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Year : 2020  |  Volume : 6  |  Issue : 2  |  Page : 75-80

MRS Showing a Singlet Peak at 3.8 ppm in Three Patients with CNS Tuberculomas

1 Department of Radiodiagnosis, Rama Medical College, Kanpur, Uttar Pradesh, India
2 Department of Ophthalmology, Rama Medical College, Kanpur, Uttar Pradesh, India
3 Sanjay Gandhi Postgraduate Institute, Lucknow, Uttar Pradesh, India
4 Parth Imaging Centre, Rajkot, Gujarat, India

Date of Submission22-May-2020
Date of Decision07-Jul-2020
Date of Acceptance22-Jul-2020
Date of Web Publication29-Aug-2020

Correspondence Address:
MD, DNB, Professor Rahul S Ranjan
Department of Radiodiagnosis, Rama Medical College, Mandhana, Kanpur, Uttar Pradesh 209217
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/mamcjms.mamcjms_47_20

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Tubercular involvement of central nervous system is one of the common extrapulmonary manifestations of tuberculosis. MRI brain plays an important role in diagnosis of CNS tuberculomas. Most of the articles on MR spectroscopy of CNS tuberculomas have mentioned presence of lipid peak within it. However, few recent studies have mentioned presence of singlet peak at 3.8 ppm corresponding to Guanidinoacetate as more specific finding in CNS tuberculoma. Here we present Magnetic Resonance spectroscopy MRS findings of singlet peak at 3.8 ppm in three confirmed cases of CNS tuberculomas with review of literature.

Keywords: Central nervous system, guanidinoacetate, lipid, spectroscopy, tuberculoma

How to cite this article:
Ranjan RS, Namrata, Singh A, Mody S. MRS Showing a Singlet Peak at 3.8 ppm in Three Patients with CNS Tuberculomas. MAMC J Med Sci 2020;6:75-80

How to cite this URL:
Ranjan RS, Namrata, Singh A, Mody S. MRS Showing a Singlet Peak at 3.8 ppm in Three Patients with CNS Tuberculomas. MAMC J Med Sci [serial online] 2020 [cited 2021 May 11];6:75-80. Available from: https://www.mamcjms.in/text.asp?2020/6/2/75/293888

Key message

Singlet peak at 3.8 ppm corresponding to Guanidinoacetate on MR spectroscopy can be helpful in detection of CNS tuberculomas and differentiation from other intracranial space-occupying lesions.

  Introduction Top

It is estimated that approximately one-third of the world’s population is infected with  Mycobacterium tuberculosis Scientific Name Search at causes tuberculosis (TB).[1] Central nervous system TB is a major health concern in developing countries and is increasing in developed countries because of human immunodeficiency virus/acquired immunodeficiency syndrome (HIV/AIDS) and multidrug-resistance.[1],[2] Intracranial inflammatory granulomas are a diagnostic challenge both to clinicians and radiologists. Magnetic resonance imaging (MRI) findings are usually non-specific and differentiation from malignant lesions can be difficult at times, particularly in the absence of TB in other parts of the body such as the lungs or lymph nodes. Magnetic resonance spectroscopy (MRS) provides additional biochemical information that can be useful. Elevated lipid peak has been seen in patients with tuberculomas and has been extensively discussed in the literature. However recent studies have found presence of singlet peak at 3.8 ppm corresponding to Guanidinoacetate as more specific marker of CNS tuberculoma on MRS.

