Neuro

Question 1

Central Sulcus

Answer 1

This anatomic landmark separates the frontal lobe from the parietal lobe,
and is useful to find if you haven’t learned the lazy Neuroradiolgisf s go to descriptor “fronto-parietal region.”

Question 2

Practically speaking, this is the strategy I use for finding the central sulcus:

Answer 2

Pretty high up on the brain, maybe the 3rd or 4th cut, I find the pars marginalis. This is called the “pars bracket sign” - because the bi-hemispheric symmetric pars marginalis form an anteriorly open bracket. The bracket is immediately behind the central sulcus. This is
present about 95% o f the time - it’s actually pretty reliable.

Question 3

Central Sulcus Trivia - Here are the other less practical ways to do it.

Answer 3

Superior frontal sulcus / Pre-central sulcus sign: The posterior end o f the superior frontal sulcus joins the pre-central sulcus

Inverted omega (sigmoid hook) corresponds to the motor hand

Bifid posterior central sulcus: Posterior CS has a bifid appearance about 85%

Thin post-central gyrus sign - The precentral gyrus is thicker than the post-central gyrus (ratio 1.5 : 1).

Intersection - The intraparietal sulcus intersects the post-central sulcus (works almost always)

Midline sulcus sign - The most prominent sulcus that reaches the midline is the central sulcus (works about 70%).

Question 4

Superior frontal sulcus

Answer 4

often intersects the pre CS

Question 5

inverted omega

Answer 5

On the central sulcus

represents the motor hand

Question 6

intraparietal sulcus

Answer 6

intersects the post CS

Question 7

precentral is

Answer 7

thick

Question 8

postcentral is

Answer 8

thin

Question 9

the post cs is bifid

Answer 9

about 85% of the time

Question 10

Homunculous Trivia

Answer 10

The inverted omega (posteriorly directed knob) on the central sulcus /
gyrus designates the motor cortex controlling hand function.

ACA territory gets legs,

MCA territory hits the rest.

Question 11

Normal Cerebral Cortex

Answer 11

As a point of trivia, the cortex is normally 6 layers thick, and the hippocampus is normally 3 layers thick. I only mention this because the hippocampus can look slightly brighter on FLAIR compared to other cortical areas, and this is the reason why (supposedly).

Question 12

Dilated Perivascular Spaces (Virchow-Robins):

Answer 12

These are fluid filled spaces that accompany perforating vessels. They are a normal variant and very common. They can be enlarged and associated with multiple pathologies; mucopolysaccharidoses (Hurlers and Hunters) / ‘gelatinous pseudocysts” in
cryptococcal meningitis, and atrophy with advancing age. They don’t contain CSF, but instead have interstitial fluid. The common locations for these are: around the lenticulostriate arteries in the lower
third of the basal ganglia, in the centrum semiovale, and in the midbrain.

Question 13

Cavum septum pellucidum

Answer 13

-100% of preterm infants,

• 15% of adults.
• Rarely, can cause hydrocephalus
• Anterior to the foramen of Monroe
• Between frontal horns

Question 14

Cavum Vergae

Answer 14

• Posterior continuation of the cavum septum pellucidum (never exists without a cavum septum pellucidum)
• Posterior to the foramen of Monroe
• Between bodies of lateral ventricles

Question 15

Ventricular Anatomy

Answer 15

You have two lateral ventricles that communicate with the third ventricle via the interventricular foramen (of Monro), which in turn communicates with the fourth ventricle via the cerebral aqueduct.

The fluid in the fourth ventricle escapes via the median aperture (foramen of Magendie), and the lateral apertures (foramen of Luschka). A small amount of fluid will pass downward into the spinal subarachnoid spaces, but most will rise through the tentorial notch and over the surface of the brain where it is reabsorbed by the arachnoid villi and granulations into the venous sinus system.

Blockage at any site will cause a noncommunicating hydrocephalus. Blockage of reabsorption at the villi / granulation will also cause a noncommunicating hydrocephalus.

Question 16

Arachnoid Granulations

Answer 16

These are regions where the arachnoid projects into the venous system
allowing for CSF to be reabsorbed. They are hypodense on CT (similar to CSF), and usually round or oval. This round shape helps distinguish them from clot in a venous sinus (which is going to be linear). On MR they are typically T2 bright (iso to CSF), but can be bright on FLAIR (although this varies a lot and therefore probably won’t be tested). These things can scallop the inner table (probably from CSF pulsation).

Question 17

Basal Cisterns overview

Answer 17

People say the suprasellar cisterns look like a star, with the five corners lending themselves nicely to multiple choice questions. So let us do a quick review; the top of the star is the interhemispheric
fissure, the anterior points are the sylvian cisterns, and the posterior points are the ambient cisterns.
The quadrigeminal plate looks like a smile, o r … I guess it looks like a sideways moon, if you
don’t like smiles.

Question 18

The Ambient Cistern is

Answer 18

a bridge between the

Interpeduncular C. ► Quadrigeminal C.

Question 19

suprasellar cistern star

Answer 19

Anterior interheispheric cistern

sylvian cistern sylvian cistern

 ambient cistern        ambient cistern

         quadrigeminal plate citern (sideways moon)

Question 20

Midbrain tectum vs tegmentum

Answer 20

Cerebral peduncle Cerebral peduncle
(usbstantia nigra) (substantia nigra)
tegmentum tegmentum
(red nucleus) (red nucleus)
tectum (aqueduct) tectum

Question 21

Foramen rotundum

Answer 21

showing Foramen Rotundum (FR) in the coronal and sagittal planes is a very common sneaky trick.

On the coronal view, FR looks like you are staring into a gun barrel.

On the sagittal view, think about FR as being totally level or horizontal.

Question 22

Foramen spinosum and ovale

Answer 22

With regard to the relationship between Spinosum and Ovale, I like to think of this as the footprint a
woman’s high heeled shoe might make in the snow, with the oval part being Ovale, and the pointy
heel as Spinosum.

Question 23

Hypoglosal canal

Answer 23

The Hypoglossal Canal is very posterior
and inferior.
This makes it unique as a skull base foramen.

Question 24

Jugular foramen overview

Answer 24

The jugular foramen has two parts which are

separated by a bony “jugular spine.”

Question 25

Pars Nervosa

Answer 25

The nervous guy in the front. This contains the Glossopharyngeal nerve (CN 9), along with it’s tympanic branch - the “Jacobson’s Nerve

Question 26

Pars Vascularis

Answer 26

This is the “vascular part” which actually contains the jugular bulb, along with the Vagus nerve (CN 10), Auricular branch “Arnold’s Nerve,” and the Spinal Accessory Nerve (CN 11)

Question 27

Bony Anatomy: Orbital Fissures and the PPF overview

Answer 27

The relationship between the Superior Orbital Fissure (SOF), the Inferior Orbital Fissure (IOF), Foramen Rotundum (FR), and the Pterygopalatine Fossa (PPF) is an important one, that can really lead to some sneaky multiple choice questions (mainly what goes through what - see chart page 17 volume 2 ``` sagittal top to bottom sof iof fr ppf ``` ``` coronal sof iof fr ppf ```

Question 28

Anatomy: Cavernous Sinus whts in it

Answer 28

CN 3, CN 4, CN VI, CN V2, CN 6, and the carotid - run through it.

Question 29

Anatomy: Cavernous Sinus whats not in it

Answer 29

CN 2 and CN V3 - do NOT run through it.

Question 30

Anatomy: Cavernous Sinus anatomy trivia

Answer 30

The only other anatomy trivia I can think of is that CN6 runs next to the carotid, the rest of the nerves are along the wall. This is why you can get lateral rectus palsy earlier with cavernous sinus pathologies.

Question 31

Anatomy: Internal Auditory Canal - “IAC’ overview

Answer 31

The thing to remember is “7UP, and COKE Down” - with the 7th cranial nerve superior to the 8th cranial nerve (the cochlear nerve component). As you might guess, the superior vestibular branch is superior to the inferior one.

Question 32

Anatomy: Internal Auditory Canal - “IAC’ ideal sequence

Answer 32

The ideal sequence to find it is a heavily T2 weighted sequence with super thin cuts through the IAC.

Question 33

Anatomy: Internal Auditory Canal - “IAC’ sagittal

Answer 33

ante/superior post/superior CN7 Superior vestibular CN8 inferior vestibular

Question 34

Contents Foramen Ovale

Answer 34

CN V3, and Accessory Meningeal Artery

Question 35

Contents Foramen Rotundum

Answer 35

CN V2 ("R2V2"),

Question 36

Contents``` Superior Orbital Fissure

Answer 36

C N 3 , CN 4, CN V I, CN6

Question 37

Contents Inferior Orbital Fissure

Answer 37

CN V2

Question 38

Contents Foramen Spinosum

Answer 38

Middle Meningeal Artery

Question 39

Contents Jugular Foramen

Answer 39

Pars Nervosa: CN 9, | Pars Vascularis: CN 10, CN 11

Question 40

Contents Hypoglossal Canal

Answer 40

CN 12

Question 41

Contents Optic Canal

Answer 41

CN 2 , and Opthalmic Artery

Question 42

Contents Cavernous Sinus

Answer 42

CN 3, CN 4, CN VI, CN V2, CN 6, and the carotid

Question 43

Contents Internal Auditory Canal

Answer 43

CN 7, CN 8 (Cochlear, Inferior Vestibular and Superior | Vestibular components). “7 Up - Coke Down”

Question 44

Contents Meckel Cave

Answer 44

Trigeminal Ganglion

Question 45

Contents Dorello's Canal

Answer 45

Abducens Nerve (CN 6), Inferior petrosal sinus

Question 46

Vascular Anatomy overview

Answer 46

Arterial vascular anatomy can be thought o f in four sections. (1) The branches o f the external carotid (commonly tested as the order in which they arise from the common carotid). (2) Segments o f the internal carotid, with pathology at each level and variants. (3) Posterior circulation, (4) Venous anatomy

Question 47

(11 Branches of the External Carotid

Answer 47

Some Administrators Love Fucking Over Poor Medical Students ``` from first off to last branch Superior Thyroid 9anterior) Ascending Pharyngeal (superior Lingual (anterior) Facial (Anterio thens uperior) Occipital (posterior superior) Posterior Auricular (posterior superior) Maxillary (anterior) Superficial Temporal (supeior) ```

Question 48

THIS VS THAT: External vs Internal Carotid via Ultrasound internal

Answer 48

no branches posterior low resistance (continous diastolic) no change in waveform with temporal tap

Question 49

THIS VS THAT: External vs Internal Carotid via Ultrasound external

Answer 49

branches anterior high resistance waverform areacts to temporal tap

Question 50

Segments of the Internal Carotid Internal Carotid

Answer 50

• The bifurcation of the IAC and ECA usually occurs at C3-C4 • Cervical ICA has no branches in the neck - if you see branches either (a) they are anomalous or more likely (b) you are a dumb ass and actually looking at the external carotid. *Remcmber finding branches is a way you can tell ICA from ECA on ultrasound. • Low resistance waveform with continuous forward flow during diastole • Flow reversal in the carotid bulb is common

Question 51

Segments of the Internal Carotid Cl (Cervical)

Answer 51

Atherosclerosis: The origin is a very common location Dissection: Can be spontaneous (women), and in Marfans or Ehlers- Danlos, and result in a partial Homer’s (ptosis and miosis), followed by MCA territory stroke. Can have a retropharyngeal course and get “drained” by ENT accidentally. Pharyngeal infection may cause pseudoaneurysm at this level. to the level of the carotid canal The internal carotid artery (C1 segment) enters the skull base through the carotid canal, where it begins a series of 90° turns which lead it to eventually terminate as the middle and anterior cerebral arteries.

Question 52

Segments of the Internal Carotid C2 (Petrous)

Answer 52

Not much goes on at this level. Aneurysms here can be surprisingly big (thats what she said). in the carotid canal It first turns 90° anteromedially within the carotid canal as the C2 segment to run through the petrous temporal bone.

Question 53

Segments of the Internal Carotid C3 (Lacerum)

Answer 53

Not much here as far as vascular pathology. The anatomic location is important to neurosurgeons for exposing Meckel’s cave via a transfacial approach from the carotid canal to the level of the petrolingual ligament As it exits the carotid canal it lies superior to the foramen lacerum (C3 segment) and then turns 90° superiorly and then immediately another 90o turn anteriorly to groove the body of the sphenoid

Question 54

Segments of the Internal Carotid C4 (Cavernous)

Answer 54

This segment is affected by multiple pathologies including the development of cavernous - carotid fistula. Aneurysms here are strongly associated with hypertension, from the petrolingual liament to the dural ring enter the medial aspect of the cavernous sinus (C4 segment). Within the cavernous sinus the abducens nerve is intimately related to the artery on its lateral side.

Question 55

Segments of the Internal Carotid C5 (Clinoid)

Answer 55

Aneurysm here could compress the optic nerve and cause blindness. in the dural ring At the anterior end of the cavernous sinus, the ICA makes another 90° turn superiorly (C5 segment) and a final 90° turn posteriorly

Question 56

Segments of the Internal Carotid C6 (Ophthalmic - Supraclinoid):

Answer 56

Origin at the “dural ring” is a buzzword for this artery. Common site for aneurysm formation. to pass medial to the anterior clinoid process (C6 segment)

Question 57

Segments of the Internal Carotid | C7 Communicating

Answer 57

Aneurysm here may compress CN III and present with a palsy. The terminal ICA (C7 segment) abruptly divides into the middle and anterior cerebral branches and gives off two smaller posterior branches, the anterior choroidal artery and the posterior communicating artery.

Question 58

Internal carotid anatomy total

Answer 58

Course The cervical segment of the ICA courses posterior to the ECA after its origin and ascends in the neck within the carotid sheath. As it ascends on the pharyngeal wall and the buccopharyngeal fascia, it is consecutively crossed laterally by the pharyngeal branch of the vagus nerve (CN X), glossopharyngeal nerve (CN IX), and the stylopharyngeus and styloglossus muscles. The internal carotid artery (C1 segment) enters the skull base through the carotid canal, where it begins a series of 90° turns which lead it to eventually terminate as the middle and anterior cerebral arteries. It first turns 90° anteromedially within the carotid canal as the C2 segment to run through the petrous temporal bone. As it exits the carotid canal it lies superior to the foramen lacerum (C3 segment) and then turns 90° superiorly and then immediately another 90o turn anteriorly to groove the body of the sphenoid and enter the medial aspect of the cavernous sinus (C4 segment). Within the cavernous sinus the abducens nerve is intimately related to the artery on its lateral side. At the anterior end of the cavernous sinus, the ICA makes another 90° turn superiorly (C5 segment) and a final 90° turn posteriorly to pass medial to the anterior clinoid process (C6 segment). The terminal ICA (C7 segment) abruptly divides into the middle and anterior cerebral branches and gives off two smaller posterior branches, the anterior choroidal artery and the posterior communicating artery. Branches Except for the terminal segment (C7), the odd-numbered segments usually have no branches. The even-numbered segments (C2, C4, C6) often have branches, although they are inconstant and usually small, therefore often not visualized even on high-resolution digital subtraction angiography. The exception is the ophthalmic artery, which is seen in nearly all cases

Question 59

what branche first posterior communicating or anterior choroidal

Answer 59

p comm

Question 60

ICA lateral vs anterior

Answer 60

ACA is antioer | MCA is lateral

Question 61

Acute CN3 Palsy (unilateral | pupil dilation)

Answer 61

classic neurology boards question - grab a relax hammer STAT! ``` The answer is PCOM aneurysm until proven otherwise (although it can also be caused by an aneurysm at the apex of the basilar artery or its junction with the superior cerebellar / posterior cerebral arteries). ``` The reason is the relationship between the CN3 and vessels (arrows).

Question 62

Circle willis anatomy

Answer 62

23

Question 63

Vascular Variants Fetal Origin o f the PCA

Answer 63

Most common vascular variant (probably) - seen in up to 30% of general population. ``` Definitions vary on what a fetal PCA is. Just think of this as a situation where the PCA is feed primarily as an anterior circulation artery (occipital lobe is feed by the ICA). ``` Therefore, the PCOM is large (some people define this vessel as PCOM larger than P 1). Another piece of trivia is that anatomy with a fetal PCA has the PCOM superior / lateral to CN3 (instead o f superior / medial - in normal anatomy).

Question 64

Vascular Variants Persistent Trigeminal Artery

Answer 64

Persistent fetal connection between the cavernous ICA to the basilar. A characteristic “tau sign” on Sagittal MRI has been described. It increases the risk of aneurysm (anytime you have branch points).

