Hello, I just thought I’d introduce myself and give you a brief history of where I’m at. I was initially sent to a Balance Clinic to see a Neuro back in Nov 23 and the Neuro thought I may have silent migraines but not all my symptoms added up. She sent me for an MRI which came back as ?SJC, then I got referred for a CT guided venogram and that concluded severe (R) SJC. She referred me to Dr Parker (Radiologist ENT, Sydney) where I had a head/neck venogram to check my pressure. The balance neuro said to me that I wouldn’t need surgery if that came back clear.
In the meantime I did make an appt with Dr Elliot (ENT, Sydney) for the end of this month.
So I did the head/neck venogram this week and it came back all normal.
I’m just wondering what the next step will be?
Do I still see Dr Elliot for a consult as of course I still have my ongoing symptoms? Is the standard of care for SJC surgery to have an abnormal pressure test?
Many thanks for your thoughts and advice,
Vesna
My symptoms: light headed, tinnitus both ears, R sided head pressure and pain, R ear pain, neck pain/stiffness and cracking, R shoulder/rib pain, R sided pressure on my throat, TMJ.
Not sure what SJC stands for; is it jugular compression?
A venogram doesn’t always show compression if the head’s in neutral position and the compression is positional, it’s strange that the CT guided venogram showed compression but that the pressure was okay!..I would still see Dr Elliot if you can, & push for a regular CT if you’ve not had one? Then at least you can see if the styloids are elongated, angled or wide which could cause the pain you’re experiencing.
@Vesna - Stylojugular compression would definitely be contributing to your symptoms. I hope Dr. Elliott is more on top of that situation than the previous doctors you’ve seen. Because the internal jugular vein can get squashed between the styloid process & the C1 vertebra, having your styloid shortened &/or your C1 vertebra shaved will reduce the pressure on your jugular vein so it can open more fully. That usually helps to reduce the symptoms which are caused by intracranial hypertension (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.
@Isaiah_40_31, the intracranial hypertension isn’t high blood pressure in the brain. It’s not resulted “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.”
That was my understanding for the last many years, @vdm. This is the first time anyone has said differently. Please correct me then as I want to be giving out accurate information.
I thought IH was the result of high pressure in the brain caused by excess blood plus CSF which also naturally occurs there.
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.
Thanks @vdm
Some really good information contained there for both hyper- and hypo-
I’ve had the ‘joy’ (not) of dealing with both. For me, the hyper- took years to show or be identified as it was slowly developing. Where as the hypo- showed up post-surgery after a faulty valve on a VP shunt sprung a leak allowing an unregulated/excessive drainage.
