Vague Sypmtoms of Tuberculoma

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    Brain tuberculoma Ir J neurol 2012; 11(1) 35

    Figure 1. Contrast-enhamced T1 weighted magnetic

    resonance imaging (MRI) showed multipleenhancing lesions with central hypointesnity

    tuberculomas and brain lymphoma. Cerebraltoxoplasmosis was another possibility. The first chestX-ray was reported normal. The second chest X-raywith under penetrated films showed miliarytuberculosis. On chest CT-scan, tree-in-bud appearancewas present which was in favor of miliary tuberculosis.

    Lumbar puncture (LP) was performed for thepatient.Cerebrospinal fluid (CSF) pressure was 280

    mm H2O. Findings of CSF analysis were as follows:glucose, 50 mg/dl; protein, 57 mg/dl; red blood cells(RBC), 2/ mm3; white blood cells (WBC), 0/ mm3;CSFWright, VDRL and cytology were negative. CSF smearand culture for fungal infection and tuberculosis werenegative. Complete blood count (CBC) was normal(WBC: 5600 /mm3, hemoglobin: 14 mg/dl). A purifiedprotein derivative (tuberculin/PPD) had 5 millimeterinduration. Erythrocyte sedimentation rate waselevated as high as 60 mm in 1 hour. Serum Wrightand VDRL were negative. Serum glucose, creatinine,urea, sodium, potassium, calcium and liver enzymes

    were within normal limits. Smear from gastric lavagewas positive for acidfast bacilli.

    As the patient was drowsy on arrival, anti-TBdrugs were started immediately because of clinicaland radiological suggestion of tuberculosis. Theregimen consisted of isoniazid, rifampin, ethambutol

    and pyrazinamide with appropriate dosages andvitamin B6 was also added to the above drugs.Drowsiness got better after several days and hergeneral condition improved after two weeks, but shehad fever occasionally. After one month she becameafebrile. The patient was discharged from hospitalafter one month with a good general condition. Shewas visited after one month at the clinic without anyneurological deficits. Ethambutol and pyrazinamidewere discontinued and treatment was continued byINH and rifampin. She completed the one year courseof treatment without any complications. At the

    moment, after about two years, the patient is in a goodgeneral condition, without any symptoms or signs. Onthe last brain MRI, brain tuberculomas still are presentbut with smaller sizes and without enhancement.

    In conclusion, the patients with brain tuberculomamay have nonspecific symptoms or show differentneurological deficits in respect to the site of thelesions. CNS tuberculoma is a non-threateningcondition with a good prognosis and effective therapyoptions. Enhanced brain and spine MRI should beconsidered to confirm that the diagnosis is notoverlooked.2 In our reported case, the patient have

    had malaise, low grade fever and nausea since severalweeks before admission and on examination, wefound only mild neurological deficit without obvioussystemic signs. The brain CT and MRI showednonspecific multiple lesions and the first routine chestX-ray did not show definite abnormality. The PPD testwas negative. But we continued our work up andfound other evidences that suggested tuberculosis asthe best impression. Therefore, it seems thatphysicians should consider tuberculosis, as animportant differential diagnosis of CNS diseases,especially in developing countries.

    References

    1. NaserpourFarivar T, Johari P, KouhpayeHR, et al. Application of PCR andAdenosine deaminase assay test for the

    diagnosis of tuberculous meningitis

    infection. Ir J Neurol. 2010; 8:651-8.2. Li H, Liu W, You C.Central nervous system

    tuberculoma. J Clin Neurosci. 2012; 19691-.