Question 65

Sag - C o n n e c ted B a s ila r an d ICA

Answer 65

L o o k s like a “T ” au

Question 66

Anastomotic Vein of Trolard

Answer 66

Connects the Superficial Middle Cerebral Vein and the Superior Sagittal Sinus

Question 67

Anastomotic Vein of Labbe

Answer 67

Connects the Superficial Middle Cerebral Vein and the Transverse Sinus

Question 68

Trolard =

Answer 68

top

Question 69

labbe =

Answer 69

lower

Question 70

Superficial cerebral veins

Answer 70

Superior Cerebral Veins Superior Anastomotic Vein of Trolard Inferior Anastomotic Vein of Labbe Superficial Middle Cerebral Veins

Question 71

Deep cerebral veins

Answer 71

Basal Vein of Rosenthal Vein of Galen Inferior Petrosal Sinus

Question 72

cerebral veins collateral pathways

Answer 72

The dural sinuses have accessory drainage pathways (other than the jugular veins) that allow for connection to extracranial veins. These are good because they can help regulate temperature, and equalize pressure. These are bad because they allow for passage o f sinus infection / inflammation, which can result in venous sinus thrombosis.

Question 73

cerebral veins inverse relationship

Answer 73

There is a relationship between the Vein o f Labbe, and the Anastomotic Vein o f Trolard. Since these dudes share drainage o f the same territory, as one gets large the other get small.

Question 74

Vein o f Labbe

Answer 74

Large draining vein, connecting the superficial middle vein and the transverse sinus

Question 75

Vein o f Trolard

Answer 75

Smaller (usually) vein, connecting the superficial middle vein and sagittal sinus

Question 76

Basal veins o f Rosenthal

Answer 76

Deep veins that passes lateral to the midbrain through the | ambient cistern and drains into the vein o f Galen. Their course is similar to the PCA.

Question 77

Vein o f Galen

Answer 77

Big vein (“great”) formed by the union o f the two internal cerebral veins.

Question 78

Venous Gamesmanship overview

Answer 78

``` An embolus o f venous gas is common and often not even noticed. The classic location is the cavernous sinus (which is venous), but if the volume is large enough, air can also be seen in the orbital veins, superficial temporal veins, frontal venous sinus, and petrosal sinus. ```

Question 79

Venous Gamesmanship why does this happen

Answer 79

Peripheral (or central IV) had some air in the tubing. Thats right, you can blame it on the nurse (which is always satisfying). “Nurse Induced Retrograde Venous Air Embolus ”

Question 80

Venous Gamesmanship significance

Answer 80

Don’t mean shit. It pretty much always goes away in 48 hours with no issues.

Question 81

Venous Gamesmanship most common spot and the other sights

Answer 81

cavernous sinus orbital veins and superficial temporal

Question 82

The Concha Bullosa

Answer 82

This is a common variant where the middle concha is pneumatized. It’s pretty much o f no consequence clinically unless it’s fucking huge - then (rarely) it can cause obstructive symptoms.

Question 83

CN 3 Palsy

Answer 83

Think Posterior Communicating Artery Aneurysm

Question 84

CN 6 Palsy

Answer 84

Think increased ICP

Question 85

Increased ICP >

Answer 85

Brain Stem Herniates Interiorly —► CN 6 Gets Stretched

Question 86

Brain Myelination overview

Answer 86

The baby brain has essentially the opposite signal characteristics as the adult brain. The T1 pattern of a baby is similar to the T2 pattern of an adult. The T2 pattern o f a baby is similar to the T1 pattern of an adult. This appearance is the result o f myelination changes. The process o f myelination occurs in a predetermined order, and therefore lends itself easily to multiple choice testing. The basic concept to understand first is that immature myelin has a higher water content relative to mature myelin and therefore is brighter on T2 and darker on T1. During the maturation process, water will decrease and fat (brain cholesterol and glycolipids) will increase. Therefore mature white matter will be brighter on T1 and darker on T2.

Question 87

Brain Myelination testable trivia

Answer 87

the T1 changes precede the T2 changes (adult T1 pattern seen around age 1, adult T2 pattern seen around age 2). Should be easy to remember (1 fo r Tl, 2 for T2).

Question 88

Brain Myelination take home point

Answer 88

Tl is most useful for assessing myelination in the first year (especially 0-6 months), T2 is most useful for assessing myelination in the second year (especially 6 months to 18 months).

Question 89

Brain Myelination order of progression

Answer 89

Just remember, inferior to superior, posterior to anterior, central to peripheral, and sensory fibers prior to motor fibers. The testable trivia is that the subcortical white matter is the last part of the brain to myelinate, with the occipital white matter around 12 months, and the frontal regions finishing around 18 months. The “terminal zones” o f myelination occur in the subcortical frontotceporoparietal regions - finishing around 40 months.

Question 90

Brain Myelination another form of testable trivia

Answer 90

the brainstem, and posterior limb of the internal capsule are normally myelinated at birth.

Question 91

Brain Myelination Pattern

Answer 91

Inferior to Superior, Posterior to Anterior

Question 92

Immature | Myelin

Answer 92

High water low fat t1 dark t2 bright

Question 93

mature myelin

Answer 93

low water high fat t1 bright t2 dark

Question 94

Pituitary development overview

Answer 94

Both the Anterior and Posterior Pituitary are T1 Bright at Birth (anterior only T1 bright until 2 months).

Question 95

Pituitary birth

Answer 95

Ant T1 Hyper Posterior T1 Hyper

Question 96

pituitary adult

Answer 96

ant t1 iso, t2 iso posterior t1 hyper, t2 hypo

Question 97

Brain Iron

Answer 97

Brain Iron increases with age (globus pallidus darkens up).

Question 98

skull bone marrow signal

Answer 98

Calvarial Bone Marrow will be active (T1 hypointense) in young kids and fatty (T1 hyperintense) in older kids

Question 99

Sinus Development overview

Answer 99

Sinus Development: The sinuses form in the following order: 1- Maxillary, 2- Ethmoid, 3- Sphenoid, 4- Frontal Most are finished forming by around 15 years.

Question 100

Sinus Development detailed

Answer 100

Order Visible on CT Maxi.l..l ary 1. Present at _5 month Ethmoid 2 Present at birth 1. year Frontal 4 Not Present at Birth 6 years Sphenoid 3 not present at birth 4 years

Question 101

Congenital Malformations overview

Answer 101

This is a very confusing and complicated topic, full o f lots o f long Latin and French sounding words. If we want to keep it simple and somewhat high yield you can look at it in 5 basic categories: (1) Failure to Form, (2) Failure to Cleave, (3) Failure to Migrate, (4) Development Failure Mimics, and (5) Herniation Syndromes.

Question 102

Failure to Form • Dysgenesis / Agenesis of the Corpus Callosum overview

Answer 102

``` A classic point o f trivia is that the corpus callosum forms front to back (then rostrum lastl. Therefore hypoplasia o f the corpus callosum is usually absence o f the splenium (with the genu intact). ```

Question 103

Failure to Form • Dysgenesis / Agenesis of the Corpus Callosum front to back

Answer 103

``` rostrum genu body isthmus splenium ```

Question 104

Failure to Form • Dysgenesis / Agenesis of the Corpus Callosum gamesmanship

Answer 104

With agenesis of the corpus callosum, a common trick is to show colpocephaly (asymmetric dilation o f the occipital homs). When you see this picture you should think: (1) Corpus Callosum Agenesis (2) Pericallosal Lipoma

Question 105

Colpocephaly

Answer 105

(asymmetric dilation of the occipital homs).

Question 106

Failure to Form - Dysgenesis / Agenesis of the Corpus Callosum Continued other common ways to show this

Answer 106

The steer horn appearance on coronal vertical ventricles - widely spaced (racing car) on axial

Question 107

Why are the lateral ventricles widely spaced when you have no corpus callosum ?

Answer 107

``` There are these things called “Probst bundles” which are densely packed WM tracts - destined to cross the CC - but can’t (because it isn’t there). So instead they run parallel to the interhemispheric fissure - making the vents look widely spaced. ```

Question 108

Failure to Form - Associations - Intracranial Lipoma overview

Answer 108

Dysgenesis / Agenesis o f the Corpus Callosum is associated with lots o f other syndromes/ malformations (Lipoma, Heterotopias, Schizencephaly, Lissencephaly, e tc...). Some sources will even say it is the “most common anomaly seen with other CNS malformations. ” — whatever the fuck that means.

Question 109

Failure to Form - Associations - Intracranial Lipoma trivia

Answer 109

. CNS Lipomas are congenital malformations, not true neoplasms. • “ Maldifferenitation o f the Meninx Primitiva " - is a meaningless French sounding explanation for the frequent pericollasal location. • Non Fat Sat T1 is probably the most helpful sequence (most non-bleeding things in the brain are not T1 bright). • These things d o n ’t cause symptoms (usually) are rarely treated.

Question 110

Intracranial lipoma

Answer 110

``` The most classic association with CC Agenesis. 50% are found in the interhemispheric fissure, as shown here. The 2nd most common location is the quadrigeminal cistern (25%). ```

Question 111

Anencephaly overview

Answer 111

Neuro Tube Defect (Defect at the top o f head) The Top of the Head is Absent (Above the Eyes) Reduced /Absent cerebrum and cerebellum. The hindbrain will be present. Mercifully, not compatible with life. Potential to he awful at Jeopardy

Question 112

Anencephaly Classic Image Appearance:

Answer 112

Incredibly creepy “Frog Eye” appearance on the coronal plane (due to absent cranial bone / brain with bulging orbits).

Question 113

Anencephaly Secondary Signs / Gamesmanship:

Answer 113

• Antenatal Ultrasound With Polyhydramnios (hard to swallow without a brain) • AFP will be elevated (true with all open neural tube defects)

Question 114

Iniencephaly overview

Answer 114

Neural Tube Defect (Defect at the level o f the cervical spine) Deficient Occipital Bone with Defect in the Cervical Region. Inion = Back of Head / Neck Extreme Retroflexion of the Head. Enlarged foramen magnum. Jacked up spines. Often visceral problems. Usually, not compatible with life. When they do survive, they tend to have a natural talent for amateur astronomy

Question 115

Iniencephaly classic imaging appearance

Answer 115

“Star Gazing Fetus” - contorted in a way that makes their face turn upward (hyper-extended cervical spine, short neck, and upturned face). It’s every bit as horrible as the Frog Eye thing (both would make incredible Halloween costumes.)

Question 116

Iniencephaly secondary sigs/gamesmanship

Answer 116

AFP will be elevated | true with all open neural tube defects

Question 117

Failure to Form - Open Neural Tube Defects - Encephalocele ( meningoencephalocele)

Answer 117

Neural tube defect where brain + meninges herniate through a defect in the cranium. There are lots o f different types and locations — but most are midline in the occipital region. There are numerous associations: - most classic = Chiari III

Question 118

Rhombencephalosynapsis

Answer 118

vermis is absent note the vertical lines across the cerebellum

Question 119

Rhombencephalosynapsis classic imaging appearance

Answer 119

Transversely oriented single lobed cerebellum as shown above (this is an Aunt Minnie). Absence of the vermis results in an abnormal fusion of the cerebellum. Small 4th Ventricle Rounded Fastigial Point, Absent Primary Fissure

Question 120

Rhombencephalosynapsis associations

Answer 120

Holoprosencephaly Spectrum

Question 121

Joubert Syndrome

Answer 121

Vermis is Absent (or Small)

Question 122

Joubert Syndrome classic imaging appearance

Answer 122

“Molar Tooth” appearance of the superior cerebellar peduncles (elongated like the roots of a tooth). Small Cerebellum Absence of pyramidal decussation (whatever the fuck the means) Large 4th Ventricle “Batwing Shaped” Absent Fastigial Point, Absent Primary Fissure

Question 123

Joubert Syndrome associations

Answer 123

``` Retinal dysplasia (50%), Multicystic dysplastic kidneys (30%). Liver Fibrosis (“COACH” Syndrome) ```

Question 124

Failure to Form - Cerebellar Vermis Gamesmanship:

Answer 124

If you are faced with this level of trivia (on an intermediate level exam), first start by looking for the two markers of normal vermian development: (1) the primary fissure and (2) fastigial point - both of which arc best seen mid sagittal. The ‘fastigial po in t” is normal angular contour (not round) along the ventral surface of the cerebellum. The primary cerebellar fissure is a deep trapezoid shaped cleft along the posterior cerebellum. Absence or abnormal morphology of these landmarks should trigger a multiple choice brain reflex indicating the vermis is not normal.

