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190]

Review A r tic le

Tuberculoma of the brain - A diagnostic dilemma:

Magnetic resonance spectroscopy a new ray of
hope
Subhasis Mukherjee, Departments of Pulmonary Medicine and 1Radiodiagnosis, College of Medicine and Sagar Dutta
Medical College and Hospital, Kamarhati, Kolkata, 2Department of Anatomy, North Bengal Medical
Runa Das1,
College and Hospital, Sushrutanagar, Siliguri, Darjeeling, West Bengal, India
Shabana Begum2
Address for correspondence:
Dr. Subhasis Mukherjee, 181/2B, Roypur Road, Kolkata ‑ 700 047, West Bengal, India.
E‑mail: drsubhasismukherjee@yahoo.in

Abstract
Tuberculoma of the brain is an important clinical entity. The main challenge in the management of brain tuberculoma is its diagnosis.
Appearance in computed tomography (CT) scan of brain is common and consists of solitary or multiple ring‑enhancing lesions
with moderate perilesional edema, but these are not specific for tuberculoma as neurocysticercosis (NCC), coccidiomycosis,
toxoplasmosis, metastasis and few other diseases may also have similar appearance on CT scan brain. Cerebrospinal fluid
examination is often normal and biopsy and tissue culture from the lesion though the diagnosis of choice is technically too
demanding and not feasible in most of the times. All these put the clinicians in a great dilemma as regard to a confidant
diagnosis of tuberculoma of the brain. With advancement of imaging techniques, magnetic resonance imaging (MRI) of brain
with magnetic resonance spectroscopy (MRS) has shown a great hope in this context as MRS shows a specific lipid peak
in cases of tuberculoma which is not seen in any other differential diagnoses of tuberculoma. This review article is written to
have an overview regarding the current diagnostic approach for brain tuberculoma with special emphasis on the role of MRS.
Extensive literature review of the articles published in English was conducted using Google search, Google Scholar, PubMed
and Medline using the keywords such as ring‑enhancing lesions, etiology, tuberculoma, NCC, CT scan brain, MRI, MRS, images.

Key words: Magnetic resonance spectroscopy, neurocysticercosis, ring‑enhancing lesion, tuberculoma

INTRODUCTION tuberculosis is still quite prevalent. The idea behind this

Overall, tuberculosis of the central nervous system (CNS)
accounts for approximately 1% of all of the diseases
caused by Mycobacterium tuberculosis, but it comprises 10–15%
of extrapulmonary tuberculosis.[1,2] Tuberculoma is the
second commonest manifestation of CNS tuberculosis
and constitutes a sizable proportion of intracranial space
occupying lesions (SOL) in the developing countries where
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DOI:
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review article is to have a clear understanding regarding
the diagnostic protocol of tuberculoma of the brain in
the present context as there has been a long prevailing
uncertainty and grey areas in the diagnosis of tuberculoma
of brain.
METHODS
Extensive literature review of the articles published in
English was conducted using Google search, Google
Scholar, PubMed and Medline using the keywords
such as ring‑enhancing lesions, etiology, tuberculoma,
neurocysticercosis (NCC), computed tomography (CT)
scan brain, magnetic resonance imaging (MRI), magnetic
resonance spectroscopy (MRS), images. Review articles,
original articles and case reports in this field that were
published in the English language were considered for this

