Summary
Experimental work on antibiotics, notably streptomycin, gives hope that an effective chemotherapeutic agent against tuberculosis may soon be discovered. Tuberculous meningitis would be a suitable choice for the clinical trial of new remedies but the development of an effective line of treatment will depend on early diagnosis and a knowledge of pathology.
Excluding Pott's paraplegia, the commonest forms of tuberculosis of the nervous system are meningitis and, rarely, the large tuberculoma.
The diagnosis and treatment of large tuberculomata are briefly discussed and the fact that these lesions are by no means inoperable is emphasized.
A series of 25 cases of tuberculous meningitis is discussed and the clinical picture described. The course of the illness can usually be divided into three stages: the prodromal phase, the stage when neurological signs and symptoms appear, and the terminal stage.
The chief neurological signs and symptoms are divided into five groups: those of meningeal irritation, those of increased intracranial pressure, mental changes, epilepsy and focal signs. These groups are discussed and an attempt made to correlate them with the underlying pathology. The absence of meningism in infants and the consequent difficulty in diagnosis is pointed out. Emphasis is laid on the production of focal signs by vascular occlusion and consequent infarction of brain tissue and it is pointed out that even when an effective chemotherapeutic agent is available, cases will have to be treated before these changes have taken place in order to achieve recovery rather than mere survival, Early diagnosis will therefore be imperative.
Changes in the cell or protein content of the C.S.F. were the most constant abnormal finding at the time when our patients were first seen and were present in every case but one. Although a fall in the C.S.F. chlorides was the rule, at least in the later stages of the disease, the average value of 37 estimations in this series of 25 cases was little lower than that of 37 estimations clone early in the illness in 15 recovering cases of pneumococcal meningitis. The fall in the C.S.F. chlorides is to some extent related to the vomiting which is so common in all types of meningitis, while the chloride content may even rise if the patient is uraemic. Thus in our experience there is no such thing as a pathognomonic level, and in the early stages of the illness or if the patient is vomiting persistently or is uraemic, the chloride level in the C.S.F. has little diagnostic significance.
The differential diagnosis from other conditions which may cause similar changes in the C.S.F. is discussed. It is essential to differentiate tuberculous meningitis from such pyogenic conditions as brain abscess and atypical or partially treated purulent meningitis since these are remediable conditions. So long as the diagnosis is uncertain the patient should be given the benefit of the doubt and treated appropriately.