WEEKLY clinicopathological exercises; tuberculous meningitis, tuberculous endometritis, miliary tuberculosis.
Explore the source record for details and available documents.
SEARCH · PubMed Health
Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Tuberculous meningitis usually results from hematogenous seeding of the central nervous system from a primary pulmonary source of infection. Initially, the meningitic process can mimic a flu-like syndrome, followed rapidly by the development of profound neurologic deficits. Computed tomography scanning or magnetic resonance imaging of the head often demonstrates a characteristic pattern of basal cistern involvement with Mycobacterium tuberculosis. The incidence of tuberculous meningitis in the more developed countries has increased during the past 5 years because of the growing number of cases in patients with acquired immunodeficiency syndrome, the spread among the homeless, and the expanding immigrant population. The significant morbidity and mortality rates associated with tuberculous meningitis--generally considered to be a disease of the past--emphasize the need for greater clinical awareness, early diagnosis, and prompt treatment.
Tuberculous meningitis leads to a high mortality rate. However, it responds well to chemotherapy if the treatment is started early. Neuroimaging is one of the most important initial investigations. There were 42 patients diagnosed with tuberculous meningitis in Kuala Lumpur Hospital based on clinical criteria, cerebrospinal fluid analysis and response to anti-tuberculous treatment over a 7 year period. Relevant information was obtained from patients' medical case notes and neuroimaging findings were evaluated. Male to female ratio was 3:1. The three major ethnics and the immigrant groups in Malaysia were represented in this study. The majority of the cases involved the Malays followed by immigrants, Chinese and Indians. The patients' age ranged from 18 to 62 years old with the mean age of 34.4 years. There were 95.2% (n = 40) of patients who presented with various neuroimaging abnormalities and only 2 (4.8%) patients had normal neuroimaging findings. Hydrocephalus and meningeal enhancement were the two commonest neuroimaging features. Other features include infarction, enhancing lesion, tuberculoma, abcess, oedema and calcification. Contrasted CT scan is an adequate neuroimaging tool to unmask abnormal findings in tuberculous meningitis.
Tuberculous meningitis generally is considered to be relentlessly progressive, unless specific therapy is administered. The "aseptic meningitis" of a 56-year-old diabetic patient proved to be tuberculous and regressed spontaneously. Review of the literature shows that spontaneous healing of tuberculous meningitis has been described and demonstrated previously. Awareness of this entity and its recognition are important because this disease may be a focus for subsequent tuberculosis of other organ systems.
Tuberculous meningitis may rarely be followed by the development of syringomyelia despite appropriate chemotherapy. In the present paper, we report a case of tuberculous meningitis in a 23-year-old Vietnamese male complicated by a rapidly progressive myelopathy due to granulomatous arachnoiditis which culminated in the development of a syrinx. The relevant literature is reviewed. The present case supports the hypothesis that vasculitic thrombosis of spinal cord vessels leading to ischemic myelomalacia is the mechanism causing postinflammatory syringomyelia.
Tuberculous meningitis is a very serious form of tuberculosis. In the absence of randomized controlled trials of alternative treatment regimens, its management depends on employing potent drugs that penetrate well into the cerebrospinal fluid (CSF). The penetration of isoniazid, rifampin, and streptomycin into the CSF of 27 Chinese patients was studied using fluorimetric and microbiologic procedures. Isoniazid rapidly diffused into the CSF, peak concentrations in excess of 3 mg/L, or over 30 times its minimal inhibitory concentration (MIC) against Mycobacterium tuberculosis being attained within 4 hr. In contrast, rifampin and streptomycin penetrated very slowly across the meninges, and CSF levels only slightly in excess of their MICs against M. tuberculosis were achieved. The penetration of the drugs into the CSF correlated poorly with differences in their partitioning between octanol/water and cyclohexane/water but could be predicted using a simple model based on their renal clearance rates and plasma protein binding. It is recommended that patients with tuberculous meningitis should be treated for at least 9 months with a combination of isoniazid, rifampin, and pyrazinamide, which may be supplemented in the first 2 mo with streptomycin.
