Spontaneous Intracranial Hemorrhage:

 

• HTN: Basal ganglia, thalamus, pons, cerebellum

• Amyloid angiopathy: Microbleeds, lobar hemorrhages

• Arteriovenous malformation: Any location

• Cavernous malformation: Any location

• Venous sinus thrombosis: Subcortical white matter

• Neoplasm: Any location

 

Multiple Scerosis

•  

  • Multiple perpendicular callososeptal T2 hyperintensities characteristic of MS

    • Perivenular extension: "Dawson fingers"

  • Bilateral, asymmetric linear/ovoid FLAIR hyperintensities

    • > 85% periventricular/perivenular

    • 50-90% callososeptal interface

    • May also commonly involve subcortical U-fibers, brachium pontis, brainstem, spinal cord common

  • Transient enhancement during active demyelination

    • > 90% disappear within 6 months

  • Rare: Large tumefactive enhancing rings

  • T1: Hyperintense lesions suggest worse prognosis

    • Correlate with disability, atrophy, progressive disease

  • Advanced imaging techniques show disease in normal-appearing white matter

• Top Differential Diagnoses

  • Acute disseminated encephalomyelitis (ADEM)

  • Neuromyelitis optica

  • Autoimmune-mediated vasculitis

MCDONALD CRITERIA (click)

 

RP Search pattern MS followup Brain MR with contrast:

 

Look for enhancing lesion which is new* most important

Look for new non enhancing lesion* next most important

If see lesions, characterize on diffusion as some acute plaques restrict diffusion

Sync up axials or sag images and compare changes in white matter plaque burden, look in periventricular, juxtacortical, infratentorial, spinal cord

periventricular means right up against the vent, orient perp to the vent

think about PML as enhancing lesion in Tysabri tx

think about a tumefactive plaque

 

MS Search Pattern for followup

RP method

 

Axial Flair vs. Axial Flair

Axial post t1 FS vs. axial post t1 fs

Sag Flair vs Sag Flair

Sync all images by relative location

 

Look for new enhancing lesions

Look for new nonenhancing lesions

^ using axials, scan multiple times on post contrast because you will miss lesions - RP

Use sagittals to document dawson's fingers and corpus callosum atrophy (confirm this on t1 sag tho)

Use sag to look at periventricular lesions that are high up that aren't noticed on axials

Use sag to analyze posterior fossa including cerebellum, medulla-pons-midbrain.  Dont overcall subtle brainstem lesions - RP

Use sag to look at up upper cervical cord to exclude lesions

Use mcdonald criteria 

 

Clinicians stop reading when they see the following:  No new enhancing or nonenhancing lesions.  

Impression if unchanged:  MS plaque burden, unchanged.

 

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Infarcts / Strokes:

 

think about atypical infarcts including if in parasgaittal cortex of frontal / parietal lobes think about watershed infarcts

Think about venous infarcts cuz they are frequnetly missed

 

Re. followup of mechanical thrombectomy

When see hyperdensity within the infarct, can be contrast staining from the procedure vs. petechial hemorrhage

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Trauma:

 

KNOW THAT YOU WILL MISS NONDISPLACED SKULL FRACTURES ACC TO RP.  ALSO THESE ARE NOT CLINICALLY RELEVANT SO NO HARM DONE.  In fact I remember a case from 9/16/2015 where the fx was miscalled and was actually a normal suture line.  Use coronals to identify sutures or fx on coronal plane.

 

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For Glioblastoma Multiforme Followup:

 

look at pre surg images.

 

look at the "brain lab".  that is the day of the surgery

 

the initial post contrast MRI should show a resection cavity.  This should not have enhancement at the margins of the cavity on the initial scan.  If it does, that could mean unresected tumor.

 

The followup studies could demonstate enhancement at the margins of the resectino cavity due to "granulation tissue". 

Things to know about:  entities of pseudoprogression.  In theory progression would be seen as nodular enhacement within the cavity which is new.  

Also keep in mind the surrounding flair edema can represent tumor progression.  GBM is always deadly and will always recur.  

 

Document any nodular enhancement and the degree of flair abn and the interval change.  keep in mind that pseudoprogression exists as an entitiy.

 

 

Major Components of GBM Followup:

Craniotomy description:

The patient is status post right-sided frontoparietal craniotomy. 

Dural Changes:
There is postoperative change with linear enhancement of the underlying thickened dura.

