Embryonic development of the meninges has been studied for more than a hundred years [3]. The primary meninx (also known as primitive meninx or meninx primitiva) give rise to the meninges, the calvaria, and the dermis of the scalp. Differentiation of the meninges progresses from a basal to apical direction. The meninges even provide a stem cell niche. During development and growth of the rostral central nervous system, the dura mater regulates events in the underlying brain and overlying skull through the release of soluble factors and cellular activity [4]. Interactions of the dura mater with the brain and skull are so dynamic that they exhibit mechanical and biochemical reciprocity. The dura mater has a profound influence on cell migration and differentiation in multiple regions of the embryonic and infant brain and skull [4].

Early experiments on quail and chick chimeras showed that neural crest-derived cells, generated from caudal forebrain and midbrain levels, contribute to the meninges associated with the forebrain [5]. In contrast, mesoderm-derived cells give rise to the meninges of the midbrain and the hindbrain. Histological observations in human fetuses also suggest that the cranial meninges originated from both the neural crest and the mesoderm [3,6]. The most striking diversity of the neural crest derivatives is found in its cephalic domain where the neural crest replaces the role of mesoderm [7]. The neural crest is a vertebrate-specific migratory stem cell that generates diverse cell types and structures. Comparative analysis suggests that neural crest cells in the vertebrates evolved at least 3 specific features—multipotency, longrange migration, and cellular communication systems for guidance [8].

Although the pathogenesis of dural arteriovenous fistula (DAVF) still remains unclear, sinus thrombosis, head trauma, surgery, and hormonal influence are the predisposing factors that initiate this disease. Current classifications of DAVF mainly focus on the presence of leptomeningeal reflux related to cerebral venous hypertension leading to cerebral infarction or hemorrhage. Presentation patterns can be different according to lesion location. Progression of DAVF may reveal 3 phases (proliferative, restrictive and late restrictive), especially in the cavernous sinus DAVF [9]. Regardless of the locations or phases of DAVF, presence of the cortical venous reflux is an important feature to access bleeding risk of DAVF. However, direct communication from the fistula to the pial vein leading to brain edema or hemorrhage due to the pial venous reflux may occur in some areas of the calvarial convexity [10].

The pial venous reflux from the trans-dural or trans-osseous feeders to the pial veins requires that the fistula crosses the subarachnoid space via the transdural emissary-bridging vein [11,12]. Such crosses may be possible either through the isolated cortical vein (caused by reasons like thrombosis or adhesion in the cortical vein) or other channels (like the emissary-bridging vein, which does not drain into the cortical vein in the subarachnoid space and does drain directly into the venous sinus or the extradural vein via certain trans-dural segments, as in the spinal DAVF) [13].

Such dural shunts with the direct pial venous reflux seem to be observed at the overlapped border of the primary meninx forming meninges and calvaria, which are separately originated from the neural crest in meninges, and mesoderm in calvaria, as in the areas like the parietal convexity [3,14].