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Current Research in Medicine and Medical Sciences

Universal Research Publications. All rights reserved

Review Article
TUBERCULOMA OF BRAIN A REVIEW
Jini. K. Bose, Treesa. P. Varghese, Panayappan L, Lincy George, Kirshnakumar K
Department of Pharmacy Practice
St.James College of Pharmaceutical Sciences, Chalakkudy-680307, Kerala
Corresponding author: stjamesdruginfo@gmail.com
Received 22 January 2014; accepted 14 March 2014
Abstract
Tuberculoma is usually caused by Mycobacterium tuberculosis that mainly affects the lungs and brain. Cerebral
tuberculoma is the formation of non neoplastic, granuloma like lesions in the central nervous system. It can occur in any
part of the brain. Various diagnostic techniques are, smear test for acid fast bacilli, presence of granuloma on
histopathology, imaging techniques such as CT and MRI. Patient with tuberculoma should receive antitubercular drug
treatment. Depending upon the clinical symptoms, conformation of diagnosis, early institution of specific antitubercular
treatment and close clinical monitoring for ADR are the key to the successful management of tuberculoma. This review
article is focused to review the pathogenesis and treatments of tuberculoma.
2014 Universal Research Publications. All rights reserved
Key words: tuberculoma, granuloma, antitubercular drugs.
tissue, but in the developmental stage capsule becomes rich
INTRODUCTION
Tuberculoma is an intracranial mass occurring secondary to in collagen, and surrounding inflammatory reaction will
dissemination of tuberculosis, elsewhere in the body. disappear5. Tuberculomas may appear as small single or
Tuberculoma may be solitary or multiple1. The incidence multiple nodules or as larger irregular lesions with a central
rate of brain tuberculoma is 1.4%. It is a potentially area of caseous necrosis.
curable disorder but delay of diagnosis can lead to Rupture of tuberculomas into the subarachnoid space
increased mortality and morbidity rate. Tuberculoma results in the development of tuberculosis meningitis,
affects 12-30% of all intracranial masses. It is more which may present as acute or chronic meningitis6.
common in people with poor immune system, young RADIOLOGICAL FEATURES OF TUBERCULOMA
children, HIV infected individuals and drug resistant strains CT scan and MRI scan are the important imaging
of mycobacterium tuberculosis2. Chance of occurance of techniques for diagnosing tuberculoma. Tuberculoma
tuberculosis is 20 times more in HIV positive individuals appears as a round or lobulated mass with irregular walls
when compaired to HIV negative individuals. The main and show homogenous ring enhancement after
clinical symptoms are intracranial hypertension, papillary administration of radio contrast. In CT scan appearance of
edema, hemiplegra, hemiparesis, epilepsy, pulmonary tuberculoma round or oval mass lesion that is isointense or
tuberculosis3. Diagnosis is mainly based upon the clinical hypotense on the plain of CT scan is observed. But the MRI
features like cerebrospinal fluid changes and imaging findings of tuberculoma depend upon the stage of
characteristics.
evolution. MRI has greater sensitivity and specificity than
CT scan.
PATHOGENESIS
Mycobacterium tuberculosis is an aerobic, nonmotile non
spore forming acid fast bacillus4. Primary tuberculosis
infection is associated with hematological spread, organism
is found in different organs and lie dormant. Such dormant
foci get distributed in the brain when organism reaches the
brain and/or meninges from acute primary lesion via blood
stream to establish focal lesion known as tuberculomas.
Intracranial tuberculoma orginates as small tubercles and
Figure 1. Axial T1
develop to form mature tuberculoma. Mature forms are
Isointense
to
gray
matter.
composed of fibroblast, epithelial cells and lymphocytes. In
May
have
central
region
of hyperintensity representing
early stage of tuberculoma formation, there is an
caseation.
inflammatory reaction and a capsule poor in collagenous

