AUTHOR=He Xingchen , Lin Yijia , Chen Jing , Wu Xinyi , Lv Jindan , Liu Heng , Wang Xue , Li Min , Zhong Tianyu , Zhang Yanhong , Weng Xuliang TITLE=Reversible splenial lesion syndrome associated with Graves’ disease and hepatic dysfunction: a case report JOURNAL=Frontiers in Neuroscience VOLUME=Volume 19 - 2025 YEAR=2025 URL=https://www.frontiersin.org/journals/neuroscience/articles/10.3389/fnins.2025.1691469 DOI=10.3389/fnins.2025.1691469 ISSN=1662-453X ABSTRACT=BackgroundReversible splenial lesion syndrome (RESLES) has been confirmed to induce severe psychiatric symptoms. This syndrome is a rare clinical condition with an etiology that remains unclear. According to current literature, the primary cause of RESLES may be associated with cytotoxic cerebral edema. First reported in 1999, reversible splenial syndrome may be triggered by bacterial or viral infections, epileptic seizures, metabolic disorders, hyperosmolar cerebral edema, and other factors. In this study, we report the case of RESLES in a patient with Graves’ disease and liver dysfunction.Case presentationThe patient was a 17-year-old female adolescent with persistent headaches, dizziness, and nausea with vomiting. Magnetic resonance imaging (MRI) suggested RESLES as the diagnosis. On admission, the patient presented with elevated free triiodothyronine (FT3) and free thyroxine (FT4), low thyroid-stimulating hormone (TSH), and positive thyroid-receptor antibodies (TRAb), meeting the diagnostic criteria for Graves’ disease. Concurrently, the levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were also elevated. After hormone therapy, the patient’s symptoms resolved, and imaging results returned to normal.ConclusionThis study presents a case of a patient with RESLES characterized by Graves’ disease and liver function abnormalities, who was sensitive to anti-thyroid drug (methimazole) and hormone therapy (methylprednisolone sodium succinate) and had a favorable prognosis. This study contributed to expanding the clinical understanding of RESLES and suggests that, in clinical practice, autoimmune hyperthyroidism may be a novel trigger for RESLES, while concurrent liver dysfunction in this context requires further investigation.