Etiology
Pathophysiology
Cerebrospinal fluid (CSF) absorption occurs both via the arachnoid granulations and along nerve root sheaths, especially along the olfactory nerve through the cribriform plate.[11] It is thought that there is increased resistance to CSF outflow along one or both of these pathways, but abnormalities of these absorption pathways in patients with IIH remain unproven. With CSF absorption block, intracranial pressure must rise for CSF to be absorbed. Although interstitial and intracellular edema have been reported in brain biopsy specimens, study with current methods of analysis has concluded that the histologic features of the brain parenchyma are normal, and the findings of previous studies are artifacts of slide preparation.[12][13] In addition, changes in cerebral hemodynamics, including increased cerebral blood volume and decreased cerebral blood flow, have been reported, but their significance is unclear.
The relationship between papilledema and loss of vision is complex and usually due to intraneuronal ischemia related to increased CSF pressure transmitted along the optic nerve sheath.[14] With the loss of axons, papilledema can regress while vision worsens. More often, however, the more severe the papilledema, the worse the loss of vision. This is true for large case series, but occasionally patients have marked papilledema and little loss of vision.[15]
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