Question 125

Classic Dandy Walker 3 key findings

Answer 125

``` 1 Hypoplasia of the Vermis (usually the inferior part) 2 Hypoplastic Vermis is Elevated and Rotated 3 Dilated Cystic 4th Ventricle ```

Question 126

Classic Dandy Walker axial

Answer 126

On axial, there is the nonspecific appearance o f an enlarged posterior fossa CSF space. It can look like a retrocerebellar cyst on axial only (although it’s not a cyst - it’s the expanded 4th ventricle). The cerebellar hemispheres will be displaced forward and laterally but their overall volume and morphologic characteristics should be preserved.

Question 127

"TORCULAR-LAMBDOID INVERSION" overview

Answer 127

This classic buzzword(s) describes the torcula (confluence o f venous sinuses) above the level of the lambdoid suture, secondary to elevation of the tentorium. It’s worth mentioning that this inversion is often NOT seen in the “variant” version of Dandy Walker.

Question 128

"TORCULAR-LAMBDOID INVERSION" quick

Answer 128

- Normal - Lambdoid Above Torcula - Dandy Walker - Torcula Above Lambdoid ' High-Inserting Venous Confluence "

Question 129

“C la s s ic ” Dandy W a lk e r trivia

Answer 129

Often identified on OB screening US. Otherwise, presents with symptoms of increased intracranial pressure (prior to month 1) Most Common Manifestation = Macrocephaly (nearly all cases with the first month) Associations: Hydrocephalus (90%), Additional CNS malformations (~ 40%) (agenesis of the corpus callosum, encephaloceles, heterotopia, polymicrogyria, etc...).

Question 130

Failure to Form - Dandy walker and Friends from least to most severe

Answer 130

Mega Cisterna Magna Blake Pouch “Variant” DWM “Classic” DWM

Question 131

Variant DWM name

Answer 131

hypoplastic rotated vermis

Question 132

Mega Cisterna Magna

Answer 132

Overview: normal variant. focal enlargement of the retrocerebellar CSF space Vermis: normal 4th Ventricle: normal Cerebellar Hemispheres: normal Posterior Fossa: normal Torcula: normal Hydrocephalus: no Trivia: no supratentorial abnormalities

Question 133

Blake Pouch

Answer 133

Overview: sac like cystic protrusion through the foramen of magendie into the infra/retro cerebellar region Vermis: normally formed but upwardly displaced 4th Ventricle: dilated Cerebellar Hemispheres: normal Posterior Fossa: normal Torcula: normal Hydrocephalus: yes Trivia: choroid from the 4th ventricle swinging into the pouch is classic (but not always present) the pouch only communicates with the 4th ventricle not the internal CSF

Question 134

“Variant” DWM

Answer 134

Overview: hypoplastic vermis with dilation of the 4th ventricle Vermis: hypoplastic (less severe) 4th Ventricle: dilated Cerebellar Hemispheres: hypoplastic Posterior Fossa: normal Torcula: normal Hydrocephalus: 25% of cases Trivia: Diagnosis on antenatal ultrasound must be done after 18 weeks (prior to 18 weeks the vermis hasnt finished forming).

Question 135

“Classic” DWM

Answer 135

Overview: hypoplastic, elevated, rotated vermis with cystic dilation of the 4th ventricle Vermis: hypoplastic and rotated 4th Ventricle: markedly dilated Cerebellar Hemispheres: normal in size but diplaced anteriolaterally Posterior Fossa: expanded Torcula: high insertion Hydrocephalus: 90% of cases Trivia: Diagnosis on antenatal ultrasound must be done after 18 weeks (prior to 18 weeks the vermis hasnt finished forming).

Question 136

Failure to Cleave - Holoprosencephaly ( HPE)

Answer 136

This entity also occurs along a spectrum with the common theme being some element of abnormal central fusion. Although, it isn’t actually a fusion problem. Instead, it is a failure to perform the normal midline cleaving. In the normal embryology, the fancy latin word '"P-lon ” starts out like a peanut butter sandwich, then mom cuts the bread into two perfect halves (separate lateral hemispheres). The sandwich cutting (cleavage) always occurs back to front (opposite of the formation of the corpus callosum), so in milder forms the posterior cortex is normal and the anterior cortex is fused.

Question 137

Holoprosencephaly least to most severe

Answer 137

lobar seim-lobar alobar

Question 138

lobar holoprosencephaly

Answer 138

Overview: Focal areas of incomplete fusion anteriorly (usually the fomix) Ventricles: Variable mild fusion of the frontal horns of the lateral ventricles. Thalamus: normal Absent structures: septum pellucidum, corpus callosum (partial vs normal) Horrible things: ..... Outcome: survive into adulthood

Question 139

semi-lobar holoprosencephaly

Answer 139

Overview: The back is cleaved (not the front), >50% fusion of the frontal lobes. Ventricles: the body of the lateral ventricles are 1 chamber. occipital and temporal horns are partially developed. Thalamus: fused (partial or complete) Absent structures: Septum Pellucidum, Corpus Callosum (partial), Anterior Interhemispheric Fissure, Anterior Falx Cerebri Horrible things: cleft lip/palate, borat brother bilo (hes the retard) Outcome: surbibe into adulhood but terrible at jeopardy.

Question 140

alobar holoprosencephaly

Answer 140

Overview: Zero midline cleavage. Cerebral hemispheres are fused and there is a single midline ventricle Ventricles: Single Ventricle (distinct lateral and third ventricles are absent) Thalamus: Fused Absent structures: Septum Pellucidum, Corpus Callosum, Interhemispheric Fissure, Falx Cerebri Horrible things: Cyclops Monster Face (one eye, one nose hole, etc) Outcome: Mercifully Bad (stillborn / dead < 1 year)

Question 141

Face predicts Brain, BUT Brain doesn’t predict Face Possible BUZZWORDS for HPE spectrum.

Answer 141

Monster Cyclops Eyes Cleft lips / Palates Pyriform Aperture Stenosis (from nasal process overgrowth) Solitary Median Maxillary Incisor (MEGA-Incisor)

Question 142

Arhinencephaly

Answer 142

“Minor” HPE expression. Midlinc olfactory bulbs / tracts are absent. “Can’t Smell” - is the clinical buzzword. Could be tested as Kallmann Syndrome (which also has hypogonadism, & mental retardation).

Question 143

Meckel-Gruber Syndrome

Answer 143

Classic triad: 1. Occipital Encephalocoele 2. Multiple Renal Cysts 3. Polydactyly Also strongly associated with Holoprosencephaly

Question 144

Septo Optic Dysplasia | overview

Answer 144

This “Minor” HPE expression could be referred to by its French sounding name, for the sole purpose of fucking with you — ”de Morsier Syndrome ” The classic findings are inferred by the name. Absent Septum Pellucidum “Septo ” and Hypoplastic “Optic ” structures such as the Optic Chiasma (circle) and Optic Nerves

Question 145

Septo Optic Dysplasia trivia

Answer 145

Associated with Schizenccphaly

Question 146

Septo Optic Dysplasia gamesmanship

Answer 146

The other thing they can show is an azygos anterior cerebral artery - which is basically a common trunk of the AC As. This is rare , but associated with SOD and lobar HPE.

Question 147

Cortical Formation prologue

Answer 147

The brain is said to form “inside-out, ” as neurons that will eventually make up the cortex are originally birthed from a thick slurry surrounding the fetal ventricles. Sleep inducing texts will refer to this as the “proliferative neuroepithelium.” I prefer the term “Lazarus Pit,” or just the “Pit.” It is from this Periventricular Pit, where cells will make “the climb” to the cortex.

Question 148

Cortical Formation Act 1 - Proliferation

Answer 148

Before making “the climb” to the cortex the neuronal-glial stem cells are bom into (and molded by) the darkness of the periventricular Lazarus Pit. It is there that they learn the truth about despair, first by dividing into additional stem cells in a symmetric fashion (1 stem cell splits into 2 stem cells). Later this process will change to asymmetric proliferation (1 stem cell splits into 1 stem cell and 1 differentiated cell - glial cell or neuron). This process continues for several cycles until the stem cells receive the signal to undergo apoptosis - they expect one o f us in the wreckage brother. The number of neurons in the cortex is determined by the frequency and number of symmetric / asymmetric divisions by these stem cells. Disturbance in this process will therefore result in either too many, too few, or improperly differentiated neurons.

Question 149

Cortical Formation Act 2 - Migration (RISE)

Answer 149

From the periventricular proliferative pit of despair, cells will make the climb. As they climb to freedom, they are guided by structural cells, chemical signals, and the chant “Deshi, Deshi, Basara, Basara.” They make the climb in 6 waves, with the first generation forming the “pre-plate” and the second generation forming the more permanent "cortical plate.” In other words, the younger cells always moving past the older ones becoming more superficial in their final position, (hence the idea - “inside out” or “outside last"). Disturbance in this mechanism (guidance, timing of detachment e tc...) will result in undermigration, over-migration, or ectopic neurons.

Question 150

Cortical Formation Act 3 - Organization

Answer 150

At this point you may think the cells have given everything to the cortex, and they don’t owe them anymore. But, they haven’t given everything... not yet. There is still the process of cortical folding (gyrification). The process actually occurs simultaneously with and depends heavily on the first two steps. The differential speed of cortex expansion (relative to the deeper white matter) is probably the key mechanism for brain folding. For this expansion to occur properly there needs to be the right number of cells (act 1) migrated in the right order (act 2). There is the additional mechanism of continued differentiation into structural cell types which organize into horizontal / vertical columns creating an underlying cytoarchitecture need for structure and function. Disturbance in these mechanisms will result in an absence of or excessive number of folds.

Question 151

Failure to Proliferate: Hemimegalencephaly

Answer 151

Rare, but unique (Aunt Minnie), malformation characterized by enlargement (from hamartomatous overgrowth) of all or part/s of one cerebral hemisphere. The presumed cause is a failure in the nonnal neuronal differentiation in the involved hemisphere - resulting in an “abnormal mixture of normal tissues” - which defines a hamartoma. This process is often mixed with other errors in migration resulting in associated polymicrogyria, pachygyria, and heterotopia.

Question 152

Hemimegalencephaly

Answer 152

big side with big ventricle = hemimegalencephaly hamartomatous overgrowth of all or part of a cerebral hemisphere, seocndary to differentiation/migration failure.

Question 153

Rasmussen’s Encephalitis

Answer 153

small side with big ventricle = atrophy the shrunken half is atrophic resultingin ex acuo dilation ofthe ventricle zebra viral (or maybe autoimmune disease that annihilates half the brain just like an old grandpa brain (only thing is this is just half the braina nd the kid is usually less than 10)

Question 154

Dyke-Davidoff-Masson (Cerebral Hemi-Atrophy):

Answer 154

This is another zebra that can look a lot like Rasmussen encephalitis - but also has weird unilateral skull thickening and expanded sinuses. The superior sagittal sinus and fissure are moved across the midline. It is supposedly caused by an in utcro or childhood stroke (supposedly). Since literally anything is fair game on this exam. I’m including it for completeness (it’s probably low yield).

Question 155

Lissencephaly | “Classic” Type 1

Answer 155

``` Smooth Surface Thick Cortex Colpocephaly Figure 8 Shape Undermigration Failure to migrate both in amount an in order - with a reverse outside-in pattern. Large numbers of neurons do not even reaching the cortical plate, depositing diffusely between the ventricular and pial surfaces. The distribution is fucked with 4 thick layers formed instead of 6 ``` ``` As a result of this disorganized / inadequate migration the process of cortical folding does not take place. Smooth Surface, Thick Cortex Colpocephaly is Common. “Figure 8” shaped brain on axial -due to shallow, vertical Sylvan fissures Autosomal Inheritance (M=F) Associated with CMV (maybe) ```

Question 156

Double Cortex | Band Heterotopia

Answer 156

``` Undermigration Considered the mildest form of Classic Lissencephaly Disorganized migration results in a second layer of cortical neurons deep to the more superficial cortex. This creates the classic “double cortex” appearance. ``` ``` Associated with seizure disorders. Gyral pattern is normal (or mildly simplified). Subcortical band of heterotopic gray matter X-Linked Inheritance (F>M) ```

Question 157

Lissencephaly "cobblestone" Type 2

Answer 157

``` Overmigration Instead of failing to migrate an adequate number of neurons to the cortical surface (as is the case in the classic type of lissencephaly), this pathology is the result o f an over migration. This over migration results in an additional layer o f cortex composed on gray matter nodules. These nodules come in a variety o f shapes and sizes (unilateral, bilateral, small, large, symmetric or asymmetric). Most commonly It is commonly located adjacent to the Sylvian fissures ``` ``` Cobblestoned Cortex (variable in size / location) Associated with congenital muscular dystrophy, and retinal detachment - "muscle- eye-brain disease ```

Question 158

Periventricular nodular heterotopia

Answer 158

``` Failed Migration Neurons in the periventricular (subependymal) region were too lazy to migrate to the cortex. The result is nodular grey matter deposition along the ventricle borders. Most common location for grey matter heterotopia. Associated with seizure disorders. ```

Question 159

THIS VS THAT: heterotopia vs supendymal tubers of TS

Answer 159

``` THIS VS THAT: Heterotopias follow grey matter on all sequences and NOT enhance. Subependymal tubers o f TS are usually brighter on T2 relative to grey matter and may also be calcified. ```

Question 160

Failure to Organize: Polymicrogyria “PIKIG”

Answer 160

I’ve heard people blame this on TORCH infections, toxic exposure, chromosomal issues, God’s wrath for “stuff the Democrats do.” There are likely many causes. I wouldn’t expect someone to ask for “the cause,” other than perhaps the broad category of failed organization. Having said that. I’ve read some PhD papers saying that layer 5 gets obliterated (by infection, toxins, wrath, etc..) after completion of normal migration. With layer 5 gone the other more superficial layers overfold and fuse resulting in an excessive number of small folds - the hallmark finding.

Question 161

Failure to Organize: Polymicrogyria “PIKIG” classic look

Answer 161

Fine undulating / bumpy cortex. This anomaly come in a variety of shapes and sizes (unilateral, bilateral, small, large, symmetric or asymmetric). Most common location is adjacent to the Sylvian fissure Fine Undulations / Bumps bilaterally.

Question 162

Failure to Organize: Polymicrogyria “PIKIG” trivia

Answer 162

Zika Virus is the most common cause of PMG in Brazil and South America

Question 163

Failure to Organize: Schizencephaly— “Split Brain”

Answer 163

Just like polymicrogyria there are likely many causes and I wouldn’t expect someone to ask for “the cause,” other than perhaps the broad category of failed organization. Having said that, one popular theory is the idea of a vascular insult. What is this vascular insult ? Well, you could say it’s the cortex’s reckoning (it damages the radial glial fibers). These radial glial fibers are in charge (or at least they “feel in charge”) of the ropes used by neurons to “make the climb.” Although, I’ve head it’s best to make the climb as the child did - without the rope. I mention this because about 30% of patient’s with schizencephaly also have non-CNS vascular stigmata (example = gastroschisis - which supposedly occurs from a vascular insult to the abdominal wall).

Question 164

Failure to Organize: Schizencephaly— “Split Brain” classic look

Answer 164

Schizencephaly literally means “split brain” with the defining feature being a cleft (lined with grey matter) connecting the CSF spaces with the ventricular system. How wide this cleft is depends on the flavor; Closed Lip (20%) or (2) Open Lip (80%), although in both cases the cleft should span the full thickness of the involved hemisphere. The clefts can be unilateral or bilateral.

Question 165

Failure to Organize: Schizencephaly— “Split Brain” closed lip

Answer 165

Closed Lip (20%) - Less Common, Less Seve i In this fonn, the "Lip” will ;appear closed without a I CSF filled cleft. To make ! the call you want to look I for is the grey matter i running across the normally j uniform corona radiata. j Sometimes you can see a “nipple” o f grey mater j pouching at the ependymal (ventricular) surface

Question 166

Failure to Organize: Schizencephaly— “Split Brain” open lip

Answer 166

``` Open Lip (80 %) - More Common, More Severe This one is more obvious. To make the call you want to see a CSF-filled cleft (lined with grey matter) extending from the ventricle to the pial surface. IThe gray matter lining is often weird looking j(kinda nodular like a heterotopia). ```

Question 167

Failure to Organize: Schizencephaly— “Split Brain” associations

Answer 167

Absent Septum Pellucidum (70%), Focally Thinned Corpus Callosum, Optic Nerve Hypoplasia (30%), Epilepsy (demonic possession)

Question 168

Porencephalic Cyst

Answer 168

Least Severe brain cleft/hole from a prior ischmic event resulting in ecneaphalomalacia. cyst/cleft can communcate with the subarachnoid space (external) micmiching an open lip schizencephaly or communicated only with the ventricular system (internal)

Question 169

Hydranencephaly

Answer 169

bilateral ICA occlusion causes massive destruction of both cerebral hemispheres. only the cerebellum, midbrain, andthe falx (usually) remain hepres is the most classic, but in utero infection with toxo or CMV are also described causes

Question 170

Developmental Failure Mimics— Hydranencephaly and the Porencephalic Cyst These can be thought of along a spectrum of severity

Answer 170

``` These things may look like a severe developmental anomaly but the underlying mechanism is different. They are “acquired.” Classically by a vascular insult - but really from anything that can cause encephalomalacia (focal necrosis of both the gray matter and white matter with eventual cystic degeneration). This would include a trauma after birth (this doesn’t have to happen in utero). Understanding that the brain develops normally first - then gets crushed, helps to remember the key findings. In particular, the absence of a gray matter lining along the defect. It’s almost like someone took an icecream scoop to the brain. In the case of Porenchephaly, they just took one scoop. In the case of Hydranencephaly, the glutinous pig took pretty much the entire brain - leaving only the cerebellum, midbrain, and the falx. ```

Question 171

THIS v s THAT open lip schizencephaly

Answer 171

``` Brain cleft / hole from a prior event (maybe ischemic) resulting in damage to the structural cells needed to properly organize the cortex. Not Normally Formed ``` ``` CSF-filled cleft extending from the ventricle to the pial surface. ``` Cleft is Lined with Gray Matter

Question 172

THIS v s THAT porencephalic cyst

Answer 172

``` Brain cleft / hole from a prior ischemic / traumatic event resulting in encephalomalacia. Normally formed - but massive insult make it look developmental. ``` ``` CSF-filled cleft extending from the ventricle and/or the pial surface. ``` Cleft is NOT Lined with Gray Matter

Question 173

The brain appears screwed with corticle mantle

Answer 173

falx present - sever hydrocephalus falx gone - Holoprosencephaly - Alobar —Anterior falx usually missing in the semi-lobar form —lobar (mild 1 subtype should still have the nax

Question 174

the brain appears to be screwed without cortical mantle

Answer 174

hydranencephaly

Question 175

“Cephalocele”

Answer 175

is an umbrella term for a herniation of the cranial contents through a defect in the skull. While retaining the suffix “cele” they are then sub-classified based on (1) location, and (2) what is in the herniation sac

Question 176

cephalocele locations

Answer 176

``` nasal frontoethmoid transsphenoid parietal occipital ```

Question 177

HERNIATION SAC CONTENTS Meningocele

Answer 177

-CSF & Meninges -NO BRAIN

Question 178

HERNIATION SAC CONTENTS Meningo- Encephalocele

Answer 178

Meningo- Encephalocele -CSF, Meninges, and BRAIN *For the purpose of fucking with you, Meningoencephaloceles are sometimes called Encephaloceles

Question 179

Cystocele

Answer 179

CSF, Meninges, | Brain, and Ventricle

Question 180

Myelocele

Answer 180

Spinal Cord

Question 181

Chiari Malformations quick type 1

Answer 181

Herniation of cerebellar tonsils (more than 5 mm) Classic Association (not always present): • Syrinx (cervical cord)

Question 182

Chiari Malformations quick type 2

Answer 182

``` Relatively less tonsillar herniation. Relatively more cerebellar vermian displacement ``` Classic Features - Low lying torcula - Tectal beaking - Hydrocephalus - Clival hypoplasia

Question 183

Chiari Malformations quick type 3

Answer 183

Features o f Chiari 2 AND Occipital Encephalocele

Question 184

Chiari Malformations quick type 4

Answer 184

``` Historically used to describe severe cerebellar hypoplasia without herniation. The term has fallen out of favor with the powerful men and women who control the Chiari nomenclature. We shall not speak of it again ```

Question 185

Chiari Malformations quick type 1.5

Answer 185

Hybrid term used to describe conditions that have features of both type 1 and type 2. Not associated with neural tube defects, despite the significant downward movement of the tonsils and brain stem.

Question 186

Chiari Type I classicly

Answer 186

Classically defined as i or both tonsils > 5mm below the level of the Basion Opisthion.

Question 187

Chiari Type I classic mechanism

Answer 187

Congenital underdevelopment of the posterior fossa, leading to overcrowding, and downward displacement.

Question 188

Chiari Type I non-classic mechanism

Answer 188

Post traumatic defonnity - acquired later in life.

Question 189

Chiari Type I clinical symptoms

Answer 189

``` 1) Occipital headache from pressure of the cerebellar tonsils - worse with sneezing (2) Weakness, spasticity, and loss of proprioception from pressure on the cord ```

Question 190

Chiari Type I classic association

Answer 190

(not always present): | • Syrinx o f the cervical cord

Question 191

Chiari Type I less-classic association

Answer 191

``` (but still highly testable) association: -Klippel-Feil Syndrome (congenital C-spine fusion). NOT associated with a neural tube defect ```

Question 192

Chiari Type II findings

Answer 192

Thinned Corpus Callosum Tectal Beak clival hypoplasia ``` *Also note (^3 the long skinny 4th ventricle, and the “towering cerebellum.” ``` ``` Interdigitated Cerebral Gvri (most classically demonstrated on axial CT) ``` Low Lying Torcula Opposite o f Dandy Walker

Question 193

Chiari Type II classic mechanism

Answer 193

Neural Tube Defect “sucks” the cerebellum downward prior to full development o f the cerebellar tonsils.

Question 194

Chiari Type II classic assocation

Answer 194

-Lumbar myelomeningocele / Spina Bifida only seen in pts with neural tube defect

Question 195

Chiari Type III

Answer 195