 

Lesion:

Again seen is heterogeneous nodular enhancement involving the resection cavity in the  right frontoparietal lobe.  The irregular and nodular enhancement has increased medially and along the lateral aspect of the thalamus (axial image 84) when compared to the prior study. The verall size of the resection cavity and heterogeneously enhancing lesion appears otherwise stable when compared to the prior study. There is surrounding localized mass effect without midline shift.  

Surrounding FLAIR Abn:

There is associated surrounding FLAIR hyperintensity extending into the right frontal lobe, right parietal lobe, right external capsule, right internal capsule, right occipital lobe, and right temporal lobe. The degree of surrounding FLAIR hyperintensities is similar when compared to the prior study but has increased along the medial aspect in the area of increased enhancement (axial image 36).

 

Characterization on gradient image:

There is gradient echo blooming and restricted diffusion in this region consistent with  blood products. 

 

Other things:

 

Hemorrhage can restrict diffusion

 

use diffusion to evaluate tumors, look at original tumor to see if restricted diffusion.  if did, then use that on followup for recurrence

 

Flair hyperintensity in WM can also be due to Radiaition traetment and not just tumor

 

if see FLAIR extending in tract like fashion, means wallerian degeneration and due to injury from the surgery and can be correlated with clinical weakness 

 

Use cerebral blood volume maps to look for increased vsacularity of regio to detect recurrence

 

use FLAIR and gyral swelling to evaluate for abn

 

use non con T1 to look for REAL enehacnemetn and not just T1 hyperintensity which could be ascribed to subacute hemorrahge.

 

neurorads usually mention the craniotomy, the underlying epidural collection and dural thickening with enhancement as a rule

 

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new thoughts on follow up GBM

 

saw case where there is new FLAIR abn above lesion.  This displays gyral edema, also this area has thin peripheral enhancement and diffusion restriction.  The ddx includes radiation necrosis.  This was actually favored by RP because it fit the time frame (about 6 mths post).  Things to do to differentiate this was:  Perfusion looking at CBV in lesion (inc in tumor, dec. in RadNec), doing spectroscopy, or doing PET-MR (altho the nucs people told me radiation changes are hypermetabolic on PET).  

 

 

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MS Thoracic spine:

 

first label the t spine on the sag

then use a narrow window and label potential lesions on t2W or stir sag

then use axials to confirm the finding, zoom in on cord and know that some lesions are subtle

try to find as many lesions as can, keep in mind a de novo diagnosis is different than a follow up

use post con to find enhancing acute lesions which acc. to RP is not that frequent a finding

 

Acc. to RP, lesions can be extremely questionable inthe thoracic spine.  sometimes you see it sometimes you dont and you can flip flop from case  to case on same patient whether something is "real" or not.  So know that they can be subtle or completely false even.

 

scrutinze the stir axials, the central H shaped gray should be nromally hyperintense relative to the surrounding white matter.  sometime the spatial resolution of the iamges is limiting.

 

MS lesions if they are seen almost never enhacne on post.  

 

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Code BAT Head CT:

 

pull up prior if there, see if patient has had strokes before

look for hemorrhage

use MIPs to make it easier to find hemorrahge

 

if no hem, then good to call

 

while on phone, look for CT evidence of acute infarct

Dense MCA or Dense Basilar 

Focal hypoattenuation in vascular distribution, use small window size, use narrow window width, use 5 mm axials

check insula for loss of G-W diff

 

check for prior infarcts, usu locs are cerebellum, BG, temporal

 

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General Brain MR tips:

 

Look in ventricles

Easy to miss small ditzel in the ventricles.  some might be benign ventircular cysts.  Dont want to miss concerning intraventricular tumor.  

 

 

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Lumbar MRI for mets:

 

Look from T11-all sacral segments, look for cdecreased t1 signal (marrow replacement) with increased signal on STIR, that is a metastasis

 

look for pedicular widening highly specific for mets

 

don't be afraid to call diffuse mets if thats what you see

 

think about path fractures and mention compression fractures***

 

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follow up for VP shunts:

 

 

There is no loss of gray-white matter distinction or other sign of acute infarction.

ﾠ

There are bilateral approach VP shunt catheters with their tips grossly unchanged in positioning. The ventricular system remains slit-like in size. Given differences in technique this is minimally increased in size is stable when compared to the prior study. Again seen are areas of encephalomalacia and gliosis involving the right temporal lobe and both parietal lobes.ﾠ There is no mass effect or midline shift.ﾠ

ﾠ

There is no intracranial hemorrhage or extra-axial collection.

