Bright	Dark
T1	- contrast - fat/cholesterol (lipoma, teratoma, dermoid, lipomatous ependymoma, cholesteatoma) ** to differentiate fat from other T1-bright lesions, look for chemical shift artifact (dark band at edge of fat on one side, light band at the other)  - melanin - early subacute blood (intracellular metHb 3-7 days) and late subacute blood (extraceullar metHb, 1-4 weeks) - subacute thrombus (i.e. venous sinus) - protein-rich fluid (colloid, rathke’s cleft, ectopic posterior pituitary, craniopharyngioma – also cholesterol and blood) - minerals (microcalcifcations, iron, manganese – hepatic encephalopathy, copper) - laminar necrosis (from global hypoxemia or immunosuppression – appears 2 weeks after insult) – may appear as cortical ribbon - slowly flowing fluid	- CSF - Edema    - flow voids - calcium (bone) – although microcalcifications often appear as bright on T2 due to their interaction of water molecules
T2	- Edema (from tumor, infection, inflammation, ischemia, vasculitis, radiation-induced, chemo-induced, migraines, etc) - late subacute blood (extracellular metHb) - CSF (virchow robin spaces) - Demyelination - Myelinolysis  - Degeneration	- contrast - acute blood (deoxy Hb)/early subactue blood (intracellular metHb), chronic blood (hemosiderin)   - melanin - mucous/protein (i.e. colloid/rathke cyst - hypercellular tumors (high nucleus to cytoplasm ratio – medullo, lymphoma, highest grade parts of high grade gliomas) ** - tends to be dark but not black - minerality (iron, copper, calcium) - flow voids/turbulent flow – of blood  and CSF (jets can appear dark) - air - fibrous tissue/bone
Diffusion	- T2 shine through - acute ischemia (<2-3 weeks) - highly cellular tumors (lymphoma, medullo/PNET, meningioma, chordoma, germinoma, hemangiopericytoma, pinealblastoma, cortical part of high-grade gliomas – cyst part typically does not restrict in gliomas) - abscess (cystic part restricts 2/2 pus) - mucinous metastasis like breast or colon adenocarcinoma (mucus restricts) - epidermoid - prion disease (CJD, kuru – cortical ribboning) - toxic (carbon monoxide, methanol, Wernicke, maple syrup urine, gluteric aciduria, methyl malonic aciduria other inborn errors of metabolism diseases) - adrenoleukodystrophy	- old stroke (> 3 weeks) - necrosis (i.e. core of GBM/mets)
GRE/SWI		Blooming - air - blood of any age - mineralization - inflammation

Source papers:

Clinical applications of diffusion weighted MR imaging: A review

Differential Diagnosis of Bright Lesions on Diffusion-weighted MR Images

Intracranial Lesions with High Signal Intensity on T1-weighted MR Images: Differential Diagnosis

Differential diagnosis of intracranial lesions with high signal on T1 or low signal on T2-weighted MRI.

GRE T2-Weighted MRI: Principles and Clinical Applications

MRI of the Brain: a primer 

Sympathetic storming 

Epidemiology 
- Typically occurs in young patients with significant/diffuse brain injury - TBI/DAI, SAH, big IPH, etc.
- Archetypally a young male with bad DAI -- likely no true gender predilection but rather trauma tends to affect male > female. And perhaps age predilection because young people have a more robust sympathetic response, or maybe because the degree of neurological injury that is typically associated tends to be mortal in older adults, or maybe because high grade SAH or IPH or diffuse injury occurs more in middle age than late age

Pathophys
- Poorly understood
- Originally believed to be exclusively a function of deep white matter injury; however its also seen in bilateral/diffuse cortical injury
- Perhaps decrease in the dampening signals? exaggerated sympathetic response to all stim, instead of only to severe/noxious stim.

Clinical Presentation 
- Paroxysmal bouts of tachycardia, hypertension, diaphoresis, fever, mydriasis
- Characteristically waxing/waning, rather than constant (i.e. alcohol withdrawal)
- Typically occurs 3-5 days after the initial injury, and resolves on the scale of days to weeks but can start as early as immediately after the injury and last for years

Treatment 
- Very severe (i.e. uncontrollable blood pressures leading to problematic sequelae) - precedex gtt and/or esmolol gtt
- Less severe/transitioning off gtts/on the floor - clonidine, propanolol, gabapentin (especially useful for controlling storming that directly follows stim - like turning/bathing/etc)
- Some people believe that opiates like morphine are an integral part of treating storming, some people don't.
- You can always snow people into the ground with propofol or drips of benzos or narcotics, but it's an inelegant solution and some people believe that they are suboptimal ways of treating storming.

Aging of stroke

Time	DWI	ADC	T2	CT
30 mins	First becomes visible - bright	First starts to become visible – dark – in animal stroke models ADC changes visible in < 5 mins	Invisible	invisible
6-8 hours	Clearly Bright	Clearly Dark	First starts to become visible – bright (edema)	First start to become visible - loss of grey-white, insular ribbon, etc
24 hours	Clearly Bright	Clearly Dark	Clearly bright	Clearly dark
1-4 days	Clearly Bright	Max darkness	Clearly bright	Clearly dark
7 days	Max brightness	Clearly dark	Clearly bright	Clearly dark
10-15 days	Signal starts to fade	Reverses from dark to bright, sometimes becomes invisible	Clearly bright	Clearly dark
2-3 weeks	Signal fading/reversing	Becomes bright	Clearly bright	Clearly dark
>30 days	Dark	bright	Max brightness	Clearly dark

UCAS (prospective) 

- 2001-2004 in Japan 

- N=5720 patients, 6697 aneurysms (3050 : treatment before rupture @ median of 48 days, 3647: not treated before rupture) 

- Rupture rate of 0.95% per aneurysm-year ; rupture rates associated with 35% mortality, 29% mRS 3-5 

Rupture rates according to location and size:  

Whereas ISUIA found increased rates in all posterior circulation aneurysms, UCAS found higher rupture rates with Acomm and Pcomm (but not more with say, BTAs..... however the total number of VA/BTA aneurysms was small (see below chart)

Graphical representations of rupture rates by location and size: 

Multivariate analyses of predictors of rupture: 

*smoking status (former or current) not associated with rupture rate! 

