**5. Pathophysiology**

The pathogenesis of cAVMs is not well understood; they are considered congenital and can undergo growth, remodeling or regression over the period. The size of cAVMs varies widely, and cAVM can remain clinically silent for decades. In cAVM blood flows directly between them without capillary bed and not intervening neural parenchyma in nidus. cAVMs is a high-flow and high-pressure system. Particularly the small AVMs are having significantly higher pressure in the feeding arteries; hence the small AVMs are more lethal than the larger ones and bleed more frequently.

Familial cAVMs have been reported, but it is not clear whether these are coincidental or indicate a familial occurrence. Angio-architecture of cAVMs is direct arterial to venous connections without an intervening capillary network. Both the arterial supply and the venous drainage may be by single or multiple vessels. The high-flow arteriovenous communication potentiates a variety of flow-related phenomena such as the development of afferent and efferent pedicle aneurysms, which occur in 20–25% of patients, and arterialization of the venous limb. Aneurysms can be a source of bleeding with cAVMs and may indicate a grave prognosis [9]. Abnormal flow and a vascular steal phenomenon have been suggested to underlie some clinical symptoms associated with cAVMs [10]. Histopathological studies demonstrate areas of chronic ischemia and gliosis in the region of the cAVM malformation. Angio-structure of cAVM is typically composed of arterial feeder, nidus, draining vein and intervening gliotic neural parenchyma. The arterial feeder can be single or multiple originating from pial or perforating or dural arteries, and it can be a direct feeder supply as terminal branch or indirect feeder supply enpassage. Nidus is a compact tangle of dysplastic, thin-walled vessels of varied length connecting feeding arteries to draining veins. cAVM nidus can either be globular or conical in shape and may be compact or diffuse. Within the nidus, arterial blood is shunted directly into draining veins without passage through a normal, highresistance arteriolar-capillary network.