Current Research in Medicine and Medical Sciences 2014; 4(1): 7-8

Figure 2. Axial T2
Isointense to gray matter.
May have central region of hypointensity representing
gliois and abundant monocyte infiltration.
Lesions are surrounded by vasogenic oedema7.
TREATMENT
Based upon clinical, laboratory and imaging findings
suspectable patients should be started with antitubercular
medicine. Duration of treatment is mainly based upon the
part that is affected. Patients with CNS tuberculosis should
receive 12 30 months of antitubercular treatment1.
Isoniazid, rifampin, pyrazinamide and ethambutol is the
four-drug regimen that is most commonly recommended,
also second line agents such as aminoglycoside and
fluroqunolones can also be added. Adverse drug reactions
associated with antitubercular drug include, discolouration
of urine associated with rifampicin, changes in serum uric
acid levels in patients receving pyrazinamide and
alterations in visual activity in patients receiving
ethambutol5, 8, 9 and 17. Other ADRs associated with
antitubercular drugs are gastrointestinal reactions,
dermatological reactions and elevation of liver enzyme
levels 10, 11. New intracranial tuberculoma or expansions of
older existing lesions require no change in antitubercular
treatment. Adjuent corticosteroid therapy will help to
reduce neurological symptoms. Today the use of
dexamethasone as an adjunct therapy for 4-8 weeks in CNS
tuberculosis is mostly accepted1. This is very effective.
Dexamethasone reduces the deleterious effect of the
immune response and reduces the incidence of
hydrocephalus and brain infarction1, 16. If there is no
response to the therapy within 8 weeks, a stereatactic
biopsy of the tuberculoma should be performed 15.
CONCLUSION
Early recognition and timely treatment of tuberculoma is
critical to prevent the considerable mortality and morbidity

associated with the condition. Mainly tuberculomas are

treated by chemotherapy with antitubercular drug, a
minimum of 10 months treatment is required. In severe
cases surgical excision of the tuberculoma can be
performed.
REFERENCE
1. Applied therapeutics The Clinical Use of Drugs. Ninth
edition Mary Anne Koda-Kimble,Lioyd Yee Young,
Page No: 61; 1-23
2. Pharmacotherapy, a pathophysiological approach, 7 th
edition by Joseph.T.Dipiro, Gray.C.Yer, page number:
1849, 1842-1843, 1847.
3. Pharmacology for health care professionals by
Christine M. Thorp page number 87, 60-61.
4. Robbins basic pathological basis of disease, by Kumar,
Abbas 8th edition, page number: 875.
5. Clinical pharmacy and therapeutics by Roger Walker,
Clive Edward,3rd Edition ,page number :584-590
6. Text book of pathology, Harsh Mohan, 5th edition,
page number: 154-165,901.
7. http//radiopadia.org/articles/cns-tuberculosis-1
8. Pharmacotherapy, a pathophysiological approach, 7 th
edition by Joseph.T.Dipiro, Gray.C.Yer, page number:
1849, 1842-1843, 1847.
9. Rang and Dales pharmacology, 7th edition, page
number: 634-635.
10. Introduction to clinical pharmacology, 7th edition by
Elsevier, page number: 175-179.
11. Essentials of concepts of altered health status by
Lippincott Williams, 2nd edition, page number: 313,
475 -478
12. Pharmacology and therapeutics for dentistry, sixth
edition by Yagiela, Dowd. Page no: 615
13. Goodman and Gilmans pharmaceutical basis of
therapeutics by Joel. G. Hardman, Lee E. Limbard 10
th
edition page no; 1273-1286
14. Park text book of preventive and social medicine by K.
Park,17th edition ,page no;138
15. http://tuberculosis/TB resourcesabouttuberculosis.html
16. http://www.medscape.com/viewarticle/558713_9
17. Text book of therapeutics ,drug and disease
management, Eighth edition ,Richard A. Helms, David
J. Quan, Eric T. Herfindal, page

Source of support: Nil; Conflict of interest: None declared

Current Research in Medicine and Medical Sciences 2014; 4(1): 7-8