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).
This 67-year-old male man has had a progressively worsening pain on the left cranium over 2 weeks that intractable to some analgesics. There was no recent head trauma or other medical disease in his history. On admission, the general physical and neurologic investigations were not remarkable. Routine laboratory evaluations including coagulation profiles and platelet function were within normal limits.\nBrain computed tomography (CT) scans revealed an isodense left-sided CSDH with marked cerebral shifting (). There was no evidence of source of this hemorrhage with temporal predilection on the CT angiogram. On magnetic resonance (MR) image subsequently obtained, the abnormal intensity within the subarachnoid space and the brain parenchyma was not visible. The patency without steno-occlusion in both transverse and sigmoid sinuses was clearly delineated on T2-weighted sequences (). This patient has received a trephination and SDH drainage, after that he was sent home with resolution of headache. Approximately 2 weeks later, however, he developed an excruciating pain in the temporal and parietal regions with recurrence of subdural collection. The site and density of hematoma was similar to the first presentation (). He was immediately returned for subdural irrigation and decompression through the prior burr-holes. The patient's clinical course was not eventful, but he complained of a mild headache again. Follow-up CT scanned just prior to discharge was strikingly for the newly-formed thin hematoma at the operative site (). Another evacuation of this subacute subdural clot was not deemed to be necessary.\nAt this time, an active intervention was sought for this patient who had an intractably recurring CSDH. On the 7th day after the second surgery, angiography was performed to rule out an occult vascular lesion. A flow-guided type microcatheter (Prowler 10™, Cordis Neurovascular, Miami Lakes, FL, USA) was positioned in the main trunk of the MMA for selective angiography. The frontal and parietal branch of the MMA was appeared normally, and the abnormal membrane staining on the affected side was not detected. A left external carotid angiogram disclosed a dural AVF between the petrosquamosal branch of the MMA and the transverse-sigmoid sinus without retrograde cortical venous draining. The AV shunt had no connection to the internal carotid artery and its branches. It was suggested that the bleeding from the draining venous system of the dural AVF led to refractory CSDH. The microcatheter was introduced into the petrosquamosal branch of the MMA, thereafter polyvinyl alcohol particles ranging 150 to 250 µm were distally injected (). After trans-arterial obliteration of the feeder and fistula, the AV shunt disappeared. The recurrent hematoma of this patient did not increase, and his complaints of headache gradually subsided. The brain CT at one year following the embolization therapy revealed complete regression of the subdural hematomas ().