``` Occipital Encephalocele, (meningoencephalocele) containing cerebellum and/ or the brainstem, occipital lobe, and sometimes even the fourth ventricle. PLUS features of o f Chiari 2 ```

Question 196

Chiari Type III Classic Associations

Answer 196

``` • Syrinx (cervical) • Tethered cord • Hydrocephalus • Agenesis of the corpus callosum Only seen in patients with a neural tube defect (NTD). Encephalocele = NTD ```

Question 197

Special Topic - Mesial Temporal Sclerosis

Answer 197

This is a pattern of findings (hippocampal volume loss + gliosis / scar), which classically result in intractable seizures. The etiology is not certain, but it is most likely developmental (hence the inclusion in this section).

Question 198

Special Topic - Mesial Temporal Sclerosis clinical trivia

Answer 198

This is the most common cause of partial complex epilepsy.

Question 199

Special Topic - Mesial Temporal Sclerosis clinical trivia 2

Answer 199

Surgical removal can “cure” the seizures / demon. Alternatively, perfect W / i intracranial positioning of a tooth (from a red haired woman) has been described as therapeutic in the Kazakhstani literature.

Question 200

Special Topic - Mesial Temporal Sclerosis imaging findings

Answer 200

• Reduced Hippocampal Volume (best seen when compared to the opposite site). *10% o f the time volume loss is bilateral - other findings are necessary to exclude fuckerv • Increased T2 Signal (from gliosis / scar) • Loss of Normal Morphology (loss of normal interdigitations) • Atrophy of the ipsilateral fornix and maxillary body • Contralateral amygdala enlargement

Question 201

Special Topic - Mesial Temporal Sclerosis mri epilepsy protocol trivia

Answer 201

• T1 - Superior for Cortical Thickness, Eval of Grey / White • FLAIR - Superior for Cortical / Subcortical Hight Signal (Gliosis) • T2* / SWI - Superior for Blood Breakdown Products (for other things that can cause seizures; calcifications of tuberous sclerosis, Sturge-Weber, Cavemomas, Gangliogliomas etc..)

Question 202

Monro-Kellie Hypothesis

Answer 202

The Monro-Kellie Hypothesis is the idea that the head is a closed shell, and that the three major components: (1) brain, (2) blood - both arterial and venous, and (3) CSF, are in a state o f dynamic equilibrium. As the volume o f one goes up, the volume o f another must go down

Question 203

Intracranial Hypotension

Answer 203

if you are leaking CSF, this will decrease the overall fixed volume, and the volume o f venous blood will increase to maintain the equilibrium. The result is meningeal engorgement (enhancement), distention o f the dural venous sinuses, prominence o f the intracranial vessels, and engorgement o f the pituitary (“pituitary pseudo-mass”). The development o f subdural hematoma and hygromas is also a classic look (again, compensating for lost volume).

Question 204

Idiopathic Intracranial Hypertension (Pseudotumor Cerebril

Answer 204

Classic scenario o f a fat middle-aged women with a headache. Etiology is not well understood (making too much CSF, or not absorbing it correctly). It has a lot o f associations (hypothyroid, cushings, vitamin A toxicity). The findings follow the equilibrium idea. With increased CSF the ventricles become slit-like, the pituitary shrinks (partially empty sella), and the venous sinuses appear compressed. You can also have the appearance o f vertical tortuosity o f the optic nerves and flattening o f the posterior sclera. Changes in intracranial pressure can create a downward displacement o f the brainstem stretching the 6th cranial nerve - it is said that 1/3 o f patients with pseudotumor cerebri have sixth nerve paresis as their only neurologic deficit

Question 205

Hydrocephalus communicating

Answer 205

``` -All Ventricles are Big (25% o f the time the fourth ventricle is normal) -Level o f obstruction between basal cisterns and arachnoid granulations - CSF can exit all the ventricles ```

Question 206

Hydrocephalus communicating true obstruction

Answer 206

Blood, Pus, and Cancer - Anything that plugs up the villi - the three most common causes being SAH, Meningitis (TB or Bacterial), and Carcinomatous Meningitis.

Question 207

Hydrocephalus communicating without obstruction

Answer 207

Brain Atrophy (ex-vacuo) Normal Pressure Hydrocephalus -see discussion below Choroid Plexus Papilloma - Tumor that secretes CSF. - Discussed more later in the chapter

Question 208

Hydrocephalus non-communicating

Answer 208

``` -Upstream Ventricles are Big -Level o f Obstruction is within the ventricle System - CSF can NOT exit all the ventricles ```

Question 209

Hydrocephalus non-communicating level of obstruction

Answer 209

``` Foramen of Monro = • Colloid Cyst Aqueduct = ’ • Aqueduct Stenosis • Tectal Glioma 4th Ventricle = • Posterior Fossa Tumor • Cerebellar Edema / Bleed ```

Question 210

Hydrocephalus non-communicating level of obstruction

Answer 210

``` Foramen of Monro = • Colloid Cyst Aqueduct = ’ • Aqueduct Stenosis • Tectal Glioma 4th Ventricle = • Posterior Fossa Tumor • Cerebellar Edema / Bleed ```

Question 211

Normal Pressure Hydrocephalus

Answer 211

it s not well understood - and idiopathic. The step 1 trivia is “wet, wackv. and wobbly” - describing the clinical triad of urinary incontinence, confusion, and ataxia. The key points clinically are the patient is elderly (60s), and the ataxia comes First and is most pronounced.

Question 212

Normal Pressure Hydrocephalus buzz phrase

Answer 212

The buzz-phrase is “ventricular size out of proportion to atrophy.” The frontal and temporal horns of the lateral ventricles are the most affected. “Upward bowing of the corpus callosum” is another catch phrase. On MR1 you may see transependyma 1 flow and/or a flow void in the aqueduct and 3rd ventricle. This is treated with surgical shunting

Question 213

Syndrome of Hydrocephalus in the Young and Middle-aged Adult (SHYMA

Answer 213

Similar to NPH but in a middle aged population - and more headaches less peeing of the pants (HA+Wacky+Wobbly). Communicating Hydrocephalus + Middle Aged + Headache = SHYMA.

Question 214

Communicating Hydrocephalus + | Elderly + Ataxia -

Answer 214

NPH

Question 215

Congenital Hydrocephalus

Answer 215

There are several causes of hydrocephalus that can be present at birth or be related to fetal development. These conditions are typically diagnosed prior to birth via routine ultrasound

Question 216

Congenital Hydrocephalus big 4

Answer 216

The big 4 are: (1) Aqueductal stenosis, (2) Neural tube defect - usually Chiari II, (3) Arachnoid cysts, and (4) Dandy-Walker.

Question 217

Aqueductal Stenosis

Answer 217

This is the most common cause of congenital obstructive hydrocephalus. Classically from a web or diaphragm at the aqueduct (hence the name). Because of the location you get a “non-communicating” pattern with a dilation of the lateral ventricles and 3rd ventricle with a normal sized 4th ventricle. You can have a big noggin (macrocephaly) with thinning of the cortical mantle.

Question 218

Aqueductal Stenosis treatment

Answer 218

Treatment is going to be either shunting or | poking a hole in the 3rd ventricle (third ventriculostomy).

Question 219

Aqueductal Stenosis clinical trivia

Answer 219

Question header may describe “sunset eyes” or an upward gaze paralysis

Question 220

Aqueductal Stenosis clinical trivia 2

Answer 220

A male with "flexed thumbs ” should make you think about the x-linked variant. (Bickers Adams Edwards syndrome).

Question 221

Arachnoid Cysts

Answer 221

As the name implies, these are cysts located in the subarachnoid space. They are CSF density, without any solid components, or abnormal restricted diffusion. You wouldn’t even notice them expect that they can exert mass effect on the adjacent brain, or in the context of this discussion block a CSF pathway (obstructive type).

Question 222

Normal CSf shunt

Answer 222

The most basic shunt consists of a proximal tube (usually placed in the frontal horn of the lateral ventricle just anterior to the foramen of Monro), a valve to control flow, and a distal tip (usually dumped in the peritoneum, but can be placed in the pleural space or right atrium).

Question 223

Shunt Evaluation Options

Answer 223

Your first line options for shunt evaluation are going to be (a) non-con CT or (b) rapid single shot T2 sequence - mainly looking at catheter position and ventricle size. *May need to verify shunt settings with a plain film post magnet. If the ventricles are big (shunt is not working) you might follow that up with a radiograph series (neck, chest, abd) to make sure the catheter is intact. Ultrasound or CT can be used to inspect the distal tip for a fluid collection. Alternatively (if you are a weirdo) you can inject < 0.4ml pertechnetate into the shunt reservoir and take images to look for leakage or blockage (remember to not aspirate when you inject).

Question 224

CSF Shunt Malfunction undershunting

Answer 224

Proximal obstruction: - Proximal > Distal - Most common cause = ingrowth of choroid piexus and particulate debris / blood products - Can also be from catheter migration Distal Obstruction: -Pseudocyst (loculated flu id along the distal tip) -Catheter migration (more common in children)

Question 225

CSF Shunt Malfunction overshunting

Answer 225

-"Slit Like Ventricles” - can be meaningless or suggest too much shunting. - The big fear is that not enough CSF will cause subdural hygroma or hematoma formation via Monroe Kelly mechanics (less CSF - more blood).

Question 226

CSF Shunt Malfunction infection

Answer 226

-Usually within 6 months of placement -Blood cultures are usually negative (fluid from the shunt should be cultured instead). -Mild enhancement after catheter placement can be normal - be on guard for fuckery. -The best sign is debris within the ventricles, ideally shown with DWI - this is the weapon of choice for diagnosis of ventriculitis. -Late stigmata may include ventricular loculations - which can cause restricted flow / obstruction and in some case isolate or "trap" the 4th ventricle — as shown in diagrams.

Question 227

CSF Shunt Malfunction hydrothorax

Answer 227

Either deliberately or via migration the catheter can end up in the pleural space. A little bit of pleural fluid doesn’t mean shit. But, if the volume gets large enough and the patient becomes symptomatic - then revision might be needed.

Question 228

CSF Shunt Malfunction ascites

Answer 228

Usually the ascites from a VP shunt isn’t symptomatic, although there are reports of inguinal hernias and hydroceles forming secondary to the increased abdominal pressure.

Question 229

Cytotoxic Edema

Answer 229

This type o f edema can be thought about as intracellular swelling secondary to malfunction o f the Na/K pump. It tends to favor the gray matter, and looks like loss of the gray-white differentiation. This is classically seen with stroke (or trauma), and is why EARLY signs o f stroke involve loss o f the GM-WM interface.

Question 230

Vasogenic Edema

Answer 230

This type o f edema is extracellular, secondary to disruption o f the blood-brain barrier. It looks like edema tracking through the white matter (which is less tightly packed than the gray matter). This is classically seen with tumor and infection. You can also see this type o f edema as a LATE stage o f cerebral ischemia. A response to steroids is characteristic o f vasogenic edema.

Question 231

Cytotoxic Edema quick

Answer 231

Failed Na/K Pump (BBB intact) Classic = Ischemia (EARLY) White Matter + Gray Matter - “blurring

Question 232

Vasogenic Edema quick

Answer 232

``` Increased Capillary Permeability (BBB NOT intact) Classic = Tumor, Infection, Ischemia (LATE) White Matter (Spares Gray Matter ```

Question 233

Subfalcine (Cingulate) Herniation

Answer 233

This is just a fancy way of saying midline shift (deviation of ipsilateral ventricle and bowing of the falx). The trivia to know is that the ACA may be compressed, and can result in infarct.

Question 234

Descending Transtentorial (Uncal) Herniation

Answer 234

The uncus and hippocampus herniate through the | tentorial incisura. Effacement of the ipsilateral suprasellar cistern occurs first.

Question 235

Descending Transtentorial (Uncal) Herniation Things to know

Answer 235

• Perforating basilar artery branches get compressed resulting in “Duret Hemorrhages classically located in the midline at the pontomesencephalic junction (in reality they can also affect cerebellar peduncles). CN 3 gets compressed between the PCA and Superior Cerebellar Artery causing ipsilateral pupil dilation and ptosis • “Kemohan’s Notch / Phenomenon” - The midbrain on the tentorium forming an indentation (notch) and the physical exam finding of ipsilateral hemiparesis - which Neurologists call a “fa ls e localizing sign. " Of course, localization on physical exam is stupid in the age of MRI, but it gives Neurologists a reason to carry a reflex hammer and how can one fault them for that.

Question 236

Ascending Transtentorial Herniation

Answer 236

Think about this in the setting of a posterior fossa mass. The vermis will herniate upward through the tentorial incisura, often resulting in severe obstructive hydrocephalus.

Question 237

Ascending Transtentorial Herniation Things to know

Answer 237

The “Smile” of the quadrigeminal cistern will be flattened or reversed ``` “Spinning Top ” is a buzzword, for the appearance of the midbrain from bilateral compression along its posterior aspect ``` ``` Severe hydrocephalus (at the level of the aqueduct). ```

