Brain Tumor Res Treat.  2024 Jan;12(1):58-62. 10.14791/btrt.2023.0039.

Spontaneous Regression of Glioma–Mimicking Brainstem Lesion in a Child: A Case Report

• Kang SH
• Park HJ
• Hyun JW
• Gwak HS

• KMID: 2552339
• DOI: http://doi.org/10.14791/btrt.2023.0039

Abstract

Differential diagnosis of focal brainstem lesions detected on MRI is challenging, especially in young children. Formerly, brainstem gliomas were classified mainly based on MRI features and location. However, since 2016, the World Health Organization’s brainstem lesion classification requires tissue biopsy to reveal molecular characteristics. Although modern techniques of stereotactic or navigation-guided biopsy ensure accurate biopsy of the lesion with safety, biopsy of brainstem lesions is still generally not performed. Here, we report a focal brainstem lesion mimicking brainstem glioma in a 9-year-old girl. Initial MRI, MR spectroscopy, and 11 C-methionine positron emission tomography (PET) features suggested low-grade glioma or diffuse intrinsic pontine glioma. However, repeated MR spectroscopy, perfusion MRI, and 18 fluorodeoxyglucose PET findings suggested that it was more likely a non-tumorous lesion. As the patient presented not with a neurological manifestation but with precocious puberty, the attending oncologist chose to observe with regular follow-up MRI. The pontine lesion with high signal intensity on T2-weighted MRI regressed from the 6-month follow-up and became invisible on the 1.5-year follow-up MRI. We reviewed brainstem glioma–mimicking lesions in the literature and discussed the key points of differential diagnosis.

Keyword

Glioma; Brainstem; Diffuse intrinsic pontine glioma; Brainstem tumors; Case reports

Figure

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  Fig. 1 Initial MRI revealed an intra-axial T1 low-intensity (A) and T2 high-intensity (B) lesion with no enhancing lesion (C) at the upper pons. Diffusion-weighted imaging (D), magnetic resonance spectroscopy (E), and 11C-methionine positron emission tomography (F) findings showed a suspicion of glioma.

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  Fig. 2 Repeated neuroimaging study 1.5 months after the initial examination revealed no definite change in the T2 high-intensity lesion (A), neither an elevated choline peak nor a suppressed N-acetylaspartate peak on magnetic resonance spectroscopy (B), no hyperperfusion on perfusion MRI (C), and no hyper uptake on 18fluorodeoxyglucose positron emission tomography compared with normal brain parenchyma (D).

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  Fig. 3 Gradual regression of the T2 high-intensity lesion was noticed on the 6-month follow-up MRI (A). The lesion became invisible on the 1.5-year follow-up MRI (B) and remained regressed on the recent 6.5-year follow-up MRI (C).

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