Evidence is presented that dural fistulae are preceded by sinus thrombosis and that their danger lies in arterialized venous pressure within the cranium or the orbit. Arterial side occlusion leads to recurrence, while venous side occlusion leads to permanent cure. Vein of Galen aneurysms embrace some features of cerebral arteriovenous malformations (AVM's), namely a reticulum, and some features of dural fistulae, namely evidence of previous sinus anomaly and direct drainage into a sinus. These aneurysms are also permanently cured by venous side thrombosis, although the dangers inherent in their reticulum demand that this be done in stages or preceded by arterial side embolization. A very limited experience with venous end occlusion of cerebral (and spinal) AVM's suggests that they, too, can be permanently cured by venous side occlusion without excision. Their reticulum demands maximum, multistage, preliminary arterial side embolization together with intraoperative hypotension during the venous occlusion stage in order to minimize intracerebral hemorrhage or swelling. Schematic models of both fistulae and malformations are presented, together with reasons why particulate embolization is safer than glue embolization. The theory is advanced that dural fistulae, vein of Galen aneurysms, and AVM's are venous- rather than arterial-based lesions, which is consistent with the experience that permanent cure has been effected by venous side occlusion without excision in all three anomalies. It is speculated that there may be a developmental link between AVM and the venous malformation, the AVM being essentially a fistulized venous malformation.