Solitary calcified neurocysticercosis with leptomeningeal enhancement mimicking tuberculous meningitis: MR spectroscopy as a diagnostic adjunct

Case description

A previously healthy 9-year-old girl presented with three generalized tonic-clonic seizures following minor head trauma. She was afebrile and hemodynamically stable with transient Todd’s paresis. Admission weight was 21.6 kg (<3rd percentile, WHO standards). Brain CT demonstrated a calcified right temporal lesion without hemorrhage or midline shift.

MRI (1.5 Tesla) revealed a solitary 11 × 10 mm calcified ring-enhancing lesion in the right temporal lobe with marked perilesional edema. Diffuse bilateral sulcal and basal cisternal enhancement was also present, classically described in tuberculous meningitis [1] (Fig. 1A, B). History was non-contributory for tuberculosis exposure; reassessment revealed no meningeal signs or cranial nerve deficits, remaining discordant with the MRI pattern.

Fig. 1.

Baseline neuroimaging and MR spectroscopy. (A) Axial FLAIR MRI demonstrating a right temporal calcified lesion (open arrow) with prominent perilesional edema (solid arrow). (B) Axial post-contrast T1-weighted MRI showing ring enhancement of the lesion (black arrow) and diffuse bilateral cerebral convexity sulcal and leptomeningeal enhancement (white arrows), closely mimicking tuberculous meningitis. (C) MR spectroscopy (TE 30 ms; intermediate TE 135 ms also acquired for lactate confirmation by phase reversal) demonstrating an acetate peak at 1.92 ppm and a lactate doublet at 1.33 ppm, with absent lipid peak and normal choline/creatine ratio, favoring NCC over tuberculoma.

Lumbar puncture was unremarkable: protein 17 mg/dL, glucose 73 mg/dL, 4 cells/mm³ (100% lymphocytes). Xpert MTB/RIF Ultra, adenosine deaminase, Gram stain, bacterial cultures, and viral PCR were negative. Serum and CSF NCC IgG ELISA were both negative – reduced sensitivity in calcified neurocysticercosis (NCC) is well recognized [2]. The combination of extensive leptomeningeal enhancement with a normal CSF profile was atypical for infective meningitis (Table 1).

Table 1.

Sensitivity of cerebrospinal fluid diagnostic tests for tuberculous meningitis ^a.

Diagnostic Test	Sensitivity
CSF – AFB Smear Microscopyb	10–20%
CSF – Xpert MTB/RIF Ultra	89.4%
CSF – M. tuberculosis Culture	50–70%
CSF Adenosine Deaminasec	89%

^a Data adapted from Ssebambulidde et al. (Reference 5).

^b Sensitivity improves to approximately 52% with CSF volumes > 6 mL and extended microscopy time.

^c Pooled estimate from meta-analysis; interpretation limited by variable cut-off thresholds and overlap with other meningitis types.

AFB = acid-fast bacilli; CSF = cerebrospinal fluid.

MR spectroscopy (MRS) was performed with mycobacterial cultures pending. Multivoxel spectra (voxel size 10 ×10 ×15 mm; TE 30 and 135 ms) demonstrated a clear acetate peak at 1.92 ppm and a lactate doublet at 1.33 ppm, interpreted by an experienced neuroradiologist. A dominant lipid peak and elevated choline/creatine ratio – more characteristic of tuberculoma – were absent [3] (Fig. 1C). This metabolic profile favored NCC over tuberculoma and substantially influenced clinical management (Table 2).

Table 2.

Characteristic MR spectroscopy profiles in neurocysticercosis and tuberculoma^#.

Metabolite	Peak (ppm)	NCC	Tuberculoma
Acetatea	1.92	May be present	Usually absent
Lactateb	1.33	May be present	May be present
Lipidc	0.9–1.3	Usually absent	Often prominent
Cho/Crd	3.2 / 3.0	Usually not elevated	May be elevated
NAAe	2.0	Reduced or near-normal	Markedly reduced
Succinatef	∼2.4	Variable	Usually absent

Metabolite patterns may overlap across lesion stages; interpretation must integrate clinical context and conventional MRI findings.