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Mukherjee, et al.: MR spectroscopy in tuberculoma of the brain
review. In addition to the literature search using the internet,
textbooks both in the field of Pulmonary Medicine and
Radiology were also consulted.
Epidemiology and pathogenesis of tuberculoma of the brain
Tuberculoma has been defined as a mass of granulation
tissue made up of a conglomeration of microscopic
tubercles. The tuberculoma may be single or less commonly
multiple, and their sizes may vary from a few millimeters
to a diameter of 3–4 cm.[1]
The current understanding of the pathogenesis of CNS
tuberculosis remains largely unaltered for last 80 years
since the pioneering work by Arnold Rich and Howard
McCordock in 1933.[1,3] CNS tuberculosis is a two‑staged
process. In the first stage, there are seeding of the tubercule
bacilli forming “Rich foci” predominantly within the brain
parenchyma following a hematogenous dissemination
during primary or postprimary phase of the infection. After
a quiescent period of about months or a few years, the
second stage starts where either the bacilli and its antigenic
components are released into the subarachnoid space
causing tuberculous meningitis; or instead of rupturing
into the subarachnoid space, the intracranial tubercles may
enlarge within the brain parenchyma and give rise to a SOL
known as tuberculoma. The tuberculoma is walled off
from the brain parenchyma by a thick fibrous capsule.[1,3]
Clinical presentations
Unlike tubercular meningitis, which has a stormy
presentation, tuberculoma of the brain has an insidious
course, but sometimes both may co‑exist in the same
patient.[4] Tuberculomas may attain a considerable size
before producing symptoms. Clinical presentations are
not due to tubercule bacilli or its antigens but due to
pressure effects of SOL. Usual presentation is a single or
repeated episodes of focal seizures (60–100%), signs of
raised intracranial tension (56–93%) and focal neurological
deficits  (33–68%). [4] Exact nature, distribution and
frequency of the neurological manifestations will depend
on the site of the lesions, size of the lesions, number of
tuberculomas and their rate of increase in size. In adults,
supratentorial location is common for tuberculomas, but
in children infratentorial the location is commoner.[2,5] The
symptoms are due to increased intracranial pressure and are
common for all intracranial SOL. In the developing world,
tuberculoma accounts for around 20–30% of SOL in the
brain and in the pediatric population, the percentage may
even be higher.[4]
Diagnostic approach
The conventional diagnostic principle can broadly be
divided into:
• Search for tuberculosis elsewhere in the body
The Journal of Association of Chest Physicians| Jan-Jun 2015 | Vol 3 | Issue 1
• M e t i c u l o u s s e a r ch f o r a n y p e r i p h e r a l
lymphadenopathy
• Chest X‑ray to look for any evidence of pulmonary
tuberculosis, military mottlings, mediastinal
lymphadenopathy or pleural effusion
• Sputum for Ziehl‑Neelsen staining
• Ultrasound of the abdomen to look for any
hepatosplenomegaly or the intra‑abdominal
lymphadenopathy.
If one or more of the above are found to be positive, these
can be taken as a surrogate evidence favoring a diagnosis
of intracranial tuberculoma.
• Neuroimaging
In developing countries like India, single enhancing lesion
in CT brain has been found to be the commonest lesion
in children and young adults with focal seizures.[6‑8] The
etiology of these lesions also differ from the western
counterparts with infective causes like NCC and
tuberculoma being the commonest etiologies in India.
It often becomes difficult to differentiate between
tuberculoma and NCC because both the diseases are
prevalent and share common clinic‑radiological features.[8]
Different modalities of brain imaging are the cornerstones
for a diagnosis of intracranial tuberculomas, these are also
very useful to assess the extent of the lesions. But, the
conventional imaging’s like CT scan and MRI of brain have
got definite limitations in regard to a specific and confidant
diagnosis of tuberculoma as the findings are not specific to
tuberculoma and can be found in certain other conditions
mimicking tuberculoma, especially NCC.[9,10]
• Computed tomography scan of the brain
Computed tomography scan appearances may vary
according to the stages of the disease. Noncontrast CT
scan of the brain may be normal or may show irregular
hypodense lesion due to cerebritis during the early stage
of the disease. With the development of inflammatory
granuloma and central caseation, lesion appears hypodense
or less commonly isodense with an irregular outline on
noncontrast CT brain which enhances and shows a ring
like an appearance with contrast. Sometimes, calcifications
and target lesions are found. The lesions are usually larger
than 20 mm, but sizes may vary from 1 to 6 cm. Lesions are
commonly solitary, but multiple lesions are not infrequent.
These are surrounded by considerable amount of vasogenic
edema that frequently produces mass effect and midline
shift.[4,9,11‑16] In the Indian scenario, a single ring‑enhancing
lesion in CT scan of brain has been found to be the
commonest radiological finding in a young adult with a new
4
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Mukherjee, et al.: MR spectroscopy in tuberculoma of the brain

onset partial seizure, and the two most common etiologies
are NCC followed by tuberculoma.[8,9]
Neurocysticercosis on the other hand classically presents
with multiple, small (<20 mm) lesion with ring‑enhancement,
presence of eccentric nodules, moderate vasogenic edema
that usually does not result in midline shift.[4,12,13,16,17]
So, although CT scan of brain is primary investigation
of choice and is very sensitive (100%) in detecting
ring‑enhancing lesions, it lacks specificity and has got a
pretty low negative predictive value (31%).[11,18] This clearly
emphasizes the limitation of CT scan of the brain with
contrast as the sole diagnostic modality of intracranial
tuberculoma.

