obliterate the lumen of the sinus on the cardiac side of the clot.

The danger of further extension of the clot being thus obviated, the bone is nibbled away in the backward direction till at least half an inch of healthy vessel is exposed on the occipital side of the thrombus. A second gauze plug is then introduced so as to obliterate the sinus lumen in that region also.

In the interval between the two plugs the sinus is freely laid open, all clot and granulations being gently curetted and washed away. Some bleeding may take place during these procedures, from the mouths of certain vessels entering the sinus between the two compressed regions. This is in itself a favourable symptom, insomuch as it proves that the thrombotic process has not extended in those directions. This hæmorrhage may be controlled with gauze plugs. The parietal sinus wall in direct relation to the thrombus is freely cut away, after which the whole field is lightly packed with gauze and the ear sewn back into position. The main portion of the wound is left open, the sinus plugs being brought to the surface whilst those inserted into the combined middle ear and antrum emerge from the external auditory meatus.

All gauze-plugs may be withdrawn after twenty-four to thirty-six hours, the wound cleansed and lightly repacked. This process is continued daily till all is healed.

When the clot extends into the jugular bulb, and when the jugular vein appears to be involved, it is necessary to expose and ligature the vein in the neck, thus preventing further extension of coagulation and diminishing the risk of general infection. This measure should be carried out before the lateral sinus is laid open. With fresh gloves and another set of instruments, the vein is exposed so as to allow the application of two ligatures, and the division of the vessel between those two ligatures. If possible, the ligatures should be applied above the level of the entrance of the common facial vein. In all cases, however, the application must be carried out, if possible, below the lower limit of the thrombus. After the vein has been divided, the upper end may be dissected in such a manner as to allow of its being brought to the surface of the wound and there anchored.

Elsewhere the neck-incision is sewn up and protected with collodion gauze. The surgeon then returns to the mastoid and sinus regions, completing the exposure of the sinus and laying it open freely to the surface. At the termination of these procedures, an attempt may be made, by irrigation between the open sinus above and jugular vein below, to wash away all thrombus contained in the intervening portion of the vessel.

Finally, both sinus and aural regions are packed with gauze, in a manner similar to that described above. Dressings are reapplied as circumstances demand, and the wounds allowed to heal by granulation.

The great frequency of a streptococcus pyogenes infection justifies one in the early administration of anti-streptococcic serum (20 to 40 c.c. of Burroughs Wellcome’s ‘Pyogenes’) followed by an autogenous vaccine as soon as that can be prepared.

Main Points in the Differential Diagnosis between

In typical cases no great difficulty will be experienced in diagnosing between brain abscess, meningitis, and lateral sinus thrombosis. In many cases, however, two or more of these conditions may be co-existent. Thus, both brain abscess and lateral sinus thrombosis are often complicated by the presence of a meningeal infection. Again, the undue prominence of abdominal, cardiac, or pulmonary symptoms—more especially in cases of lateral sinus thrombosis—demand the full consideration of enteric fever, endocarditis, and pneumonia. Thus, in a case recently under my care at the hospital, and in which I had the benefit of the wide experience of my Aural colleague, Mr. West, operative procedures were carried out on the mastoid region, the patient dying some days later from enteric fever. Again, the question of differential diagnosis between tuberculous meningitis, brain tumour and brain abscess is always cropping up. Thus, a short time ago, I explored both temporo-sphenoidal lobes in a boy suffering from double otitis media and presenting well-marked general cerebral symptoms, only to find that he was a subject of tuberculous meningitis.

The diagnosis is often difficult, and no trouble must be spared in the complete investigation of the case. Lumbar puncture should invariably be carried out, the fluid being examined both cytologically and bacteriologically. In all cases of doubt one would be wise to call in further advice before undertaking exploratory operation.

Cavernous sinus thrombosis.

Thrombosis of the cavernous sinus arises either as an osteo-phlebitis or as a thrombo-phlebitis. In the former case, the thrombus is dependent on disease of the bones related to the sinus—arising more especially as the result of prolonged sphenoidal sinusitis—whilst, in the latter instance, the sinus becomes infected through one of the many vascular communications connecting it with other neighbouring regions. Thus the radicles of the ophthalmic vein, by means of their communication with orbital, ethmoidal, and upper nasal vessels, and their connexion at the inner canthus of the eye with radicles of the angular vein, afford the most ready means of infection. Again, infection may spread from the auditory region along the superior petrosal sinus, and from the tonsillar and pharyngeal regions along the various emissary veins connecting the cavernous sinus on the one hand with the deep cervical vascular system on the other.

The two cavernous sinuses intercommunicate by means of the circular sinus, and consequently thrombosis of the one sinus is liable to involve its fellow. According to Macewen,[57] bilateral trouble occurs in 50 per cent. cases, the infection often spreading from one sinus to the other within twenty-four to thirty-six hours.

Thrombosis of the cavernous sinus is often associated with meningeal infection or brain-abscess.

Symptomatology.

(a) Symptoms dependent on the formation of the thrombus and its extension to neighbouring venous and lymphatic channels.

