Benign gynecologic tumor, such as uterine adenomyosis, has been suggested to develop hypercoagulability. Although some cases of cerebral infarction associated with adenomyosis have been reported, the mechanism of hypercoagulation initiated by adenomyosis is still not clear, and the therapeutic strategy is uncertain. A 44-year-old woman was presented to our department with headache, left hand weakness, and gait disturbance during her menstrual phase. She had a history of adenomyosis and infertility treatment for 18 years and heavy menstrual bleeding. Magnetic resonance imaging on admission showed multiple hyperintense lesions in cortical and subcortical areas in the cerebrum and cerebellum on diffusion-weighted imaging. Transesophageal echocardiography showed neither embolic sources nor existence of foramen ovale. Her laboratory data revealed anemia, a high D-dimer level, and elevated levels of a mucinous tumor marker. She had adenomyosis and no malignancy was detected. Anticoagulation therapy with intravenous heparin followed by rivaroxaban did not prevent recurrence of cerebral infarction. We discontinued rivaroxaban, and started warfarin therapy with pseudomenopause treatment, which prevented recurrence for 6 months. Five months after her last pseudomenopause treatment, multiple cerebral infarctions occurred. Total hysterectomy was performed, which prevented recurrence of the multiple cerebral infarctions for 2 years without anticoagulation therapy. Our findings reveal for the first time that anticoagulation therapy, including novel oral anticoagulants, had no preventive effect against cerebral infarctions associated with adenomyosis in a middle-aged woman. Although pseudomenopause treatment temporarily prevented recurrence, resection of the adenomyosis might be the most effective therapy in these cases.

This study aimed to explore whether cerebrospinal fluid (CSF) levels of matrix metalloproteinases (MMPs), and their inhibitors (TIMPs) were associated with brain amyloid deposition, cortical glucose metabolism, and white matter lesions (WMLs) in individuals with amnestic mild cognitive impairment (MCI). A total of 33 individuals with amnestic MCI (mean age, 75.6 years) underwent ¹¹C-Pittsburgh compound B positron emission tomography (PiB-PET), ¹⁸F-fluorodeoxyglucose positron emission tomography, magnetic resonance imaging or computed tomography, and CSF analysis. PET uptake of the frontal and temporoparietal lobes and posterior cingulate gyrus was assessed using the cerebellar cortex as the reference region. WMLs were assessed by the Fazekas scale. CSF levels of MMPs and TIMPs were measured with bead-based multiplex assays. After adjusting for covariates, multiple linear regression analysis showed that CSF levels of MMP-2 were negatively correlated with global PiB uptake (p = 0.035), especially in the parietotemporal lobe and posterior cingulate gyrus (p = 0.016 and p = 0.041, respectively). Moreover, CSF levels of MMP-7 were positively correlated with the severity of WMLs (p = 0.033). CSF levels of MMP-2 and MMP-7 are associated with brain amyloid deposition and severity of WMLs, respectively. These findings provide valuable insights into the role of MMPs in amyloid β catabolism and blood–brain barrier integration at the MCI stage.