Management of Tuberculous Infections of the Nervous System

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Chapter 148 Management of Tuberculous Infections of the Nervous System

Infection of the central nervous system (CNS) by Mycobacterium tuberculosis is invariably secondary to a primary focus elsewhere in the body. The avium, bovine, and atypical mycobacteria are rarely isolated from the nonimmunocompromised host. The primary sites are usually pulmonary, bone, and gastrointestinal tract; genitourinary sites are less common. The incidence of CNS tuberculosis (TB) is a reflection of the overall incidence of TB in a population. A third of the global population (i.e., 2 billion people) harbors the M. tuberculosis bacillus and is at risk of developing active disease. It is still a leading cause of mortality from a single infectious disease.¹ The epidemiology of the disease has been greatly affected by the advent of the human immunodeficiency virus (HIV);²^–⁵ emergence of multidrug-resistant TB (MDR TB) and extensively drug-resistant strains of TB (XDR TB); widespread intravenous drug abuse; inadequate case detection, diagnosis, and therapy; collapse of health infrastructures due to economic crisis and war; and continuing poverty.

The health burden related to TB has prompted the implementation of World Health Organization’s (WHO’s) Stop TB Strategy, which includes the following goals: (1) TB incidence should fall by 2015, (2) prevalence and death rates should be halved by 2015 from the baseline of 1990, (3) at least 70% of incident smear-positive cases should be detected and treated in the Direct Observation of Treatment (DOTS) program, and (4) at least 85% of detected incident smear-positive cases should be successfully treated.⁶ The WHO has also been publishing an annual report on global control of TB since 1997 to provide a comprehensive and up-to-date assessment of the TB epidemic and progress in controlling the disease. The trends suggest that neither the prevalence nor the death rate would be halved in Africa and Europe by 2015. An estimated 37% of incident TB cases are not being treated in the DOTS program, 96% of incident case with MDR TB are not being diagnosed and treated according to guidelines, the majority of HIV-positive TB cases do not know their HIV status, and of those who do, the majority do not have access to antiretroviral therapy.¹

In the United States,⁷ the average decline of 5% per year in the TB case rate plateaued, and from 1986 to 1992 there was an increase in the number of reported cases.⁴ Subsequent to aggressive management of TB, the average annual percentage decline in TB was 7.3% per year during the period from 1993 to 2000 and 3.8% during the period from 2000 to 2008, along with a 75% reduction in drug resistance.⁸

HIV and TB Coinfection

An estimated 9.27 million new cases of TB (15% of which were among HIV–positive patients) were reported in 2007, with Asia and Africa accounting for almost 90% of them. There were 1.75 million deaths, 25% in HIV-positive individuals. There is a clear synergistic relation between HIV and TB. Being HIV-positive increases the likelihood of developing TB 20 to 37 times.^1,⁹ In Asia and the Pacific region, as much as 40% to 70% of HIV patients have TB.¹⁰ The tubercle bacillus has been demonstrated to enhance the replication of HIV by transcriptional activation.^11,¹² The increased susceptibility and accelerated natural history of TB with HIV infection leads to more rapid creation of drug resistance.

TB of the nervous system, which merits the attention of a neurosurgeon, occurs in several forms, and more than one form may be present in the same individual (Table 148-1). This chapter deals only with tuberculomas, tuberculous meningitis (TBM), and tuberculous spinal arachnoiditis. Pott’s disease of the spine and tubercular encephalopathy are extensively described in orthopedic and neurologic texts. The significant threat to life and/or a risk of subsequent severe handicap merits the classification of all CNS-related TB as severe extrapulmonary TB.

