Cranioplasty


- just like for a decompressive hemicrani - when you're making a giant trauma flap incision, you have to think about positioning such that you can reach the back of the head/most posterior aspect of incision. If someone has excellent neck mobility, you can just put them flat and turn head all the way over. If someone doesn't have good neck mobility (ie. c-collar, really old, arthritis, contractures) then you put a bump under the shoulder to get you access to back of head. similar principle for shunt - shoulder bump to straighten out neck for optimal tunneling.
- putting someone on a horse-shoe means that you can reach more posterior around their head more easily - think about your hand/wrist position relative to head vs them being flat on a table, and having the table block you
- shave around the incision area only
- cover eyes well with tegaderm, and then again with the 1000 drape, put drape as low across brow as you can to get the biggest field, but make sure to shield eyes - chlorhexadine is very caustic to corneas
- stuff xeroform into the ears only if you intend to use a chlorhexadine prep - it is ototoxic. if you are painting betadine or using alcohol only this step is skiappable
- prep and drape wide - you will have to tunnel a drain out of your flap
- feel bone edges under incision - if you have bone under incision you can cut all the way down. if you do not, you have to be careful - go thru skin with knife and then carefully bovie/dissect because its scalp - dura - brain. you will definitely not have any bone over the squamous temporal bone, because if you did a good decompression originally, you put a burr hole right at the pterion/over root of zygoma, and you kerrison'd all the way flush to the floor of the middle fossa for good temporal lobe decompression.
- for temporalis muscle, carefully dissect it off the dura - if you don't dissect between temporalis muscle and scalp, you can have a better chance of not causing a frontalis palsy. this is also a good place to find the bone edge and begin to develop the plane between periostium and dura.
- if you are lucky, there will be a good plane between periostium and dura, and you can follow that plane all the way around - you are not done until you see all bone edges. Put screws into the bone flap, push it flush all the way against anterior aspect of bone. if temporalis muscle is large and  healthy, you can just close (fascia on fascia) anterior temporalis muscle against posterior. If its kind of bad looking, consider putting in a mesh over the cranial defect where temporal bone used to be, to buttress it and prevent a hollowing defect later on.
- if you are not lucky, the whole thing will be scarred down and socked in and you just have to create a plane - find the bone, do not violate dura.
- leave a subgaleal drain, use hemovac (same width of drain all the way around vs JP which is a wider drain; HMV hurts less coming out, creates a smaller hole to close when removed). Always leave drain because it will bleed a lot and you will not be able to use aggressive electrocautery because otherwise it won't heal well.
- tunnel your drain before you close, tunnel it outside of your flap becusae it will heal better. do not sew in drain until you finish closing, otherwise you'll shift the position of the drain in head and where you tunnel it out may not be as sterile as the rest of your field so do that last.
- close galea with 3-0 vicryl with C-23 needle
- close skin with either absorbable sutures or staples - for healthy people who will heal well, choose absorbable - it looks nicer, plus you don't have to hurt people 2 weeks later when you take them out. If there is any question about whether someone will heal an incision though, use staples - you can hypothetically leave staples in forever. also they are faster.
- if you are struggling to close, either because scalp is really scarred or tight, consider nylon sutures with horizontal mattress-  you can use it to pull the scalp incrementally closer together

Differential Diagnosis of Intra-Axial Brain Tumor based on appearance in Adults

Intra-axial: 75% astrocytic tumor or mets

Tumors that invade the corpus callosum and cross midline
- GBM (rarely has leptomeningeal spread)
- Lymphoma (can have leptomeningeal spread, typically homogenously enhancing but in immunocompromised hosts can appear ring-enhancing or heterogenous)
- Mets (can have leptomeningeal enhancement, often cystic)