  Case Report Top

A 27 year female presented to Neurology out patient department (OPD) with single episode of seizure. The patient was conscious, oriented and vital parameters were within normal limits. Neurological examination revealed normal muscle power in all the limbs and intact sensory system. Contrast MRI brain showed multiple small conglomerated ring-enhancing lesions in right fronto-parietal lobe displaying hyperintense core on T2 weighted images (WIs) and hypointense on T1WIs and fluid attenuated inversion recovery (FLAIR) and rim was isointense on FLAIR and hypointense on T2WIs [Figure 1]A. MRS at the site of lesions showed increased lipid peak, decreased N-acetylaspartate peak with increased Ch/Cr ratio (choline/creatine) . An additional peak was also noted at 3.8 ppm that was seen on both short TE (35 ms) [Figure 1]B and intermediate TE (144ms) [Figure 1]C spectroscopy sequences; though more prominent on short TE sequences that did not invert on intermediate TE sequences. Therefore, diagnosis of CNS tuberculomas was made. Additional peaks were also seen at 2.2 to 2.5 ppm (glutamine/glutamate peak), that were more prominent on short TE MRS. Patient responded to Anti-tubercular therapy with resolution of lesions in subsequent MRI at 3 month interval.
Figure 1 (A) Contrast MRI brain showing conglomerated ring enhancing lesions in the right fronto-parietal lobe (red arrow). Lesions showing peripheral T2 hypointense rim with central hyperintense area. (B) MR spectroscopy at short TE (35ms) showing lipid peak at 1.3 ppm (blue arrow), singlet Guanidinoacetate peak at 3.8 ppm (red arrow) and multiple Glutamine/Glutamate peak at 2.2 to 2.5 ppm (yellow arrow). (C) MR spectroscopy at intermediate TE (144ms) showing lipid peak at 1.3 ppm (blue arrow), inversion of lactate peak, singlet Guanidinoacetate peak at 3.8 ppm (red arrow) which is less prominent than at short TE MRS; however did not invert on intermediate TE and multiple Glutamine/Glutamate peak at 2.2 to 2.5 ppm (yellow arrow) which are less prominent than at short TE.

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A 37 year male presented with insidious onset weakness in right upper and lower limb since three weeks. On examination power in right upper and lower limb muscles was 3/5. Contrast MRI brain revealed single slightly incomplete, ring enhancing lesion in the left high parietal lobe in postcentral gyrus with perilesional edema [Figure 2]A. Lesion showed central T2 hyperintense area and peripheral T2 hypointense rim. MRS at low TE revealed elevated lipid peak with a singlet peak at 3.8 ppm [Figure 2]B. MRS at intermediate TE was not done in this case. Diagnosis of CNS tuberculoma was supported by positive cerebrospinal fluid PCR (polymerase chain reaction) for mycobacterium tuberculosis (another MRI differential being demyelination in view of incomplete rim enhancement) and patient was put on anti- tubercular treatment.
Figure 2 (A) Contrast MRI brain showing single slightly incomplete ring enhancing lesions in the left high parietal lobe in post-central gyrus (red arrow). Lesions showing peripheral T2 hypointense rim with central hyperintense area. (B) MBR spectroscopy at short TE (35ms) from lesion in left high parietal lobe showing lipid lactate peak at 1.3 ppm (blue arrow), singlet Guanidinoacetate peak at 3.8 ppm (red arrow) and multiple Glutamine/Glutamate peak at 2.2 to 2.5 ppm (yellow arrow).

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A 55 year female presented to neurology OPD with single episode of seizure. Contrast MRI brain revealed two ring enhancing lesions in right parietal lobe with perilesional edema showing central T2 hyperintense portion and peripheral hypointense rim [Figure 3]A. No restricted diffusion or susceptibility on Gradient sequences was seen. MR spectroscopy MRS at the site of lesions showed increased lipid peak, decreased N-acetylaspartate peak with increased Ch/Cr ratio. An additional peak was also noted at 3.8 ppm that was seen on both short [Figure 3]B and intermediate TE spectroscopy sequences; though more prominent on short TE sequences that did not invert on intermediate TE sequences. Additional peaks at 2.2 to 2.5 ppm were also seen on mainly short TE MRS. Therefore, diagnosis of CNS tuberculomas was made. Follow-up MRI at 4 month interval showed resolution of lesion and therefore, diagnosis of CNS tuberculoma was confirmed.
Figure 3 (A) Contrast MRI brain showing two closely abutting ring enhancing lesions in the right parietal lobe (red arrow). Lesions showing peripheral T2 hypointense rim with central hyperintense area. (B) MR spectroscopy at short TE (35ms) showing lipid peak at 1.3 ppm (blue arrow), singlet Guanidinoacetate peak at 3.8 ppm (red arrow) and multiple Glutamine/Glutamate peak at 2.2 to 2.5 ppm (yellow arrow).

