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Although neuroradiologists and skull base neurosurgeons are aware of the existence of veins within the clivus, such vessels have seldom been described in the literature. The aim of the present study is to elucidate the detailed venous structure of the clivus. Computed tomography digital subtraction venography (CT-DSV) images of 50 unruptured aneurysm cases were examined retrospectively. Eighteen emissary veins were identified in 14 (28.0%) cases. A half of the emissary veins connected the inferior petrosal sinus with the inferior petro-occipital vein (IPOV) in the middle clivus. The clival diploic vein (CDV) was identified in 14.0% of cases, 42.9% of which had the clivus of the presellar type. The CDV was connected to the posterior intercavernous sinus or the rostral end of the basilar plexus superiorly, and was connected to the IPOV, anterior condylar vein, marginal sinus, or the anterior condylar confluence. The CDV provides collateral channels between the cavernous sinus and the internal jugular vein and the inferior petrosal sinus and the IPOV. Understanding of the emissary veins in the clivus and the CDV is valuable for skull base surgery, especially for endonasal endoscopic skull base procedures.

Sinus pericranii (SP) is a rare, usually asymptomatic condition characterized by a large communication between the intra- and the extracranial venous drainage pathways in which blood may circulate bidirectionally through dilated veins of the skull. We describe our diagnostic and therapeutic experience with SP, with a special focus on the vascular analysis of digital subtraction angiography (DSA). DSA images of 15 patients were evaluated with regard to the delay in opacification of the scalp vessels, the absence or distortion of the superficial cortical veins in the vicinity of the SP, the drainage patterns of the superior sagittal sinus, and the degree of maturation of the venous outlets of the brain. SP were classified either as “dominant”, if the main stream of contrast flow used the SP to drain the brain bypassing usual venous outlets, or as “accessory”, if only a small part of the venous outflow occurred through the extradiploic vessels. All patients presented with a nonpulsatile, soft-tissue mass. The lesion was on the midline in 14 of 15 patients, frontal in 12 patients, and parietal in 2 patients. In 13 patients, associated intracranial venous anomalies were present, eight of which were developmental venous anomalies. Seven patients had a dominant SP, and eight an accessory SP. SP can be considered the cutaneous sign of an underlying venous anomaly. If treatment is contemplated, analysis of the drainage pattern of the SP has to be performed. Treatment should be avoided in dominant SP or if its accessory role constitutes the only collateral pathway of an underlying venous anomaly.

For more than a century, available data concerning collateral venous outflow from the brain have received insufficient attention, as existing theories did not assign practical importance to them. Ideas concerning arterial blood supply and circulation of cerebrospinal fluid were considered more relevant. But available data afford a schematic model of cerebral venous outflow that does have important pathophysiological consequences. Principal outflow through the internal jugular veins can be substituted completely by the large vertebral plexuses, through communications at the cranial base. Emissary veins of the skull vault are small and few in number. Outflow from the deep venous system through the great vein of Galen can be substituted by choroidal, thalamic and striate anastomoses toward the basal vein. So-called intracerebral venous anastomoses through the centrum semiovale towards the convexity are nonexistent or negligible. Instead, a venous watershed exists separating paraventricular white matter from a layer of subcortical white matter. In most infants, the cavernous sinus is not yet connected to the cerebral veins. Once such communications have been formed, important collateral pathways exist through basal and Sylvian veins via the cavernous sinus to the pterygoid plexuses. Simultaneous hindrance of principal and collateral venous outflow will lead to elevated venous pressure and eventual insufficiency of cerebral blood flow (CBF). This will cause increased intracranial pressure, and ventricular enlargement due to periventricular atrophy. The slow phase of the two-compartment model of CBF coincides with the paraventricular white matter area of the deep venous system. In the neonate CBF was found to be still very low, and in the two compartments CBF increases at a different rate to a maximum in childhood. In hydrocephalus, measurement of CBF in the slow deep compartment, rather than the fast cortical one, will be most informative.

We report an unique case of a giant aneurysm of the occipital artery, with a venous connection to the transverse sinus via an emissary vein. Because of this connection, the term arteriovenous aneurysm is used.

The venous drainage of the craniocervical junction is made up of jugular veins and particularly the vertebral veins and their anastomoses. The anterior and posterior condylar veins join to form the plexus of the vertebral vein, the supply functions of which can be modified by the presence of the mastoid anastomotic emissary veins which increase the possibilities of drainage at that level.