Cases reported "Tuberculosis, Meningeal"

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1/9. Late clinical manifestation of cerebral tuberculomas in two children with tuberculous meningoencephalitis.

    We report on two children with cerebral tuberculomas leading to late dramatic clinical exacerbation after appropriate antituberculous chemotherapy and high-dose corticosteroids. A 6-year-old girl with tuberculous meningoencephalitis initially fully recovered. However, after 9 months of continuous therapy she presented with acute increased intracranial pressure caused by tuberculomas requiring rapid drainage of CSF. A 16-year-old boy with miliary pulmonary tuberculosis and severe meningoencephalitis had reached a stable condition for more than 10 months although still suffering from a left-dominant spasticity and motor dysphasia. Fifteen months after initiation of therapy he presented with an acute central paralysis of the left facial nerve, progressive hemiplegia, severe ataxia and increasing lethargy caused by a cerebral tuberculoma with a perifocal oedema. Prolonged treatment with antituberculous chemotherapy and high-dose corticosteroids led to complete recovery in the younger patient and marked improvement in the older patient who remains severely handicapped. CONCLUSION: 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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2/9. Endoscopic third ventriculostomy in tuberculous meningitis.

    INTRODUCTION: We report our preliminary experience with two cases of tuberculous meningitis (TBM) in which endoscopic third ventriculostomy (ETV) was performed to treat non-communicating hydrocephalus. For many years, the insertion of ventriculoperitoneal shunts has been the standard treatment for hydrocephalus in patients with TBM, although the indications for and timing of surgery are not uniformly accepted. Shunt insertion is associated with a high incidence of complications, particularly with long-term follow-up. An alternative treatment for hydrocephalus in this group of patients would clearly be of great benefit. The indications for ETV have increased in the last decade, and there are reports of some effectiveness of the procedure in patients with hydrocephalus due to bacterial meningitis. To our knowledge, ETV has not been described in the management of TBM. methods: We report the early results of our preliminary experience with ETV in two patients who presented with neurological compromise due to hydrocephalus and raised intracranial pressure. The clinical context and pre-operative investigation of these patients are presented. The emphasis is placed on the distinction between communicating and non-communicating pathologies as a guide to management options. We detail our surgical findings and the peculiar endoscopic challenges that the condition presented to us. Follow-up in these patients included clinical and investigational data suggesting early effectiveness of the procedure in converting non-communicating hydrocephalus into a communicating one, which can then be treated medically. DISCUSSION: Endoscopic third ventriculostomy is presented as a new application of a procedure accepted for other indications in the treatment of non-communicating hydrocephalus. There are particular aspects of the use of this procedure related to the unique pathology of TBM that are significantly different. We explain our rationale for endoscopy in these patients, and suggest a protocol in which endoscopy may play a role in the management of patients with raised intracranial pressure due to tuberculous hydrocephalus.
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3/9. Tuberculous radiculomyelitis (arachnoiditis) associated with tuberculous meningitis.

    Abstract. A 17-year-old man who presented with progressive quadriparesis is reported. About 8 months prior to admission, he had miliary tuberculosis, and that improved with anti-tuberculous therapy. He had also developed tuberculous meningitis and tuberculous myelitis, respectively. He regularly took anti-tuberculous drugs until this illness. Neurological findings were compatible with cervical cord lesion. CSF analysis indicated a predominate lymphocytic pleocytosis with a high protein level and low sugar profile. MRI findings revealed a multi-loculated arachnoid cyst at C1-C3 level with pressure affecting the adjacent spinal cord and evidence of myelitis at C3-T1 level. Hemi-larminectomy and removal of the arachnoid cyst were performed, but without improvement. A CSF culture yielded M. tuberculosis, that was susceptible to anti-tuberculous drugs.
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4/9. The treatment of multiple intracranial tuberculous abscesses: a case report.

    A Chinese female aged 2 years 8 months with tuberculous meningitis developed hydrocephalus requiring insertion of a ventriculoperitoneal shunt. After adequate anti-tuberculosis chemotherapy for 14 weeks, multiple intracranial tuberculous abscesses developed. The lesions increased in size and number accompanied by clinical deterioration. Repeated drainage operations were performed in view of the increased intracranial pressure. The child made a remarkable recovery after an initial stormy course.
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5/9. mycobacterium tuberculosis meningitis: a report of twelve cases and a literature review.