^# Data adapted from Pretell et al.^⁶ and Maheshwarappa et al.^⁷

^a Acetate reflects anaerobic parasitic metabolism and is the key discriminating peak favoring NCC over tuberculoma.

^b Lactate is non-specific and may be present in both entities; supportive only in context of the overall spectral pattern.

^c A dominant lipid peak reflects caseous necrosis; its prominence in tuberculoma is the principal MRS distinguishing feature and was absent in this case.

^d Cho/Cr represents the ratio of choline (3.2 ppm) to creatine (3.0 ppm); elevated ratio reflects high cellular membrane turnover in active tuberculoma.

^e NAA reflects neuronal integrity; may be reduced in active perilesional inflammation and can recover following resolution of edema and treatment.

^f Succinate may be variably present in viable or degenerating NCC lesions; absence is consistent with calcified-stage disease and does not exclude NCC.

Cho/Cr = choline/creatine ratio; MRS = magnetic resonance spectroscopy; NAA = N-acetylaspartate; NCC = neurocysticercosis; ppm = parts per million.

Fundoscopy excluded ocular cysticercosis [4]. Levetiracetam was initiated for seizure control. Despite calcification, ongoing inflammatory activity was evidenced by ring enhancement, perilesional edema, leptomeningeal enhancement, and MRS metabolic activity. Corticosteroids followed by albendazole (15 mg/kg/day for 21 days) were given [4]. CSF mycobacterial culture returned negative for Mycobacterium tuberculosis.

Follow-up MRI at two months showed near-complete resolution of ring enhancement, perilesional edema, and leptomeningeal enhancement (Figs. 2D, 2E). Repeat MRS demonstrated complete disappearance of the acetate peak with near-resolution of lactate (Fig. 2F). The child remained seizure-free at 18-month follow-up with no neurological sequelae.

Fig. 2.

Follow-up imaging after therapy. (D) Axial FLAIR MRI showing a residual calcified focus (open arrow) with near-complete resolution of perilesional edema (solid arrow). (E) Axial post-contrast T1-weighted MRI demonstrating near-total resolution of ring enhancement (black arrow) and near-complete resolution of bilateral leptomeningeal enhancement (white arrows). (F) Follow-up MR spectroscopy demonstrating complete resolution of the acetate peak and near-complete resolution of the lactate peak, consistent with resolution of previously observed metabolic signature.

This case demonstrates that a solitary calcified NCC lesion may produce diffuse leptomeningeal enhancement closely resembling TBM despite a normal CSF profile and absence of clinical meningitis. Leptomeningeal enhancement should therefore be interpreted alongside clinical and CSF findings rather than in isolation. When conventional investigations remain inconclusive, MRS may provide valuable metabolic information to support differential diagnosis and avoid unnecessary empirical antitubercular therapy.

Ethics declaration

Written informed consent to take part in the study and to publish the article has been obtained from all participants or their legal representatives. The privacy rights of participants have been observed.

This study was performed in compliance with relevant laws, regulatory frameworks and guidelines where the research took place. Ethics committee approval was not required under relevant laws and institutional guidelines. Ethics committee approval was not required for this anonymized single-patient case report in accordance with the institutional policy of Daya General Hospital, Thrissur, India. All patient information has been anonymized.

This research follows the CARE guidelines and the CARE checklist.

CRediT authorship contribution statement

K Rajagopalan: Investigation, Supervision. G Shyamnath: Formal analysis. Khan Rahman: Writing – review & editing, Writing – original draft, Conceptualization.

Declaration of Generative AI and AI-assisted technologies in the writing process

During the preparation of this work the authors used AI-assisted tools to support language polishing and grammatical correction. The authors reviewed and edited the content as needed and take full responsibility for the content of the published article.

Institution

Daya General Hospital and Surgical Speciality Centre, Thrissur, is accredited by the Joint Commission International (JCI) and the National Accreditation Board for Hospitals and Healthcare Providers (NABH).

Funding

This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.

Declaration of Competing Interest

All authors listed below have reviewed and completed this declaration. In accordance with Elsevier’s competing interests policy, authors must disclose any financial and personal relationships with other people or organizations that could inappropriately influence or bias their work.

Data Availability

All relevant data supporting the findings of this report are included within the article. Additional details are available from the corresponding author upon reasonable request while maintaining patient confidentiality.