Patients with inflammatory bowel disease (IBD) have been reported to have an increased risk of thromboembolism. Cerebral venous thrombosis (CVT) is a rare but serious extraintestinal manifestation of IBD. Due to its highly variable manifestation and low incidence, CVT is not usually readily recognized by physicians. Herein, we report a case of a 35-year-old male presenting with CVT associated with ulcerative colitis (UC). The patient was admitted with chief complaints of bloody diarrhea that had started 3 days prior. Sigmoidoscopy showed hyperemic and edematous mucosa, friability, and shallow ulcers from the sigmoid colon to the rectum suggestive of IBD. Three days later, the patient started complaining of a headache, and gradually developed a decreased level of consciousness. Magnetic resonance imaging of the brain revealed CVT with hemorrhagic infarctions. An angiogram was obtained to evaluate the extent of CVT, and anticoagulation therapy was initiated with intravenous heparin. During hospitalization, he was diagnosed with UC and treated with 5-aminosalicylic acid. After discharge, the patient was recovered without neurological deficit, and remission of UC was also obtained. The presence of headache or acute worsening of neurological status in a patient with IBD should alert the health professionals about the possibility of CVT.

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Patients with inflammatory bowel disease (IBD) have an elevated risk of venous thromboembolism compared with the general population. The most common sites of venous thromboembolism in IBD patients are the deep veins of the legs, the pulmonary system, and portal and mesenteric veins. However, cerebral venous thrombosis is rarely associated with IBD. This report describes a case of cerebral venous thrombosis in a patient with Crohn's disease. A 17-year-old girl, diagnosed 4 years earlier with Crohn's disease, presented with headache and vomiting. Magnetic resonance imaging of the brain with venography showed venous thrombosis in the cortical veins, superior sagittal sinus, right transverse sinus, and right internal jugular vein. The patient immediately started anticoagulation therapy with intravenous heparin infusion followed by daily oral rivaroxaban 10 mg. Follow-up imaging after 2 weeks showed resolution of the thrombosis, with recanalization of the cortical veins, superior sagittal sinus, right transverse sinus, and right internal jugular vein. She continued rivaroxaban therapy for 6 months, and remained well, without neurologic sequelae. A high level of concern for cerebral venous thrombosis may be important when treating active IBD patients, because anticoagulation treatment can prevent fatal complications.

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