A 45-year-old man was admitted for a progressively worsening headache over 2 weeks. He denied history of recent head trauma or anticoagulation and antiplatelet medication. General and neurologic examinations were not remarkable on admission. Routine laboratory investigations including coagulation profiles and platelet function were within normal limits. Head computed tomography (CT) on admission revealed an isodense CSDH on the right hemisphere with mild midline shift (Fig. a). A CT angiography (CTA) was performed to rule out any intracranial vascular malformation. A DAVF was noticed at the transverse sinus with dilated cortical venous drainage (Fig. b). So, a digital subtraction angiography (DSA) of the external carotid artery and DAVF embolization was planned.\nNo anomaly was noticed during selective angiography of the internal carotid and vertebral arteries and the left external carotid artery. Selective angiography of the right external carotid artery showed that the DAVF was located at the transverse sinus and fed by posterior branch of the middle meningeal artery (MMA), the occipital artery, and the posterior meningeal artery and drained to the occipital cortical veins with venous ectasia (Fig. a-b). The DAVF was classified as type IV according to the Cognard classification. The embolization was performed via the MMA. The Headway duo catheter was used and accessed to the DAVF, and Onyx was injected until the shunt disappeared (Fig. c-d). The patient experienced an uneventful recovery. His CSDH gradually resolved in 1 month (Fig. ). No neurologic deficit was noticed.\nA PubMed search of published studies written in English and Chinese was conducted on June 30th, 2017. The following key words were used in relevant combinations: dural arteriovenous fistula, dural arteriovenous malformation, subdural hematoma, subdural haematoma, subdural hemorrhage, and subdural haemorrhage. The reference lists of the identified articles were also manually searched for additional studies. Studies of which full text could not be obtained or those without sufficient individualized description of the isolated SDH cases mixed in larger case series were excluded.\nFinally, 13 articles containing 14 patients were identified [–]. In all 15 patients (9 females, 60%) including 1 case in our institution were included for the final interpretation (Table ). The inflicted patients were aged from 27 to 82 years (55.5 ± 8.6).Of note, 12 (80%) of the 15 patients were aged between 40 and 60 years of age, and 8 (53.3%) patients were between 50 and 60 years. Sides of the DAVF or SDH were obtained in 13 patients with 9 (69.2%) located at the left side and 4 at the right side. The intracranial locations of DAVF were anterior fossa (2), middle fossa (2), frontal region (2), parietal region (3), temporal region (2), and occipital region (2). The types of SDH were CSDH (7/15), acute SDH (ASDH) (7/15), and undefined SDH (1/15). Of the 12 patients feeding artery could be identified, MMA was the commonest feeding artery (8/12, 66.7%). Multiple feeding arteries were identified in 3 (25%) patients. The causes of DAVF were only defined in 3 patients (2 iatrogenic and 1 traumatic), with the rest undefined or not mentioned. Cognard classifications (Table ) of the DAVF were reported or deduced from the reports in 12 patients, with type I, type III, and type IV in 7, 2, and 3 patients respectively. The treatment strategies included hematoma evacuation (2/15), CSDH drainage and DAVF embolization (5/15), craniotomy and DAVF resection (3/15), DAVF embolization and hematoma evacuation (1/15), DAVF embolization (2/15), and not applicable or not mentioned (2/15). Of the 12 patients with direct description of outcome, 7 (58.3%) patients were neurological intact, 3 (25%) patients with neurological deficits, and 2 (16.7%) died.
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).