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  Discussion Top

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.[3],[4] Tuberculoma is the second commonest manifestation of CNS tuberculosis after meningitis and constitutes a sizable proportion of intracranial space occupying lesions (SOL) in the developing countries. Tuberculoma of the brain is an important clinical entity.

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.[3] 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.[3],[5] CNS tuberculosis is a two-staged process. In the first stage, there are seedings of the tubercule bacilli forming “Rich foci” predominantly within the brain parenchyma following a hematogenous dissemination during primary or post-primary phase of the infection. After a quiescent period of about months or a few years, the second stage starts where either the bacilli or 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 an SOL known as tuberculoma. The tuberculoma is walled off from the brain parenchyma by a thick fibrous capsule.[3],[5]

The main challenge in the management of brain tuberculoma is its diagnosis. Appearance in computed tomography (CT) scan of brain is common to other infective/inflammatory granulomas 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 confident diagnosis of tuberculoma of the brain. With advancement of imaging techniques, MRI of the brain with MRS has shown a great hope in this context.

Conventional MRI brain is better than CT scan brain for diagnosis of tuberculomas, but the findings are not always specific for tuberculoma and are often difficult to differentiate between tuberculoma and NCC in a conventional MRI. A non caseating tuberculoma is hyperintense on T2 weighted and appears hypointense on T1 weighted images. But, a caseating tuberculoma is seen as iso to hypointense on both T1- and T2-weighted images, with an iso to hyperintense rim on T2-weighted images. On contrast image nodular or ring like enhancing lesions are seen. The diameter of these enhancing lesions usually ranges from 1 mm to 5 cm. The type of enhancement varies and may show complete ring, open rings, lobular patterns or may be irregular. Sometimes target lesions are found.[6],[7],[8],[9]

MRS 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 N-acetyl aspartate (NAA) and creatinine and a choline/creatinine ratio of >1. Lipid peak in MRS in the context of a ring-enhancing lesion is more specific for tuberculoma and has not been seen in any cases of NCC, the other common differential diagnosis of a ring enhancing lesion.[8],[12],[13],[14],[15],[16],[17],[18],[19] This is because of the fact that one of the characteristic features of mycobacterium is the presence of a lipid-rich cell wall that contributes to the lipid peaks in tuberculomas. Although in vivo spectroscopy is known to show only lipid in T2 hypointense tuberculoma, the lesion with variegated appearance shows Cho at 3.22 ppm along with lipid. As these lesions show a large amount of cellularity and minimal solid caseation, the cellular regions appear brighter on T1-weighted magnetization transfer (MT) imaging and show Cho peak on spectroscopy along with lipid. Predominance of cellularity in such variegated tuberculoma is responsible for prominent Cho peak and may cause difficulty in its differentiation from neoplastic lesions.[19],[20]

In a recent study by Morales et al.[21] spectroscopic peaks representing lipids and glutamate/glutamine (Glx) as well as a peak at 3.8 ppm were well defined in 77% (10/13), 77% (10/13) and 69% (nine of 13) cases of tuberculomas, respectively. In their study, Lipid and Glx (glutamine/glutamate) peaks were also present in most of the malignant lesions, 79% (15/19) and 74% (14/19) respectively; however, a singlet peak at 3.8 ppm was present in only 10% (two of 19) of the tumor cases. They found that a singlet peak at 3.8 ppm is present in the majority of tuberculomas and absent in most malignant tumors, can act as a useful marker to differentiate these lesions.

In their study, the peak at 3.8 ppm was present on both short- and long/intermediate-TE spectra (eight of nine cases with a well-defined peak at 3.8 ppm on short-echo MRS also demonstrated the peak on long-echo MRS). Similar findings were also seen in our cases in which singlet peak was more prominent at short TE spectroscopy, however were also seen on intermediate TE spectroscopy sequences and did not invert on it.

