Migraine has numerous similarities with idiopathic intracranial hypertension headache with (IIH) or without papilledema (IIHWOP). It is known that the two conditions are completely indistinguishable on clinical basis, so that an IIHWOP is found between 10 and 86% of chronic migraine (CM) series [
31‐
34]. They also share main risk factors (obesity, female sex, sleep disorders) [
35], some treatments such as topiramate [
36] but also migraine-specific treatments as MAb anti-CGRP Receptor [
37], suggesting the causative involvement of CGRP also in IIH/IIHWOP-related headache. Finally, both conditions show a high prevalence of significant dural sinus stenosis [
38,
39], considered a neuro-radiological marker of IIH/IIHWOP [
40]. These similarities indicate a close pathogenetic link between CM and IIHWOP and that a derangement of intracranial pressure (ICp) control associated with dural sinus stenosis is probably a shared mechanism between the two. There is evidence that sinus stenosis-associated increased ICp is a very common condition in the general population, found in up to 11.1% of individuals without persistent headache or other symptoms or signs of IIH/IIHWOP [
41]. Their prevalence raises to 44.8% in unselected chronic headache series [
38] and up to 86% in chronic migraine cases with prospectively assessed refractoriness [
33]. On this basis, it has been proposed [
35] that an unacknowledged IIHWOP associated with sinus stenosis can occur almost asymptomatically in many individuals but that in subjects with a predisposition to migraine, it represents a powerful and modifiable [
33,
34] risk factor for the progression and refractoriness of migraine [
42]. IIHWOP was recently mentioned in a reference paper on chronic migraine risk factors [
43].
IIH/IIHWOP is associated with profound cerebral fluid dynamics rearrangements such as redistribution of venous flow towards extracranial, epidural, and vertebral veins [
44]; increase in resistivity [
45,
46] and pulsatility indices [
46]; arterial hypoperfusion [
47]; and reduced cerebrovascular response to hypoxia [
25] which resolve after treatment [
19,
46]. Could the impact of IIH on cerebral fluid dynamics imply a perfusion risk? Ideally, relocating the pathogenesis of migraine in the context of IIH/IIHWOP could allow us to attempt an answer to our initial questions. However, to illustrate the putative role played by TVS in the control of cerebral perfusion and to propose the possible finalistic significance of the migraine attack, it is necessary to summarize some mechanisms involved in cerebral perfusion and CSF turnover dynamics which occur on the venous side of the cerebral circulation [
48].