Tuberculoma is a benign, non-cancerous mass caused by a localized tuberculosis infection that most commonly appears in the lungs or brain. It results from infection by the Mycobacterium tuberculosis bacteria. Symptoms vary depending on the location of the tuberculoma but often include headaches, fever, and neurological deficits. Diagnosis involves imaging tests like CT or MRI scans showing characteristic lesions, as well as spinal fluid and tissue analysis. Treatment primarily consists of a prolonged course of multiple antibiotic medications over 9-12 months.

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

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 ≈1/6th 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.