1. As a part and parcel of miliary tuberculosis.
2. Haematogenous spread from a tuberculous focus from the lungs, mediastinal lumph nodes, mesenteric lymph nodes, bones, joints, genitourinary tract etc.
3. From a caseous focus in the brain (Rich’s focus) to the subarachnoid space or the ventricle. Sometimes there may be rupture of meningeal tuberculoma which is responsible for meningitis.
Trauma, contact with infected individual, past history of measles and whooping cough are important predisposing factors. Past history of tuberculosis or active tuberculosis elsewhere in the body may be present in about 75 % of cases. Human bacilli are mostly responsible though in some instances bovine type of bacilli are the causative agents.
The disease is common in children between 2-5 years of age.
Weakness, lassitude, loss of appetite, low grade pyrexia, loss of weight are usually complained of, which persist for about 2-3 weeks.
Stage of Meningeal irritation
This stage is not so much conspicuous as in pyogenic meningitis. Fever (low grade), headache, vomiting, photophobia, convulsion may appear. Kernig’s sign is usually present but nuchal rigidity is less pronounced in the early stage though it gradually develops. Meningeal cry is present. Sometimes, all these features are very much masked till late stage develops and this is called lucid interval.
Stage of Meningeal compression
Oculomotor palsy with ptosis, squint and diplopia may develop. Involuntary movements particularly tremors may be present. Reflexes are lost but may be brisk if rigidity is present. Plantar reflex may be extensor in type. Papilloedema may sometimes develop and in 25 % of cases choroidal tuberclesmay be seen. This is diagnostic sign of tuberculous meningitis at the bed side.
Stage of Paralysis of Coma
The features are same as in pyogenic meningitis.
Clinical examination may also reveal evidences of tuberculosis in other parts of the body.Evidences of primary complex or miliary tuberculosis may be present.
1. Blood shows high ESR with moderate leucocytosis.
2. Chest X-ray may show evidences of tuberculosis in the form of primary complex or miliary tuberculosis.
3. CSF: Colour is clear, cob-web or spider-web coagulum is formed on standing overnight, pressure is increased to 100- 500 cmm, polymorphs dominate in early stages, lymphocytes dominate in later stages, Pleocytosis is a common finding. Protein is increased 100-400 mg/100 cc. Sugar and chloride levels are diminished but chloride level is diminished to a greater extent as vomiting is a prominent feature.
Smear, staining and culture may be done from centrifuged deposit or from cob-web coagulum, for demonstration of acid fast bacilli but they are usually negative. Animal inoculation test can also be performed
Here neck stiffness develops later on in course of the disease. Convulsion, coma, delirium are rare. Kernig’s sign is less pronounced. History of sweating, vomiting or diarrhoea precedes the onset of neck stiffness. Bradycardia is usually absent. Cranial nerve palsies are absent. CSF shows increased pressure with diminished protein and chloride content but no hypercellularity.
Fever is absent, severe headache at the onset develops suddenly, and cranial nerve palsies are present, ophthalmoscopic examination reveals subhyaloid haemorrhage. CSF shows frank blood.
Rapid progress, usually terminating fatally, convulsion, coma, hyperpyrexia are very common and develop early. CSF does not show characteristic finding of meningitis.
Three stages of meningitis are well-pronounced. High temperature, toxaemia, sometimes rash, involuntary movements and cranial nerve palsies are seen, bulging of anterior fontanelle is common, CSF shows characteristic finding. Blood examination reveals leucocytosis with increased polymorphs.
Here signs of meningeal irritation are present in presence of a background of carcinoma in some parts of the body. The metastasizing tumours are usually from carcinoma of breast, leukaemia or lymphoma. CSF shows apart from elevated pressure, high protein, low sugar and pleocytosis. Cytologic study shows malignant cells. CT scan shows contrast enhancement of the basal cisterns or shows hydrocephalus without mass lesion indicating diagnosis. MRI shows enhancing foci. Myelography shows deposits on multiple nerve roots.
Treatment is to be followed as in cases of pulmonary tuberculosis. Rifampicin 450 mg along with Isoniazide 300 mg, Ethambutol 800 mg and Pyrazinamide 1500 mg daily to be continued for 2 months followed by Rifampicin and Isoniazid for 4-7 months. Steroids are to be added either orally or parenterally. Though controversial, it is indicated to reduce raised intracranial pressure, when hydrocephalus develops surgical drainage is beneficial.
Same as in pyogenic meningitis.