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115 cases of cerebral tuberculoma were treated in our department between 1986 and 1996. The series of 115 patients comprised of 64 women and 51 men, whose age ranging from 13 to 60 years (mean of 26 years). Symptom duration before treatment was from 3 weeks to 2 years (mean of 8 months). Intracranial hypertension is the most frequent reason of consultation (50 cases). Ophthalmologic symptoms were encountered in 34 patients, 19 of them had total blindness or light perception only and remaining 15 had poor vision. Fundoscopic examination, achieved in 80 patients, has shown an optic nerve atrophy in 15 cases, papillary oedema in 35 cases, and no abnormality in 30 cases. Physical examination showed focal signs in 95 cases: 16 had hemiplegia, 29 hemiparesis, 1 monoplegia, 5 aphasis, 22 cranial nerves lesions, and 22 cerebellar syndrome. Epilepsy is noted in 27 cases. Poor general state is found in 9 cases. The tuberculoma is found in conjunction with pulmonary tuberculosis, 12 cases, lymph node tuberculosis 2 cases and vertebral tuberculosis 6 cases. Contamination by family members was established in only 11 cases. Laboratory studies: Anaemia is found in 20 patients. From 37 tuberculin skin tests carried out, 26 were positive. Mycobacterium tuberculosis was isolated in only one systematic sputum culture. Radiological findings: Skull x-rays were obtained in all patients and showed signs of intracranial pressure in 31 patients: an enlarged sella in 11 cases, and digitiforms impressions in 20 cases. A computed tomography (CT) scan (Fig. 1a and 2) carried out in 98 patients, was complemented by magnetic resonance imaging (MRI) (Fig. 1b) in 6 patients, and showed the presence of 66 supra-tentorial tuberculomas, 7 of which had multiple locations, and 49 were infratentorial, 11 of which were located in the brainstem. Hydrocephalus was found in 14 cases. Extracerebral localisation of tuberculosis was found in 16 patients, 10 had tuberculous cavity, 4 had mediastinal lymph node and 2 had miliary tuberculosis. Neuropathological examination of all patients operated, by excision or biopsy revealed area of caseous necrosis surrounded by inflammatory granulation tissue containing many granuloma (epitheloid and giant cells) with scattered giant cells in all cases. Acid fast bacilli were found in only 4 cases. Medical: It consisted of tuberculous chemotherapy, corticosteroids and phenobarbital in all patients, including those with infratentorial tuberculoma. This treatment was undertaken in only 19 patients and comprised rifampicin, isoniazid, pyrazinamide for 2 months, followed by 10 months of rifampicin and isoniazid. Surgical: Surgical treatment was recommended in 96 patients for diagnostic and therapeutic reasons. Three approaches were used:
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Twelve deaths (7 patients were operated and 5 were not) were recorded in our series, which means a mortality rate of about 10.4%. Three patients died after tuberculous meningitis, two cases of miliary tuberculosis, two patients after antituberculous drugs were discontinued by the patient. One patient with cardiovascular disease. The cause of death was unknown in one case. One patient with a sudden deterioration in neurologic status that was associated with paradoxical expansion of a cerebellar tuberculoma. Clinical follow-up was 1 year on average for medically treated patients, and 15 months for operated patients. The clinical outcome (Table 1) was marked by cerebellar syndrome regression in 73% of the surgically managed patients and in 27% of the medically treated patients. Improvement of vision was seen in 50% of the medically treated patients and 27% of the operated ones. Regression of neurologic deficit occurred in 50% of the medically treated patients and 30% of operated patients. Recurrence was seen in five patients, who discontinued antituberculous therapy after a good evolution. A good result was seen after the anti-tuberculous drugs were restarted.
The frequency of CNS tuberculoma is closely related to tuberculous endemic, which is still high in developing countries. In India, 20% of intracranial processes are tuberculomas;4 this number reaches 47% if only children under 15 are considered. In Europe, tuberculomas represents only 0.15% of intracranial processes.3,12 This percentage is increasing because of HIV infection.14,22 Lecuit in 1994 reports the incidence of 10% of intracranial tuberculoma in tuberculous HIV patients, mainly when tuberculous meningitis coexists.18 In HIV negative patients, tuberculoma is the only expression of cerebral tuberculosis in 60% of cases.8 Pathologically, tuberculoma is characterised by multiple confluent epitheloid granulomas with large areas of caseating necrosis and numerous Langerhan’s giant cells. On Ziehl-Nielsen stain, tubercule bacillus was rarely detected. Tuberculoma is characterised by its clinical heterogeneity, which particularly depends on the variable location, size and number of the tuberculomas. Lisa and Deangelis emphasise the high frequency of seizures (50% - 80%), but intracranial hypertension or neurologic deficit can also be seen.20 No obvious clinical symptoms of extra-cerebral tuberculosis were found in 40% of cases.24 The tuberculin test is positive in 25% of patients only, chest x-ray is of normal aspect in 50% (16% in our series), and cerebrospinal fluid analysis are normal in 70% of cases.19 The CT scan is the most important examination.16 It shows supratentorial lesions more often than infratentorial ones.9,23 The centre of lesion is spontaneously hyper-, iso-, or hypodense, surrounded by an oedematous peripheral zone. Macroscopic calcifications can invariably be seen according to the stage of the lesions. MRI has better sensitivity for small lesion screening as it specifies their morphology and their location, owing to its three dimensional images.13 However, it does not show any specific lesions. The radiological differential diagnosis includes a number of intracranial space-occupying lesions. Cerebral tuberculomas can be mistaken for abscesses, mycotic granulomas, parasitic cysts, primary (gliomas and lymphomas) or metastatic tumors. The treatment of cerebral tuberculoma is becoming more conservative. It combines three antituberculous antibiotics. The addition of fluoroquinolones may be of interest.5,25 We emphasise the efficiency of steroids in reducing the perilesional oedema and threatening intracranial hypertension.1,2,17,21 Anticonvulsant treatment is mandatory for seizure control. The indication of medical treatment alone is justified because it is safe, efficient, and cheap. It has to be attempted first in all cases with strict CT scan and MRI follow-up.11 Finally, medical management is obviously indicated when surgical treatment is impossible, because of the location, the multiplicity of lesions, or the severely altered general condition of the patient.1 Surgical treatment is currently suitable in cases of threatening intracranial hypertension, or rarely for diagnostic purposes.12,16 Some authors operate on the chronic cases and the calcified tuberculomas because they are resistant to medical treatment.10,15 Stereotaxic biopsy can be complicated by meningeal contamination.8 However it seems important for deeply localised tuberculomas, multiple lesions, and brainstem tuberculomas. It is useful for diagnostic confirmation before establishing medical treatment. The prognosis is currently quite good; the post-operative mortality is estimated at 16%.6,21 In medically managed patients, the mortality is difficult to determine because of the absence of large series. This disease, however, is considered severe, because of the important complications it can cause. These complications recover in 5 to 60% of cases in some series.14,17
Tuberculosis and cerebral tuberculoma are still frequent in our country. The diagnosis is based on a group of arguments, clinical, epidemiological and neuroradiologic. The treatment is becoming increasingly medical but surgery is still indicated in cases of dangerous intracranial pressure or for diagnostic confirmation. Stereotaxic biopsy can be diagnostic in cases of multiples lesions, deep tuberculomas or brainstem lesions.
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http://www.panarabneurosurgery.org/ |