The validity of trauma, at least of ordinary blunt injuries to the skull, as an exciting cause is open to argument. Of course, if a tubercu lous focus is pierced or crushed, this may result in starting a general nailiary; tuberculosis with meningitis. We observe this after forcible repression of a spondylitis or tuberculous coxitis, after operations on the cervical glands, etc.
Less certain is the inciting part played by cranial injuries, striking the head against level ground, falling from a bed or chair, bumping the head on the furniture, etc., if no cerebral symptoms of any kind immedi ately follow the accident itself. At any rate to assume this connection as established, it is requisite that the interval between the injury; to the skull and the onset of meningitis should correspond approximately to that which is required for the experimental production of tuberculous meningitis in animals.
Robert Koch found that eighteen to nineteen days elapsed after intravenous injection before a microscopically discernible miliary tuber culosis appeared; L. Martin found the time was shorter or longer, depend ing upon the nature of his researell animals and the concentration of his cultures. From this experimental evidence WC MUSt conclude that in those cases in which death follows the injury within a few hours or clays, the injury merely offers an opportunity for a meningitis which was already; anatomically present to come into clinical view. We shall however accept thc traumatic etiology in those cases in which at least eight to ten days, usually indeed three to four weeks, intervene between the cranial injury and the first appearance of meningeal symptoms. Observations of this kind have been repeatedly described and we our selves have very frequently' made them with especial attention to this point. Death from meningitis occurs so remarkably frequently about the third or fourth week after a fall or a blow that it is impossible to consider it merely a coincidence.
In comparison with infectious disease and traumatism, the other suggested supplementary causes of tuberculous meningitis, such as sunstroke, mental overexertion, violent mental excitement, etc., play at most a vague and secondary part.
It should be mentioned that chronic nontuberculous otitis media can very frequently be demonstrated in individuals afflicted with tuber culous meningitis and no doubt is a predisposing cause. The digestive
disturbances which sometimes precede meningitis, especially in young, otherwise healthy children are to be esteemed rather as prodromal symptoms than as the cause of the disease.
Pathology.—The most striking nieningeal changes arc the miliary tubercles and the inflammatory exudate; corresponding to these in the ventricles, the granular ependyrnitis (which however is only partly tuberculous), and the internal hydrocephalus. The changes in and on the vessels, not discernible macroscopically, are important, since they cause more or less circumscribed circulatory disturbances in the brain, and their resulting symptoms.
The tubercles are found chiefly at the base of the cerebrum and cerebellum, especially numerous within the region covered by the artery of the Sylvian fossa, somewhat less frequently and less numerous on the convexity. The fact that the miliary tubercles are arranged along the ramifications of the medium-sized and smaller arteries has always appeared a support for the theory of leptomeningeal infection through the blood. ...Although this assumption seems natural, yet it should not be forgotten that the same arrangement exists also in those cases in which a direct infection of the subdural and subarachnoidal fluid is much more probable.
The fact that Louis Martin found the same distribution of tubercles in his animals, after Ile had injected cultures through the atlanto-occipital joint into the .subarachnoflal space, without injuring the vessels, agrees with the latter view. It may be assumed that the lymphatic sheaths of the vessels then undertake the distribution, probably because they arc wider or possess stronger currents than the other lymph-spaces.
The inflammatory exudate, of a peculiar gelatinous consistence, is located chiefly at the base of the brain between the optic chiasm and ihe cerebral peduncles. By virtue of its serofibrinous consistence it adheres quite firmly to the ineshes of the pia mater and, when the brain is removed, does not run out like serous inflammatory (edema which often is much more widely disseminated.