Tuberculoma.

simple ppt

1. Tuberculoma

2. Definition Tuberculomas  or tuberculous granulomas are a well defined focal mass that results from Mycobacterium tuberculosis infection, and is one of several morphological forms of tuberculous disease.

3. Tuberculosis of the central nervous system  can result from either haematogenous spread from distant systemic infection (e.g. pulmonary tuberculosis) or direct extension from local infection (e.g. tuberculous otomastoiditis ).

4. A tuberculoma is a benign non- neoplastic mass (a tumor-like mass that is not a cancer) caused by a localized tuberculosis infection. They are rare even in patients with tuberculosis, but usually appear in the lungs or brain. They usually respond to the same antibiotics used to treat the tuberculosis, but can also present with complications such as meningitis.

5. Incidence The incidence of TB is increasing worldwide . Some reports keep TB as the "leading cause of death due to a single infectious agent" and the seventh leading cause of death and disability worldwide .

6. Risk factors Many factors predispose a person to TB. 95% of their patients had low social, economic, and nutritional conditions. CNS tuberculomas are seen in 0.55% to 15% of systemic TB cases, Intracranial tuberculomas are seen in about 1% of all patients with TB, [6] whereas intradural spinal tuberculomas are reported to be 2% to 5% of CNS tuberculomas . [1

7. Types of intracranial tuberculoma Intracranial manifestations of tuberculosis are protean and can affect all compartments Manifestations include: extra-axial tuberculous meningitis ( leptomeningitis ): most common tuberculous pachymeningitis : rare intra-axial intracranial tuberculous granuloma  ( tuberculoma ) focal tuberculous cerebritis intracranial tuberculous abscess tuberculous rhombencephalitis tuberculous encephalopathy

8. ETIOLOGY AND PATHOPHYSIOLOGY TB is an infectious disease caused by the obligate aerobic bacillus, Mycobacterium tuberculosis . It is transmitted through inhalation of as few as 1 to 10 aerosolized droplets containing the bacteria. As the bacteria multiply in the alveoli and macrophages of the lung, the complex cell-mediated immune response generates a granulomatous reaction, resulting in a tubercle and caseating necrosis (a small rounded lesion with a necrosing center).

9. Its outer waxy capsule makes it more resistant to destruction. As a result, this bacterium can persist in old necrotic and calcified lesions and is capable of reinitiating growth. If the bacteria are not contained, the infection can be hematogenously spread to other sites.

10. The location of TB spread to the CNS is directly related to the pattern of blood flow and usually spreads to the cerebral hemispheres and basal ganglia in adults and to the cerebellum in children. The ratio of intramedullary to intracranial lesions are found to relate to spinal cord versus brain weight, about 1:42. Spinal lesions are most often found in the thoracic spine and often present as subacute cord compression.

11. A tubercle that ruptures in the subarachnoid space results in TB meningitis, whereas deep lesions cause tuberculomas or abscesses. The tuberculoma capsule is composed of fibroblasts, lymphocytes, epithelioid cells, and Langhans giant cells, and its core is a necrotic caseous center. When this core liquefies, the lesion becomes a tuberculous abscess, packed with AFB. Vascular inflammation, vasculitis , and edema, which can occur around the lesions, are products of the immune response and can cause additional clinical complications.

12. Epidemiology Tuberculosis remains a leading cause of morbidity and mortality in the developing world. It may account for ≈1/6 th of the 3 million of global mortality due to Mycobacterium tuberculosis infection. CNS involvement is thought to occur in 2-5% of patients with tuberculosis and up to 15% of those with AIDS-related tuberculosis .

13. Although CNS involvement by tuberculosis is seen in all age groups, there is a predilection for younger patients, with 60-70% of cases occurring in patients younger than 20 years of age . In endemic regions, tuberculomas account for as many as 50% of all intracranial masses .