Table 148-1 Tuberculosis of the Nervous System

Anatomic Area	Manifestation
Intracranial Tuberculosis
Parenchymal	Tuberculoma
	Abscess
	Tubercular encephalopathy
Meningeal	Chronic meningitis
Calvarial	Osteomyelitis
Spinal Tuberculosis
Vertebral	Pott’s disease of the spine
Meningeal	Arachnoiditis
Parenchymal	Tuberculoma

Tuberculomas

Incidence

The incidence of tuberculomas in India, which comprised 20% to 30% of all intracranial space-occupying lesions in the 1950s and 1960s, has declined since 1980.¹³^–¹⁶ Although TB is widely prevalent in Nigeria¹⁷ and Taiwan,¹⁸ tuberculomas are rare. Tuberculomas are increasingly reported in industrialized nations and account for 1% to 2% of all intracranial lesions.¹⁹^–²²

Location

Tuberculomas can occur at any site in the brain, most commonly the various lobes and the cerebellum. Unusual sites of tuberculomas include the dura mater,²⁰^–²³ subdural space, orbital fissure, intraventricular, brain stem,^21,²⁴^–²⁶ pituitary gland,²⁷^–³¹ and hypothalamus.³² Spinal intramedullary tuberculomas are rare.³³^–³⁹

Pathologic Features

The typical mature tuberculoma is a solid, creamy white, well-defined, avascular mass with multiple nubbins encased in a firm gliotic capsule and extending into and compressing the surrounding brain. The cut section is pale yellow with an often gritty caseating central core.⁴⁰ The immature form consists of multiple small tubercles, some with caseating or liquefied centers dispersed within an edematous brain. Severe edema, possibly caused by an allergic response,⁴⁰ may surround these tubercles. Tuberculomas vary in size from 1.5 to 8 cm. Giant tuberculomas can occupy an entire cerebral hemisphere,⁴¹ and many adhere to the dura. The dural attachment can be tenuous or so firm that the tumor resembles a meningioma.

Microscopically, the central zone of caseous necrosis is surrounded by tuberculous granulation tissue consisting of epithelioid cells, Langerhans giant cells, and some lymphocytes, polymorphonuclear leukocytes, and plasma cells (Fig. 148-1). Acid-fast bacilli, although sparse, are usually present in both layers. The brain surrounding a tuberculoma may show degenerated axons and nerve cells, thrombosed vessels, and occasionally, swollen astrocytes and oligodendroglial cells. The changes in the small vessels can lead to microhemorrhages or microinfarcts, and these areas may coalesce.⁴² Smaller satellite tuberculomas may surround the main mass.

FIGURE 148-1 A photomicrograph of a typical tuberculoma with Langerhans giant cells, epithelioid cells, and lymphocytes. Hematoxylin and eosin stain, magnification ×100.

Tuberculomas can take several unusual forms,^43,⁴⁴ representing the spectrum of inflammatory reaction: (1) incipient tuberculoma, which may appear as an irregular, fleshy, gray cortical mass with associated meningeal tuberculomatosis or even grape-like clusters of tuberculoma along cerebral vessels; (2) subdural cyst overlying an intracerebral tuberculoma; (3) cystic tuberculoma; (4) tubercular abscess; (5) extensive edematous encephalopathy without a tuberculoma; (6) severe cerebral edema with a small, “inconsequential” tuberculoma; and (7) rarely, tuberculoma that has spread transdurally to the calvarium.

TB is a classic example of a disease the resistance to which is mediated by cellular immunity. The nature of the immunologic compromise in HIV, with its major effect on cellular immunity, increases host susceptibility to TB and abscess formation. Chronic inflammatory granulomas seen in immunocompetent patients are less common in patients with HIV.⁴⁵ Organisms belonging to the Mycobacterium avium–intracellulare complex are the most common cause of systemic bacterial infection in patients with HIV and have been demonstrated in 50% of such patients coming to autopsy.⁴⁶ Tubercular abscess is a distinct entity from a tuberculoma with central liquefaction. The abscess has a wall of chronic inflammatory cells without tubercular granulomas, and the “pus” contains a large number of acid-fast bacilli.

