Case Presentation:

A 24‐year‐old white man presented with a 1‐month history of progressively worsening headache and blurred vision. He also reported a 27‐kg weight loss and persistent diarrhea with hematochezia in the previous 6 months since his diagnosis of ulcerative colitis. Ulcerative colitis (UC) was refractory to therapy with corticosteroids and 6‐mercaptopurine (6‐MP). He appeared cachectic with temporal wasting, but otherwise had a normal physical examination. Laboratory study was remarkable for pancytopenia, which was likely related to 6‐MP. Given his severe headache, a noncontrast CT of the brain was performed with findings of increased density in Ihe region of The left Transverse sinus. A subsequent magnetic resonance venogram (MRV) confirmed a thrombosis in the left transverse sinus and the superior sagittal sinus. Anticoagulation with unfractionated heparin was administered with gradual improvement in the headache. Given the unusual location of the thrombosis, a thrombophilia workup was done, which was significant for a homozygous methylene tetrahydrofolate reductase (MTHFR) mutation with a mild hyperhomocysteinemia (homocysteine of 21 μmol/L). Hyperhomocysteinemia was treated with vitamin B6, vitamin B12, and folate.


Headaches are problems commonly encountered by internists. Most headaches are benign, but caution is warranted for IBD patients presenting with headaches. Cerebral venous thrombosis is a rare cause of headaches. Thromboembolisms in general occur up to 3‐ to 4‐fold higher among IBD patients with an even higher prevalence seen in UC compared to Crohn's disease (CD). Cerebrovascular thrombotic complications account for fewer than 10% of all thromboembolisms associated with IBD. and there have been fewer than 40 cases of cerebral venous thrombosis in UC reported in literature. The majority of thrombosis occurs in patients with active IBD, although it could also exist with the disease in remission. Coagulation abnormalities are also reported to be abnormal in about 30% of cases with cerebral thrombosis and IBD. Similar to our patient, hyperhomocysteinemia has been linked, but this genetic predisposition is not an independent risk factor for thromboembolism. Therapy for thromboembolism is anticoagulation, although clinicians must be cognizant of the increased risk of mucosal bleeding from UC lesions. Prompt recognition and treatment of cerebral venous thrombosis is important because its overall prognosis is dismal, with more than half suffering a major neurological complication or death.


Cerebral venous thrombosis is a rare complication in patients with ulcerative colitis. Hospitalists should be aware of this potentially fatal and disabling disorder and should have a lower Threshold for neuroimaging in IBD patients presenting with headaches.

Author Disclosure:

C. Kim, none.