Superior Sagittal Sinus Thrombosis
OBJECTIVES
To discuss the clinical presentation of cerebral venous thrombosis.
To discuss the management of superior sagittal sinus (SSS) thrombosis.
To discuss the management of anticoagulant therapy in pregnancy.
VIGNETTE
A 30-year-old woman was evaluated 3 years earlier due to severe bifrontal headaches and dizziness. After 3 days, she noted that her left leg became “limp.” Then, her left arm also became weak. She also had slurred speech and left facial weakness. She then had a spell characterized by turning of her head to the left associated with jerking of her left limbs with secondary generalization. A diagnosis of SSS thrombosis was made. She was found to have elevated IgA antiphosphatidylethanolamine antibody. She was treated with intravenous and fractionated heparin and was discharged on warfarin (target INR 2.0 to 3.0). Three years later, while on warfarin, she became pregnant.

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At the age of 27, our patient suddenly experienced severe right frontal headaches associated with left leg weakness. CT showed a small right frontal lobar hemorrhage. MRI showed a hemorrhagic infarction involving the right frontoparietal lobe and the left posterior parietal lobe. Magnetic resonance venography (MRV) and catheter cerebral angiography documented an occlusion of the anterior portion of the SSS. Subsequently, the patient had a single seizure characterized by head deviation to the left, followed by rhythmic clonic movements of the left arm and leg, followed by loss of consciousness. She received intravenous phenytoin and was referred for further evaluation and management.
Past medical history was fairly unremarkable except for abruptio placenta at 8 months of gestation. She smoked a pack of cigarettes daily and was not on oral contraceptives. Physical examination showed extensive livedo reticularis. There was residual weakness of her left hamstrings, foot dorsiflexors, and plantar flexors. Patellar and ankle reflexes were brisk (left greater than right). Ancillary investigations showed persistent elevation of IgA antiphosphatidylethanolamine titers. She was treated with intravenous unfractionated heparin followed by warfarin. She also received oral phenytoin and folic acid.
Three years later, while still on warfarin, she became pregnant. She discontinued warfarin on the first day she recognized she was late for her menses. A fetal ultrasound was normal. Neurologic examination was stable.
The patient was treated with 81 mg of aspirin daily and subcutaneous enoxaparin (initially 60 mg twice daily and then 80 mg twice daily). She also received folic acid, prenatal vitamins, vitamin D, and calcium supplements. On her 37th week of gestation, enoxaparin was discontinued and she received subcutaneous unfractionated heparin. Following an unremarkable delivery, she was allowed to breast-feed her baby, and warfarin was restarted.

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