The liquefaction produced by hydrolytic enzymes released from brain tissue is thought to allow tubercle bacilli to proliferate, leading to abscess formation. Enzyme inhibitors from dead bacilli and necrotic tissue in caseous material have been reported to prevent liquefaction in tuberculous lesions.⁴⁷ The vessels in the reactive border zone of tuberculomas show marked proliferation of the basement membrane into several concentric layers associated with fragmentation. This basement membrane, consisting mainly of glycoproteins, may act as a newly formed antigen, initiating a cellular antibody reaction that results in vasculitis and brain damage.⁴⁸

Clinical Features

Tuberculoma is a disease of the young, with 70% of patients younger than 30 years. However, it is uncommon in children under 4 years of age. Both sexes are equally affected.^40,⁴⁹

The signs and symptoms of tuberculomas resemble those of other intracranial space-occupying lesions. As they enlarge gradually, the clinical picture is one of a slowly progressive lesion, although in at least 50% of patients, the symptoms are less than 6 months in duration. Features helpful in distinguishing tuberculomas from other brain tumors are constitutional symptoms, such as weight loss, fever, or malaise; a history of active or known TB elsewhere in the body; close contact with a patient with an open case of TB; a high frequency of seizures, even in association with a cerebellar lesion; a positive result on the Mantoux test; and an increased sedimentation rate. Infants and young children may have an enlarging head. The clinical diagnosis is often presumptive. Pyrexia is variable and may not be present in more than 20% to 25% of patients,⁴⁹ and the Mantoux test result may be negative.⁴⁰ The clinical course may uncommonly show spontaneous remissions and relapses.²⁴ Clinical evidence of an active focus of TB, such as the lungs and lymph glands, may be present in only 33% of patients ⁴⁰ and in approximately 10% of close relatives. Rare signs include scalp swelling, cerebrospinal fluid (CSF) rhinorrhea, features of a pituitary tumor,²⁷^–³¹ unilateral proptosis, and trigeminal neuralgia.⁴⁰ The clinical picture may be confusing when multiple lesions are present. Intramedullary tuberculomas with no evidence of extracranial TB are clinically indistinguishable from intramedullary tumors; the diagnosis may be suspected on magnetic resonance imaging (MRI) and is usually established at surgery.

Extrapulmonary manifestations, particularly CNS involvement, are frequently seen in patients with HIV.⁵⁰ Seizures, headaches, and an altered mental state are common presentations, but fever is often absent. The infection is usually a reactivation of latent TB.⁵¹

The clinical setting of a rare but well-described paradoxical response to antituberculous drugs ⁵²^–⁵⁶ has been reviewed by Hejazi and Hassler.⁵⁴ Most of these patients were young adults in whom inoperable intracranial tuberculomas located in high-risk regions had developed while they were receiving adequate antitubercular therapy. Frequently, intracranial tuberculomas develop or enlarge at a stage when systemic TB is responding to therapy. This paradoxical response is attributed to the load of antigenically active dead bacteria in a setting of a hypersensitive cell-mediated response. In this group of patients, associated TBM was a common feature. In TBM, symptoms of increased intracranial pressure (ICP) and development of focal neurologic signs, such as motor weakness, cerebellar signs, field defects, visual compromise, and behavioral problems in children, necessitate a search for expanding tuberculomas.

Radiographic Features

An abnormal chest radiograph is a pointer to the diagnosis of a tuberculoma.⁵⁷^–⁶⁰ More sensitive is a computed tomography (CT) scan of the chest in picking up a tubercular involvement. Calcification occurs in fewer than 6% of tuberculomas and is rarely extensive or dense,⁴¹ with the striking exceptions of the Inuit (Eskimos) and North American Indians, in whom nearly 60% of tuberculomas are known to have calcifications.⁴⁶ Calcification does not indicate an inactive lesion. Cerebral angiography invariably reveals an avascular mass, although surface tuberculomas adherent to the dura may show some peripheral vascularity.^41,⁶⁰ An associated vascular spasm may be seen that is ascribed to tuberculous vasculitis. These angiographic findings may also be seen on magnetic resonance angiography.

