6/ Ventriculitis = 🔥 of the ventricles
Encephalitis =🔥 of the enkephalos (Greek for “brain,” the brain parenchyma)
The cranial nerves are named: vestibular neuritis, optic neuritis etc... & then there is angiitis / vasculitis of the CNS (@AaronLBerkowitz’s favorite) 😉
7/ So …what, then, is cerebritis??
Vague inflammation of the “cerebrum”? Wouldn’t that be covered by “encephalitis"?
And is “lupus cerebritis” the same thing as other forms of “cerebritis"?
For the last question, the short answer is:
8/ Non-lupus cerebritis is inflammation of any intracranial structures.
Its most often caused by an infectious, pyogenic pathogen & tends to be invasive, invading many/any anatomic regions-- dura, subdural space, arachnoid, parenchyma...its not a well localized inflammation.
9/ Another way to think about non-lupus cerebritis is to think of it as a “pre-abscess.”
In the early phase bacterial invasion results in perivascular inflammation & softening of the brain tissue
Look for T2 hyperintensity, DWI restriction, & poorly defined enhancement.↕️
10/ Untreated the inflammatory response results in a walled off abscess, and/or subdural empyema depending on the location of the inflammation.
Microbiology can be difficult to diagnose because the CSF may be sterile, and aspiration may be necessary.
10/ Of course, a forming abscess is not the only thing that causes patchy diffusion restriction and enhancement.
The differential for non-lupus cerebritis includes:
💥High grade neoplasms
💥Subacute infarcts
💥Mets
💥Radiation necrosis
💥Demyelinating disease
11/
There is potentially a role for advanced neuroimaging like MR spectroscopy especially in cases where aspiration/biopsy would have high morbidity.
12/ So then...Is lupus cerebritis related at all? Basically, no.
Lupus cerebritis is an outdated term which has been replaced with neuropsychiatric SLE (NPSLE). But even NPSLE is a vague umbrella term which covers everything from headaches to stroke.
Kivity et al. BMC med
13/ The pathophysiology is complicated and may be antibody-mediated, vasculopathy, hypercoaguable state, cytokine-induced neuroloxic, and loss of neuroplasticity.
13/ Many of these neuropsychiatric symptoms have no MRI findings.
Cerebrovascular dz is a notable exception.
If “lupus cerebritis” shows up in an imaging report the likely pathophysiology is cerebrovascular disease.
Lupus Cerebritis = Stroke until Proven Otherwise
14/ ⚠️This DOES NOT mean that lupus cerebritis = vasculitis.
Remember, that vasculitis, by definition[!], involves inflammation. You CANNOT look at diffusion restriction on an MRI & determine vasculitis.
15/ In these patients, the most common pathology finding is thrombotic-vasculopathy. This may be due to:
✨antiphospholipid antibodies
✨immune complex/compliment activation.
SLE pts also can have:
✨cardiac emboli (Libman-Zachs endocarditis)
✨accelerated atherosclerosis.
16/ Can something other than cerebrovascular disease be going on?
Absolutely.
Given chronic immune suppression, SLE pts are at risk for infections (including the “non-lupus” form of “cerebritis”!) & can have demyelination, encephalitis, sz-related MRI.
17/
But keep cerebrovascular dz high on Ddx.
LP and advanced neuroimaging can be helpful here. Vessel Wall Imaging has been reported to help differentiate which is interesting.
“Unfortunately, your 55yo loved one has suffered a very large stroke affecting a large portion of the brain. Surgery would reduce the change of death, but not the disability from the stroke.”
Goals for the scroll (⬅️credit @sigman_md 😂):
1⃣ How difficult it can be to diagnose spiral epidural abscesses (SEA)
2⃣ What exactly is the spinal epidural space
3⃣ How these should be treated
4⃣ And why decompress?
3/ Diagnosing SEA = super tricky. The symptoms & labs are so non-specific!
✅Back pain ⏫(but back pain--who doesn't?)
✅Fever is often present, but not always.
✅WBC may be elevated, but sometimes just mildly. ✅Blood cultures are only positive about 60% of the time.
1/ A #tweetorial about simulation in NCC
Today @namorris opened his remarks on Sim in NCC @ #NCS2021 w/ a simple question about the correct first line treatment for SE? Everyone got it.
Then he posed a tougher question.
How often does that happen?
No one voted "always"
2/
Even the most groundbreaking research won’t benefit our patients if we aren’t delivering it correctly.
I so highly encourage you to check out Nick’s talk on-demand if you have access to #NCS2021.
It is 🚨critical🚨 that we teach more effectively!
3/ Convinced?
Some practical, take-aways from this talk about finding right Simulation Solution.
1/🧵
In the early days of fellowship, I remember checking our SAH patients’ transcranial dopplers (TCD), scanning the Vmeans & if they were ~<70 cm/sec throughout thinking:
“Great. Perfect. TCDs globally low. Nothing to worry about here!”
🚨Note. This is not a #tweetorial about if large vessel vasospasm is the cause of DCI or just an epiphenomenon OR if treating vasospasm is the way to improve functional outcomes …That is important!... but that is not this tweetorial. pubmed.ncbi.nlm.nih.gov/21285966/
3/ Given #TCDs is a pretty large topic, this @medtweetorial will be told in 3 parts:
Part 1⃣:
⭐️Basic principles of TCDs
⭐️Use of TCDs to detect Vasospasm
Part 2⃣: The Pulsatility Index - why it matters
Part 3⃣: The Utility of TCDs as an ancillary test in BDT