Dural arteriovenous fistulas (DAVFs) can occur as a complication of cerebral venous sinus thrombosis (CVST). The incidence of DAVFs following a diagnosis of CVST is reported to be between 0.9% and 13%. It is believed that a thrombus in the cerebral venous system causes stagnation of blood flow, which leads to an increase in venous pressure and the enlargement of preexisting physiological arteriovenous shunts or neoangiogenesis, which could result in the development of a DAVF. The prognosis in cases of DAVF is directly related to the anatomy of the venous drainage as presented in the Borden and Cognard classifications, as well as other venous drainage characteristics such as the presence of pseudophlebitis, distant venous sinus location, single drainage, and venous thrombosis. It is noteworthy that the clinical management of CVST differs from that of DAVF; anticoagulation therapy is the mainstay of treatment for CVST; however, its use is typically withheld or restricted in cases of CVST associated with aggressive DAVFs, mainly due to the increased risk of hemorrhage. A 72-year-old man experienced repeated episodes of word-finding difficulties. He had a history of hypertension and dyslipidemia. One year prior, he had been diagnosed with chronic lymphocytic leukemia, which was Chronic lymphocytic leukemia diagnosed 1 year earlier had been treated with ibrutinib and venetoclax, resulting in partial remission. Routine admission laboratory tests, including coagulation profiles and platelet function, were within normal limits, and head CT and cardiologic studies were unremarkable. Brain MRI showed a left temporal lesion. MR angiography (MRA) and MR venography (MRV) were performed, confirming a sinodural venous thrombosis. Anticoagulation with a novel oral anticoagulant (NOAC) was initiated; however, the patient was readmitted 20 days later with mild to moderate pure motor dysphasia, and a follow-up MRI revealed extension of the temporal lesion. Radiologically, the lesion was compatible with venous infarction secondary to extensive venous thrombosis. Ophthalmologic examination was unremarkable and excluded papilledema. Diagnostic angiography confirmed bilateral transverse sigmoid sinus thrombosis and showed a high-grade DAVF fed by transosseal arterial feeders originating from the occipital artery and draining directly into the vein of Labbé. Furthermore, the arterialized vein of Labbé drained into the partially thrombosed left transverse sinus and torcula, and most importantly, there was retrograde drainage through the temporal veins and superior anastomotic vein. This bidirectional drainage caused venous congestion in both the temporal and frontal lobes. The DAVF was consequently classified as Borden-Shucart type III and Cognard type IV. Immediately after diagnosis, we performed balloon angioplasty of the right transverse sigmoid sinus and embolization of the DAVF using dual-lumen balloon-assisted and ethylene vinyl alcohol (EVOH)-based techniques, achieving complete occlusion of the fistula. The patient had a rapid clinical recovery with speech improvement as early as 12 hours after the procedure, which allowed NOAC therapy to be restarted. At neurological follow-up on postoperative day 30, the patient had achieved complete speech recovery. Fluid-attenuated inversion recovery (FLAIR) MRI performed 2 months after the embolization procedure showed complete resolution of the previously observed abnormalities, and a diagnostic angiogram performed 3 months after embolization confirmed the stable and complete exclusion of the arteriovenous fistula. We present a case of DAVF associated with the vein of Labbé, secondary to sinodural vein thrombosis, presenting with nonhemorrhagic neurological deficits after cerebral venous congestion due to venous hypertension. The patient was successfully treated endovascularly with complete clinical recovery. We discuss the relationship between CVST and DAVF, the therapeutic challenges of this association, and the technical aspects of the embolization procedure.