Intracranial dermoid cyst rupture causing aseptic meningitis

Case presentation

A 65-year-old woman presented to the Emergency Department with an acute onset of severe, positional vertigo, nausea, vomiting and a non-pulsatile sensation of fullness in her right ear, without headache or fever. No history of head trauma was reported. Neurological examination revealed a persistent nystagmus on both right and left lateral gaze, which remained unchanged despite the performance of canalith repositioning maneuvers, further suggesting a central vestibular involvement, mandating urgent neuroimaging.

Initial non-contrast computed tomography (CT) (Figure 1) revealed a large, heterogeneous, low-attenuating mass [negative Hounsfield units (HU)] in the right temporal fossa, measuring approximately 4.5 cm × 3.8 cm × 3.2 cm, with scattered small fat-density components in subarachnoid spaces, suggesting a ruptured dermoid cyst. Subsequent magnetic resonance imaging (MRI) (Figure 2) confirmed the fat component of the lesion. It appeared hyperintense on T1-weighted, showed signal drop-out on fat-suppressed sequences and was markedly hypointense on T2*-weighted sequences due to chemical shift artifact and susceptibility effects at the fat-water interface. Small fat droplets exhibiting the same signal characteristics were widely dispersed throughout the prepontine, suprasellar, and Sylvian cisterns, as well as within the subarachnoid sulci of the right hemisphere. Post-contrast sequences showed dural enhancement and thickening around the droplets and mass, suggesting a reactive pachymeningeal inflammatory process.

Figure 1 Axial non-contrast CT (A-C) images show a large, heterogeneous, hypodense (negative HU) mass in the right temporal fossa (A: black arrow), with scattered small fat-density components in subarachnoid spaces (B,C: white arrowhead), suggesting a ruptured dermoid cyst. AR, area; CT, computed tomography; DS, standard deviation; HU, Hounsfield units; MED, mean value.

Figure 2 Axial MRI images demonstrated the presence of a hyperintense on T1-weighted (A: white arrow) lesion, markedly hypointense on T2*-weighted sequences (B: white arrow), with associated dural thickening and enhancement, consistent with pachymeningitis, nearby the main dermoid cyst (C: white arrowhead) and adjacent to the small fat droplets in the subarachnoid spaces (D: white arrowhead). MRI, magnetic resonance imaging.

Surgical exploration and subsequent histopathological examination confirmed the presence of lipid material and hair debris, with epidermal and dermal components. Since post-operative microbiological cultures and laboratory tests were negative for infectious agents, a sterile inflammatory process was confirmed, establishing the final diagnosis of a ruptured dermoid cyst with associated aseptic chemical meningitis.

However, long-term radiological follow-up is mandatory, because recurrence of the cyst could happen due to its congenital nature and typically slow growth rate.

All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Declaration of Helsinki and its subsequent amendments. Written informed consent was obtained from the patient for the publication of this article and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

Discussion

Intracranial dermoid cysts are benign, rare congenital tumors, more commonly affecting young women, usually located in posterior fossa or parasellar regions (1). These lesions arise from inclusion of ectodermal elements during embryonic neural tube closure, and contain both epidermal and dermal elements, such as hair follicles, sebaceous, and sweat glands (1-4).

They are typically asymptomatic, until they reach a considerable size causing mass effect or rupture. In case of rupture (traumatic or spontaneous), it can present with a variable range of symptoms, such as headaches, nausea/vomiting, signs of increased intracranial pressure, seizures, cranial nerve palsies and focal neurological signs (2-4). The acute vestibular syndrome of our case was atypical, likely determined by specific temporal location causing compression or meningeal irritation of adjacent vestibular structures. Imaging is fundamental for diagnosis, providing location, size, and confirming the fat content of the lesion. These lesions in CT usually appear as hypodense with negative HU, while in MRI images show hyperintensity on T1-weighted sequences and hypointensity on T2*-weighted sequences (1-4). Leaked droplets in subarachnoid spaces or ventricles, with the same signal characteristics, are a pathognomonic sign for rupture. These could ensue an aseptic chemical meningitis, that can manifest, like in our case, as a pachymeningeal enhancement and thickening adjacent to the lesions (2-4).

Main differential diagnoses are epidermoid cysts (lack dermal appendages) and teratomas (contain mature tissue from all three germ layers, midline/suprasellar/pineal regions) (1,3).

Management is regular surveillance or for symptomatic dermoid cysts surgical resection, to alleviate mass effect and prevent complications. Following rupture, extensive rinsing of the subarachnoid space is crucial to mitigate risks of obstructive hydrocephalus or meningitis (2,3).

This presentation of a ruptured dermoid cyst complicated by chemical meningitis manifesting as acute vestibular syndrome is atypical in literature and reinforces the diagnostic value of post-contrast MRI in revealing pachymeningeal irritation and underscores the need to include this rare entity in the differential diagnosis of central vestibular syndromes.

Acknowledgments

None.

Footnote

Funding: None.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://qims.amegroups.com/article/view/10.21037/qims-2026-1-0060/coif). C.A.M. serves as an unpaid editorial board member of Quantitative Imaging in Medicine and Surgery. The other authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Declaration of Helsinki and its subsequent amendments. Written informed consent was obtained from the patient for the publication of this article and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

References

1. Lakhani DA, Morris MO, Deng F. Intracranial Dermoid Cyst. Radiology 2024;311:e232952. [Crossref] [PubMed]
2. Sood A, Khandelwal S, Luharia A, Mishra GV. Ruptured intracranial dermoid cyst. BMJ Case Rep 2024;17:e262513. [Crossref] [PubMed]
3. Tudela Martínez JI, García Jiménez Á, Martínez García F, Alcaraz Pérez P, Contreras Espejo L, Velázquez Marín F. Teaching NeuroImage: Ruptured Intracranial Dermoid Cyst Presenting as Bilateral Tonic-Clonic Seizures in a Young Woman. Neurology 2025;105:e213915. [Crossref] [PubMed]
4. Tolebeyan AS, Kuruvilla DE. Headache in Ruptured Intracranial Dermoid Cysts. Curr Pain Headache Rep 2020;24:31. [Crossref] [PubMed]