ﾠ

The patient is status post suboccipital craniectomy.ﾠ There is no acute calvarial fracture.ﾠ Again seen is evidence of Chiari malformation. There is a non fused posterior arch of C1.ﾠ There is a polyp versus retention cyst within the left maxillarysinus.ﾠ There is no significant mastoid air cell disease. ﾠ

 

Talk about shunt catheters

 

talk about ventricular size  and comparison to prior

 

can mention the encephalomalacia adjacent to the catheters (the tracts)

 

Somtimes patients might have chirai malformation

 

there may be suboccip crani

 

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Temporal Bone:

 

anaomtay:

 

 

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Re. WHITE MATTER FLAIR HYPERINTENS:

 

Scattered punctate foci of nonenhancing T2/FLAIR signal in the white matter of the frontoparietal lobes. These are nonspecific, and may be the sequela of very mild chronic small vessel ischemia.  These have also been described with migraine headaches. 

 

 

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CTA Head Findings:

 

Re. Intracranial aneurysms:

 

1. Approximately 90% of such aneurysms arise from the anterior circulation, and 15-30% of these patients have multiple aneurysms 4. 

2. anterior circulation: ~90%

   1. ACA/ACoA complex: 30-40%

   2. supraclinoid ICA and ICA/PCoA junction: ~30%

   3. MCA (M1/M2 junction) bi/trifurcation: 20-30%

3. posterior circulation: ~10%

   1. basilar tip

   2. SCA

   3. PICA

 

 

 

 Re. AVM:

LOCATION:

• supratentorial: ~85% 

  • superficial (two-thirds)

  • deep (one-third)

• infratentorial: ~15%

Incidence

• solitary AVMs (98%)

 

 

 

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re. infarcts / stroke

 

look at the m2 segments in the sylvian fissure on every head ct, could see a hyperdense vessel ehre nicely outlined by darrk csf

 

usually look at the proximal mca (m1 segent for this)

 

however, saw a good case of this 

 

and was positive on diffusion

 

--

 

also re. ifnart

 

 

there is a thing called fogging

 

after the infarct

 

you can see pseudoimporovement of the region of infarct where it looks normal again

 

but then it will become encephalomalacic

 

strange

 

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re. serach pattern for MRI brain:

 

use T1 imaging to check the marrow of the skull to exclude marrow infiltration

 

also subcutaneous swelling could theoretically be lymphoma infiltration (I saw a case which was initially called soft tissue swelling from trauma and turned out to be lymphoma).  Though this seems very rare

 

Re. Workup of seizure with Brain MR:

 

looking for mesial temporal sclerosis or migrational disorder in peds:

 

good website for examples

 

 

 

Re. Brain tumors (RP ppt)

-Need to know areas of tumors

-these include:

CP angle

 

parenchymal lobes (Frontal, Parietal, Temporal, Occipital

 

Suprasellar

Posterior Fossa / Cerebellarntraventricular/ periventricular

Pineal

-think about tumor type:

cyst with enhancing nodule

gyral swelling without enhancement

cystic rim enhnacing tumor with lots of surrounding edema

hetero internally with lipid or hemorrhage

 

Re. Head CT:

Its all about hemorrahge, hydrocephalus, and herniation

 

Orbit:

Look for enhancing abnormalities.  Don't overlook orbital pathology on Brain MR.

 

Re. Aneurysm clips or coils:

Use Scout film to figure out difference

 

 

Re Inpatient followup Head CT:

Three types of cases

Post hemorrhage followup:

Look for worsening hem, or improving

 

Hydrocephalus followup:

Check positions of catheters

Check temporal horns for worsening or improvement fo hydro

Check for any intraventricular finding to explain hydro

 

Infarct fu:

Check for evolution of the infarct

Check for new infarcts 

Check for hemorrhagic transformation

 

Re. Normal pressure hydrocephalus:

Check high fronto-parietal lobes sulci (near vertex) and see if degree of sulcation is in proportion with the degree of hydro.  If more hydro than atrophy, consider NPH as diagn.  Per RP and LB

 

Re. Teeth:

check for periapical lucency

 

Re. Paravertebral or posterior mediastinal masses:

Could be asked to eval one on MR

Try to exclude nerve sheath tumors like shwanoma or neurofibroma which are well defined, with pronounced enhancement, and with widening of neural canals

Could be extramedullary hematopoesis

Could be lipoma or atypical lipomatous tumor

 

Re. Lytic lesions on CT:

measure the inside of the lesion.  If measures fat, than unlikely to be a true met or malignant lesion, more likely to be focal osteoporosis / osteopenia

 

Seizure workup:

 

For sezirure workup:

http://www.radiologyassistant.nl/en/p4f53597deae16/role-of-mri-in-epilepsy.html