Computed Tomography and Magnetic Resonance Imaging

Reviews from Africa,⁶¹ Asia,⁵⁸^–⁶⁵ the West,⁶⁵ and the Middle East⁵⁹ have pointed out that most tuberculomas are similar in appearance on CT (Fig. 148-2). The CT scan image of a tuberculoma is characterized by (1) a lesion that appears isodense with the brain or slightly hyperdense and enhances strongly with contrast, revealing a dense, unbroken ring of enhancement; (2) in some cases, an enhancing disc or nodular mass with a regular or irregular margin; and (3) combinations of rings and discs, which may coalesce. Uncommonly, tuberculomas may present as a nonenhancing lesion or even a strongly enhancing lesion that is indistinguishable from a meningioma. Welchman⁶¹ described the rather rare target sign, wherein a central focus of calcification and occasional enhancement is surrounded by a peripheral ring of contrast enhancement. The target sign is not specific for CNS TB and may lead to an erroneous diagnosis of TB.⁶⁶

FIGURE 148-2 A contrast-enhanced CT scan shows multiple rings and discs surrounded by areas of low attenuation, indicating edema characteristic of TB. The larger rings are abscesses. Courtesy of Rajiv Gupta and Harsh Mahajan from Mahajan Imaging, New Delhi.

Multiplicity is common in CT scans of patients with tuberculomas. Bhargava and Tandon ^57,⁵⁸ found that 50% to 60% of cases may demonstrate multiple lesions.

Microtuberculomas

The CT scan also picks up small lesions that are less than 1.5 cm in size, disc-like or ring shaped, and single or multiple; have slightly increased attenuation that enhances with contrast; and are surrounded by disproportionately extensive low-attenuating white matter edema. Bhargava and Tandon ⁵⁸ labeled them microtuberculomas. Careful review of these cases suggests that not all of those lesions are tuberculous in etiology. Indian neurologists and neurosurgeons encounter these lesions frequently in children and young adults, but reports have come from other countries as well. The patients usually present with focal epilepsy and no neurologic deficit. Although some of these cases are definitely tuberculomas, as proved by biopsy, others result from a variety of causes.⁶⁷^–⁷⁵

Goulatia et al.⁷⁰ suggested that edema and increased vascular permeability due to seizures may be responsible for the CT appearance. Chandy et al.^68,⁶⁹ found cysticercosis as the most common cause, and Ahuja et al.⁶⁷ noted that 12 of their 38 patients were seropositive for cysticercosis and two were seropositive for TB. On CT scan, tubercular lesions tend to be larger than 20 mm, more frequently irregular in outline, with a midline shift. Cysticercus cysts, in contrast, tend to be smaller than 20 mm, with a regular outline and no midline shift.⁷³ When first seen, they could represent tuberculomas, abscesses, cysticercus granulomas, focal meningoencephalitis, astrocytomas, or metastases. A prospective study of the predictive value of CT diagnosis of intracranial TB concluded that “although the sensitivity of CT in the diagnosis of intracranial tuberculomas is 100%, and its specificity is 85.7%, the positive predictive value is only 33%.” The low positive predictive value of making a diagnosis of intracranial TB based on CT alone has been cited as a reason for obtaining histologic confirmation by open or stereotactic biopsy.⁷⁴ Nearly 30% to 40% of these lesions may regress, either spontaneously or as a result of anticonvulsant drugs alone (Fig. 148-3).

FIGURE 148-3 A contrast-enhanced CT scan of a patient who had right focal motor seizures shows (A) a disc-like lesion with disproportionate surrounding low attenuation, which (B) disappeared 2 months later on anticonvulsant therapy alone.

