Evidence map›Paper›PMID 41357835›Full record

ArticleFrontiers in neuroscience2025

Reversible splenial lesion syndrome associated with Graves' disease and hepatic dysfunction: a case report.

Xingchen He, Yijia Lin, Jing Chen, Xinyi Wu, Jindan Lv, Heng Liu, Xue Wang, Min Li, Tianyu Zhong, Yanhong Zhang and 1 more

Abstract readCase Reports
In one paragraph

Article in Frontiers in neuroscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

11 authors.

Xingchen HeDepartment of Neurology, The Affiliated Guangzhou Hospital of TCM of Guangzhou University of Chinese Medicine, Guangzhou, China.
Yijia LinDepartment of Neurology, The Affiliated Guangzhou Hospital of TCM of Guangzhou University of Chinese Medicine, Guangzhou, China.
Jing ChenDepartment of Neurology, The Affiliated Guangzhou Hospital of TCM of Guangzhou University of Chinese Medicine, Guangzhou, China.
Xinyi WuDepartment of Neurology, The Affiliated Guangzhou Hospital of TCM of Guangzhou University of Chinese Medicine, Guangzhou, China.
Jindan LvDepartment of Neurology, The Affiliated Guangzhou Hospital of TCM of Guangzhou University of Chinese Medicine, Guangzhou, China.
Heng LiuDepartment of Neurology, The Affiliated Guangzhou Hospital of TCM of Guangzhou University of Chinese Medicine, Guangzhou, China.
Xue WangDepartment of Neurology, The Affiliated Guangzhou Hospital of TCM of Guangzhou University of Chinese Medicine, Guangzhou, China.
Min LiSleep Research Institute of Traditional Chinese Medicine, Guangzhou Medical University, Guangzhou, China.
Tianyu ZhongDepartment of Neurology, The Affiliated Guangzhou Hospital of TCM of Guangzhou University of Chinese Medicine, Guangzhou, China.
Yanhong ZhangDepartment of Neurology, The Affiliated Guangzhou Hospital of TCM of Guangzhou University of Chinese Medicine, Guangzhou, China.
Xuliang WengDepartment of Neurology, The Affiliated Guangzhou Hospital of TCM of Guangzhou University of Chinese Medicine, Guangzhou, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Reversible 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 presentation: The 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. Conclusion: This 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.

Indexed as

case reportcytotoxic edemaGraves’ diseaseliver dysfunctionreversible splenial lesion syndrome

Identifiers

PMID41357835
PMCPMC12675446

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