Question 238

Cerebellar Tonsil Herniation

Answer 238

``` Can be from severe herniation after downward transtentorial herniation. Alternatively, if in isolation you arc thinking more along the lines of Chiari (Chiari I = 1 tonsil - 5 mm). ```

Question 239

Osmotic Demyelination or Central Pontine Myelinolysis most classic scenario

Answer 239

Asshole drunk Hobo shows up to the ER with a low Na. Like most asshole drunks in the ER, he starts out demanding a cheeseburger and a Sprite (not a fucking Sierra Mist!), then threatens to leave against medical advice. .. .after finishing the burger. Family Medicine Resident begs him to stay (a decision he will soon regret). The Resident eventually tires of his bullshit and decides to correct his hyponatremia as rapidly as possible - with the goal of expediting discharge. 2 days later the guy is still in house, acting like a massive prick - acutely encephalopathic with spastic quadriparesis. Neurology gets consulted and writes "pseudobulbar palsy” in the chart. Family Medicine Resident doesn’t know what the fuck that means, but is humble enough to ask. A below average 2nd year medical student explains to him that it is slurred speech, sensitive gag reflex, and being an even bigger cry baby than normal- “labile emotional response”. Coma, the above MRI, death, then a lawsuit follow (in that order).

Question 240

Osmotic Demyelination or Central Pontine Myelinolysis MRI

Answer 240

T2 bright in the central pons (spares periphery) Earliest change: restricted diffusion in lower pons

Question 241

Osmotic Demyelination or Central Pontine Myelinolysis trivia

Answer 241

Osmotic Demyelination or | Central Pontine Myelinolysis

Question 242

Wernicke Encephalopathy classic scenario

Answer 242

Very friendly Hobo - known for singing songs from the 70s (mostly Supertramp’s goodbye stranger) - starts acting squirrelly. “His tempo seems o ff’ - notes the feminine male nurse. An above average medical student suggests he is exhibiting the clinical triad o f ( 1) acute confusion. (2) ataxia, and (3) ophthalmoplegia, but is dismissed by the Medicine intern who talks non-stop about going into Cardiology (“Cards” - he calls it). Only moments later the same Intern will suggest to his Attending the same triad of findings before stating “my medical student” seems disinterested and may benefit from more call. Still desperate to honor the clerkship, the student suggests thiamine (vitamin B it deficiency as the etiology, and says the symptoms could progress to chronic memory loss and confabulation (Korsakoff psychosis) or even death. The cycle repeats - additional call is assigned, and a formal letter of reprimand is issued to the student.

Question 243

Wernicke Encephalopathy imaging findings

Answer 243

• T2/FLAIR bright classically seen in medial/dorsal thalamus (around the 3rd ventricle), periaqueductal gray, mamillary bodies, and the tectal plate. • Enhancement is classic in the mamillary bodies

Question 244

Wernicke Encephalopathy treatment

Answer 244

thiamine replacement

Question 245

Marchiafava-Bignami most classic scenario

Answer 245

• Swelling / T2 bright signal at the corpus callosum (represents an acute demyelination) • Order is progressive - typically beginning in the body, then genu, and lastly splenium • “Sandwich sign” on sagittal imaging - describes the pattern of preference for central fibers with relative sparing of the dorsal and ventrals fibers • Chronic Phase: Thinned corpus callosum + cystic cavities favoring in the genu and splenium

Question 246

Marchiafava-Bignami imaging

Answer 246

• Swelling / T2 bright signal at the corpus callosum (represents an acute demyelination) • Order is progressive - typically beginning in the body, then genu, and lastly splenium • “Sandwich sign” on sagittal imaging - describes the pattern of preference for central fibers with relative sparing of the dorsal and ventrals fibers • Chronic Phase: Thinned corpus callosum + cystic cavities favoring in the genu and splenium

Question 247

Direct Alcoholic Injury:

Answer 247

Most Common / Classic Finding(s): Brain Atrophy. Particularly the cerebellum and especially the cerebellar vermis

Question 248

Copper & Manganese Deposition

Answer 248

Tl Bright Basal Ganglia -Non-Specific and related To Liver Disease. -Can be seen without hepatic encephalopathy -Also seen in TPN, Wilson’s Disease, -Also seen in Non-Ketotic Hyperglycemia (HNK) in which it’s often unilateral

Question 249

Methanol Toxicity:

Answer 249

“Drinking Windshield Wiper Fluid” as an idiotic attempt to get drunk. Can also be seen from consuming “poorly adulterer moonshine” - or "West Virginia Budweiser.” Classic Findings: Optic nerve atrophy, hemorrhagic putaminal and subcortical white matter necrosis

Question 250

H IS VS THAT: Carbon Monoxide vs Methanol

Answer 250

Carbon Monoxide: CT Hypodensity / T2 Bright: Globus Pallidus (carbon monoxide causes “globus ” warming Methanol T2 Bright: Putaminal - which may be hemorrhagic, and thus CT Hypcrdense.

Question 251

PRES (Posterior Reversible Encephalopathy Syndrome]: classic features

Answer 251

• Asymmetric cortical and subcortical white matter edema (usually in parietal and occipital regions *but doesn’t have to be - superior frontal sulcus is also common). • Does NOT restrict on diffusion (helps tell you it’s not a stroke).

Question 252

PRES (Posterior Reversible Encephalopathy Syndrome]: classic historr

Answer 252

Acute Hypertension or Chemotherapy

Question 253

PRES (Posterior Reversible Encephalopathy Syndrome]: etiology

Answer 253

Poorly understood auto regulation fuck up.

Question 254

Post Chemotherapy two main looks

Answer 254

(1) PRES - As above, chemo is a classic cause. BUT! It tends to have a “non-classic” look relative to the hypertension type. It will often spare the occipital lobes, and instead target the basal ganglia, brainstem, and cerebellum. (2) Leukoencephalopathy (treatment induced): The classic look would be centered in the periventricular white matter - bilateral, symmetric, confluent, T2/FLAIR bright changes (history is obviously key to the diagnosis).

Question 255

Post Chemotherapy

Answer 255

It is fairly common. There are lots of named offenders. Methotrexate seems to be the one people write the most papers about (especially in kids with ALL)

Question 256

Post Chemotherapy Other Misc trivia

Answer 256

Can progress to brain atrophy. “Mineralizing Microangiopathy - the vocab word to use if there are calcifications “Disseminated necrotizing leukoencephalopathy” - severe white matter changes, which demonstrate ring enhancement, classically seen with leukemia patients undergoing radiation and chemotherapy. It is bad news and can be fatal (it believes in nothing Lebowski).

Question 257

Post Radiation

Answer 257

The quick and dirty version is that after radiation therapy to the brain you can see T2 bright areas and atrophy corresponding to the radiation portal. You can also sec hemosiderin deposition and mineralizing microangiopathy (calcifications involving the basal ganglia and subcortical white matter). There is a latent period, so imaging findings don’t typically show up for about two months post therapy. Now... if you want to get crazy, you can discuss changes at different time periods.

Question 258

Post Radiation Acute (Days-Weeks):

Answer 258

Too rare to give a fuck about (at least for the test)

Question 259

Post Radiation Early Delayed (1-6 months):

Answer 259

The classic look is similar to chcmo - high T2/FLA1R signal in the periventricular white matter. This is reversible change (usually).

Question 260

Post Radiation Late Delayed (6 months):

Answer 260

Described as a “mosaic" pattern with high WM signal changes again favoring the deep white matter. Can appear “mass-like” and expansile. Classically sparing of the U-Fibcrs & Corpus Callosum. Progressive... but reversible (mostly)

Question 261

Post Radiation Long Term Sequela Radiation-Induced Vasculopathy

Answer 261

Strokes and Moya-Moya type of look

Question 262

Post Radiation Long Term Sequela Mineralizing Microangiopathy

Answer 262

1 mentioned this on the previous page. This is a delayed finding — like two years following treatment. Think calcifications (basal ganglia and subcortical white matter) - hence the term “mineralizing.”

Question 263

Post Radiation Long Term Sequela Radiation-Induced Vascular Malformations

Answer 263

The most classic types are capillary telangiectasias / cavernous malformations. The most classic scenario is a kid getting whole brain radiation for ALL. Remember the key finding is blooming on GRE/SWI sequences.

Question 264

Post Radiation Long Term Sequela Radiation-induced Brain Cancer

Answer 264

* XRT is the “most important risk factor” for primary CNS neoplasm. * Most common type is a meningiomas (70%) - usually seen ~ 15 years post XRT * More aggressive types Gliomas, Sarcomas, etc, have a shorter window < 10 years

Question 265

Chasing the Dragon” - Heroin Inhalational leukoencephalopathy

Answer 265

Most toxic lcukoencephalopathies (either from chemotherapy, immunosuppressives, antibiotics, or the aristocratic art of paint thinner huffing) all create a similar non-specific pattern of widespread high T2/FLAIR signal in the supra and infratentorial white matter. The “Chasing the Dragon” pattern is also not specific - but it does have a catchy name, so people love collecting cases of it to show in conference (“catchy name” = high yield for boards). The most classic look (diagrams are FLAIR sequences):

Question 266

Chasing the Dragon” - Heroin Inhalational leukoencephalopathy imaging

Answer 266

Symmetric “Butterfly” in the Centrum Semiovale High Signal in the Posterior Limb of the Internal Capsule High Signal in the Deep Cerebellar White Matter Sparing of the dentate nucleus (arrows)

Question 267

Multiple Sclerosis overview

Answer 267

Size can be helpful. A single lesion > 15 mm in size suggests the underlying etiology is not vascular. Certain locations will also make you think “not vascular." When you think “not vascular pattern" you should think dcmyelinating. When you think dcmyelinating you should think MS first (it’s by far the most common).

Question 268

Multiple Sclerosis vascular

Answer 268

Size can be helpful. A single lesion > 15 mm in size suggests the underlying etiology is not vascular. Certain locations will also make you think “not vascular." When you think “not vascular pattern" you should think dcmyelinating. When you think dcmyelinating you should think MS first (it’s by far the most common).

Question 269

Multiple Sclerosis mcdonalds criteria

Answer 269

* Usually targets women 20-40 (in children there is no gender difference). * There are multiple sub-types with the relapsing-remitting form being the most common (85%). * Clinical history o f "separated by time and space ” is critical.

Question 270

Multiple Sclerosis epidemiologial trivia

Answer 270

* Usually targets women 20-40 (in children there is no gender difference). * There are multiple sub-types with the relapsing-remitting form being the most common (85%). * Clinical history o f "separated by time and space ” is critical.

Question 271

MS Vascular vs perivascular pattern

Answer 271

``` Vascular Pattern Perivascular Pattern (MS Corpus Callosum RARE COMMON Juxtacortical RARE COMMON Infratentorial RARE COMMON Basal Ganglai COMMON RARE ```

Question 272

Additional MS Related Trivia

Answer 272

• Most Classic Finding: T2/FLA1R oval and periventricular perpendicularly oriented lesions. • Involvement o f the calloso-septal interface is 98% specific for MS (and helps differentiate it from vascular lesions and ADEM). • In children the posterior fossa is more commonly involved. • Brain atrophy is accelerated in MS. • Solitary spinal cord involvement can occur but it is typically seen in addition to brain lesions. • The cervical spine is the most common location in the spine (65%). • Spinal cord lesions tend to be peripherally located. • FLAIR is more sensitive than T2 in detection o f juxtacortical and periventricular plaques. • T2 is more sensitive than FLAIR for detecting infratentorial lesions • MR spectroscopy (discussed later in the chapter) will show reduced N AA peaks within the plaques.

Question 273

MS Active vs Not Active

Answer 273

Acute demyelinating plaques should enhance and restrict diffusion (on multiple choice tests and occasionally in the real world).

Question 274

Tumor vs MS

Answer 274

You can sometimes get a big MS plaque that looks like a tumor. It will ring enhance but classically incomplete (like a horseshoe), with a leading demyelinating edge.

Question 275

Tumor =

Answer 275

Complete Ring

Question 276

Demyelination =

Answer 276

Incomplete Ring

Question 277

Multiple Sclerosis Variants

Answer 277

ADEM Acute Hemorrhagic Leukoencephalitis Devics Marburg Variant

Question 278

ADEM

Answer 278

(Acute Disseminated Encephalomyelitis): Typically presents in childhood or adolescents, after a viral illness or vaccination. Classically has multiple LARGE T2 bright lesions, which enhance in a nodular or ring pattern (open ring). Lesions do NOT involve the calloso-septal interface.

Question 279

Acute Hemorrhagic Leukoencephalitis

Answer 279

(Hurst Disease): This a fulminant form o f ADEM with | massive brain swelling and death. The hemorrhagic part is only seen on autopsy (not imaging).

Question 280

Devics

Answer 280

(neuromyelitis optica): Transverse Myelitis + Optic Neuritis. Lesions in the Cord and the Optic Nerve

Question 281

Marburg Variant:

Answer 281

Childhood variant that is fulminant and terrible leading to rapid death. It usually has a febrile prodrome. “MARBURG!!! ” = DEATH

Question 282

Subcortical Arteriosclerotic Encephalopathy ISAE1

Answer 282

Also referred to as Binswangcr Disease - for the purpose of fucking with you. It’s best thought of as a multi-infarct dementia that ONLY involves the white matter

Question 283

Subcortical Arteriosclerotic Encephalopathy ISAE1 trivia

Answer 283

• Strong association with Hypertension. • It’s seen in older people - 55 and up • If they show you a case that looks exactly like SAE but that patient is 40 and has migraines they are leading you to the genetically transmitted form of this disease called CADASIL. • It favors the white matter of the centrum semiovale (white matter superior to the lateral ventricles / corpus callosum). • Classically spares the subcortical U fibers

Question 284

WTF are “U Fib e rs” ?

Answer 284

``` They are the fibers under the cortex, that look like “U”s. They come up a lot, as being spared or not spared. ```

Question 285

CADASIL

Answer 285

(Cerebral Autosomal Dominant Arteriopathv with Subcortical Infarcts & Leukoencephalopathy) Basically it is SAE in a slightly younger person (40), with migraines.

Question 286

CADASIL classic scenario

Answer 286

40 year old presenting with migraine headaches, strokes, then eventually dementia. CADASIL is actually the most common hereditary stroke disorder.

Question 287

CADASIL step 1 trivia

Answer 287

NOTCH3 mutations on chromosome 19

Question 288

CADASIL classic imaging findings

Answer 288

Severe white matter disease (high T2/FLAIR signal) involving multiple vascular territories, in the frontal and temporal lobe. The occipital lobes are often spared. Temporal lobe involvement is classic.

Question 289

Dementia Disorders nucs

Answer 289

FDG PET for dementia is a worthless and expensive component o f the workup. Like most imaging exams it is ordered with no regard to the impending collapse o f the health care system under crippling rising costs (with inevitable progression into a Mad Max style dystopian future or even better Mega-City 1). As such, it is standard practice in most academic centers to obtain the study. The idea is that “demented brain” will have less perfusion and will have less metabolism relative to “not demented brain.” PET can assess perfusion ( 15O-H20) but typically it uses l8FDG to assess metabolism (which is analogous to perfusion). Renal clearance o f 18FDG is excellent, giving good target to background pictures. Resolution o f PET is superior to SPECT. HMPAO, and ECD (tracers that are discussed in more depth in the nukes chapter) can also be used for dementia imaging and the patterns o f pathology are the same. It’s important to remember that external factors can affect the results; bright lights stimulating the occipital lobes, high glucose (>200) causes more competition for the tracer and therefore less uptake, e tc .. .e tc ... so on and so forth.

Question 290

On FDG PET the motor strip is always preserved | in a

Answer 290

dgsenerative type o f dementia.

Question 291

Alzheimer Disease

Answer 291

``` Most common cause Tauopathy, Amyloid Cascade, and Neurofibrillary Tangles are all buzzwords people use when they pretend to understand the pathophysiology. ```

Question 292

Alzheimer Disease Risk Factor(s):

Answer 292

``` The biggest one is Age. A more obscure one (but certainly testable) is Downs Syndrome. Downs patients nearly always get AD, and they get it earlier than normal - that extra 21st isn’t doing them any favors. ```

Question 293

Alzheimer Disease | Most Classic Feature(s):

Answer 293

``` hippocampal atrophy (which is first and out of proportion to the rest of the brain atrophy). They could ask temporal horn atrophy > 3 mm , which is seen in more than 65% of cases. ```

Question 294

Alzheimer Disease FDG Pattern

Answer 294

``` Low posterior temporoparietal uptake - "headphones ” or "ear muffs. ” 11C PiB (Pittsburgh compound B) is an even better way to waste money making this diagnosis. It works as an Amyloid Binding Tracer. ```

Question 295

Multi-infarct Dementia

Answer 295

2nd most common Also called “Vascular Dementia” - for the purpose of fucking with you.

Question 296

Multi-infarct Dementia Risk Factor(s):

Answer 296

``` • McDonalds, Burger King, Taco Bell, Pizza Hut • Hypertension, • Smoking (tobacco), and • CADAS1L ```

Question 297

Multi-infarct Dementia Most Classic Feature(s):

Answer 297

Cortical infarcts and lacunar infarcts are seen on MR1. Brain atrophy (generalized) is usually advanced for the patients age

Question 298

Multi-infarct Dementia FDG Pattern:

Answer 298

``` Multiple scattered areas of decreased activity. No specific lobar predominance. Unlike the neurodegenerative dementias - this one could knock out the motor strip (if the strokes happen to involve that region). This is different that AD and DLB. ```

Question 299

Dementia with LewyDodies

Answer 299

``` 3rd most common Alpha synuclein and synucleinopathy are buzzwords people use when they pretend to understand the pathophysiology ```

Question 300

Dementia with LewyDodies Clinical Scenario

Answer 300

``` There is a triad of classic features. (1) Visual hallucinations (2) Spontaneous parkinsonism, (3) Fluctuating ability to concentrate / stay alert ``` ``` Clinical picture can be similar to Parkinson’s dementia - the major difference in DLB, the dementia comes before the Parkinsonism ```

Question 301

Dementia with LewyDodies Most Classic Feature(s):

Answer 301

``` Mild generalized atrophy without lobar predominance (unlike multi-infarct). Hippocampi will be normal in size (unlike AD) ```

Question 302

Dementia with LewyDodies FDG Pattern

Answer 302

``` decreased FDG uptake in the lateral occipital cortex, with sparing of the mid posterior cingulate gyrus (Cingulate Island Sign). ```

Question 303

Picks

Answer 303

Also be referred to a “frontotemporal dementia ’’ - for the purpose of fucking with you.

Question 304

Picks clinical

Answer 304

Onset is earlier than AD (like 40s-50s). Classic presentation is described as “compulsive or inappropriate behaviors.” In other words, acting like an asshole (fucking prostitutes, and buying miracle weight loss potions from Dr. Oz - when you aren’t even going to the gym or trying to cat right). Just being a real Prick.

Question 305

Picks classic features

Answer 305

Severe symmetric atrophy of the frontal lobes (milder volume loss in the temporal lobes).

Question 306

Picks | FDG Pattern

Answer 306

Low uptake in the frontal and temporal lobes.

Question 307

FDG PET-Brain quick Alzheimers

Answer 307

``` Low posterior temporoparietal cortical activity -Identical to Parkinson Dementia -Posterior Cingulate gyrus is the first area abnormal ```

Question 308

FDG PET-Brain quick Multi Infarct

Answer 308

Scattered areas o f decreased | activity

Question 309

FDG PET-Brain quick Dementia with Lewy Bodies

Answer 309

Low in lateral occipital cortex Preservation o f the mid posterior cingulate gyrus (Cingulate Island Sign

Question 310

FDG PET-Brain quick Picks / Frontotemporal

Answer 310

Picks / Frontotemporal

Question 311

The Defias Brotherhood of Neurodegeneration

Answer 311

Fahr Disease (syndrome) Hallervorden Spatz Amyotrophic Lateral Sclerosis Cortico-basal Degeneration Huntington Disease Leigh Disease Hurler Syndrome MELAS Syndrome Parkinson Disease (PD) ``` “Parkinson- Plus” Multi- System Atrophy (MSA) ``` ``` Parkinson- Plus” Progressive Supranuclear Palsy (PSP) ``` Wilson Disease

Question 312

Fahr Disease | syndrome

Answer 312

``` Also called “Bilateral Striatopallidodentate Calcinosis", and sometimes "Primary Familial Brain Calcification ” for the sole purpose of fucking with you on the exam. Many are asymptomatic. Others go insane and start stumbling around ```

Question 313

Fahr Disease (syndrome) Imaging

Answer 313

``` Extensive Calcification in the Basal Ganglia and Thaiami. *Globus is typically involved first ```

Question 314

Hallervorden Spatz

Answer 314

``` Also called PKAN (pantothenate kinaseassociated neuropathy) for the sole purpose of fucking with you on the exam. Etiology: Iron in the Globus Pallidus T2 Dark Globus with central bright area of necrosis “Eye o f the Tiger”. No enhancement. No Restricted Diffusion. ```

Question 315

Hallervorden Spatz Imaging

Answer 315

T2: Dark Medial Basal Ganglia (Globus), | with centraI high signal dot (necrosis

Question 316

Amyotrophic Lateral Sclerosis

Answer 316

Upper motor neuro loss in the brain and spine. Most people die within 5 years (unless you are really good at physics).

Question 317

Amyotrophic Lateral Sclerosis Imaging

Answer 317

Does NOT show gross volume loss. T2/FLAIR tends to be Normal (rarely can be bright in the posterior internal capsule).

Question 318

Cortico-basal Degeneration

Answer 318

Tauopathy (whatever the F that means). Awesome clinical manifestations like the “Alien limb phenomenon ” -50% of cases.

Question 319

Cortico-basal Degeneration Imaging

Answer 319

Asymmetric frontoparietal atrophy.

Question 320

Huntington Disease

Answer 320

``` One of those AD repeat sequence things. What Sequence ? 38 CAGs Mother Fuckers. Yes, I still remember that worthless factoid from Step 1. Why? It’s a curse. My mind is like a bear trap, you gotta chew your leg off to get out. So, between Step 1 & the CORE exam. I’ve got tons of worthless bullshit up there. Remember these poor guys turn into huge assholes - then start flopping around. ```

Question 321

Huntington Disease Imaging

Answer 321

Caudate Atrophy and reduced FDG uptake. The frontal horns will become enlarged and outwardly convex (from the atrophy pattern)

Question 322

Leigh Disease

Answer 322

Mitochondrial Disorder | Elevated Lactate peak at 1.3 ppm

Question 323

Leigh Disease Imaging

Answer 323

T2/FLA1R bright lesions in the Brainstem, Basal Ganglia , and Cerebral Peduncles. They can restrict, but do NOT enhance.

