Decreased CSF absorption in arachnoid granulations has also been postulated to be a potential cause of IIH.Obesity, specically in those with a more central distribution of adipose tissue, increases the intra-abdominal pressure leading to elevated pulmo­nary and cardiac lling pressures, which in turn decreases venous return to the heart, generating an elevated pressure in the venous system that builds up to the cerebral venous sinuses [15]. Due to elevated pressure, the gradient prevents resorption of CSF into the sinuses through the arachnoid granulations. Furthermore, accord­ing to Fargen’s unifying theory, the increased ICP can result in collapse of the venous sinus in susceptible segments, thus gener­ating stenosis, which in turn increases even more from the pres­sure in the dural sinuses due to venous outow obstruction, in a vicious feedback loop [16]. Therefore, venous hypertension is likely the most reasonable explanation for IIH and why increased ICP is not married to ventricular caliber [17]. This is further vali­dated in studies showing that as SSS pressure elevates, so does CSF pressure secondary to decreased, pressure-dependent absorp­tion of CSF across arachnoid granulations [17–19]. This is the most presently accepted mechanism for the pathophysiology of IIH and will be discussed further later in the chapter.