Presumed Hippocampal Endometriosis Presenting as Catamenial Epilepsy: Diagnostic Challenges, MRI Follow-Up, and Comparative Review of Reported Cerebral Endometriosis Case

Mihaela Camelia Tîrnovanu, Ștefan-Dragoș Tîrnovanu, Elena Cojocaru, M Holicov, Vlad Constantin Donica, Roxana Covali, Awad Dmour, Norina Consuela Forna, Paul-Dan Sîrbu, Alin Ciubotaru
In: Journal of Clinical Medicine · 2026 · vol. 15(18) , pp. 7062 · doi:10.3390/jcm15187062 · W7212310961
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A 48-year-old woman with catamenial epilepsy and a right hippocampal lesion, lacking pelvic endometriosis symptoms, experienced complete neurological resolution and MRI regression following progestin therapy, supporting conservative management of presumed cerebral endometriosis.

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Abstract

Background: Cerebral endometriosis is an exceptionally rare manifestation of extrapelvic endometriosis and remains a diagnostic challenge because its clinical and imaging features may mimic more common neurological, inflammatory, vascular, or neoplastic disorders. Catamenial neurological symptoms may provide an important diagnostic clue, but histological confirmation is rarely available. Case presentation: We report the case of a 48-year-old woman with epilepsy beginning at 41 years of age, associated with short-term memory loss and a catamenial pattern of seizures. She had no typical symptoms of pelvic endometriosis, including dysmenorrhea, dyspareunia, or cyclic pelvic pain. Neuropsychological test for memory had normal scores. Brain magnetic resonance imaging (MRI) revealed a right hippocampal lesion with T2/FLAIR hyperintensity and later pseudonodular contrast enhancement, raising suspicion of focal cortical dysplasia, infection, tumor infiltration, or a hippocampal tumor. Magnetic resonance spectroscopy (MRS) was inconclusive and did not provide clear support for tumor-like infiltration. Because of the temporal association between symptoms and menstruation, cerebral endometriosis was considered. The patient received hormonal therapy with progestins, including desogestrel and dienogest, after which antiepileptic therapy was discontinued. Neurological symptoms resolved completely. Follow-up MRI demonstrated marked regression or disappearance of the previously described right hippocampal hyperintense lesion, with preserved bilateral hippocampal morphology. Conclusions: This case highlights the importance of considering cerebral endometriosis in women of reproductive or perimenopausal age presenting with catamenial epilepsy and unexplained intracranial lesions, even in the absence of pelvic endometriosis symptoms. Recognition of menstrual cyclicity, careful neuroimaging follow-up, and multidisciplinary evaluation may support diagnosis and guide individualized treatment. The favorable clinical and radiological response to progestin therapy in this case adds to the limited evidence regarding conservative management of presumed cerebral endometriosis. Cerebral endometriosis is a very rare condition, and only eight case reports were found in the literature.

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