To the best of our knowledge, there have been no reports illustrating normalization of the sizes of cerebral veins and dural sinuses after decreasing CSF pressure in patients with IIH. Gideon et al (8) and Mattle et al (9), by means of MR flow measurement, showed mean blood flows in the superior sagittal sinus of 457 mL/min and 420 mL/min, respectively, in healthy control volunteers and also showed a tendency toward a lower mean flow volume in the superior sagittal sinus (mean, 345 mL/min) in patients with IIH than in control volunteers (8). The flow volume in the superior sagittal sinus in the present patient was low at the time of admission and increased to within normal range, probably because of resolution of the intracranial hypertension. On the other hand, MR imaging in cases of spontaneous intracranial hypotension may reflect an increase in the venous volume throughout the brain, which shows diffuse dural enhancement, prominent dural sinuses, and an engorged epidural venous plexus, with a return to normal appearance with elevation of CSF pressure (10, 11). Fishman and Dillon (10) speculated that the changes were a consequence of the Monro-Kellie rule (10, 12), which states that CSF volume fluctuates reciprocally with changes in intracranial blood volume. We also speculate that normalization in the sizes of cerebral sinuses and veins and in the flow volume of the superior sagittal sinus after normalization of CSF pressure are a consequence of reductions in CSF volume and pressure.
I've read other papers indicating that reducing CSF pressure can cause twisted tortuous cerebral veins to normalize. I'll post them later if I can find them again. (Should really stop reading on my phone)
Above linked paper is an interesting read. It speaks of fluctuating csf pressure. This could make iih diagnosis difficult. Also, some iih mris show white matter lesions in the same areas as MS lesions. In light this and of recent official link between ccsvi, ms, and csf flow/pressure by zamboni, I wonder if MS isn't subclinical fluctuating iihyper/hypotension in rr phase and subclinical constant iihyper/hypotension in progressive forms.
Some cases might be caused by stenosis/valve issues, others caused by muscle, bone, or csf production abnormalities. Different treatments for different causes of the same thing??