Acute ring-enhancing change in a previously solidly enhancing meningioma.

Abstract

Background: Meningiomas are typically slow-growing, benign extra-axial tumours that exhibit stable radiological characteristics over long periods. Although peritumoural oedema and mass effect may develop gradually, acute structural changes with rapid neurological deterioration are unusual, particularly in World Health Organisation (WHO) grade I lesions. Ring enhancement is extremely rare and is often associated with necrosis, haemorrhage, or cyst formation.

Methods: We describe an adult patient with multiple right frontal meningiomas who had been followed radiologically for almost a decade. Serial MRI scans demonstrated stable tumour morphology and slow intermittent growth. Six weeks after her most recent surveillance MRI, she developed new focal neurological symptoms prompting urgent re-imaging and subsequent surgical intervention. Imaging findings and histopathology were reviewed in detail.

Results: A 72-year-old woman presented with an acute onset of left-sided tremor, weakness, and mild headache. MRI revealed that the largest meningioma, previously solidly enhancing without surrounding oedema, had developed new ring enhancement with marked vasogenic oedema and mass effect. Other incidental meningiomas were unchanged. Dexamethasone produced partial symptomatic improvement before surgical excision.Histopathology demonstrated a WHO grade I meningothelial meningioma with a broad central zone of infarction and viable tumour only at the periphery, without haemorrhage, cystic change, or brain invasion. No molecular evidence of atypia was identified, including a negative TERT promoter mutation and methylation profiling consistent with "Meningioma, Subclass Benign 1". The Ki-67 proliferation index was approximately 3%.

Conclusion: This case illustrates a rare presentation of acute ring enhancement and substantial peritumoural oedema in an otherwise benign meningioma without identifiable degenerative features. The updated histopathology indicates that spontaneous central infarction, rather than degenerative change or atypical biology, likely accounted for the abrupt radiological and clinical deterioration. Prompt recognition of new neurological symptoms in patients under long-term surveillance remains crucial, as rapid changes may reflect evolving tumour biology despite stable prior imaging.