Question 324

MELAS Syndrome

Answer 324

Mitochondrial Disorder Lactic Acidosis, Seizures, and Strokes Elevated Lactate “doublet” at 1.3 ppm

Question 325

MELAS Syndrome Imaging

Answer 325

with a nonvascular distribution (usually occipital and parietal). Underlying WM is normal

Question 326

Hurler Syndrome

Answer 326

Lysosomal Storage Disease / | Mucopolysaccharidoses

Question 327

Hurler Syndrome Imaging

Answer 327

(1) Macrocephaly with Mctopic “beak” (2) Enlarged Perivascular Spaces (3) Beaked Inferior L 1 Vertebral Body

Question 328

Parkinson Disease (PD)

Answer 328

Classic Clinical Hx: Resting tremor, Rigid / Slow movements (shuffling gate, etc..). Etiology: Reduced dopaminergic input to striatum (whatever the fuck that means).

Question 329

Parkinson Disease (PD) imaging

Answer 329

DAT Scan - loflupane 123 - This exotic Nukes study is certainly fair game for an “intermediate level” exam., commas instead of periods Impossible to diagnose on CT or MR alone - but supposedly has mild midbrain volume loss with a “butterfly” pattern (this would have to be stated, it is too subtle to show). Worth noting in the sparing of the midbrain and superior cerebellar peduncles. This is a fairly high yield piece of trivia as it helps distinction Parkinsons from multi-system atrophy.

Question 330

Wilson Disease

Answer 330

AR copper metabolism malfunction. Once the liver fills up with copper it starts spilling over into other organs including the brain.

Question 331

Wilson Disease trivia

Answer 331

Trivia: “Kayser-Fleischer Rings” - seen in 95% of patients. Prepare the Slit Lamp. Trivia: Cortical Atrophy is the most common CT finding (although obviously non-specific). Trivia: T 1 Bright BG is the most common initial MR findings (supposedly).

Question 332

“Parkinson- Plus” Multi- System Atrophy (MSA)

Answer 332

``` This is a monstrously complex entity, that is actually 3 separate renamed entities (“P”, “ Q " an(j “A”). The highest yield pearl is the appearance of the Cerebellar subtype MSA-CI Trivia: 1-123 M1BG can be used to differentiate PD from MSA, by looking at the cardiac/mediastinal ratio (which is normal in MSA, and abnormal in PD) ```

Question 333

“Parkinson- Plus” Multi- System Atrophy (MSA) imaging

Answer 333

Cerebellar Hemisphere / Peduncle Atrophy with a Shrunken Flat Pons & an enlarged 4th vent. Hot Cross Bun Sign (loss of the transverse fibers)

Question 334

“Parkinson- Plus” Progressive Supranuclear Palsy (PSP)

Answer 334

``` • Also called Steele-Richardson-Olszewski for the purpose of fucking with you. • PSP = Most Common Parkinson Plus • Unlike PD & MSA, PSP is a Tauopathy (whatever the fuck that means). ```

Question 335

“Parkinson- Plus” Progressive Supranuclear Palsy (PSP) imaging

Answer 335

Micky Mouse Sign: Tegmentum Atrophy with Sparing of the Tectum & Peduncles. *If needed anatomy refresher - page 14 Hummingbird Sign: Midbrain volume loss with a concave upper surface + relative sparing of the Pons

Question 336

Wilson Disease imaging

Answer 336

Panda Sign: T2 Bright Tegmentum with normal dark red nuclei & substantial nigra T1 and T2 Bright Basal Ganglia T2 Bright Dorsal Medial Thalamus

Question 337

Deep Brain Stimulators

Answer 337

``` I want to quickly touch on deep brain stimulators. These things are used in the treatment of Parkinson disease, essential tremor, and chronic pain. It is common to get a CT immediately after DBS placement to evaluate for correct positioning of the electrode or any obvious complications (bleeding, etc...). Knowing the “correct” position is the most useful piece of trivia. For Parkinson Disease, the electrodes are typically positioned in the sub thalamic nucleus with the tips of the electrons located 9 mm from the midline (just inside the upper most margin of the cerebral peduncle). ```

Question 338

Introduction to MRI Spectroscopy overview

Answer 338

The general idea is that the various metabolites which exist on the cellular level (choline, lactate, N-acetylaspartate “NAA,” etc... etc..., so on and so forth...) occur in different concentrations depending on the pathology. For example, “NAA” is a neuronal marker. Things that destroy neurons (like tumors) will decrease NAA. So, in general the lower the NAA the higher the grade tumor. You will see a graph like this one, with “PPM” on the X-Axis, and “Intensity” on the Y-Axis.

Question 339

Introduction to MRI Spectroscopy itnensity

Answer 339

``` Intensity is going to tell you “how much” of a thing there is. It’s not a raw number, and better thought of as a ratio. ```

Question 340

Introduction to MRI Spectroscopy PPM

Answer 340

PPM stands for parts per million. Better understood as a percent of the Larmor Frequency (1 ppm = 1 millionth of the Larmor frequency). This is important because each metabolite will have a unique frequency distribution. For example NAA is at 2.0 ppm.

Question 341

Introduction to MRI Spectroscopy why are the numbers backward ont he scall

Answer 341

I’m going to answer this with the same explanation I received as a small child when I asked why I couldn’t just eat my dessert first, and my vegetables last — “because I’m your mother that’s why!”

Question 342

Introduction to MRI Spectroscopy hunters angle

Answer 342

This is a method to quickly decide if the MRS is normal or not. Under normal conditions Choline, Creatine, and NAA should ascending in that order. Using a line to connect the tips gives you a 45 degree~ish angle. If it slopes the other way (as shown) then it is not normal.

Question 343

Reversed Hunter's | Angle in a

Answer 343

High Grade | Glioma (GBM)

Question 344

MRI Spectroscopy High Yield Pearls Lipid

Answer 344

``` 0.9-1.4 Product of brain destruction - lipids are present in necrotic brain tissue (necrosis marker). Necrotic Tissue (spilling of membrane lipids). Elevated with high grade tumors, brain infarcts, and brain abscess. ```

Question 345

MRI Spectroscopy High Yield Pearls Lactate

Answer 345

``` 1.3 Product of anaerobic metabolism. Absent under normal conditions. Brain tumor has outgrown its blood supply - is forced into anaerobic pathways for metabolism. Also elevated with cerebral abscess. Classic Trivia: It’s normal to see lactate elevated in the first hours of life Classic Trivia: Lactate and Lipid peaks superimpose - you need to use an intermediate TE (around 140) to causes an “inversion” of the lactate peak (so you can see it) ```

Question 346

MRI Spectroscopy High Yield Pearls Alanine

Answer 346

1.48 Amino Acid Found in Meningiomas

Question 347

MRI Spectroscopy High Yield Pearls N-acetvlaspartate “NAA”

Answer 347

``` 2.0 Neuronal Marker (Neuron Viability). Usually the tallest peak. Glial tumors have NAA. The higher the Glial tumor grade, the lower the NAA Classic Trivia: NAA peak is super high with Canavans ```

Question 348

MRI Spectroscopy High Yield Pearls Glutamine - “GLX”

Answer 348

2.2-2.4 Neurotransmitter Increased with Hepatic Encephalopathy

Question 349

MRI Spectroscopy High Yield Pearls Creatine - “C r”

Answer 349

3.0 Energy | Metabolism Decreased in tumor necrosis.

Question 350

MRI Spectroscopy High Yield Pearls Choline - “Co”

Answer 350

``` 3.2 Cell Membrane Turnover More turnover more Choline (thus elevated in high grade tumor, demyelination, inflammation). ```

Question 351

MRI Spectroscopy High Yield Pearls Myoinositol - “ml”

Answer 351

``` 3.5 Cell Volume Regulator and Byproduct of Glucose Metabolism. - Elevated in low grade gliomas. - Elevated in Alzheimer’s (decreased in other dementias) - Elevated in Progressive multifocal leukoencephalopathy (PML) - Reduced in high grade gliomas - Reduced in Hepatic Encephalopathy ```

Question 352

h is vs THAT: Demyelinating vs Dysmyelinating

Answer 352

Demyelinating disease Example = MS Disease that destroys normal myelin Dysmyelinating disease Example = Mctachromatic leukodystrophy disease that disruptst he normal formation and turnover of myelin

Question 353

Leukodystrophy

Answer 353

Fucked White Matter in a Kid Leukodystrophy (ALD) “X-Linked Metachromatic Alexander Disease Canavan Disease Krabbe Pelizaeus- Merzbacher

Question 354

Leukodystrophies & Friends

Answer 354

On the prior page, I introduced the vocab work "dysmyelinating” disease. Leukodystrophies are the classic example o f this group o f pathologies. Technically speaking Leukodystrophies can occur from deficiencies in lysosomal storage, peroxisomal function, or mitochondrial dysfunction. I'm gonna hit on mitochondrial diseases separately as they tend to be more asymmetric and favor the grey matter. Where as the classic forms target the white matter in a more symmetric and extensive manner

Question 355

Leukodystrophy (ALD) “X-Linked

Answer 355

``` Normal Head Size Parieto-occipital Predominance “Extends across the Splenium of the Corpus Callosum” Sex-linked recessive (peroxisomal enzyme deficiency) Male Predominant Can Enhance & Restrict ```

Question 356

Metachromatic

Answer 356

``` Normal Head Size Frontal Predominance Periventricular and Deep White Matter - Tigroid Pattern (stripes of milder disease). Most common Leukodystrophy. U-fibers are relatively spared ```

Question 357

Alexander Disease

Answer 357

``` Weird Bie Head Frontal Predominance Also hits the cerebellum and middle cerebellar peduncles Can Enhance ```

Question 358

Canavan Disease

Answer 358

``` Weird Bin Head Diffuse Bilateral subcortical U fibers. “Subcortical Predominance” Elevated NAA (MRS). ```

Question 359

Krabbe

Answer 359

``` Small Head Centrum semiovale and periventricular white matter with parietooccipital predominance High density foci on CT (in the thalamus, caudate, and deep white matter). Earlv sparine of the subcortical U fibers ```

Question 360

Pelizaeus- | Merzbacher

Answer 360

``` Normal Head Size Typically diffuse “total lack of normal myelination” with extension to the subcortical U fibers. Patchy variant is also described as “tigroid” - although that term is more classic for Metachromatic No enhancement. No restricted diffusion ```

Question 361

Leukodystrophies & Friends continued

Answer 361

As discussed on the prior page Leukodystrophies can occur from deficiencies in lysosomal storage, peroxisomal function, or mitochondrial dysfunction. The classic forms tend to target the white matter in a more symmetric and extensive manner. This is different than mitochondrial diseases which are more asymmetric and favor the grey matter. Grey Matter needs more oxygen than White Matter (and White Matter needs more oxygen than trial lawyers). Inability to process oxygen (mitochondrial dysfunction) - helps me remember the grey matter > white matter thing.

Question 362

MELAS

Answer 362

Mitochondrial Enccphalomyopathy, Lactic Acidosis, and Stroke-like episodes. This is a mitochondrial disorder with lactic acidosis and stroke like episodes. Tends to have a parietooccipital distribution

Question 363

MELAS BUZZWORD(s

Answer 363

migrating infarcts

Question 364

typical MRS pattern for MELAS

Answer 364

increased lactate and decreased naa

Question 365

Leigh Disease

Answer 365

Also called Subacute Necrotizing Encephalo-Myelopathy - for the purpose of fucking with you. White Matter Distribution: Focal areas of subcortical white matter. Gray Matter Distribution: Basal ganglia and Periaquaductal Gray

Question 366

Leigh Disease trivia

Answer 366

Head size tends to be normal.

Question 367

Brain tumors approach

Answer 367

The strategy is as follows; (1) decide if it's single or multiple, (2) look at the age o f the patient - adults and kids have different differentials, (3) look at the location - different tumors occur in different spots, (4) now use the characteristics to separate them. The strategy centers around narrowing the differential based off age and location till you are only dealing with 3-4 common things, then using the imaging characteristics to separate them. It's so much easier to do it that way.

Question 368

Multiple Masses approach

Answer 368

multifocal primary from seeding mets (50% at solitary) syndromes (example nf2)

Question 369

single mass adult approach

Answer 369

cortical intraventricular cp angle infratentorial

Question 370

single mass kid approach

Answer 370

supratentorial skull base/dura sella/parasella pineal gland

Question 371

Before we get rolling, the first thing to do is to ask yourself is this a tumor, or is it a mimic?

Answer 371

Mimics would be abscess, infarct, or a big MS plaque. This can be tricky. If you see an incomplete ring - you should think giant MS plaque. If they show you diffusion, it is either lymphoma or a stroke (or an abscess) - you’ll need to use enhancement to straighten that out (remember lymphoma enhances homogeneously). Yes... GBM can restrict, but for multiple choice it is way more likely to be lymphoma.

Question 372

intra-Axial” vs “Extra-Axial”

Answer 372

The Brant and Helms discussion on brain tumors will have you asking “ intra-axial” vs “extra-axial” first. This is not always that simple, but it does lend itself very well to multiple choice test questions (therefore it’s high yield).

Question 373

Basically yo u need to memorize the "signs o f extra-axial location "

Answer 373

• CSF Cleft Displaced Subarachnoid Vessels Cortical Gray matter between the mass and white matter Displaced and expanded Subarachnoid spaces • Broad Dural Base / Tail • Bony Reaction

Question 374

Why Do Things Enhance

Answer 374

Understanding the WHY is very helpful for problem solving. Let me first answer the question “Why D O N 'T things enhance?” They DON’T enhance because o f the blood brain barrier. So, when things DO enhance it's because either: (a) They are outside the blood brain barrier (they are extra-axial), or (b) They have melted the blood brain barrier. In other words, extra axial things (classic example is meningioma) will enhance. High grade tumors (and infections) enhance. Low grade tumors ju st aren't nasty enough to take the blood brain barrier down

Question 375

Why Do Things Enhance exceptions

Answer 375

Gangliogliomas and Pilocytic Astrocytomas are the exceptions - they are low-grade tumors, but they enhance.

Question 376

Multiple Masses

Answer 376

In adults or kids, if you see multiple masses you arc dealing with mets (or infection). Differentiating between mets and infection is gonna be done with diffusion (infection will restrict). If they want you to decide between those two they must show you the diffusion otherwise only one or the other will be listed as a choice.

Question 377

Mets — High Yield Trivia

Answer 377

• Most common CNS met in a kid = neuroblastoma (BONES, DURA, ORBIT - not brain) • Most common location for mets = Supratentorial at the Grey-White Junction (this area has a lot of blood flow + an abrupt vessel caliber change... so you also see hematogenous infection / septic emboli go there first too). • Most common morphology is “round” or “spherical” • Remember that mets do NOT have to be multiple. In fact, 50% of mets are solitary. In an adult, a solitary mass is much more likely to be a met than a primary CNS neoplasm. • MRCT is the mnemonic for bleeding mets (Melanoma. Renal, Carcinoid / Choriocarcinoma, Thyroid). • Usually Mets have more surrounding edema than primary neoplasms of similar size.

Question 378

Mets gamesmanship

Answer 378

“Next Step Gamesmanship ” - Because the most common intra-axial mass in an adult is a met, if they show you a solitary mass (or multiple masses) and want a next step it’s gonna be go hunting for the primary (think lung, breast, colon... the common stuff).

Question 379

Tumors that Like to be Multifocal

Answer 379

Mets — you should still think this first when you see multiple tumors Lymphoma Multiccntric GBM Gliomatosis Cerebri

Question 380

Tumors that are Multifocal from Seeding

Answer 380

Mcdulloblastoma Ependymoma GBM Oligodendroglioma

Question 381

SYNDROMES - Tumors in Syndromes are more likely to be Multifocal

Answer 381

NF 1 NF 2 “MSME” Tuberous Sclerosis VHL

Question 382

NF 1

Answer 382

Optic Gliomas | Astrocytomas

Question 383

NF 2 MSME

Answer 383

Multiple Schwannomas Meningiomas Ependymomas

Question 384

Tuberous Sclerosis

Answer 384

Subependymal Tubers IV Giant Cell Astrocytomas

Question 385

VHL

Answer 385

Hcmangioblastomas

Question 386

Cortically Based

Answer 386

Most intra-axial tumors arc located in the white matter. So when a tumor spreads to or is primarily located in the gray matter, you get a shorter DDx. High yield piece of trivia regarding the cortical tumor / cortical met is that they often have very little edema and so a small cortical met can be occult without IV contrast.

Question 387

Cortically Based ddx

Answer 387

