A case of cavernous sinus thrombosis complicated by meningitis.
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A case of cerebral venous thrombosis caused by undiagnosed homocystinuria is reported. The pitfalls regarding the diagnosis of a potentially medically treatable condition are discussed. Cerebral venous thrombosis in children has a variable type of onset and a multiplicity of causes. This type of pathology, although not frequent, is more common than previously thought. Among the different etiologies, undiagnosed homocystinuria is not routinely considered. We report a case of venous thrombosis of the left transverse cerebral sinus in a girl with drug-resistant partial epilepsy and homocystinuria. This diagnosis was considered and confirmed after the appearance of acute cerebral symptoms caused by venous thrombosis.
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A newborn boy presented within the first day of life with moaning, anemia, and thrombocytopenia. The clinical syndrome resulted from thrombosis of the posterior part of the superior sagittal sinus due to impression at birth of the tip of the occipital squama. Both computed tomography and ultrasound scans were valuable noninvasive tools for documentation of the thrombus itself and the cerebral sequelae. Color Doppler ultrasound scan confirmed the absence and reappearance of flow in the superior sagittal sinus.
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CASE REPORT: A 14 year old patient showing bilateral frontal headache during the previous four months was studied. Ophtalmoscopic examination revealed presence of bilateral papilledema. Magnetic resonance angiography showed presence of thrombosis in upper sagital and transverse sinuses. Patient was treated with oral acetazolamide (500 mg a day), one month later, headhache had disappeared and papilledema decreased. DISCUSSION: Aseptic cerebral venus thrombosis is an infrecuent condition that often is cause of neurologic complications that may become severe. Treatment should aim at decreasing intracranial pressure in order to avoid optic nerve atrophy and visual loss.
Thromboembolic disease is a well-recognized but very uncommon complication of inflammatory bowel disease. The mechanisms of the increased risk of thrombosis are not well understood: although several coagulation abnormalities have been described in inflammatory bowel disease patients, it is not clear whether they actually contribute to hypercoagulation or whether they are nonspecific markers of inflammation. Antiphospholipid antibodies (anticardiolipin antibodies and/or lupus anticoagulant) have recently been associated with an increased risk of thrombosis, particularly cerebrovascular disease in young patients. We report the case of a 33-yr-old female with severe ulcerative colitis at first attack who developed thrombosis of the superior and inferior longitudinal dural sinuses. No risk factors for thrombosis or coagulation abnormalities were observed; however, lupus anticoagulant was detected in the serum. The patient was successfully treated with osmotic agents, prophylactic anticonvulsant, and antiplatelet therapy, combined with i.v. steroids. After 6 months, the colitis is in remission, and the neurological recovery is good even if not yet complete.
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