The presence of the thrombus and its extension into ophthalmic, angular, and retinal veins leads to proptosis, paresis of the ocular muscles, disturbances of vision, and œdema. Proptosis is of rapid development, frequently reaching its maximum within a few hours, the globe being protruded in the downward and outward direction. With respect to ocular palsies, the movements of the globe are greatly restricted with squints, ptosis, and perhaps complete ophthalmoplegia. The pupil may be contracted during the earlier stages, becoming fully dilated and insensitive at a later date. The vision suffers in proportion to the degree of paralysis of ocular muscles and associated retinal hæmorrhages and thrombosis. The veins of the lids, conjunctivæ, and upper part of the face and forehead are engorged, with corresponding œdema of the soft parts. The conjunctivæ may be chemotic.

The spread of the thrombus to the opposite sinus results in the development of bilateral symptoms, whilst the involvement of the petrosal sinus may bring about thrombosis of the lateral and sigmoid sinuses, with corresponding developments.

In other cases the meningeal veins are affected at an early date, in which case the symptoms dependent on the cavernous thrombus are obscured by those resulting from the meningeal infection.

(b) Symptoms dependent on toxic absorption or resulting from the transference of infected particles to other parts of the body.

These more general symptoms closely resemble those enumerated when discussing lateral sinus thrombosis (see p. 283). Headache, however, is of the most intense type, and pain, of a severe neuralgic character, is referred along the course and distribution of the first and second divisions of the fifth nerve.

Treatment.

It has been suggested that exploration could be carried out, the thrombus evacuated, and the cavernous sinus region drained from the naso-ethmoidal region or by approach along the floor of the middle fossa of the skull—an exaggerated Gasserian ganglion operation. Both these methods have been tried, but the difficulties encountered and the want of success tended to show that cavernous sinus thrombosis was beyond the reach of the surgeon. However, of recent date, more hopeful views have been entertained, it being suggested that the globe should be removed, the sinus explored, and the orbital cavity packed with gauze. It is doubtful, however, whether the end justifies the means.

The prognosis in brain abscess, meningitis, and sinus thrombosis.

A patient may be expected to recover from brain abscess, whether temporo-sphenoidal, cerebellar, or frontal, if an early diagnosis be made, if the case be uncomplicated by meningeal infection or sinus thrombosis, and if the evacuation be carried out without any great difficulty. As Sir William Macewen[58] pointed out, ‘an uncomplicated brain abscess may be regarded as the most hopeful of all cerebral affections.’ In fatal cases, death results from general meningeal infection or from the bursting of the abscess into the lateral ventricles.

In meningitis the prognosis is bad, more especially when the process is widespread. Early exposure of the affected region and the supply of adequate drainage offer the only hope of recovery. This, even under the most favourable circumstances, is a desperate remedy.

The prognosis in lateral sinus thrombosis hinges to a large extent on the time at which operative procedures are carried out. When the case is seen and operated on at an early date in the history of the disease, recovery may be anticipated in about 50 per cent. cases. Hunter Tod states that, when all cases are considered of whatever grade, about one-third recover. Death results from pyæmia, septicæmia, meningitis, or brain abscess.

Cavernous sinus thrombosis of the infective variety almost necessarily terminates fatally. Death results from causes similar to those observed in cases of lateral sinus thrombosis.

HERNIA CEREBRI

The term Hernia cerebri was formerly used as inclusive of all those conditions in which the brain protruded through some aperture in the skull, whether such opening was congenital, traumatic, or post-operative.

Owing to the recent advances in cranio-cerebral surgery, especially with reference to the frequent adoption of decompression operations, it is advisable that the cases should be classified into two groups:—

1. Cases of hernial protrusion, including cephaloceles (see Chapter I), protrusions intentionally produced by the surgeon in a decompression operation, and those which follow after unsuccessful operations for tumour removal. It will be observed that, in all these cases, the projecting brain, though bulging through its osseous barrier, is still protected by a more or less normal scalp-covering.

2. Cases of hernia cerebri. Here, as the result of injury to scalp, bone, dura, and brain, the cerebral substance bulges through a deficiency in the vault and presents on the surface, uncovered by integument. Hernia cerebri can develop under non-infective conditions, the congested state of the bruised or lacerated brain bringing about that degree of intracranial tension which can only be relieved by the outward projection of the brain. Still it must be accepted that Hernia cerebri almost invariably implies some bacterial infection.

Hernial protrusions are dealt with elsewhere. Hernia cerebri requires some consideration. Its development, by reason of its usual bacterial agency, must always be regarded as of serious import. The congested brain bulges through the aperture in the skull and presents on the surface as a purple—sometimes black—fungating mass, bleeding freely, and associated with a considerable discharge of cerebro-spinal fluid, serum, and pus.

The effects produced by this condition vary according to the extent of the cerebritis, and the question of associated meningeal infection.

When associated with meningitis those symptoms which might result from the hernial protrusion are more or less obscured by those dependent on the meningeal infection. Under other circumstances, the symptoms vary according to the extent and position of the area involved. Thus, when the infection is limited to the surface of the brain in the immediate vicinity of the aperture in the bone, the patient may merely complain of some headache and present some symptoms of cerebral irritation. More usually, the infection spreads rapidly to the surrounding brain substance, and the patient evidences the most acute stage of cerebral irritation, passing thence rapidly into a stuporose, typhoid-like condition.