``` P-DOG: Pleomorphic Xanthoastrocytoma (PXA) Dysembryoplastic Neuroepithelial Tumor (DNET) Oligodendroglioma, Ganglioglioma ```

Question 388

PXA (Pleomorphic Xanthroastrocytoma

Answer 388

Superficial tumor that is ALWAYS supratentorial and usually involves the temporal lobe. They are often in the cyst with a nodule category (50%). There is usually no pcritumeral T2 signal. The tumor frequently invades the leptomeninges. Looks just like a Desmoplastic Infantile Ganglioglioma - but is not in an infant

Question 389

PXA (Pleomorphic Xanthroastrocytoma quick

Answer 389

``` PEDS (10-20) Will Enhance Dural Tail*** Cyst with Nodule Temporal Lobe ```

Question 390

D N E T (Dysembryoplastic Neuroepithelial Tumor)

Answer 390

Kid with drug resistant seizures. The mass will always be in the temporal lobe (on the test - real life 60% temporal). Focal cortical dysplasia is seen in 80% of the cases. It is hypodense on CT, and on MRI there will be little if any surrounding edema. High T2 signal “bubbly lesion.” Bright Rim Sign -

Question 391

Bright Rim Sign

Answer 391

Persistent rim of FLAIR signal * Looks Similar to T2-FLAIR Mismatch of Astrocytomas **discussed later

Question 392

DNET quick

Answer 392

``` PEDS (< 20) No enhancement High T2 Signal with Bright FLAIR Rim “Bubbly” Temporal Lobe ```

Question 393

Oligodendroglioma

Answer 393

Remember this is the guy that calcifies 90% of the time. It’s most common in the frontal lobe and the buzzword is “expands the cortex”. This takes after its most specific feature of cortical infiltration and marked thickening. It’s 0 likely you could get asked about this Ip/I9q deletion which I ^ will discuss later when I go into detail about Gliomas

Question 394

Oligodendroglioma quick

Answer 394

``` ADULT - (40s-50s) Can Enhance Calcification Common “Expands the Cortex” Frontal Lobe 1p /19q ``` ribbon calcifications

Question 395

Ganglioglioma

Answer 395

This guy can occur at any age, anywhere (usually temporal lobe), and look like anything. However, for the purpose of multiple choice testing the classic scenario would be a 13 year old with seizures, and a temporal lobe mass that is cystic and solid with focal calcifications. There may be overlying bony remodeling.

Question 396

Ganglioglioma quick

Answer 396

``` Any Age Can Enhance Can look like Anything Temporal Lobe Not bubly ``` Mixed Cystic & Solid

Question 397

Ventricular wall and septum pellucidum ddx

Answer 397

``` F.pendvmoma (TEDS) Medulloblastoma (TEDS) SEGA (Subependymal Giant Cell Astrocytoma) = PEDS Subependymoma (ADULT) Central Neurocytoma (YOUNG ADULT) ```

Question 398

choroid plexus ddx

Answer 398

``` Choroid Plexus Papilloma (PEDS in Trigone) (ADULT in 4th Vent) Choroid PlexusCarcinoma (TEDS) Xanthogranuloma t “Found“ in ADULTS) ```

Question 399

misc intraventricular ddx

Answer 399

mets meningioma colloid cyst

Question 400

Ependymoma overview

Answer 400

Bimodal distribution on this one (large peak around 6 years o f age, tiny peak around 30 years o f age). I would basically think o f this as a PEDS tumor. They come in two flavors:

Question 401

Ependymoma 4th ventricle

Answer 401

4th Ventricle - which is about 70% o f the time. There is frequent extension into the foramen o f Luschka and Magendie. They are the so-called “plastic tumor” or "toothpaste ” tumor because they squeeze out o f the base o f the 4 th ventricle.

Question 402

Ependymoma parenchymal supratentorial

Answer 402

Parenchymal Supratentorial - which is about 30% o f the time. These are usually big (> 4cm at presentation).

Question 403

Medulloblastoma overview

Answer 403

Let us just assume we are talking about the “Classic Medulloblastoma” which is a type o f PNET. If you want to understand the genetic spectrum o f these things, read Osborn’s Brain — seriously don’t subject yourself to that.

Question 404

Medulloblastoma epidiomology and location

Answer 404

This is a pediatric tumor - with most occurring before age 10 (technically there is a second peak at 20-40 but for the purpose o f multiple choice tests I’m going to ignore it). These guys are cerebellar arising from vermis / ROOF o f the 4th ventricle - project into 4th ventricle. They are much more common than their chief differential consideration the Ependymoma (which originates from the FLOOR o f the 4th ventricle).

Question 405

Medulloblastoma classic look

Answer 405

The classic look is a dense mass on CT, heterogeneous on T1 and T2, and enhances homogeneously. They are hypercellular and may restrict. They calcify 20% o f the time (less than Ependymoma).

Question 406

Medulloblastoma mets to

Answer 406

This is a tumor that loves to met via CSF pathways — they like to “drop met.” The buzzword is “zuckerguss” which apparently is German for sugar icing, as seen on post contrast imaging of the brain and spinal cord (leptomeningeal carcinomatosis). As a point of absolute trivia, they are associated with Basal Cell Nevus Syndrome and Turcots Syndrome.

Question 407

Gorlin Syndrome

Answer 407

Gorlin Syndrome - If you see a Medulloblastoma next look for dural calcs. If you see thick dural calcs you might be dealing with this syndrome. »'v i ‘\ They get basal cell skin cancer after radiation, and have odontogenic cysts.

Question 408

Medulloblastoma next step

Answer 408

Preoperative imaging o f the entire spinal axis should be done in any child with a posterior fossa neoplasm, especially if Medulloblastoma or Ependymoma is suspected. Evidence o f tumor spread is a statistically significant predictor o f outcome.

Question 409

M e d u llo b la s tom a quick

Answer 409

More common Originate from Vermis /ROOF o f the 4th Ventricle Can project into 4th ventricle, do NOT usually extend into basal cisterns Enhance Homogeneously (more so than Ependymoma anyway) Calcify Less (20%) Linear “icing-like” enhancement o f the brain surface is referred to as “Zuckerguss”

Question 410

Ependymoma quick

Answer 410

Less Common Originate from the vermis/ floor of the 4th ventricle Can extend into basal cisterns like tooth paste pushing though foramina o f Luschka and Magendie Enhance Heterogeneously Calcify More (50%)

Question 411

Subependymal Giant Cell Astrocytoma (SEGA):

Answer 411

This is going to be shown in the setting o f TS. They will more than likely show you renal AMLs or tell you the kid has seizures / developmental delay. Because it’s syndromic, you see it in kids (average age 11). It will arise from the lateral wall o f the ventricle (near the foramen o f Monro), often causing hydrocephalus. It enhances homogeneously.

Question 412

THIS vs THAT: SEGA vs Subependymal Nodule (SEN)

Answer 412

The SEN will stay stable in size, the SEGA will grow. The SEGA is found in the lateral ventricle near the foramen o f Monroe, the SEN can occur anywhere along the ventricle. SENs are way more common. Both SEN and SEGA can calcify.

Question 413

THIS vs THAT: SEGA vs Subependymal Nodule (SEN) pearl

Answer 413

Enhancing, partially calcified lesion at the foramen o f Monro, bigger than 5 mm is a SEGA not a SEN.

Question 414

Subependymoma

Answer 414

Found in ADULTS. Well-circumscribed IV mass most commonly at the foramen of Monro and the 4th ventricle. They can cause hydrocephalus. They typically don’t enhance. They are T2 bright (like most tumors).

Question 415

Central Neurocytoma

Answer 415

``` This is the most common IV mass in an ADULT aged 20-40. The buzzword is “swiss cheese,” because o f the numerous cystic spaces on T2. They calcify a lot (almost like oligodendrogliomas). Swiss Cheese + Calcification in the Ventricle ```

Question 416

Choroid Plexus Papilloma / Carcinoma

Answer 416

Can occur in peds (85% under the age o f 5) or adults. They make up about 15% o f brain tumors in kids under one. Basically you are dealing with an intraventricular mass, which is often making CSF, so it causes hydrocephalus.

Question 417

Choroid Plexus Papilloma / Carcinoma here is the trick

Answer 417

Brain tumors are usually supratentorial in adults and posterior fossa ▼ in kids. This tumor is an exception. Remember exceptions to rules are testable.

Question 418

Choroid Plexus Papilloma / Carcinoma trivia

Answer 418

• In Adults it’s in the 4th Ventricle, in Kids it’s in the lateral ventricle (usually trigone). • Carcinoma type is ONLY SEEN IN KIDS - and are therefore basically ONLY SEEN IN LATERAL VENTRICLE / TRIGONE • Carcinoma association with Li-Fraumeni syndrome (bad p53) • Angiography may show enlarged choroidal arteries which shunt blood to the tumor, • Carcinoma type o f this tumor looks very similar (unless it's invading the parenchyma) and is almost exclusively seen in kids. • The tumor is typically solitary but in rare instances you can have CSF dissemination

Question 419

Xanthogranuloma

Answer 419

This is a benign choroid plexus mass. You see it all the time (7%) and don’t even notice it.

Question 420

Xanthogranuloma trick

Answer 420

``` The trick is that they restrict on diffusion, so they are trying to trick you into working them up. They are benign... leave them alone. ```

Question 421

Intraventricular mets

Answer 421

The most common location o f intraventricular metastasis is the trigone o f lateral ventricles (because o f the vascular supply o f the choroid). The most common primary is controversial - and either lung or renal. I f forced to pick I’d go Lung because it’s more common overall. I think all things equal renal goes more - but there are less renal cancers. It all depends on how the question is worded

Question 422

Colloid C yst

Answer 422

These are found almost exclusively in the anterior part o f the 3rd ventricle behind the foramen o f Monro. They can cause sudden death via acute onset hydrocephalus.

Question 423

Colloid C yst appearance

Answer 423

Their appearance is somewhat variable and depends on what they are made of. If they have cholesterol they will be T1 bright, T2 dark. If they do n ’t, they can be T2 bright. The trick is a round well circumscribed mass in the anterior 3rd ventricle. If shown on CT, it will be pretty dense.

Question 424

Colloid C yst quick

Answer 424

- Anterior 3rd Ventricle | - Hyperdense on CT

Question 425

Intraventricular meningioa

Answer 425

Can occur in an intraventricular location, most commonly (80%) at the trigone of the lateral ventricles (slightly more on the left). Details on meningiomas are discussed on the following page.

Question 426

Cerebellar Pontine Angle (CPA)

Answer 426

Age is actually less o f an issue here because the DDx isn’t that big. Most of these are adult tumors, but in the setting of NF-2 you could have earlier onset.

Question 427

Cerebellar Pontine Angle (CPA) Epidemiology

Answer 427

Vestibular Schwannoma is #1 - making up 75% o f the CPA masses, #2 is the meningioma making up 10%, and the Epidermoid is #3 making up about 5%. The rest are uncommon.

Question 428

Cerebellar Pontine Angle (CPA) Schwannoma (Vestibular)

Answer 428

These guys account for 75% of CPA masses. When they are bilateral you should immediately think NF-2 (one fo r each side). Enhances strongly but more heterogeneous than meningomas. May widen the porus acousticus resulting in a “trumpet shaped” IAC. "Ice Cream Cone IAC. ”

Question 429

Cerebellar Pontine Angle (CPA) Meningioma

Answer 429

Second more common CPA mass. One o f the few brain tumors that is more common in women. They can calcify, and if you are lucky they will have a dural tail (which is pretty close to pathognomonic - with a few rare exceptions). Because they are extradural they will enhance strongly. Radiation o f the head is known to cause meningiomas

Question 430

Cerebellar Pontine Angle (CPA) Meningioma trivia

Answer 430

•Most common location of a meningioma is over the cerebral convexity. ^Meningiomas take up octreotide and Tc-MDP on Nuclear Medicine tests (sneaky).

Question 431

Cerebellar Pontine Angle (CPA)Epidermoid

Answer 431

Can be congenital or acquired (after trauma - classically after LP in the spine). Unlike dermoids they are usually off midlinc. They will follow CSF density and intensity on CT and MR1 (the exception is this zebra called a "white epidermoid" which is T1 b r ig h t- just forget I ever mentioned it). (5%)

Question 432

Cerebellar Pontine Angle (CPA) Epidermoid key points

Answer 432

(1) Unlike an arachnoid cyst they are bright on FLAIR (sometimes warm - they don't completely null), and (2)They will restrict diffusion. Epidermoid - Follows CSF Signal - Restricts Diffusion

Question 433

Cerebellar Pontine Angle (CPA) Schwannoma quick

Answer 433

``` Enhance Less Homogeneously Invade IAC IAC can have “trumpeted” appearance ```

Question 434

Cerebellar Pontine Angle (CPA) Meningioma quick

Answer 434

``` Enhance Homogeneously Don't Usually Invade IAC Calcify more often ```

Question 435

Cerebellar Pontine Angle (CPA) Dermoid C yst

Answer 435

``` This is about 4x less common than an epidermoid. It’s more common in kids / young adults. Usually midline, and usually are found in the 3rd decade. They contain lipoid material and are usually hypodense on CT and very bright on T l. They are associated with NF2. ```

Question 436

Cerebellar Pontine Angle (CPA) Dermoid C yst trivia

Answer 436

•These are usually midline • Most common location for a A dermoid cyst is the suprasellar 4 9 1 1 cistern (posterior fossa is #2)

Question 437

Cerebellar Pontine Angle (CPA) The Ruptured Dermoid

Answer 437

It is possible for a dermoid cyst to explode -rare in real life, common on multiple choice. Sometimes this is after a trauma, but usually it’s spontaneous. The most common clinical scenario is “headache and seizure” - which is pretty much every brain tumor, so that is not helpful.

Question 438

The Ruptured Dermoid buzzword

Answer 438

“Chemical Meningitis ”

Question 439

The Ruptured Dermoid aunt minnie

Answer 439

Fat droplets (typically shown as low density on CT, or High Signal on T i l floating in the ventricles and/or subarachnoid space.

Question 440

THIS vs THAT: Dermoid vs Epidermoid

Answer 440

The easy way to think o f this is that the | Epidermoid behaves like CSF, and the Dermoid behaves like fat.

Question 441

I AC Lipoma

Answer 441

It can occur, and is basically the only reason you get a Tl when you are working up CPA masses. It will fat sat out - because it’s a lipoma. There is an association with sensorineural hearing loss, as the vestibulocochlear nerve often courses through it

Question 442

Arachnoid C yst

Answer 442

Common benign lesion that is located within the subarachnoid space and contains CSF. They are increased in frequency in mucopolysaccharidoses (as are perivascular spaces). They are dark on FLAIR (like CSF), and will NOT restrict diffusion.

Question 443

How can yo u tell an epidermoid | from an arachnoid cyst?

Answer 443

The epidermoid restricts, | the arachnoid cyst does NOT.

Question 444

Infratentorial

Answer 444

Most are PEDS (Hemangioblastoma is the exception).

Question 445

Infratentorial | Atypical Teratoma I Rhabdoid Tumor “AT/RT”

Answer 445

Highly malignant tumors (WHO IV), and rarely occur in patients older than 6 years. The average age is actually 2 years, but they certainly occur in the first year of life. They can occur in supra and infratentorial locations (most common in the cerebellum). These are usually large, pissed off looking tumors with necrosis and heterogeneous enhancement. They believe in nothing Lebowski. They fuck you up. They take the money

Question 446

Infratentorial THIS vs THAT: AT/RT v s Medulloblastoma

Answer 446

``` Both are WHO Grade 4 destroyers (AT/RT is worse) that are often seen in the posterior fossa of a kid. Technically they are both subtypes of Medulloblastoma - but that’s the kind of knowledge that causes you to miss multiple choice questions. For the purpose of multiple choice: • AT/RT is a 2 year old • Medulloblastoma is a 6 year old • AT/RT has calcifications • Medulloblastoma does not ```

Question 447

Infratentorial Medulloblastoma & Ependymoma

Answer 447

discussed with intraventricular

Question 448

Infratentorial Juvenile Pilocytic Astrocytoma (JPA):

Answer 448

Just think cyst with a nodule in a kid. They are WHO grade 1, but the nodule will still enhance. This will be located in the posterior fossa (or optic chiasm).

