Hello everyone
I have just written a very long text, and when rereading it I noticed that it is extremely unstructured and actually all boils down to the two questions,
does my internal jugular vein look constricted respectively occluded in my MRI/CT?
and can a calcification of the ligament cause symptoms even if it is only a short piece and is not fused to the styloid, like in my picture
(I wasn’t able to properly trace the jugular veins on my CT…)
I’ll put the text in a spoiler anyway, in case anyone is bored or wants to know a bit more and my thought process behind that question…
Summary
Hello everyone
I am new here and recently registered after I had a CT scan to determine the length of my styloid.
As I only have jugular symptoms apart from a slight stinging in my throat, the likelihood was very low, but I still wanted to have it checked to at least see if the styloid is not elongated.
After the CT it is now definitely clear that the styloid is not elongated (6mm/8mm) as measured by the radiologist. One look was enough for me to see that the remeasurement is definitely not necessary. But a small piece is calcified on both sides.
The reason why I am still writing here is as follows.
Half a year ago my psychiatrist had an MRI/MRA done because after two years of therapy she was of the opinion that the likelihood of my complaints actually having a somatic cause was quite high.
When I received the first MRI images six months ago, I quickly noticed the mastoid emissary vein on the right side and the different diameters of the right and left transverse sinus. However, as there was nothing in the report about either, I assumed that this was an anatomical variation. (later I saw a case report that linked pulsatile tinnitus (flow noises) with a dilated mastoid emissary vein).
The MRI findings were generally unremarkable.
My psychiatrist then ordered a neurological examination. Due to a shingles infection a few years ago, a lumbar puncture was carried out in addition to an EEG. I was pleased that the opening pressure was finally being measured because I had been thinking about the possibility of a change in pressure for some time. I then had to learn that this is not done automatically and the neurologist felt it was unnecessary because the MRI findings showed no signs of intracranial hypertension and I showed no signs of paralysis. (For me this also meant crossing IIH off my list of possible causes).
This neurological examination didn’t reveal anything significant either.
However, it turned out that my partner suffered a presyncope attack with brief loss of vision in the next day and had a severe headache for the next few hours. The emergency ophthalmologist I had urged her to see diagnosed an eye migraine. Two days later, I coerced her to go to the hospital emergency department again. Here, after several hours of waiting and an unremarkable CT scan, she was sent home again with medication for migraines. However, two hours after she returned home, her phone rang and she was asked to come back to the hospital. only by chance, a neuroradiology specialist had seen her images and was of the opinion that certain things could not be ruled out. So she went back, they did an MRI and wanted to send her home on the basis of the provisional report. However, the definitive report arrived at the last minute. Diagnosis: sinus vein thrombosis and three small strokes.
I think this event had a strong influence on the fact that I began to doubt my radiological findings. As a result, I started to think (perhaps a little too intensively) about what could be the cause of my complaints.
That’s when I came across Eagles syndrome and CSF leak, somehow both would have fitted apart from the respective leading symptoms (the headaches only have a diffuse orthostatic component, I only have a slight stinging sensation in my throat), but since there are cases of both where these symptoms are absent, I still wanted to have both checked out.
Regarding the CSF leak, this MRI was performed. I did not receive a report on this and when I asked here about the prominent mastoid emissary vein and whether there were any signs of an elongated styloid. They said that they only looked explicitly for signs of a CSF leak.
Shortly afterwards, a CT scan was performed. Question: Eagles syndrome?
The findings were initially unremarkable, but I then sent the radiology specialist an e-mail with pictures of the calcified parts of the ligament and said that I would be interested to know why these “structures” were not mentioned. Answer: These structures are calcifications of the ligament and usually do not cause any complaints, and if they do, then mainly when they are fused with the styloid. He therefore did not mention them, but would be happy to add them as additional findings.
I had actually hoped either not to see anything at all and to rule this out completely or to see a clearly elongated styloid and then to see whether this could be responsible for the symptoms.
However, this CT raised more questions than it answered.
Can such a mildly calcified ligament cause symptoms?
Even though every report from this specialist radiologist contains the last statement “normal venous blood vessels”, I would say that my internal jugular vein is narrowed or completely occluded. Or am I completely wrong?
If it is really narrowed, the calcification would be exactly where the narrowing of the vein is. I also made a 3D model of it (yes, the quality is pretty bad) and it looks to me as if the ligament is pinching off the vein. However, I don’t know if that makes any sense.
What would also speak in favor of this in my eyes would be the dilation of the mastoid emissary vein, which then takes over a large part of the flow, which would possibly also explain why I suffer a presyncopal attack every time I lean my head to the right in the neck and stretch my arm upwards or do overhead work, because then the flow in this vein is inhibited.
The discussion of the CT scan with the ENT is still pending, but as the radiologist’s findings show “inconspicuous venous blood vessels”, I assume that nothing will come of it.
I am now wondering whether it makes sense to address this theory or whether it is complete nonsense?
