1/"You can put this diagnosis in the differential as many times as you want in your life, but you will only be right once," I told my fellow.
Ađź§µabout a dx you hear about but are rarely lucky enough to see #medtwitter#FOAMed#FOAMrad#medstudent#neurorad#radres#neurosurgery
2/Pt had a calcified lesion in the posterior fossa found incidentally on a trauma CT, that was now enlarging. It had very coarse, stippled appearing calcifications, like grains of sand or dirt
3/It also had very jagged, irregular margins, almost as if the grains of calcium had just been piled up together haphazardly
4/On MRI, it was very T2 dark (from the calcs) & demonstrated mild enhancement. It was extraaxial, but didn't appear to arise from the meninges. Rather, it was in the lateral cerebellomedullary cistern, where CN 9-11 arise.
5/So went back to the CT--left SCM & trapezius atrophy but no cord palsy! This means it's a CN11 lesion--not just affecting it from mass effect, then it would affect 10 also. Calcified schwannomas are rare. CN11 schwannomas are rare. Calcified CN11 schwannomas likely don't exist
6/Googling "calcified lesion CN11" gave us CAPNON--a rare, non-neoplastic, reactive process. It affects CNs & when it does, usually 11.We were right! So I've had my 1 time to be right about this. If you haven't, now you know what to look for to make this dx a feather in your CAP!
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@TheAJNR 2/Vascular cognitive impairment, or its most serious form, vascular dementia, used to be called multi-infarct dementia.
It was thought dementia directly resulted from brain volume loss from infarcts, w/the thought that 50-100cc of infarcted related volume loss caused dementia
@TheAJNR 3/But that’s now outdated. We now know vascular dementia results from diverse pathologies that all share a common vascular origin.
It’s possible to lose little volume from infarct & still result in dementia.
So if infarcts are common—which contribute to vascular dementia?
@TheAJNR 2/In the lumbar spine, it is all about the degree of canal narrowing & room for nerve roots.
In the cervical spine, we have another factor to think about—the cord.
Cord integrity is key. No matter the degree of stenosis, if the cord isn’t happy, the patient won’t be either
@TheAJNR 3/Cord flattening, even w/o canal stenosis, can cause myelopathy.
No one is quite sure why.
Some say it’s b/c mass effect on static imaging may be much worse dynamically, some say repetitive microtrauma, & some say micro-ischemia from compression of perforators
1/Do radiologists sound like they are speaking a different language when they talk about MRI?
T1 shortening what? T2 prolongation who?
Here’s a translation w/an introductory thread to MRI.
2/Let’s start w/T1—it is #1 after all! T1 is for anatomy
Since it’s anatomic, brain structures will reflect the same color as real life
So gray matter is gray on T1 & white matter is white on T1
So if you see an image where gray is gray & white is white—you know it’s a T1
3/T1 is also for contrast
Contrast material helps us to see masses
Contrast can’t get into normal brain & spine bc of the blood brain barrier—but masses don’t have a blood brain barrier, so when you give contrast, masses will take it up & light up, making them easier to see.