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.
Fig. 83. A Fracture of the Anterior Fossa which was followed by the Development of Meningitis.
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.
Fig. 84. Basal Meningitis secondary to Temporo-sphenoidal Abscess.
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.