*previous SAH not predictive of rupture - however only 3% of the cohort had ever had a SAH 

Criticisms: 

- Japanese population: which has the same incidence of aneurysm, but a higher risk of SAH compared to the rest of the world. Unclear if this data can be applied to US or european populations.
- Same selection bias as ISUIA - non-randomized data; the aneurysms believed to be high risk were all treated.

ISUIA (prospective) 
- 1991-1998
- N=4060 patients (1692 no surgery, 1917 surgery, 451 endovascular)
- Overall rupture rate -- 3% over 4.1 years of follow up; 65% mortality with ruptures

Rupture rates by location, size and presence of previous SAH*

 *All aneurysms examined in this study were unruptured, however some people in the study had a history of SAH from another source/another aneurysm. Those were designated as "group 2" --- vs "group 1", which denotes those who had no history of SAH.

Graphical representation of rupture rates by size and history of SAH: 

Multivariate model of predictors of aneurysmal rupture: 

Size: 

<7 mm (ref) 

7–12 mm, [RR] 3·3 [95% CI 1·3–8·2], p=0·01  

> 12 mm, [RR]17·0 [8·0–36·1], p<0·0001

Location:**

ICA (ref)

Basilar tip - [RR] 2·3 [1·1–4·8], p=0·025

Cavernous - [RR]  0·15 [0·04–0·64], p=0·01

Pcomm - [RR] 2·1 [1·1–4·2], p=0·02

Age: [RR] 1·007, [0·98–1·03], p=0·56 

- Morphological characteristics such as multiple lobes, presence of a daughter sac, and a family history of subarachnoid haemorrhage were not predictive of SAH 

**other locations not statistically significantly associated with rupture


Table comparing the observation vs intervention cohorts. 

Criticisms of the study: 
- Data from 1991-1998 -- before the era of widespread use of aspirin and statins, which decrease the rate of aneurysmal rupture. Also really before the era of endovascular techniques, which have significantly altered practice patterns such that the data from the people who were observed during this study is unlikely to apply to people we would observe today.
- Not randomized -- (most) everyone who was believed to be a high rupture risk underwent surgical or endovascular interventions; thus there's a selection bias for the low-risk aneurysms, thus possibly leading to an artifically lower rupture rate in the observation group.
- Selection bias of older, sicker patients --  The 5 year KM mortality in this group was 12.7% -- you would expect <1% in an age-matched control cohort. The observation group was likely enriched for poor surgical (and poor mid-90s era endovascular) candidates -- many died from cancer, heart disease, etc; About half of the patients died from intracranial hemorrhage events, many of which were NOT counted as rupture events but as censored -- patients who died from intracranial hemorrhage that could not be definitively attributed to the aneurysm were counted as censored. Another group (I can't remember which, but I think it was the TEAM group) re-analyzed the data counting all these censorship events as rupture events and found the overall annual rupture rate to be 1.2% vs 0.8% - a 50% difference although a small absolute difference.
- 32% censorship/crossover for treatment  -- enough said.
- <22% with >4 years of fu -- enough said.

- Included cavernous carotid aneurysms - which are known to have a very, very low rupture rate. 

Pretty Anatomy

Posterior choroidal vessels - lateral and medial. Lateral makes a more sharp C shape, while medial makes a curvy, swoopy "3" shape 

Lateral choroidal - makes clear C shape in lateral and AP shots. 

Really nice anatomy, ICA injection with reflux into basilar and PCAs via a large pcomm. Demonstrates a lovely anterior choroidal (orange), MHT (pink), ILT (cyan) and a mystery vessel in green that might be an enlarged vidian. 

Case study: vertebral dissection 

Young person, trauma, some C2 fractures. Concern for R vertebral artery dissection. 

Thoughts: 

- Clots respond to flow. In a case of complete occlusion leading, the clot will propagate to the nearest point of flow-- in this case, the original occlusion/dissection was at C2-3, and the occlusion is complete. We would expect it to go all the way down to the origin. It hasn't -- there are 2 reasons. One is that there might not have been enough time. Two is that there are vessels causing flow somewhere along V1 or V2 keeping the vert patent. Big muscular branches or there's sometimes a big radiculomedullary branch (analogous to artery of adamkiewicz) that comes off around C5-6 -- this is very important; occlusion of this vessel may compromise high cervical spine vascular supply. One might think, in a case where the vert is still partially filling, if we fully occlude the vert there will be a lower stroke risk -- that might be the case, but if the vert is patent because there is flow to a large radiculomedullary branch, occluding it might lead to a devastating outcome.

- Complete occlusions typically do not have to be treated with anticoagulation as they are low embolic stroke risks. Partial or recannalized verts typically do have to be anticoagulated.