2/The etiology for dizziness depends both on how you define dizziness (i.e., vertigo, imbalance) & where you see the patient
For imaging, subtle distinctions in symptoms usually aren’t provided & many common diagnoses are without imaging findings (BPPV, vestibular migraine)
3/The most important finding on imaging for dizziness is a stroke from vertebrobasilar insufficiency (VBI)
It's a relatively uncommon etiology of dizziness, but its prevalence increases in emergent/acute dizziness populations
Missed VBI can have profound consequences/morbidity.
4/Dizziness from VBI usually isn’t isolated bc many structures are in close proximity in brainstem/cerebellum, so it's rare for an infarct to only affect vestibular structures.
I remember this bc the brainstem is a VIP & VIPs are never alone, they always have an entourage.
5/However, VBI can result in some strokes that present w/only dizziness (nodulus, CN8 root entry, labyrinth & vestibular nucleus).
Importantly, it's not uncommon for there to be a false negative on DWI in the first 24 hrs—so repeat imaging is key if suspicion is high!
6/Even in the outpatient setting, you should look for remote infarcts that may indicate VBI as a possible etiology of dizziness (remote PICA infarcts, basilar lacunes), even if there is no acute infarct at the time of exam
7/Next most important finding after stroke is tumor. Most common tumor causing dizziness is a vestibular schwannoma.
A typical ice cream cone appearance is seen—w/the scoop of ice cream as the CP angle component & cone as the long internal auditory canal component
8/Technically, these tumors should NOT be called an acoustic neuromas—as most arise from the vestibular not cochlear nerve. And they are schwannomas, not neuromas—neuromas are a nerve's response to injury, not a neoplasm
9/Next most important after tumor is inflammation. Labyrinthitis can have several different appearances on imaging.
Normally the labyrinth should look clean on imaging—clear fluid, without enhancement. Like a perfectly clean living room with no mess
10/Acute labyrinthitis is where inflammation goes crazy, like a wild party. Inflammatory cells come into the labyrinth like random people crashing your house party
And like any party—the bright lights are on = enhancement. Acute labyrinthitis enhances on post-contrast imaging
11/Chronic labyrinthitis follows acute labyrinthitis. So it’s the party aftermath. Trash fills the room
Similarly, fibroblasts & debris fill the labyrinth in the chronic stage, so you lose your normal clean fluid signal (so it’s dark T2). Party is over, so no lights/enhancement
12/Finally, hardest diagnosis is Meniere’s dz (endolymphatic hydrops)
What is endolymph? Labyrinth has layers, like Russian nesting dolls
Outer doll is the bony labyrinth, holding perilymph & a 2nd doll—the membranous labyrinth
Inside the 2nd doll/mem. labyrinth is endolymph
13/Think of the labyrinth like a worm. It has its outer skin, but inside the skin is an intestine like a Russian nesting doll. Instestine is the mem. labyrinth holding endolymph
Endolymphatic hydrops is like when the worm eats too much & the intestine gets big inside the skin.
14/To understand imaging for endolymphatic hydrops, you must understand some labyrinth anatomy
In the coronal plane, labyrinth looks like a bow tie, w/the utricle/semicircular canals on top & cochlea on the bottom. Knot in the middle is the saccule—an important marker in hydrops
15/When looking at the vestibule in the coronal plane, the utricle is on top & the saccule is on the bottom
You can remember utricle is superior bc U is for both Utricle & up
You can remember the saccule is inferior bc it hangs down like a sack.
16/So how to image hydrops?
Remember the worm. If a worm is put in dye, it’ll absorb dye into its skin, but not its intestine
Same for the labyrinth. If you give contrast, it’s absorbed into the perilymph, but not endolymph—allowing us to see the endolymph as a filling defect
17/You must give the contrast via tympanic injection or wait 2 hrs or more after IV injection. Then perilymph will be bright & endolymph dark
On delayed axial post images, vestibular structures look like a bird. Body is perilymph & eye/belly are filling defects from endolymph
18/The filling defect that looks like an eye is the saccule endolymph. I remember this bc it’s the SACCule & eyes have SACCades
The belly filling defect is the endolymph in the utricle. You can remember this bc utricle means pouch (like uterus) & the belly is just a big pouch
19/An early hydrops sign is when the saccule endolymph gets enlarged (hydropic). Bird’s eye gets huge & runs into the belly
Utricle endolymph may also be hydropic—then you see big eye & belly
Remember when you are dizzy/high, your eyes are wide and your belly get big!
20/Seeing a giant bird’s eye is a common sign of hydrops.
Bird’s eye (saccule endolymph) is usually smaller than the belly (utricle endolymph). In hydrops, this is often reversed—called SURI or saccule to utricle inversion ratio.
Larger the bird’s eye, the more hydrops.
21/But what if there’s no delayed contrast imaging? It’s not usually done & it’s burdensome to wait several hours
Is there a non-contrast finding to help us select who may benefit from delays? We can use saccular morphology. On coronals, vestibular structures look like a rabbit
22/Bunny ears are the semicircular canals, eyes/forehead are the utricle, & the nose is the saccule.
The morphology of that saccular nose is key to telling us if there is hydrops. Too large a nose or not seeing the nose at all suggests hydrops
23/Too big a nose or no nose are very specific for hydrops.
There are measurements to define too long a nose (>1.5mm)—but it’s just a screening tool to see who needs delayed contrast imaging, so look for the abnormal morphology before you break out the calipers!
24/So for every MRI for dizziness, remember the mnemonic VESTIbular to remind you what to look for:
V for vestibular schwannoma
E for endolymphatic hydrops
S & T for stroke/TIA
I for internal otitis (labyrinthitis)
Hopefully now an MRI for dizziness won’t put you off balance!
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1/The 90s called & wants its carotid imaging back!
It’s been 30 years--why are you still just quoting NASCET?
Do you feel vulnerable when it comes to identifying plaque vulnerability?
Here’s a thread to help you identify high risk plaques with carotid plaque imaging
2/Everyone knows the NASCET criteria:
If the patient is symptomatic & the greatest stenosis from the plaque is >70% of the diameter of normal distal lumen, patient will likely benefit from carotid endarterectomy.
But that doesn’t mean the remaining patients are just fine!
3/Yes, carotid plaques resulting in high grade stenosis are high risk.
But assuming that stenosis is the only mechanism by which a carotid plaque is high risk is like assuming that the only way to kill someone is by strangulation.
1/I always say you can tell a bad read on a spine MR if it doesn’t talk about lateral recesses.
What will I think when I see your read? Do you rate lateral recess stenosis?
Here’s a thread on lateral recess anatomy & a grading system for lateral recess stenosis
2/First anatomy.
Thecal sac is like a highway, carrying the nerve roots down the lumbar spine.
Lateral recess is part of the lateral lumbar canal, which is essentially the exit for spinal nerve roots to get off the thecal sac highway & head out into the rest of the body
3/Exits have 3 main parts.
First is the deceleration lane, where the car slows down as it starts the process of exiting.
Then there is the off ramp itself, and this leads into the service road which takes the car to the roads that it needs to get to its destination
3/At its most basic, you can think of the PPF as a room with 4 doors opening to each of these regions: one posteriorly to the skullbase, one medially to the nasal cavity, one laterally to the infratemporal fossa, and one anteriorly to the orbit