Multiple lesions
- usually mets
- multifocal GBM - rarer but exists
- gliomatosis cerebri
- lymphoma can appear as multiple lesions
- CNS metatstases - i.e. medulloblastoma, ependymoma, oligodendro
Genetic diseases that cause multiple tumors :
- NF1 (optic glioma, astrocytoma)
- NF2 (meningiomas, schwannoma, ependymoma of brain and spinal cord)
- Tuberous Sclerosis (SEGA, ependymoma)
- VHL (cerebellar/retinal/spinal cord hemangioblastomas, endolymphatic sac tumor)

Cortical-based

Oligodendro
- often cortical/subcortical, and are shown on MRI "extending all the way to the cortex"
- classically frontal but can be in any lobe.
- 70-90% calcified.
- usually T1 dark, T2 bright (except calcified areas - which will show up as T2 dark/T2* blooming
- 50% will enhance with Gad - usually heterogenously. Gad enhancement is not a reliable indicator of grade.
- Typically do not restrict on DWI. Often older people (40-50s+)

Ganglioglioma
- mix of glial and neuronal cells (if the glial component de-differentiates it turns into a GBM; if the neuronal component de-differentiates it turns into a neuroblastoma).
- 45% of the time it will appear as a cyst with mural nodule in a cortical area, but it can be very variable in appearance--- simple cyst with small mural nodule, complex cyst with large, heterogenous mural nodule, solid tumor only.
- The mural nodule has variable enhancement - sometimes enhances vividly
- not much edema.
- Usually affects children and young adults.

DNET:
- arise from cortical or deep grey matter.
- Predilection for temporal lobes.
- often associated with cortical dysplasia
- often cause intractable seizures.
- May be cyst with mural nodule.
- Enhances 20-30% of the time.
- T1 isodense, T2 bright with sometimes "bubbly" appearance 
- not much peritumoral edema.
- Rarely grow in size over time, excellent oncologic prognosis but often removed because of the intractable seizures they cause - seizures often stop when the tumor is resected.
- Typically affects children and young adults.

Of note: in clinical practice, DNETs and GG often appear very similar radiographically, are both T1-dark, T2-bright tumors that rarely enhance (DNET can sometimes appear as ring-enhancing but not commonly, GG are a little more likely to be cystic with mural nodule, etc), with predilections for the temporal lobe, cause seizures, and have excellent seizure freedom outcomes with resection. See this retrospective series from Turkey with 52 patients.

PXA:
- cortical tumors with cystic component and vivid enhancement with Gad. 
- 98% supratentorial. Mostly temporal.
- Often low grade/slow growing without much edema.
- T1 iso/hypointense. 50-60% cyst with mural nodule that enhances strongly. T2 - cyst often looks different than CSF due to proteinacious content.
- Avascular on angio despite vidid enhancement.
- Often affects kids and young adults.

Contain T1-bright tissue that resembles fat 

Lipoma
- always located in subarachnoid spaces - believed to be from maldevelopment of meninx primativa (subarachnoid precursor)
- pericallosal (can wrap around corpus callosum - associated with agensis of corpus callosum in 50% of cases) - 45%
- quadrigeminal cistern (associated with underdevelopment of inferior colliculus) - 35%
- suprasellar cistern - 15%
- CP angle - 10%
- sylvian fissure - 5%

Dermoid:
- Can be thought of as on the spectrum from epidermoid (only squamous epithelial tissue) to dermoid (ectodermal only) to teratomas (contain tissue from all 3 embryonic layers)
- They appear bright on T1 but there is actually no fat in them. They contain squamous epithelial tissue + ectodermal appendages like hair follicles, sweat glands, sebaceous glands - which secrete sebum which looks T1 bright (from cholesterol and other things). Technically no adipose tissue, because that is from mesenchymal tissue so it would technically be a teratoma if there was mesenchyme
- Often midline - suprasellar, subfrontal, cerebellar vermis
- They can rupture and cause a chemical meningitis - leptomeningeal enhancement
- Very rarely will transform into squamous carcinoma

