The diagnostic value of adenosine deaminase (ADA) activity was studied to evaluate its use in the differential diagnosis of tuberculous meningitis in the local setting. Cerebrospinal fluid (CSF) from 119 patients with meningitis and other conditions with central nervous system symptoms were collected and ADA activity determined by the colorimetric method of Guisti read at 628 nm. The CSF was also subjected to other laboratory examinations so as to provide the aetiological diagnosis. All 14 tuberculous meningitis patients had ADA activity greater than the cut off value of 9.0 IU/L. High ADA activity was also seen in 13 of 105 non-tuberculous cases giving a specificity of 87.6%. Even though the ADA activity determination is sensitive for tuberculosis, it was not specific enough to be used as a rapid diagnostic test. However when interpreted together with clinical signs and symptoms and other laboratory tests, it is a useful adjunctive rapid marker for tuberculosis.
Tuberculous meningitis leads to a high mortality rate. However, it responds well to chemotherapy if the treatment is started early. Neuroimaging is one of the most important initial investigations. There were 42 patients diagnosed with tuberculous meningitis in Kuala Lumpur Hospital based on clinical criteria, cerebrospinal fluid analysis and response to anti-tuberculous treatment over a 7 year period. Relevant information was obtained from patients' medical case notes and neuroimaging findings were evaluated. Male to female ratio was 3:1. The three major ethnics and the immigrant groups in Malaysia were represented in this study. The majority of the cases involved the Malays followed by immigrants, Chinese and Indians. The patients' age ranged from 18 to 62 years old with the mean age of 34.4 years. There were 95.2% (n = 40) of patients who presented with various neuroimaging abnormalities and only 2 (4.8%) patients had normal neuroimaging findings. Hydrocephalus and meningeal enhancement were the two commonest neuroimaging features. Other features include infarction, enhancing lesion, tuberculoma, abcess, oedema and calcification. Contrasted CT scan is an adequate neuroimaging tool to unmask abnormal findings in tuberculous meningitis.
We report a case of a 19-year-old immunocompetent Malay woman who presented with a worsening psychotic disorder of 1-year duration. She initially presented with social isolation with subsequent mutism and stupor. Physical examination revealed a stuporous, emaciated, dehydrated woman with Glasgow Coma Scale of 11/15 (E4V2M5). She had a blank stare, mutism and akinesia. Motor examination revealed upper motor neuron findings. Neck stiffness was present, however, Kernig's and Brudzinski's signs were negative. There were no other findings on other systems. Brain imaging and EEG were normal. Cerebrospinal fluid investigations revealed positive cerebrospinal fluid Mycobacterium tuberculosis PCR (MTB PCR). The patient was treated with empirical antituberculosis drugs and steroids. On follow-up visit 1 month later, her psychotic symptoms had fully resolved. She was able to ambulate and care for herself; she was unable to recall the symptoms she had experienced before and during admission.
We discuss the diagnostic challenge in an adult patient presented with purely ocular symptoms diagnosed with tuberculous meningitis (TBM). A 38-year-old woman presented with bilateral painless blurring of vision. There were bilateral sixth cranial nerve palsy and bilateral optic disc swelling. Optic nerve function tests were normal. Patient was lucid with no signs of meningism. Brain imaging were normal. She had a positive Mantoux test, high erythrocyte sedimentation rate but no clinical evidence of active pulmonary tuberculosis infection. Her Quantiferon-TB Gold in-tube test was negative. Cerebrospinal fluid analysis revealed a high opening pressure but no biochemical parameters to suggest TBM, hence she was treated as idiopathic intracranial hypertension. A diagnosis of TBM was finally made following a positive PCR for Mycobacterium tuberculosis Her vision improved with reduction in optic disc swelling following antituberculous treatment.
A 38-year old female with underlying systemic lupus erythematosus was admitted with tuberculous meningoencephalitis. After an initial good response to anti-tuberculous treatment, she developed cerebral infarction and profound hyponatremia. This was due to cerebral salt wasting syndrome, which has only previously been described in 2 cases. The difficulties in diagnosis and management of this case are discussed.