Tuberculous meningitis remains an illness with a substantial morbidity and mortality despite the introduction of effective antituberculous agents. The correct diagnosis is often initially unsuspected and, even when appropriately considered, may be difficult to unequivocally confirm. Since the advent of the AIDS era, the frequency of neurological disease due to mycobacterial infection has increased and the spectrum of the disease has changed. The effects of the AIDS epidemic, the role of computed tomography and magnetic resonance imaging, the value of newer laboratory techniques in establishing the diagnosis, and approaches to treatment are among the topics addressed in this review of tuberculous meningitis.
Tuberculous meningitis (TBM) is not the most common but the most serious clinical form of extrapulmonary tuberculosis. Serious complications resulting from difficulties in diagnosis and treatment of the disease makes it an important health problem. In our study, 82 patients with TBM, followed up in our clinic between January 1998-December 2002, are evaluated with their clinical and laboratory properties. 52% of our patients were females, 48% were males and their ages ranged from 15 to 70 with a mean of 32 years. The diagnosis was based on patients' history, clinical and laboratory properties, cerebrospinal fluid (CSF) findings and radiographic findings. 59% of our patients were grade II clinically, 29% were grade I, and 23% were grade III. Mostly observed complaints were headache (87%) and nausea-vomiting (63%) and fever (45%) and mostly seen physical findings were stiff neck (70%), alterations in consciousness (57%). Pleocytosis in CSF was detected in 94%, low CSF glucose level in 87%, and elevated CSF protein level in 82% of the patients. From CSF samples of 40 patients, out of total 82, Mycobacterium tuberculosis was isolated on Loewenstein-Jensen medium (49%). Nineteen patients had tuberculomas, 13 had basal meningitis, and 11 had hydrocephalus on cranial radiographic studies. 28% had miliary pattern and 26% had active infiltration and cavities on chest roentgenogram. A four-drug antituberculous regimen was administered for 88% of the patients and dexamethasone treatment was administered for 75%; 56 (68.3%) patients recovered from the illness, 14 (17%) patients had slight and 4 (4.9%) patients had serious neurological sequeales and 8 (9.8%) patients died in spite of tuberculous therapy. As a conclusion, TBM is an infectious disease with high morbidity and mortality rates. Various prognosis patterns may be observed according to the clinical grade of the patient on application. When suspected, an early diagnosis and early treatment of the disease are the most important factors which effect complication and mortality rates.
Tuberculous meningitis may rarely be followed by the development of a syrinx even after apparently successful chemotherapy. There are only six previously reported cases of this unusual complication; these are reviewed. A case is described of syringomyelia which developed 1 year after TBM. One year later magnetic resonance imaging demonstrated not only the spontaneous resolution of the syringomyelia but also the appearance of a new cavity within the brain stem. This surprising sequence of events illustrates the need for extensive studies of the natural history of syrinxes of differing aetiologies.
Tuberculous meningitis arises from the discharge of bacilli from a subjacent caseous focus into the subarachnoid space. Meningeal involvement is most marked at the base of the brain. The clinical spectrum is very broad and the outcome of therapy depends mainly on the stage of disease at the time treatment is instituted.
Tuberculous meningitis (TBM), the most severe form of Mycobacterium tuberculosis infection in humans, is associated with significant morbidity and mortality despite successful treatment with antituberculous drugs. This is due to the irreversible brain damage subsequent to the local inflammatory response of the host to M. tuberculosis. Corticosteroids have been used in conjunction with antituberculous therapy in an attempt to modulate the inflammatory response, but this strategy has been of limited success. Therefore, we examined whether combining antituberculous drugs with the immunomodulatory drug thalidomide or with a new thalidomide analog, immunomodulatory drug 3 (IMiD3), would be effective in reducing morbidity and mortality in an experimental rabbit model of TBM. Intracisternal inoculation of 5 x 10(4) CFU of Mycobacterium bovis Ravenel in rabbits induced progressive subacute meningitis characterized by high cerebrospinal fluid (CSF) leukocytosis, protein influx, release of tumor necrosis factor (TNF), substantial meningeal inflammation, and mortality by day 28. Treatment with antituberculous drugs or with antituberculous drugs plus thalidomide improved the clinical course of disease somewhat and increased survival to about 50%. In contrast, treatment with antituberculous drugs in combination with IMiD3 limited pathological neurologic changes and resulted in marked improvement (73%) in survival. IMiD3 treatment was also associated with reduced leukocytosis in the CSF and significantly lower levels of TNF in CSF and plasma. Histologically, the meningeal inflammation in animals treated with antituberculous drugs plus IMiD3 was considerably attenuated compared to that of the other treatment groups. These results suggest a potential role for IMiD3 in the management of TBM in patients.