Teratoma - contains tissue from all 3 embryonic layers.
- rare in general population - however 25-50% of fetal brain tumor
- usually pineal or suprasellar
- T1 bright from fat, can enhance

Contain Calcifications

- Oligodendro - rare, but often calicfied

- Astrocytoma - common, but infrequently calcified 

- Pinealcytoma - are not calcified in and of themselves, but contain the inherent calcifications of the pineal gland 

- Craniopharyngioma - suprasellar 

Cystic lesions with same intensity as CSF 

- Arachnoid
- Neurenteric cyst 

- Enlarged virchow-robin space 

Bright on T1

- most tumors are isodense or slightly hypodense on T1. T1 hyperintensity implies presence of one of the elements which are hyperintense on T1, which include the following: 

- Fat -> Lipoma, Teratoma 

- Cholesterol -> Craniopharyngioma, Dermoid, colloid cyst 

- Melanin -> Melanoma met

- Subacute blood (intracellular or extracellular metHb) -> Hemorrhagic tumor - melanoma met, breast/lung (uncommonly bleed), follicular thyroid met, renal cell met, choriocarcinoma met. pituitary apoplexy 

- Mineralization with paramagnetic divalent cations ( Ca, Copper, manganese )

- Proteinaceous fluid - neurentetic cyst 

Dark on T2

- Most tumors are bright on T2 dude to high water content. Low T2 signal implies:

- hypercellularity -> PNET/medullo, lymphoma, mucinous adenoCA mets, high-cellularity parts of GBM (although GBM is usually T2 bright) 

- calcifications -> oligo, astro, craniopharyngioma 

- many flow voids -> hemangioblastoma

Contrast enhancement: 

- Fundamentally based on the integrity of the BBB

Tumors that do not have a BBB will enhance vividly 

- extra-axial masses like meningioma, schwannoma

- non-CNS tumors like lymphoma, metastatic lesions (breast, lung, etc)

- CNS tumors derived from tissue that does not have a BBB - pituitary, pineal (including germinoma and other pineal gland tumors), choroid plexus 

Homogenous enhancement

- Mets

- Lymphoma (non immunocompromised) 

- Meningioma - and its great mimics, hemangiopericytoma and dural based MALT lymphomas 

- Schwannoma/neurofibroma 

- Mural nodule of hemangioblastoma, JPA

- Germinoma, other pineal gland tumors

- Pituitary adenoma

- Ganglioglioma 

Patchy Enhancement

- Mets

- GBM

- Non tumor things (like radiation necrosis) 

Ring Enhancement

- MAGICALDR

- Mets

- Abscess

- GBM

- Ischemia (subacute stroke), Infection (neurocystercercosis, toxoplasma, TB, blasto/histo/crypto, nocardia, listeria) 

- Contusion

- Alternative weird stuff (sarcoid, vasculitis, behcets) 

- Lymphoma 

- Demyelination (MS, ADEM) 

- Radiation necrosis 

Leptomeningeal Enhancement 

- leptomeningeal carcinomatosis (breast, lung, melanoma, leukemia/lymphoma) 

- from CNS tumors - GBM, medullo/PNET, ependymoma, choroid plexus carcinoma. 

- infectious - meningitis (bacterial, viral, crypto, TB)

- sarcoid 

- post-LP (<5%), post-surgery/hemorrhage/trauma 

Sources:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3876643/
http://www.radiologyassistant.nl/en/p47f86aa182b3a/brain-tumor-systematic-approach.html
http://radiopaedia.org/articles/dysembryoplastic-neuroepithelial-tumour
http://radiopaedia.org/articles/ganglioglioma
http://radiopaedia.org/articles/pleomorphic-xanthoastrocytoma
http://radiopaedia.org/articles/intracranial-dermoid-cyst-1
http://radiopaedia.org/articles/gliomatosis-cerebri
http://radiopaedia.org/articles/leptomeningeal-enhancement

	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.