14. Symptoms CNS TB presents in many different ways. A patient may be asymptomatic, have pulmonary symptoms, or have neurologic deficits alone. As one can see from the case studies, all of the patients had headaches, but one had vertigo and another fatigue.

15. CNS TB usually has signs and symptoms of increased intracranial pressure or space-occupying lesions in the brain or spine. Common complaints may include headache, stiff neck, fever, weight loss, blurry vision, confusion, lethargy, nausea, vomiting, and, for spinal cord lesions, lower extremity weakness or bowel or bladder symptoms. Signs of meningitis may include altered mental status, fever, seizure, cranial nerve deficits, papilledema , or meningismus .

16. Examinations Patients with tuberculomas will have a physical examination that is consistent with the location in the brain of the space-occupying lesion, which may include cranial nerve deficits, altered mental status, visual changes, hemiparesis , or seizures. Patients with spinal cord lesions will have a physical examination consistent with the location of the lesion in the spinal cord.

17. CT.SCAN A CT scan of the brain should be done if there is suspicion for intracranial or intramedullary TB. The CT scan should be done with and without contrast. Immature lesions are hypodense and nonenhancing . Mature lesions are isodense to hyperdense with solid, ring, or mixed enhancement. There is a typical target sign suggestive of TB. CT findings are similar to that of many other CNS lesions, including fungal infections, neurosarcoidosis , bacterial infections, and some metastatic disease.

18. MRI SCAN An MRI scan is more specific and sensitive than a CT scan and should be done with and without contrast. T1-weighted images show central isointensity . T2-weighted images show an isotense to hypertense core and a hyperintense rim, ring, or conglomerate of rings with enhancement. MRI findings may also mimic several of the aforementioned lesions.

19. Laboratory test Cerebrospinal Fluid. Lumbar punctures that remove 10 to 15 mL provide the best information. CSF studies may show normal findings or have elevated protein, decreased glucose, or pleocytosis . Results of CSF polymerase chain reaction tests may be diagnostic. Most patients will have an elevated opening pressure as well.

20. Always get an AFB smear when testing CSF. Although there are a fair amount of false negatives, with serial AFB smears (up to 4) the diagnostic yield is 87%. Mantoux Tests. Mantoux tests may be positive or negative. Other Blood Work. Sedimentation rate, C-reactive protein, and white blood cell count may also be elevated.

21. Biopsy Biopsy of the lesion should be done if the diagnosis is unclear and the lesion is in an accessible area or if neurologic compromise is present. Histopathology may show a central necrosis, lymphocytes, Langerhans giant cells, or epithelioid cells. Bacilli may or may not be present. No definitive diagnostic pathway is available for CNS TB.

22. Treatment Treatment of CNS tuberculosis is based on an anti-tubercular treatment regimen. However, multidrug-resistant tuberculosis remains a major hurdle in treatment.

23. CDC guidelines recommend a 9- to 12-month pharmacologic treatment regimen for CNS TB and offer four regimens for administering treatment. The initial phase of treatment in the first 2 months should include INH, rifampin (RIF), PZA, and EMB. The medications can be given daily throughout the first phase, daily for 2 weeks, and then twice weekly for 6 weeks, or three times weekly throughout.

24. With differing administration schedules come differing doses of the drugs. If the organism's drug susceptibilities are known, and it is fully susceptible, EMB need not be included in the initial phase.

25. PZA should be avoided in severe liver disease, gout, and, perhaps, pregnancy. The continuation phase should consist of INH and RIF for 7 to 10 months, and this timeline should be prolonged if the patient was initially slow to respond to treatment.

26. When patients with intracranial tuberculomas experience increased intracranial pressure or neurologic symptoms, corticosteroids can be added to the regimen, although their value is still under investigation.

27. Surgical intervention for intracranial tuberculomas is generally not recommended because prolonged pharmacologic therapy combined with corticosteroids is usually effective in treating these lesions. However, surgery may be warranted if immediate decompression is necessary or if biopsy is required for definitive diagnosis.