Though, lesions with size >20 mm, irregular outline and • Magnetic resonance imaging
midline shift in CT brain has been proposed to favor
a diagnosis of tuberculoma by some authors,[4,17] these Conventional MRI brain is better than CT scan brain
descriptions are not mutually very exclusive or specific for for anatomical delineation, but the findings are not
neither of the two conditions.[5,9] Moreover, pyogenic brain always specific for tuberculoma and are often difficult
abscess, brain tumors (metastasis or primary), lymphoma, to differentiate between tuberculoma and NCC in a
toxoplasmosis and cryptococcosis in immunocompromised conventional MRI. A non caseating tuberculoma is
subjects can also give rise to similar findings on CT scan hyperintense on T2‑weighted and but appears hypointense
of brain [Tables 1 and 2].[4,10,17] on T1‑weighted images. But a caseating tuberculoma is seen
as iso‑to hypointense on both T1‑ and T2‑weighted images,
Table 1: Spectrum of differential diagnoses of with an iso‑to hyperintense rim on T2‑weighted images.
single ring‑enhancing lesion in CT Brain On contrast image nodular or ring‑like enhancing lesions
Solitary ring‑enhancing lesion in CT Brain
are seen. The diameter of these enhancing lesions usually
Common
ranges from 1 mm to 5 cm. The types of enhancement
Neurocysticercosis varies and may show complete ring, open rings, lobular
Tuberculoma patterns or may be irregular. Sometimes target lesions are
Less common found.[11‑14,16,17]
Pyogenic abscess
Glioma
Metastasis In the case of NCC, the appearance depends on the stage
Lymphoma of the lesion. The wall of the cysticercus granuloma
Toxoplasmosis (in immunocompromised host) (a colloid cyst stage) becomes thick and hypointense,
Cryptococcosis (in immunocompromised host)
Sarcoidosis
and there is mild to moderate perilesional edema on T2
Larva migrans image. Cysticercus granuloma also enhances and shows a
Cryptic AVM ring pattern after administration of contrast. Usually, the
CT: Computed tomography, AVM: Arteriovenous malformation lesions are <20 mm in diameter. Calcified eccentric scolex
if seen can be diagnostic of NCC in MRI. The lesions
Table 2: Spectrum of differential diagnoses of
are often multiple and most often do not have extensive
multiple ring‑enhancing lesion in CT Brain edema.[12,13,16,17,19]
Multiple ring‑enhancing lesions in CT Brain
• Molecular tests‑molecular tests like polymerase chain
Infective reaction based studies are very sensitive but cannot
Neurocysticercosis
Tuberculoma and tubercular abscess differentiate between infection and disease and also
Pyogenic abscess lack specificity and currently are not recommended
Syphilis as a diagnostic tool.
Nocardiocis
• Brain biopsy‑although histopathology accompanied by
Toxoplasmosis
Cryptococcosis tissue culture should be the gold standard for diagnosis,
Neoplasms it is not always feasible especially in the developing
Metastasis countries with limited resources.[17]
Primary brain tumors
Primary CNS lymphoma
Inflammatory and demyelinating diseases Newer imaging modalities for the diagnosis of tuberculoma
Sarcoidosis • Magnetic resonance spectroscopy
SLE Magnetic resonance spectroscopy of brain is a new
Neuro‑Behcet’s disease
and smart technique that measures the concentration
Whipple’s disease
Multiple sclerosis of several biochemical compounds in the brain
Acute disseminated encephalomyelitis in health and various disease states. In contrast to
CT: Computed tomography, CNS: Central nervous system, SLE: Systemic lupus conventional MRI showing images, MRS demonstrates
erythematosus
spectra of resonances. The area under each peak in the

