2001
DOI: 10.1007/s004310100795
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Late clinical manifestation of cerebral tuberculomas in two children with tuberculous meningoencephalitis

Abstract: Patients with initially successful treatment of central nervous system tuberculosis should undergo an alert follow-up for the development of late cerebral tuberculomas. Treatment should consist of prolonged courses of antituberculous chemotherapy and high-dose corticosteroids.

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Cited by 7 publications
(7 citation statements)
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“…Tuberculoma formation has repeatedly been observed to coincide with tapering steroid doses (as in cases 9, 10, 11 and 17), indicating that the clinical situation might be dominated by a delayed type hypersensitivity response (Afghani and Liebermann, 1994). In contrast, the delayed occurrence of symptomatic tuberculomas in successfully treated TBM patients (as in cases 13, 18, 19 and 20) might support another hypothesis; a reaction to a local reactivation of non‐sterile granulomatous lesions (Rolinck‐Werninghaus et al. , 2001).…”
Section: Discussionmentioning
confidence: 93%
“…Tuberculoma formation has repeatedly been observed to coincide with tapering steroid doses (as in cases 9, 10, 11 and 17), indicating that the clinical situation might be dominated by a delayed type hypersensitivity response (Afghani and Liebermann, 1994). In contrast, the delayed occurrence of symptomatic tuberculomas in successfully treated TBM patients (as in cases 13, 18, 19 and 20) might support another hypothesis; a reaction to a local reactivation of non‐sterile granulomatous lesions (Rolinck‐Werninghaus et al. , 2001).…”
Section: Discussionmentioning
confidence: 93%
“…24,25 The case described by Martins et al 12 showed a much more favorable outcome than ours: in our case, the duration of the initial status epilepticus, the occurrence of an ischemic stroke, and the existence of multiple tuberculomas were clearly negative outcome factors. 22 Paradoxical enlargement of intracranial tuberculomas during adequate antituberculous chemotherapy has been reported previously, 8,10,14,16,[26][27][28] but the appearance of new extracranial lesions is more uncommon. This finding does not suggest that the ongoing treatment is inefficient, but usually justifies prolonged antituberculous chemotherapy.…”
Section: Discussionmentioning
confidence: 92%
“…21 It is out of the scope of the current article to enumerate all agents of postinfectious acute cerebellar ataxia, but consideration in diagnosis may be lent to measles, mumps, herpes simplex virus, coxsackie A and B, hepatitis A, influenza A and B, parvovirus B19, echoviruses, poliovirus, Mycoplasma pneumoniae, and Legionella pneumophilia. [18][19][20][21]24 Additional etiologies that may present with acute cerebellopathies include tick paralysis, 25 cerebellar tuberculomas, 26 and brain stem encephalitis caused by Epstein-Barr virus, Listeria monocytogenes, or enterovirus 71 infection. 19 Acute disseminated encephalomyelitis is another autoimmune phenomenon typically preceded by infection that affects the entire brain and not only the cerebellum.…”
Section: Celiac Disease Cerebellar Ataxia and Pediatricsmentioning
confidence: 99%