A 66-year-old male with a recent syncope-related fall and closed head injury presented with progressively worsening gait instability, dizziness, and headaches. The fall occurred 1 week before presentation. On examination, no focal neurologic deficits were found. Noncontrast head CT demonstrated a 7 mm right convexity mixed density subdural hematoma [ and ]. Given his significant headaches and progressive functional decline, MMA embolization was performed as primary treatment. Intraprocedural digital subtraction angiogram revealed a right parietal Cognard Grade I DAVF [ and ]. Given the absence of cortical venous reflux and benign natural history of the fistula, the remainder of the procedure did not deviate from routine MMA embolization. The right temporal and right frontoparietal branches of the MMA were embolized with n-BCA glue with indirect penetration of liquid embolic into the fistulous point. Following embolization, there was no further opacification of the fistula. The patient experienced no procedure-related complication and was discharged the subsequent day. At 1-month follow-up, there was complete resolution of his presenting symptoms and surveillance CT demonstrated no residual SDH.
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 ().