    Twelve recent cases of mycobacterium tuberculosis meningitis were presented, and the literature was reviewed. There are no particularly new or unique therapies or approaches to the management of this most serious disease. The major obstacle to successful diagnosis and treatment of tuberculous meningitis continues to be a lack of clinical suspicion of its presence. As illustrated in the cases presented, it has been our experience that patients already moribund or nonresponsive do not respond, regardless of the intervention undertaken. The most sensitive and economical method of detecting M. tuberculosis in the CSF may be LPA. However, this has not yet been widely validated or accepted. Larger volumes of CSF should be sent to the laboratory for testing and centifuged to about 5x concentrations before both acid-fast bacilli staining and culture are attempted. If tuberculous meningitis is suspected, three-drug therapy can be started immediately without jeopardizing subsequent culture confirmation of the presence of the TB bacillus. In addition, these patients must be followed closely to detect hydrocephalus at the earliest possible moment. When patients fail to respond to appropriate antituberculosis and pressure-reducing therapy, hydrocephalus should be actively sought by either CT or radioisotope cisternography. Although the decision to proceed to ventricular drainage or shunting must be individually made in adult patients with infection-related hydrocephalus, we agree with others that surgical intervention should be considered early and should be performed if the level of consciousness deteriorates, intracranial pressure increases, or ventricular enlargement or enhancing basal exudates are identified on CT.
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6/9. Symptomatic intracranial tuberculoma developing during treatment of tuberculosis: a report of 10 patients and review of the literature.

    Ten patients with intracranial tuberculomata which developed during treatment for tuberculosis are described. The initial infection was meningeal in five, miliary in three and pulmonary in two and all improved after treatment was started. However 10 days to five months (mean two months) after the start of treatment, new neurological symptoms and/or signs occurred that led to the recognition of intracranial tuberculomata. CT brain scans suggested tuberculomata in all 10 patients; there were several lesions in five and histological confirmation was obtained in three cases. Earlier CT brain scans (six weeks to five months before) were carried out in five patients and in none was a tuberculoma seen. After treatment with anti-tuberculous drugs and control of raised intracranial pressure when present, five patients made a full recovery, three were left with mild neurological deficit and in two it is too early to assess the outcome.
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7/9. Recurrent miliary tuberculosis secondary to infected ventriculoatrial shunt.

    The placing of a ventriculoatrial anastomosis because of elevated CSF pressure secondary to tuberculous meningitis resulted in repeated dissemination of mycobacterium tuberculosis from the anastomosis. The consequent clinical picture showed recurrent appearance and clearing of miliary tuberculosis of the lung in spite of antituberculosis chemotherapy. While this possibility was considered early, the diagnosis was not established until the shunt was replaced shortly before the patient's death.
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8/9. Cerebral tuberculomas developing during treatment of tuberculous meningitis.

    Cerebral tuberculomas developed in two adult Asian immigrants during treatment for miliary tuberculosis and tuberculous meningitis. Both were infected by strains of mycobacterium tuberculosis sensitive in vitro to all antituberculous drugs, and no evidence of immunodeficiency was detected. Focal neurological signs appeared and the lesions led to the death of one patient despite maximum treatment. The importance of systemic corticosteroids in controlling the raised intracranial pressure is discussed.
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9/9. Ventriculoatrial shunting for hydrocephalus complicating tuberculous meningitis.

    Relatively little attention has been focused on the management of increased intracranial pressure which develops in patients with tuberculous meningitis. In the acute phase of infection, cerebral edema is the most common cause; whereas in the subacute or chronic phases, hydrocephalus is most often implicated. patients with tuberculous meningitis may fail to show neurologic improvement or deteriorate despite appropriate medical therapy, no matter what the pathogenesis of increased intracranial pressure. The patient we describe illustrates the usefulness of ventricular shunting in patients with hydrocephalus who fail to respond to the administration of antituberculous and pressure-reducing agents.
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