They attributed singlet peak at 3.8 ppm to Guanidinoacetate due to reasons as described here. Many metabolites also resonate at 3.8 ppm, such as: mannitol, serine, alanine, trehalose, guanidinoacetate (Gua), glucose (Glc), Glx complex and ethanolamine. None of their patients received mannitol by the time of MRS, so they excluded the presence of mannitol. Similarly none of our patients have received mannitol at time of MR imaging.

Serine has been identified at 3.7 to 3.9 ppm on ex-vivo/in vitro MRS of tuberculoma samples.[22] However, since serine and also alanine peaks invert on intermediate TE MRS (144 ms) because of spin-spin coupling (J-coupling) they were unlikely candidates in their sample. Similarly in our cases MRS at intermediate TE did not show inversion of peak at 3.8 ppm. The sugar alpha-trehalose, which forms part of the wall of some fungus, has been found on in vivo and ex vivo MRS samples of cryptoccocomas and has also been described in MRS of mucormycosis and other fungal abscesses.[23],[24],[25] Trehalose has not been found in ex-vivo samples of tuberculoma.[22] Glc and the complex Glx have been postulated as metabolites responsible for a peak at 3.8 ppm in prior studies of peri-tumoral edema.[26] This peak is usually a multiplet/broad resonance with an associated secondary peak at 3.4 ppm (consistent with Glc). They did not find a secondary peak at 3.4 ppm in their cases. Similar findings were also seen in our cases. A well-defined peak at 3.8 ppm has also been found in meningiomas and in pediatric brain tumors, particularly medulloblastoma.[27],[28] It has been assigned to Gua and postulated as a potential marker to differentiate meningiomas from high-grade tumors or hemangiopericytomas.[27],[28],[29],[30] Gua is not detected in normal brain.[31] It is the intermediate metabolite of Cr synthesis by the sequential action of arginine: glycine amidinotransferase (AGAT) and guanidinoacetate methyltransferase (GAMT).[32] A prominent peak of Gua (3.8 ppm) has been reported in patients with a GAMT deficiency.[31] Overall, the significance of Gua in individual tumor types is unknown. However, the most important observation is that peaks at 3.8 ppm are typically absent in high-grade gliomas or metastases.[21],[24],[27]Thus, its presence suggests a more specific marker of inflammatory reaction and supports the diagnosis of tuberculoma in the appropriate clinical setting.

We also found a peak at 2.2–2.5 ppm in three cases with tuberculomas that were well seen on short TE MRS and less prominent on intermediate TE MRS. Similar findings were also seen in study by Morales et al in which peak of Glx (glutamine/glutamate) at 2.2 to 2.5 ppm were seen in 77% cases with tuberculomas; however it was not specific for tuberculoma and were seen in 74% of malignant tumours/gliomas. The reasons for its presence are unclear. Some studies have suggested a relationship between cell damage and elevated Glx. [33] Glx peak has been shown to be elevated in meningiomas.[33],[29],[34] Finally, Glx is detected in more gliomas than controls, thus a rise of Glx peak may relate to a role of glutamate as an excitotoxin in accelerated cell proliferation of malignant brain tumors.[35] However, there are limitations in the role of presence of peak of guanidinoacetate at 3.8 ppm in diagnosis of CNS tuberculoma. Such peaks are also found in MR spectroscopy of few brain tumors. The studies on this subject are also limited to few case studies. Furthermore, quantitative values and different spectroscopy ratios of guanidinoacetate in relation to choline, NAA are still to be established. However its role in supporting the diagnosis of CNS tuberculoma will evolve over time as more research work needs to be done.

  Conclusion Top

MRS is useful in differentiating CNS tuberculomas from other infective/inflammatory granulomas, demyelination, gliomas and metastasis. Presence of lipid peak within it has been considered since long as differentiating feature of tuberculoma; however recent studies have demonstrated singlet peak at 3.8 ppm as another supportive feature of CNS tuberculomas which was also seen in our three cases.


We are thankful to Mr. Mohan Chandra, Medical Transcriptionist, Rama Medical College in helping to prepare the Manuscript.

Financial support and sponsorship


Conflicts on interest

There are no conflicts of interest.

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