Magnetic Resonance Imaging

In a review of 100 consecutive cases of tuberculoma, Wasay et al. described the finding of a hypointense core surrounded by a hyperintense periphery as the most common signal characteristic on T2-weighted images; in T1-weighted images, the core was isointense with a hypointense rim (Fig. 148-4).⁶⁵ This hyperintense signal on T2-weighted images made lesions stand out even when there was only minimal central liquefaction.⁷⁶ On comparing MRI signal intensities with histologic results, Kim et al.⁷⁷ noted that the hyperintense and hypointense rims on T1-weighted images corresponded to layers of collagenous fibers and inflammatory cellular infiltrate, respectively, whereas the central zone consisted of caseation necrosis and cellular infiltrate. T2-weighted images did not discriminate among the various layers. Gupta et al.⁷⁸ found that granulomas that consisted predominantly of macrophages and gliosis were hypointense on T2-weighted images. This characteristic hypointensity of intraparenchymal tuberculomas is not found in most other space-occupying lesions.²² When the histologic pattern was one of marked cellular infiltration, with minimal gliosis, the appearance was hyperintense on T2-weighted images. In vivo proton magnetic resonance spectroscopy in hypointense lesions shows a marked increase in lipids compared with normal brain parenchyma^79,⁸⁰ (Fig. 148-5). In comparison to neurocysticercosis, the magnetic resonance spectroscopy of tuberculomas shows more choline and less creatinine.⁸¹^–⁸³ Although the course of TB is more fulminant in the patient with HIV, the imaging findings are similar to those in nonimmunosuppressed patients.⁸⁴

FIGURE 148-4 A, An MRI scan of a tuberculoma shows on T1-weighted images a slightly hyperintense rim (gliosis) surrounded by a complete or partial rim of slight hypointensity (inflammatory cellular infiltrate) and central isointensity or of mixed isointensity and hypointensity (caseation necrosis and cellular infiltrate). B, On T2-weighted MRI images, the granuloma was hypointense (predominantly consisting of paramagnetic free radicals in the macrophages and gliosis). This characteristic hypointensity of intraparenchymal tuberculomas is not found in most other space-occupying lesions. Lesions may be hyperintense as well on T2-weighted images when the histology is of marked cellular infiltration with minimal gliosis. Courtesy of D.C. Aggarwal, New Delhi, India.

FIGURE 148-5 A, This axial T2-weighted image shows a single lesion with edema of surrounding white matter. B, In vivo proton magnetic resonance spectroscopy of the hypointense lesions shows a characteristic lipid peak. Though the choline peak is small in this case, it is frequently as prominent as a lipid peak in tuberculomas. Courtesy of Rajiv Gupta and Harsh Mahajan from Mahajan Imaging, New Delhi.

Spinal intramedullary tuberculomas appear isointense or hypointense on T1-weighted images, and on T2-weighted images, the lesion is isointense, hypointense, or hyperintense, surrounded by a ring of hyperintensity because of the edema that commonly accompanies these lesions. On contrast enhancement, there is rim or nodular enhancement (Fig. 148-6).

FIGURE 148-6 This clinical presentation was of a progressive paraparesis. The T2-weighted image shows an intramedullary hyperintense lesion with a thin rim of hypointensity around it. The surrounding cord is swollen and edematous. The gadolinium–diethylene triamine penta-acetic acid–enhanced image highlights the lesion. Courtesy of Rajiv Gupta and Harsh Mahajan from Mahajan Imaging, New Delhi.