Tuberculous meningitis (TBM) remains a common serious neurological emergency especially in the developing world. Elevated intracranial pressure (ICP) is often a feature of severe TBM and is associated with high morbidity and mortality. The pathology associated with TBM, such as cerebral edema, hydrocephalus, tuberculoma(s), and infarcts related to arthritis, contribute to increase in intracranial volume and, therefore, elevated ICP. The three types of edema (vasogenic, cytotoxic, and interstitial) may contribute to cerebral edema. The molecular mechanisms underlying the events that ultimately lead to brain damage and cerebral edema during infection are complex. Similarly to bacterial meningitis, cerebral blood flow autoregulation is probably impaired in TBM, and the mechanisms are unclear. Although no universal guidelines are available to institute ICP monitoring in patients with severe TBM, it is be prudent to monitor patients at risk for increases in ICP. Such an approach helps to detect the secondary brain insults, allowing for a more informed approach to treatment. Treatment of elevated ICP involves a multipronged approach. The first step should be to identify focal brain lesions and hydrocephalus (which require surgical intervention) by brain imaging. Cerebral edema is treated with hyperosmolar agents. Mannitol is currently the most commonly used agent. It appears that use of hypertonic saline as an osmotic agent in infection-related cerebral edema has certain advantages. However, this needs to be established by well-designed trials. Use of steroids reduces not only cerebral edema but also the production of cytokines and other chemicals involved in the immunopathogenesis of TBM. Fever associated with TBM should be aggressively treated, because fever can worsen the impact of elevated ICP. Hyponatremia may complicate TBM and requires appropriate correction because it can aggravate cerebral edema.
Tuberculous meningitis (TBM) is a common manifestation of extrapulmonary tuberculosis. Syringomyelia is a rare complication of TBM. We report a case of syringomyelia due to TBM. A 25 year old Thai male was admitted with a history of progressive paraparesis and loss of body sensation. He had a history of TBM in the previous year, and was treated with antituberculous drugs. Physical examination revealed a temperature of 37 degrees C. Motor power was grade 3/5 with generalized hyperreflexia. He had bilateral loss of pain, temperature and vibratory sensation below the T7 level. A magnetic resonance imaging of the spine demonstrated a long segment of syrinx from C4 to the conus medullaris region. A T12-L1 laminectomy and syringosubarachnoid shunt were done. His clinical symptoms improved after surgery.
Tuberculous meningitis is an uncommon but potentially devastating form of tuberculosis. Current antituberculous drugs are highly effective when treatment is initiated early, before the onset of altered mentation or focal neurologic deficits. Because the clinical outcome depends greatly on the stage at which therapy is initiated, early recognition is of paramount importance. Patients with the meningoencephalitis syndrome and CSF findings of low glucose levels, elevated protein levels, and pleocytosis should be treated immediately if there is evidence of TB elsewhere in the body, or if prompt evaluation fails to establish an alternative diagnosis. Examination of CSF is the best diagnostic approach; with sufficient diligence, serial AFB smears and cultures will usually yield positive results, even days after therapy has been started. The CT scan is an important and highly effective tool for the diagnosis and management of patients with TBM. In a patient with compatible clinical features, the combination of basilar meningeal enhancement and any degree of hydrocephalus is strongly suggestive of the diagnosis of TBM. Serial evaluation by CT scanning is useful for following the course of hydrocephalus and tuberculoma, particularly in reference to the need for, or response to, adjunctive therapy with corticosteroids and surgery. The decision to administer corticosteroids should be based on careful correlation of the clinical and radiographic features of the case. Surgical shunting should be considered early in the patient with hydrocephalus and symptoms of raised intracranial pressure. Tuberculomas are best treated medically, often in conjunction with corticosteroids where cerebral edema is believed to contribute to neurologic decline. The recommended chemotherapy regimen is isoniazid and rifampin in all patients, together with pyrazinamide for the first 2 months.
Tuberculous meningitis is a grave, yet curable, illness. It is a rare condition nowadays and may present special problems when the clinical picture is untypical. Clinical awareness, early diagnosis and vigorous treatment are the key to therapeutic success.