Intracranial Hypertension is effectively defined as increased CSF pressure around the brain, in which the brain “floats”. That’s why in certain cases in the emergency a spinal tap can be used to drain some of the CSF and reduce the intracranial hypertension symptoms.
Now, WHY the intracranial hypertension happens: there are many reasons, among which is swollen brain (obviously if the brain expands, but the skull doesn’t, and there is the same amount of CSF, the pressure increases), lack of proper CSF drainage (in case of occluded venous system, problems with arachnoid granulations, and based on various research, allegedly with glymphatic system), aneurysms, bleeding into the brain, stroke, tumours, brain injuries, edema, and dozens of other reasons.
Under normal circumstances, it has nothing* to do with the levels of oxygen in the blood, as it’s not directly dependent on the oxygen (except that in case of lack of oxygen, the brain might start dying rather quickly and perhaps cause edema leading to intracranial hypertension consequence as per above).
It has not THAT much to do with slight variations of blood in-flow (supply via arteries into the brain), although the CSF is a byproduct of the blood flowing into the brain - see the presentation below - but it has something to do with the combined blood outflow as some of the CSF is absorbed back into the venous system inside of the skull. So even if the both IJVs are compressed but there is sufficient collateral network of veins or other measures to drain the CSF, and the absorption across the whole spinal cord is sufficient the patient might have intracranial pressure very well within normal limits even with severely occluded IJVs. Also, when upright, according to some research, many people have little blood drainage via IJVs anyways.
Another thing, if you drill a hole in the skull, or stick a spinal tap needle into the lumbar area, or someone has a skull base (or spinal dura) defect (either congenital or acquired) where the CSF can leak out, there might be massive intracranial HYPOtension even with the increased blood pressure (below the level when aneurysms start forming, or the mass of the brain reaches the bone of the skull), as simply the body won’t be able to produce enough CSF quickly enough to maintain any meaningful pressure inside the skull due to the most of the fluid leaking out immediately.
This is the presentation on how the CSF fluid is produced and absorbed under normal circumstances:
*Nothing as in “nothing under normal circumstances, as obviously there are mechanisms in the brain that start massively failing when the brain starts dying due to the lack of oxygen”.
Yes, one of the many possible reasons why intracranial hypertension sometimes happens is lack of proper blood outflow out of the brain (and Dr Kyle Fargen suggested the most likely mechanism why this self-reinforcing loop happens), but saying that intracranial hypertension is “high blood pressure in your brain, which results from the old, deoxygenated blood not being able to flow out of your brain via the IJV as quickly as the carotid arteries take fresh, oxygenated blood into your brain” is not the actual explanation of what the IH is.
The arterial blood pressure inside of the brain, unless there are aneurysms or other disorders, shouldn’t differ that much from the remaining parts of the body, so if the person has normal blood pressure, and no vasospasms, there shouldn’t be any significantly increased sustained blood pressure in the brain at all. Theoretically. Arteries aren’t veins, they don’t have valves, and therefore if some part of the arterial network cannot perfuse the blood through capillaries into the veins during the heartbeat, the blood will be perfused somewhere else. If enough of the blood paths are occluded, then the systolic/diastolic blood pressure in the whole circulatory system (brain, arm, leg) will increase. That’s why some doctors say “blood always finds a path to flow out”.
When it comes to the veins, the obstruction in veins triggers the process that Dr Kyle Fargen describes as proposed mechanism why some type IIH happens - the pressure in venous sinuses increases, making it harder for the CSF flow to enter the bloodstream through the arachnoid granulations (“one-way valves”), causing increased pressure within the brain, further compressing the veins and increasing pressure in them, making it even harder for the CSF to conquer it and enter the venous system etc. until some equilibrium is achieved.