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Introduction: Tuberculous meningitis (TBM) is a severe form of tuberculosis affecting the meninges, primarily caused by Mycobacterium tuberculosis. Diagnosis of TBM poses numerous challenges due to its nonspecific clinical presentation and the limitations of diagnostic tests like GeneXpert. Case presentation: The authors report a case of a 22-year-old female from Eastern Nepal presenting with acute-onset fever, headache, vomiting, and neck pain. Cerebrospinal fluid (CSF) analysis showed lymphocytic pleocytosis, elevated protein, low glucose levels, and cobweb coagulum indicative of TBM. However, the GeneXpert test revealed negative results. Discussion: In resource-limited settings like Nepal, where access to GeneXpert MTB/Rif is limited, CSF analysis and clinical algorithms play a crucial role in diagnosing TBM. Relying solely on GeneXpert results may lead to false negatives, so a high level of suspicion based on patient risk factors is essential. Prompt initiation of empirical antitubercular therapy is vital for a favorable outcome in TBM cases. Conclusion: Negative MTB PCR results from CSF can be misleading in diagnosis of tubercular meningitis. Therefore, comprehensive evaluations, including detailed patient history, physical examination, and CSF fluid analysis, are crucial in high tuberculous prevalence countries to ensure accurate and timely diagnosis.
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Organophosphate-induced delayed neuropathy, a central-distal axonopathy, passes through latent, progressive, static and improvement phases. During the improvement phase, the peripheral nerves regenerate unmasking the spinal cord lesion with myelopathic features. We report a case of a 16-year-old male who developed myelopathy 6 weeks following chlorpyrifos poisoning. He had a motor weakness of 4/5 in bilateral hips and 3/5 in bilateral knees and ankles. Spasticity and exaggerated reflexes with ankle clonus were present in the lower limbs. Sensory and the upper limb motor examinations were all normal. Pertinent blood, cerebrospinal fluid and nerve conduction tests were normal. Magnetic resonance imaging of the spine showed features of cord atrophy. Three months following physiotherapy, his power improved to 5/5 in bilateral knee and hip joints and 4/5 in bilateral ankles with spasticity. Organophosphate-induced delayed neuropathy can present as earlier as 6 weeks with myelopathy. Previous history of organophosphorous exposure is important in myelopathy or peripheral neuropathy.