A 60-year-old male experienced one month of escalating bifrontal headaches refractory to analgesics and antibiotics prescribed for presumed sinusitis. The headaches increased during sneezing, bending over, or bedrest and improved when he was sitting or standing. There was no history of trauma. His prior medical history was notable for hypertension and hyperlipidemia. There was no family history of coagulopathy or thrombophilia. He was married, employed, used 0.5 packs of tobacco (7.5 packs/years), consumed alcohol socially, and did not use any illicit drugs. His vital signs were notable for sinus bradycardia with a heart rate of 39 and elevated BP of 184/86 mmHg. He had no other significant findings on physical examination; detailed neurologic examination was unremarkable. Routine admission laboratory studies were within normal limits. Coagulation studies including platelet function assays were normal.\nNoncontrasted head CT demonstrated a 19 mm left isodense SDH with 10 mm of midline shift []. The collection was more prominent in the frontal region. A CT angiogram was obtained prior to surgery, and no source of bleeding was identified. He underwent a mini-craniotomy; and repeat CT imaging after the procedure [] demonstrated excellent hematoma evacuation and brain reexpansion.\nA scheduled follow up head CT obtained on postoperative day 27 was notable for recurrent SDH with a frontal predilection \n[]. The appearance and location were similar to the initial presentation. He was readmitted to the hospital and underwent SDH drainage via burr hole. On subsequent imaging with MRI, MR angiography, and MR venography, a filling defect was visible in the distal left transverse sinus and no flow was observed in the distal left sigmoid sinus or internal jugular vein. These findings were confirmed on CT venography.\nPatient underwent cerebral angiography on postoperative day 7 after SDH evacuation []. Left carotid injection was notable for a prominent left vein of Labbe with delayed wash-out, a filling defect in the left transverse sinus, and retrograde flow in the left transverse sinus with subsequent drainage into the right transverse sinus. Transvenous catheterization confirmed retrograde drainage of the left transverse sinus and venous stasis in the left vein of Labbe. Manometric readings in the left sigmoid sinus and both transverse sinuses were elevated (18-25 mmHg range). Thrombectomy with the Penumbra device and venoplasty with 7 × 20 mm balloon were performed; 10 mg of systemic abciximab was administered. Follow up venography demonstrated improved flow in the left vein of Labbe, restored normal direction of flow in the sinuses with normalized pressure (11 mmHg) in the left transverse sinus. Daily aspirin (325 mg) was initiated on the day of this intervention; patient was discharged home without neurologic deficits. A follow-up CT venogram at 6 weeks demonstrated patent venous sinuses and no recurrence of his SDH. His 3 month clinical outcome was excellent (modified Rankin score 0).
A 68-year-old woman with polycythemia vera experienced a global, nonpositional headache for one day. She subsequently became comatose. On emergent evaluation she exhibited decorticate posturing. Her Glasgow coma score was 6. There was no preceding history of trauma, infection, or dehydration. She was not on anticoagulants or antiplatelet agents. Her polycythemia vera had been managed with therapeutic phlebotomy and hydroxyurea (500 mg daily). She had no prior history of thromboembolic events. Noncontrasted head CT showed extensive left 20 mm acute SDH with 16 mm of midline shift []. She underwent emergent craniotomy and hematoma evacuation. On careful inspection of the exposed brain, a prominent and engorged cortical vein observed. No other vascular abnormalities or potential bleeding sources were identified. CT venography and MR venography detected partial superior sagittal sinus thrombosis, which leads to the empty delta sign (the intraluminal thrombus prevents central filling of the sinus; ). She was managed conservatively with hydroxyurea, hydration, and aspirin. Laboratory analyses were notable for normal coagulation panel, normal platelet function assays, hematocrit of 45.9, negative thrombophilia evaluation (protein S, protein C, antithrombin III, anticardiolipin antibody, homocysteine, lupus anticoagulant, beta-2 glycoprotein antibodies, Factor V Leiden mutation, prothrombin gene mutation). Analysis of DNA extracted from her blood revealed the presence of the V617F mutation within the JAK2 gene. Her 3-month outcome was poor (modified Rankin score 4).