TB of the pituitary gland is rare, and clues to a tubercular etiology include intense contrast enhancement, meningeal enhancement, and a thick pituitary stalk.^28,²⁹ Pachymeningeal TB typically is isointense on T1-weighted images and isointense to hypointense on T2-weighted images.^20,²³

Medical Treatment

Antituberculous Drugs

The drugs usually prescribed nearly always belong to a group of five antibiotics known to be effective in the treatment of extracranial TB (Table 148-2). The first-line agents most commonly used are isoniazid, rifampicin (rifampin), and pyrazinamide, all of which are bactericidal. Ethambutol, a bacteriostatic drug, or streptomycin, in children too young to be monitored for visual acuity, is included in the initial treatment regimen if there is a possibility of drug resistance.⁸⁵

Table 148-2 Antituberculous Drugs

The optimal duration of treatment is not definite because, apart from early trials with streptomycin,⁸⁶ there is only one controlled trial in the treatment of intracranial tuberculomas or TBM. Rajeswari et al.⁸⁷ tested the efficacy of a short-course chemotherapy in the treatment of brain tuberculoma in 108 patients and concluded that a 9-month course was effective. This is in marked contrast to the treatment of pulmonary TB, which is based on data obtained from well-controlled trials. Guidelines for treating severe extrapulmonary TB suggest an initial 2 months of four drugs followed by 4 to 6 months with isoniazid and rifampicin.⁸⁸ In practice, such guidelines are not commonly followed for CNS TB. At present, four drugs are administered for the initial 3 or 4 months, and two drugs are given for an additional 14 to 16 months.^49,⁸⁵ Occasionally, drug treatment may have to be prescribed in larger doses for 18 months to 3 years for symptomatic intracranial tuberculomas developing during treatment of TBM.^89,⁹⁰

Transient disturbance in liver function is often observed in patients taking a combination of isoniazid and rifampicin. This needs to be monitored at regular intervals. The incidence of serious liver disturbance appears to be higher in Asians.⁹¹ Pyridoxine (10 mg/day) is invariably added to prevent peripheral neuropathy due to isoniazid intake.

Most intracranial tuberculomas resolve with medical therapy.^49,⁶¹^–⁶⁴ ^,91 The clinical and radiographic improvements are a result of the reduction in the size of the tuberculoma and the perilesional edema. Regardless of their size, lesions usually start to regress after 4 to 6 weeks, and most tuberculomas resolve within 12 to 14 months of treatment. In approximately one third of cases, telltale evidence of the lesion consists of an area of calcification or sometimes just a speck of low attenuation.⁴⁹ Some ring lesions change their character and become disc-like or nodular on treatment. In general, patients with increased ICP are slower to respond than those with seizures alone.

Medical treatment may occasionally result in liquefaction of the center of the lesion without any reduction in size.²⁶ In some patients, the tuberculoma may either show no change or increase in size on use of antituberculous drugs (described earlier).^54,^56,⁹² Tuberculomas seem to enlarge and compress the surrounding brain without causing the destruction usually associated with a malignant tumor; as a result, they can resolve with minimal residual deficits. The treatment of TB in HIV-positive patients is the same as for those who are HIV negative with the exception that thioacetazone is contraindicated in the HIV-positive patients.

Drug Resistance

Drug resistance of M. tuberculosis has been recognized since the early days of streptomycin therapy. More recently, there has been an emergence of MDR TB, defined as TB that is resistant to the two most effective first-line therapeutic drugs, isoniazid and rifampicin. There are also virtually untreatable strains of MDR TB labeled as XDR TB that are also resistant to the most effective second-line therapeutic drugs: fluoroquinolones and at least one of three injectable second-line drugs used to treat TB (amikacin, kanamycin, or capreomycin). Because of the limited responsiveness of XDR TB to available antibiotics, mortality rates are similar to the preantibiotic era. The mechanism is by chromosomal mutation with emergence of resistant clones on the backdrop of inadequate drug therapy. The incidence of acquired multidrug resistance (i.e., resistance to both isoniazid and rifampicin) ranges from 0% to 48%.^93,⁹⁴ The WHO estimates that there are nearly 0.5 million new cases of MDR TB, which accounts for 5% of the total of 9 million new TB cases. The highest rate is in Baku, the capital of Azerbaijan, where 22.3% of new cases were MDR TB.⁹⁵ High rates were reported from New York City,⁹⁶ Estonia, and Latvia. A subsequent report of a decline in the prevalence of drug resistance in New York⁹⁷ and in the United States as a whole,⁹⁸ as well as the two Baltic countries,⁹⁵ highlights the effectiveness of a strong TB program and the need for continuous surveillance of drug resistance.⁹⁹

