Gabriel Susilo

JOURNAL READING 11.2016.044

 British Medical Bulletin Advance Access

TUBERCULOUS MENINGITIS : ADVANCES IN published Febuary 18, 2015.

DIAGNOSIS AND TREATMENT M.E. Torok, Department of Medicine,

University of Cambridge, Addenbrookes
Hospital.
INTRODUCTION
Tuberculous meningitis is the most frequent form of central nervous system
tuberculous. Infection caused by Mycobacterium tuberculosis, causing death or
disability in more that half of those affected.

Once the neurological symptoms of advance disease are present (e.g. coma,
seizures, raised intracranial pressure and hemiparesis), the diagnosis is
apparent but the prognosis is poor.
TUBERCULOUS MENINGITIS CLASSIFICATION
Grade 1 : GCS of 15 with no focal neurology.

Grade 2 : GCS of 15 with a focal neurological deficit, or GCS of 11-14.

Grade 3 : GCS of <10

CLINICAL FEATURES OF TUBERCULOUS MENINGITIS
Symptoms : Prodromal period with low-grade fever, malaise, weight loss followed by gradual
onset of headache (1-2 weeks). Worsening headache, vomiting, confusion, coma (>6 days).

Clinical findings : Neck stiffness, confusion, coma, cranial nerve palsies (3, 4, 6). Focal
neurological signs (monoplegia, hemiplegia, paraplegia) and urinary retention.

CSF : Raised protein, raised white cell count with neutrophils and lymphocytes.
PATHOGENESIS OF TUBERCULOUS MENINGITIS
Tuberculous meningitis was caused by release of Mycobacterium tuberculosis
into the meningeal space from focal sub-pial or sub-ependymal lesions, which
were most commonly located in the Sylvian fissure.

Its commonly observed neurological deficits : the exudate may obstruct

Cerebrospinal Fluid flow resulting hydrocephalus.
PATHOGENESIS OF TUBERCULOUS MENINGITIS
The number and types of white cells in the Cerebrospinal Fluid may help to
differentiate Tuberculous Meningitis from other meningitides. Neutrophils can
predominate in early disease, and a high proportion of neutrophils and
lymphocyte in the Cerebrospinal Fluid has been associated with an increased
likelihood of a bacteriological diagnosis and improved survival.
PATHOGENESIS OF TUBERCULOUS MENINGITIS
Death was associated with high Cerebrospinal Fluid concentrations of lactate,
low numbers of white blood cells, in particular neutrophils, and low
Cerebrospinal glucose levels.
TREATMENT OF TUBERCULOUS MENINGITIS
In contrast to pulmonary Tuberculous, the optimal therapy of Tuberculous Meningitis
has not been determined in clinical trials. Current guidelines recommend a 2 month
initiation phase with 4 drugs (rifampicin, isoniazid, pyrazinamide and ethambutol)
followed by a 10 month continuation phase of 2 drugs (rifampicin and isoniazid).
 TREATMENT OF TUBERCULOUS MENINGITIS

Drug Dose in Adults Durations Common Side Effects

Orange discolouration of bodily fluids, hepatoxicity,

Rifampicin 450 mg 12 months
gastrointestinal symptoms, headache

Hepatoxicity, peripheral neuropathy, optic neuropathy,

Isoniazid 300 mg 12 months
gastrointestinal symptoms

Pyrazinamide 1.5 g 2 months Hepatoxicity

Ethambutol 15 mg / kg 2 months Optic neuritis, red/green colour blindness, peripheral neuritis

DIAGNOSTIC TEST OF TUBERCULOUS MENINGITIS

Cerebrospinal Fluid smear and culture.

CONCLUSIONS
The best way to improve survival is by rapid accurate diagnosis and promt
initiation of therapy.

Intensified therapy with rifampicin and fluoroquinolones are going some way
towards addressing this deficiency.
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