Article Text

A focal central nervous system mass in an AIDS patient with tuberculous meningitis
  1. Miguel Martín-Luquero,
  2. Luis A Marcos,
  3. Natalia Freijanes,
  4. José Luis Pérez-Castrillón
  1. Department of Internal Medicine, Hospital Rio Hortega, University of Valladolid, Valladolid, Spain
  1. José Luis Pérez Castrillón, Department of Internal Medicine, Cardenal Torquemada s/n, 47010 Valladolid, Spain

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A 36-year-old man who had been seropositive for human immunodeficiency virus (HIV) for 2 years and who had not undergone treatment, was admitted to the hospital. He reported fever and headache during the week prior to admission. His CD4 count was 26 × 106/1. The results of the physical examination were unremarkable. Contrast-enhanced T-1 weighted magnetic resonance imaging (MRI) displayed basal meningeal involvement, but no evidence of a cerebral mass (figure 1). Cerebrospinal fluid (CSF) examination revealed 435 white blood cells/mm3, with 60% neutrophils and 40% lymphocytes, glucose 40 mg/dl, protein 199 mg/dl and adenosine deaminase 40 IU/l. The fluid smears were negative for acid-fast bacilli and a fluid culture revealed Mycobacterium tuberculosis. The M tuberculosisisolates were susceptible to isoniazid, rifampicin, ethambutol, and streptomycin. The patient received isoniazid (300 mg daily), rifampicin (600 mg daily), pyrazinamide (1500 mg daily) and ethambutol (1800 mg daily). Antiretroviral treatment with zidovudine and didanosine was initiated. The patient improved and was asymptomatic after 3 weeks.

Figure 1

Contrast-enhanced T-1 weighted MRI at presentation

One month later the fever re-appeared, the CD4 count was 42 × 106/1, and the HIV viral load was 2525 000 copies/ml. The patient also suffered from headaches and appeared lethargic. On physical examination he showed marked stiffness of the neck and left hemiparesis. Contrast-enhanced T-1 weighted MRI (figure 2) displayed a large mass with a hypo-intense centre in the perimesencephalic region.

Figure 2

Contrast-enhanced T-1 weighted MRI one month later


What is the differential diagnosis?
What is the clinical diagnosis?
What is the treatment?



The causes of focal CNS mass lesion in a patient with acquired immune deficiency syndrome (AIDS) appear in the box.

Causes of focal CNS mass lesion in AIDS

  • toxoplasmosis

  • primary CNS lymphoma

  • cryptococcosis (pseudocyst)

  • tuberculosis (granuloma)

  • syphilis (gumma)

  • abscess (cryptococcal, tuberculous or bacterial)


The patient developed a mass lesion during adequate treatment for tuberculous meningitis. The MRI findings, in association with clinical and laboratory evidence of tuberculosis, suggest the paradoxical growth of an intracranial tuberculoma.


The optimal therapy is unknown due to the rarity of the disease. It should be treated empirically with at least four drugs. The value of adjunctive steroids cannot be determined. The patient was treated with isoniazid, rifampicin, pyrazinamide, ethambutol and dexamethasone. He recovered, and a subsequent MRI displayed a partial resolution of the tuberculoma (figure 3).

Figure 3

Contrast-enhanced T-1 weighted MRI after treatment


Tuberculosis has become another serious complication of AIDS, and the combination of both poses a significant clinical problem.1 Intracranial tuberculoma are caseous foci with fibrous encapsulation which develop in association with deep-seated tubercles and which are acquired during periods of haematogenous dissemination.2 They normally present with the symptoms and signs of a mass lesion. Headache, seizures, paralysis, and personality changes may be observed. CSF protein increase is common, but pleiocytosis is rare. The diagnosis is based on characteristic computed tomography or MRI findings in association with clinical and laboratory evidence of tuberculosis.

The patient displayed an unusual reaction during adequate treatment and his lesions worsened. The pathogenesis of paradoxical reactions remains unclear; they can occur during adequate treatment, and do not indicate the presence of drug-resistant organisms as a response to inadequate treatment.3 4 The most probable explanation may be an enhanced immune response to dying tubercle bacilli following the initiation of therapy. Seven cases of paradoxical expansion of intracranial tuberculoma in AIDS patients had been previously reported.5-7 The use of highly active antiretroviral therapy in HIV disease can result in some degree of immune reconstitution that may facilitate paradoxical expansion of tuberculoma. The immune status of our patient, however, was similar.

Our patient improved under treatment with corticosteroids, which are known to inhibit T-helper type 1 activity and tumour necrosis factor-α production and to stimulate T-helper type 2 cell activity, which may contribute to the regulation of immune response in paradoxical expansion.7 Surgical intervention should be considered when medical therapy fails or for relief of intracranial pressure.

Tuberculosis must be considered in the differential diagnosis of contrast-enhancing lesions of the central nervous system in AIDS patients, including those who have been treated for tuberculosis.

Final diagnosis

Paradoxical growth of intracranial tuberculoma during adequate treatment for tuberculous meningitis.