Second-line drugs include the bactericidal drugs, fluoroquinolones, amikacin, kanamycin, ethionamide, capreomycin, prothionamide, and the bacteriostatic cycloserine. Guidelines for treating MDR TB involve the use of at least four new drugs never used by the patient, including a fluoroquinolones and at least one of the three injectable drugs (amikacin, kanamycin, or capreomycin). Resistance to pyrazinamide and ethambutol is less likely, and they can be included in the initial treatment. The initial treatment is for at least 6 months, followed by a continuation phase of 12 to 18 months with the three most active and best tolerated drugs.⁸⁸ Patients with organisms resistant to rifampicin and isoniazid have a high rate of treatment failure. Patients with HIV infections not only are more prone to TB but also are more susceptible to drug-resistant TB.¹⁰⁰^–¹⁰² Such patients require a longer duration of therapy and may still die of TB despite optimal treatment.¹⁰²

Corticosteroids are used in the presence of elevated ICP or severe cerebral edema as noted on imaging. Treatment is seldom prolonged beyond 2 to 3 weeks, during which time the corticosteroid therapy can produce dramatic improvement in the patient’s clinical state. Occasionally, patients require steroids for a much longer period.

Anticonvulsant Medications

The high incidence of seizures with tuberculomas mandates the routine use of anticonvulsants. The commonly used drugs are phenytoin, carbamazepine, oxcarbamazepine, and sodium valproate. Patients taking phenytoin and isoniazid may acquire phenytoin toxicity because high levels of isoniazid in the serum can block metabolism of the anticonvulsant.

Surgery

A tuberculoma that severely elevates ICP and threatens life or vision merits emergent surgical excision. In addition, surgical intervention comes into consideration in (1) patients who do not respond clinically or radiographically to antituberculous drugs; (2) patients whose diagnosis is in doubt, such as those with an atypical CT or MRI scan of the lesion; and (3) patients with obstructive hydrocephalus.

Complete excision of tuberculomas is usually reserved for smaller lesions in noneloquent areas of the brain. Larger lesions require subtotal excision when they cause pressure-related symptoms. An insistence on total excision at the cost of an undesirable neurologic deficit is to be discouraged. In cases of multiple tuberculomas, only the largest mass need be decompressed.

An appropriate craniotomy or craniectomy is performed over the site of the lesion. Perioperative ultrasonography and image guidance are useful for accurate localization of small, deep-seated lesions. A clear plane of cleavage ^40,⁴¹ exists between the firm, avascular tuberculoma and the edematous brain. The edema is usually not as pronounced as that associated with metastatic deposits. Tuberculous lesions are often on the cortical surface and adherent to the overlying dura. Although dural adhesions are usually separable with ease, the dural attachment at times can be extremely vascular, resembling that of meningiomas.⁴¹ After the tumor surface is identified, it is removed piecemeal from within the confines of the granuloma. The ultrasonic aspirator is a useful aid in decompression. Where the center is liquefied or necrotic, aspiration of the contents is sufficient; no attempt should be made to excise the capsule. Subcortical lesions are approached through a small corticectomy with preservation of as many vessels as possible. Parts of the tuberculoma adherent to major vessels, venous sinus, or brain stem are left in situ. The practice of frontal and temporal lobectomy or excision of edematous brain is seldom necessary to achieve decompression. Antitubercular chemotherapy is mandatory even after a complete excision of a tuberculoma. After several months of administration of antituberculous drugs, the lesion may be tough in consistency and resistant to curetting.

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