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Mukherjee, et al.: MR spectroscopy in tuberculoma of the brain

spectrum actually reflects relative concentrations of

that particular metabolite and is expressed in unit parts
per million.[20,21] Historically, first MRS of biological
tissues dates back to 1970s when Moon and Richards
used Phosphorous‑31 (P‑31) to examine red blood cells
and  same P-31 was applied to excised leg muscle from
rat by Hoult and his group.[20,21]

In modern day, proton MRS is perfor med most

commonly using 1 H as it is easy to perform and
shows better spectra compared to sodium (23Na) and
phosphorous (31P). MRS can be done within 10–15 min
and can easily be supplemented with conventional MRI
brain.[20,21] MRS has been found very useful in an array
of diseases like brain tumor, infections, ring‑enhancing Figure 1: Normal magnetic resonance spectroscopy of brain showing
lesions, abscesses, metabolic disorders, epilepsy and that N-acetylaspartate peak is highest, and there is no lipid or lactate
neurodegenerative disorders as MRS usually shows peak
different characteristic spectral peak in different
conditions.[20,21] However, MRS interpretation is best
when its result is analyzed in the context of clinical
and MRI data.

Magnetic resonance spectroscopy of normal brain

shows predominant peaks of N‑acetylaspartate (NAA),
choline, creatinine and myo‑inositol with the highest peak
being NAA. NAA is a healthy neuronal marker, choline
represents energy store and choline is a marker of cellular
turnover [Figure 1].[20,21]

Magnetic resonance spectroscopy is of great value in

the diagnosis of tuberculoma in cases of ring‑enhancing
lesions on CT scan or MRI imaging. It demonstrates a
very high lipid peak, reduction in NAA and creatinine
Figure 2: The magnetic resonance spectroscopy brain in the case of
and a choline/creatinine ratio of  >1 [Figure 2]. Lipid peak tuberculoma showing grossly diminished N-acetylaspartate peak and
in MRS in the context of a ring‑enhancing lesion is very a distinct lipid peak
much specific for tuberculoma and has not been seen in
any cases of NCC, the other common differential diagnosis
of a ring‑enhancing lesion.[8,13,22‑27] NCC demonstrates
a high lactate and proteins like alanine, succinate,
glutamate, glycine levels with some reduction of NAA
and creatinine [Figure 3].[28] A high choline peak is seen
in MRS in case of tumors, primary or secondary, because
of very high cellular turnover. MRS can also differentiate
tuberculoma or tuberculous brain abscess from pyogenic
brain abscess by the presence of elevated levels of amino
acid peaks in pyogenic brain abscess.[29]

• Other newer and advanced MRI techniques like

diffusion‑weighted MRI, magnetization transfer ratio
and three‑dimensional constructive interference in
steady state are also being studied and have shown
encouraging results in the diagnosis of tuberculoma
and tuberculous brain abscess.[24,29]
Figure 3: The magnetic resonance spectroscopy brain in the case of
neurocysticercosis showing moderately diminished N-acetylaspartate
and presence of a lactate peak but absence of a lipid peak

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Mukherjee, et al.: MR spectroscopy in tuberculoma of the brain

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Flow Chart 1: Diagnostic algorithm for a solitary ring-enhancing lesion in computed tomography brain

CONCLUSION tuberculosis outside the brain and use of newer imaging

Conventional neuroimaging like CT scan of the brain
with contrast and MRI brain ± contrast alone are
insufficient diagnostic tool for a confidant etiological
diagnosis of intracranial ring‑enhancing lesions like
tuberculoma. In patients with focal seizures with solitary
or multiple ring‑enhancing lesions in CT or MRI brain,
MRS of the brain should be done in all cases to look for
the characteristic lipid peak to confirm a diagnosis of
tuberculoma. Evidence of tuberculosis elsewhere in the
body should also be searched for in all these cases as these
can also support the diagnosis of intracranial tuberculoma.
Integration of a good clinical insight, thorough search for
techniques like MRS is the key to overcome the prevailing
diagnostic dilemma in cases of tuberculoma of the
brain [Flow chart 1].
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How to cite this article: Mukherjee S, Das R, Begum S. Tuberculoma
of the brain - A diagnostic dilemma: Magnetic resonance spectroscopy
a new ray of hope. J Assoc Chest Physicians 2015;3:3-8.
Source of Support: Nil, Conflict of Interest: Nil.

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