The pulse, usually retarded to 70-60—in infancy to 100-90—beats a minute, is likewise uneven and irregular. The instability of pulse rate, mentioned as an early symptom, its jerky racing, caused by the patient sitting up or by painful passive motions, usually persists, to be displaced after some days by a constant bradyeardia.
Respiration is often irregular,sighing, but not pronouncedly periodic.
The pupils arc usually- contracted, often uneven and either do not react or react slowly and incompletely to light. Usually the half open eyelids disclose the eyeballs now rolling irregularly, now in conjugate deviation, now making vertical uystagmatic motions. At the same time there is usually, a severe pericorneal conjunctivitis in the form of vessels extending to the Embus.
Constantly- deepening obscurity of consciousness is the next evidence of the progress of the disease. The patient lies in deep coma, unable to swallow. The head has ceased boring into the pillow: the extremities hitherto rigid or shaken by elonic spasms, gradually relax; in conse quence of inability to cough, the respiration becomes audible, rattling, and as the end approaches often assumes a periodic character; the pulse always becomes rapid (though the earlier braclyeardia in not a few cases may have been absent): the temperature rises during the last few days or hours to 40° C. (104° F.) and higher, or it may become subnormal. The sweat-glands, formerly active, cease to funetionate; the skin is pale, often grayish, or brownish, dry, desquamating, and owing to the rapid emaciation it can be lifted in folds. In deepest coma, with penetrating tracheal rales and thready running pulse death finally ensues.
The duration of the disease, in ordinarily typical cases, is about three weeks, but these limits vary widely, as we shall immediately note in portraying the chief variations.
These deviations involve the mode of onset as well as the combina tions of symptoms and additional symptoms, and the entire course of the disease, which occasionally is protracted by considerable remissions or other circumstances. The onset, usually insidious, as we have de scribed it, may be sudden, without prodromal symptoms. Not infre quently it is ushered in by convulsions, which either resemble *Jack sonian epilepsy (in which case after continuing for minutes or hours they are followed by paresis or paralysis of the extremity first attacked), or they resemble genuine epileptic attacks. Tuberculous meningitis begins with tonic spasms much less frequently than the other forms of meningitis and, especially in infancy, so rarely in comparison with the frequency of elonic convulsions that the occurrence of general clonic convulsions in infancy justifies the suspicion of tuberetdous meningitis only in the presence of more definite symptoms.
The early occurrence of convulsions in tuberculous meningitis depends often, if not always, upon an unusual involvement of the con vexity. As a rule this involvement is asymmetrical, being limited to one hemisphere, and in this to the area supplied by the arteria eerebri media. In such cases the meningeal exudate may in circumscribed localities, preferably the motor area, attain a striking thickness and firmness (through its richness is fibrin) which explains the focal symp toms (convulsions and paralyses). This form of anatomical deviation is known as "meningite en plaques." Further, these focal symptoms are often very transitory, in which respect they differ materially from the more constant symptoms of tumors. Convulsions or paralyses in different localities not infrequently interchange with or sueeeed each other; and then by recalling the topographical arrangement of the cortical motor areas, we can recognize on the one hand the localization of the irritating process on the cortex, on the other hand its transitory nature (circulatory disturbances, oedema, etc.) (Zappert).
From this last point it is comprehensible, and this should be espe cially emphasized, that the same clinical symptoms occasionally may occur also without a previous "meningite en plaques," and that therefore our diagnosis cloes not extend beyond a certain probability.
The particular cases described exhibit in their further course, the greatest conceivable difference. The course may be very stormy and contrary to the rule rush through the separate stages to death within a few day-s; however more frequently it is abnormally protracted. The headache following the initial convulsions and the changes of conscious ness may disappear; the paralyses, if any existed, diminish, and then after days or weeks the regular picture of tuberculous basilar meningitis first begins to develop. Or definite meningeal symptoms, headache, clouding of the senses, cervical rigidity, pulse and pupillary- phenomena, fever, etc., follow the initial insult but the condition suddenly and sur prisingly improves and a remission of a week or month or exceptionally, even a year occurs, whieh simulates a complete and permanent recovery.