The authors describe their experience with four cases of dural arteriovenous malformation (AVM) which led them to analyze the clinical aspects of these lesions in an attempt to understand their pathophysiology. An additional 191 previously reported cases of dural AVM's were reviewed with special attention to the mechanism of intradural, central, and peripheral nervous system manifestations. Apart from the peripheral cranial nerve symptoms, which are most likely due to arterial steal, the central nervous system (CNS) symptoms appear to be related to passive venous hypertension and/or congestion. Generalized CNS symptoms can be related to cerebrospinal fluid malabsorption due either to increased pressure in the superior sagittal sinus, to venous sinus thrombosis, or to meningeal reaction resulting from minimal subarachnoid hemorrhages. These phenomena are not related to the anatomical type of venous drainage. On the other hand, focal CNS symptoms are specifically indicative of cortical venous drainage. Seizures, transient ischemic attacks, motor weakness, and brain-stem and cerebellar symptoms can be encountered depending on the territory of the draining vein or veins. Therefore, the localizing value of focal CNS symptomatology relates to the venous territory and not to the nidus or to the arterial supply characteristics of dural AVM's. Furthermore, the venous patterns of various dural AVM's at the base of the skull are expressed by differences in their clinical presentation. Dural AVM's of the floor of the anterior cranial fossa and of the tentorium are almost always drained by the cortical veins and, therefore, have a high risk of intradural bleeding. The remarkable similarities in the manifestations of dural and brain AVM's and the differences in the manifestations of dural and spinal dural AMV's are pointed out. High-quality angiograms and a multidisciplinary approach to the study of dural AVM's will provide the best understanding of their symptoms and, therefore, the most appropriate treatment strategy.

The lateral spinal artery corresponds to the most rostral extent of the posterolateral arterial axis of the spinal cord. It supplies the posterior and lateral aspects of the spinal cord, and courses anterior to the posterior roots of the upper cervical spinal nerves (C-1 to C-4), and posterior to the dentate ligament. The lateral spinal artery anastomoses rostrally with the branches of the posterior inferior cerebellar artery (PICA) at the restiform body and laterally with the extraspinal arteries at the emergence of each nerve. It may originate either from the vertebral artery or from the PICA lateral to the medulla. Certain variations will cause an unusual but normal enlargement of the vessel in a specific portion of its course; these variations include vertebral artery duplication, a C-1 or C-2 vertebral origin of the PICA, a C-1 or C-2 occipital origin of the PICA, and an intradural course of the vertebral artery at C-2. Knowledge of these variations in the arterial supply to the area allows for an understanding of the different anatomic peculiarities present and their angiographic importance.

The authors describe three cases of clinical cerebral ischemia associated with angiographic evidence of cerebral arterial luminal narrowing presenting 7, 14, and 52 weeks after subarachnoid hemorrhage (SAH) and aneurysm clipping. Delayed vasospasm, in its usual time setting 1 or 2 weeks after hemorrhage, did not occur symptomatically in these patients. No evidence for aneurysm clip migration or rebleed was present. All patients responded favorably to volume expansion and elevation of blood pressure. This unusual occurrence of a very delayed vasospasm may further the understanding of the vasospastic process. The symptomatic onset of arterial luminal narrowing months after SAH may suggest that a proliferative vasculopathy more accurately explains the observed vessel narrowing, rather than conventional active constriction of vascular smooth muscle.