Question 449

Infratentorial Hemangioblastoma:

Answer 449

First things first - immediately think about this when you see a cyst with a nodule in an ADULT. Then think Von Hippel Lindau, especially if they are multiple. These things are slow growing, indolent vascular tumors, that can cause hydrocephalus from mass effect. 70% of the time you will see flow voids along the periphery of the cyst. About 90% of the time they are found in the cerebellum. There is an association with polycythemia

Question 450

Infratentorial Ganglioglioma

Answer 450

Occurs at any age, anywhere, can look like anything - see cortical lesions

Question 451

Infratentorial Diffuse Pontine Glioma (DPG):

Answer 451

Seen in kids age 3-10. Most common location is the pons, which is usually a high grade fibrillary glioma. It’s going to be T2 bright with subtle or no enhancement. 4th ventricle will be flattened. Imaging features arc so classic that no biopsy is needed

Question 452

Atypical Teratoma I Rhabdoid Tumor (“AT/RT”) buzzword

Answer 452

“Increased Head Circum ference ”

Question 453

Juvenile Pilocytic Astrocytoma (JPA): gamesmanship

Answer 453

if they don’t tell you the age, you can look for enhancement of the cystic wall which JPA can have (-50%) but Hemangioblastomas don’t

Question 454

Pilocytic Astrocytoma quick

Answer 454

Cyst + Nodule in Kid

Question 455

I Say Posterior Fossa Cyst | with a Nodule - PEDS,

Answer 455

JPA

Question 456

I say Posterior Fossa Cyst | with a Nodule - ADULT

Answer 456

Hemangioblastoma

Question 457

Supratentorial - Adults Tumors Astrocytomas

Answer 457

Most common primary brain tumor in adults. There is a trend towards “genetically classifying” tumors - this actually changes the way they arc treated and could be the source of trivia. I’m going to attempt to simply this - because it can get pretty fucking complicated The new way to think about these things is a spectrum of severity based on genetic classification - and the treatment and prognosis follows that.

Question 458

Supratentorial - Adults Tumors Astrocytomas simple terms

Answer 458

In the simplest terms, you have the neurons and you have the glial cells. The glial cells are the “support staff’ — there are lots of them and lots of different kinds. Astrocytes and Oligocytes share a common origin (both are support staff - “glial cells”) and have a lot of similarities. In other words, they are both “Gliomas” and are going to get lumped together in this discussion.

Question 459

Supratentorial - Adults Tumors Ribbon pattern of calcification Classic for

Answer 459

Oligodendroglioma

Question 460

Supratentorial - Adults Tumors Astrocytoma IDH Mutation (earliest genomic event) yes

Answer 460

Yes (10%) ``` Astrocytoma Grade 4 - Glioblastoma - Younger Patients -Better prognosis -Probably “Secondary GBM” from progression of a previous lowergrade tumor ``` 1p/19qd deletion positive ``` Oligodendroglioma Calcification on preoperative CT is associated with codeletion (Ip/I9q) ``` 1p/19qd deletion negative Astrocytoma Low Grade

Question 461

Supratentorial - Adults Tumors Astrocytoma IDH Mutation (earliest genomic event) no

Answer 461

no 990%0 ``` Astrocytoma Grade 4 - Glioblastoma -Older Patients -The Worst Prognosis -Probably “Primary GBM” ``` ``` Astrocytoma Higher Grade -Grade 2 - Diffuse -Grade 3 - Anaplastic T 2 - FLAIR Mismatch Sign ```

Question 462

Supratentorial - Adults Tumors Astrocytoma prognosis

Answer 462

You probably noticed me using this WHO classification (1-4). All brain tumors are bad, but 4 is the worst - this is your GBM. On the following page, I'll get into a few more details on each type but as a general rule low grade tumors don’t typically enhance (WHO 2) and higher grades do (mild for grade 3, and intense for grade 4 GBM). The exception to this rule is the pilocytic astrocytoma which often has an enhancing nodule, and the Subependymal Giant Cell Astrocytomas which enhances because of its location (Intraventricular). GBM is the beast that cannot be stopped. It believes in nothing Lebowski. It grows rapidly, it can necrose (creating the ring of enhancement, with a non-enhancing central necrotic co re), it can cross the midline, and it can restrict diffusion. Remember Turcot Syndrome (that GIpolyp thing), and NF 1 are associated with GBMs.

Question 463

Astrocytoma Grade 1 Subependymal Giant Cell Astrocytomas

Answer 463

``` Intraventricular mass near the foramen of Monro in a young patient with tuberous sclerosis. -Can cause obstructive hydrocephalus ```

Question 464

Astrocytoma Grade 1 Pilocytic Astrocytoma

Answer 464

``` - Cyst with nodule in the posterior fossa of a kid Remember these tumors break the rule - and enhance despite being low grade. ```

Question 465

Astrocytoma | Grade 2 - Diffuse

Answer 465

``` White Matter is Preferred NO ENHANCEMENT T2 Bright - FLAIR Iso (mismatch sign) ```

Question 466

Astrocytoma | Grade 3 - Anaplastic

Answer 466

``` White Matter is Preferred Mild ENHANCEMENT T2 Bright-FLAIR Iso (mismatch sign) ```

Question 467

Astrocytoma | Grade 4- GBM

Answer 467

``` White Matter is Preferred - can cross the midline. RING ENHANCEMENT (can also be diffuse heterogenous enhancement) T2 & FLAIR Bright Central locations (like the thalamus) are worse than normal. NF type 1, Turcot syndrome, Li Fraumeni syndrome ```

Question 468

T2 / FLAIR Mismatch

Answer 468

Seen with WHO 2 (diffuse) and 3 (anaplastic) astrocytoma, not with WHO 1. T2 tumor has high signal with surrounding vasogenic edema. On FLAIR the tumor signal become isointense

Question 469

Siupratentorial adults Gliomatosis Cerebri

Answer 469

A diffuse glioma with extensive infiltration. It involves at least 3 lobes and is often bilateral. The finding is usually mild blurring of the gray-white differentiation on CT, with extensive T2 hyperintensity and little mass effect on MR. It’s low grade, so it doesn’t typically enhance.

Question 470

Siupratentorial adults mets

Answer 470

The most common supratentorial mass. Just like mets favor the lower lobes in the lungs, the cerebrum is favored over the cerebellum (it is a blood flow thing). They arc usually multiple, but can be solitary — some sources say 50% of the time, so don’t be fooled a solitary lesion can totally be a met. Some other trivia worth knowing — melanoma can be T1 bright even if it doesn’t bleed. CT-MR is a good way to remember the ones that like to bleed (Choriocarcinoma / Carcinoid, Thyroid, Melanoma, Renal).

Question 471

Siupratentorial mets quick adults

Answer 471

Irregular Margin -Multifocal (25-50% solitary) -Favors Grey-White Junction

Question 472

Siupratentorial GBM quick adults

Answer 472

Spherical -Solitary ) (25%> multifocal) -Favors Deep White Matter

Question 473

Supratentorial - Adults Tumors Primary CNS Lymphoma:

Answer 473

Seen in end stage AIDS patients, and those post-transplant. EB virus plays a role. Most common type is Non-Hodgkin B cell.

Question 474

Supratentorial - Adults Tumors Primary CNS Lymphoma: classic

Answer 474

Classic picture would be an intensely enhancing homogeneous solid mass in the periventricular region, with restricted diffusion. However, it can literally look like and do anything. Classic Multiple choice test question is that it is Thallium Positive on SPECT (toxo is not).

Question 475

Supratentorial - Adults Tumors I say restricting brain tumor, you say

Answer 475

Lymphoma (although GBM can do this also)

Question 476

THIS vs THAT: P e r iv e n tr icu la r / Ep e n d ym a l E n h a n c em e n t P a tte rn s

Answer 476

thin smooth and linear Ependymitis - £ (Classic Example = CMV) thick and irregular lymphoma (rim phoma)

Question 477

Supratentorial - Peds Tumors DNET & PXA (Pleomorphic Xanthroastrocytoma):

Answer 477

Discussed under the cortical tumors .

Question 478

Supratentorial - Peds Tumors D e smo p la s t ic Infantile Ganglioglioma I As tro cy toma “DIG”:

Answer 478

These guys arc large cystic tumors that like to involve the superficial cerebral cortex and leptomeninges. Unlike the Atypical Teratoma / Rhabdoid, these have an ok prognosis (WHO 1). They ALWAYS arise in the supratentorial location, usually involve more than one lobe (frontal and parietal most commonly), and usually present before the first birthday.

Question 479

Supratentorial - Peds Tumors D e smo p la s t ic Infantile Ganglioglioma I As tro cy toma “DIG”: buzzword

Answer 479

“rapidly increasing head circumference.”

Question 480

Skull Base Chordoma

Answer 480

This is a locally aggressive tumor that originates from the notochord. WTF is the “notochord” ? It’s an embryology thing that is related to spine development. The thing you need to know is that the notochord is a midlinc structure. Therefore all Chordomas are midline - either in the clivus, vertebral bodies (especially C2), or Sacrum. You can NOT get them in the hips, ribs, legs, arms, or any other structure that is not totally midline along the axis o f the axial skeleton.

Question 481

Skull Base Chordoma facts

Answer 481

*lt is most common in the sacrum (#2 is the clivus) *When it involves the spine, it’s most common at C2 - but typically extends across a disc space to involve the adjacent vertebral body. .It’S T2 Bright *Ifs ALWAYS Midline. — it is never in a leg, arm, e tc ... ONLY MIDLINE structures.

Question 482

Ch on d ro sa r coma skull base

Answer 482

This is the main differential o f the chordoma in the clivus. The thing to know is that it is nearly always lateral to midline (chordoma is midline). These are also T2 bright, but will have the classic “arcs and rings” matrix o f a chondrosarcoma. Obviously you’ll need a CT to describe that matrix.

Question 483

Dura Meningioma

Answer 483

As described above, it is common and enhances homogeneously. The most common location is over the cerebral convexity and it has been known to cause hyperostosis.

Question 484

Dura H em an g iop e r ic y toma

Answer 484

This is a soft tissue sarcoma that can mimic an aggressive meningioma because they both enhance homogeneously. They also can mimic a dural tail, with a narrow base of dural attachment. They won’t calcify or cause hyperostosis , but will invade the skull.

Question 485

Dura metd

Answer 485

The most common met to the dura is from breast cancer. 80% will be at the gray-white junction. They will have more edema than a primary tumor o f similar size.

Question 486

Sella I Parasella - Adults Pituitary Adenoma

Answer 486

The most common tumor o f the sella. They are seen 97% o f the time in adults. If they are greater than 1 cm they are “macroadenomas.” When functional, most are prolactin secreting (especially in women). Symptoms are easy to pick up in women (menstrual irregularity, galactorrhea). Men tend to present later because their symptoms are more vague (decreased libido). On MR, 80% are T1 dark and T2 bright. They take up contrast more slowly than normal brain parenchyma. Next step = Dynamic contrast enhanced MR.

Question 487

Sella I Parasella - Adults Pituitary Adenoma thingsj to know

Answer 487

• Microadenoma under 10 mm, • Macroadenoma over 10 mm. m • Microadenomas typically form in the adenohypophysis (anterior 2/3). • Prolactinoma is the most common functional type. • Typically they enhance less than normal pituitary.

Question 488

Sella I Parasella - Adults Pituitary Apoplexy

Answer 488

Hemorrhage or Infarction o f the pituitary, usually into an enlarged gland (either from pregnancy or a macroadenoma). Here are the multiple choice trivia association: taking bromocriptine (or other prolactin drugs), “Sheehan Syndrome” in postpartum woman, Cerebral Angiography. They will be T1 bright (remember adenoma is usually T1 dark). Supposedly this is an emergent finding because the lack o f hormones can cause hypotension.

Question 489

Sella I Parasella - Adults Rathke Cleft Cyst

Answer 489

Usually an incidental finding. Rarely symptomatic. The “cleft” is between the anterior and posterior pituitary. They are variable on T1 and T2, but are usually very bright on T2. They do NOT enhance

Question 490

Sella I Parasella - Adults Epidermoid

Answer 490

Discussed on page 80. Remember these guys restrict diffusion. I say "Midline Suprasellar Mass that Restricts Diffusion ”, You say Epidermoid.

Question 491

Sella I Parasella - Adults Craniopharyngioma

Answer 491

They come in two flavors: (a) Papillary - 10% and (b) Adamantinomatous - 90%. The Papillary type is the adult type (Papi for Pappi). They are solid and do not have calcifications. They recur less frequently than the Adamantinomatous form (because they are encapsulated). They strongly enhance. The relationship to the optic chiasm is key for surgery. These things occur along the infundibulum. Pediatric type is discussed below (under on the next page with the peds tumors).

Question 492

Sella I Parasella - Peds Craniopharyngioma

Answer 492

As stated above, they come in two flavors: (a) Papillary and (b) Adamantinomatous. The kid type is the Adamantinomatous form. These guys are calcified (papillary is not). These guys recur more (Papillary does less - because it has a capsule).

Question 493

Sella I Parasella - Peds Craniopharyngioma buzzword

Answer 493

“machinery oil. "

Question 494

Sella I Parasella - Peds Craniopharyngioma imaging

Answer 494

* Tl Bright * T2 Bright * CT / GRE = Calcifications * Enhance Strongly (in the solid parts)

Question 495

Sella I Parasella - Peds Hypo tha lamic Hamar toma

Answer 495

A classic Aunt Minnie. This is a hamartoma o f the tuber cinereum (part o f the hypothalamus located between the mammillary bodies and the optic chiasm). The location is the key

Question 496

Sella I Parasella - Peds imaging

Answer 496

Tl Iso T2 Iso Do NOT enhance.

Question 497

Sella I Parasella - Peds Hypo tha lamic Hamar toma classic history

Answer 497

The Classic History is Gelastic Seizures | although precocious puberty’ is actually more common

Question 498

Pineal Region

Answer 498

There are 3 main characters here, all o f which can present | with “vertical gaze palsy” (dorsal Parinaud syndrome).

Question 499

Pineal Region G e rm in om a :

Answer 499

The most common o f the 3, and seen almost exclusively in boys (Germinomas in the suprasellar region are usually in girls). Precocious puberty may occur from secretion o f hCG. Characteristic findings are a mass containing fat and calcification with variable contrast enhancement. It is heterogeneous on T1 and T2 (because o f its mixed components).

Question 500

Pineal Region G e rm in om a : quick

Answer 500

“Engulfed" Calcification Pattern

Question 501

Pineal Region P in eo b la s tom a

Answer 501

Does occur in childhood. Unlike the pineocytoma, these guys are highly invasive. Some people like to think o f these as PNETs in the pineal gland. They are associated with retinoblastoma (“trilateral” ). They" are heterogeneous and enhance vividly.

Question 502

Pineal Region Pineoblastoma & Pineocytoma quick

Answer 502

"Expanded’’ Calcification Pattern

Question 503

Pineal Region P in eo c y tom a

Answer 503

Rare in childhood. Well-circumscribed, and non-invasive. Tend to be more solid, and the solid components do typically enhance.

Question 504

Pineal Region P in e a l Cys t

Answer 504

An incidental findings that is meaningless... although frequently obsessed over. They can have thin enhancement. Calcifications occur in 25%.

Question 505

Pineal Region P in e a l Cys t quick

Answer 505

Classically— looks like a cyst

Question 506

A Few Extra Tips op Characterization “Restriction”

Answer 506

If they show a supratentorial case with restriction it’s likely to be one o f two things (1) Abscess or (2) Lymphoma. Technically any hypercellular tumor can restrict (GBM & Medulloblastoma), but lymphoma is the one they classically show restricting. If it’s a CP angle case, then it’s an Epidermoid. Lastly, a dirty move could be to show Herpes encephalitis restricting in the temporal horns.

Question 507

A Few Extra Tips op Characterization “Midline Crossing”

Answer 507

If they show it crossing the midline, it’s most likely going to be a GBM or Lymphoma. Alternative sneaky things they could show doing this would be radiation necrosis, a big MS plaque in the coipus callosum, or Meningioma o f the falx simulating a midline cross.

Question 508

A Few Extra Tips op Characterization “Calcification”

Answer 508

If they show it in the brain it is probably an Oligodendroglioma. The trick is that Oligodendrogliomas calcify 90% o f the time by CT (and 100% by histopathology), whereas astrocytomas only calcify 20% o f the time. But astrocytoma is very common and oligodendroglioma is not. So in other words, in real life it’s probably still an astrocytoma.

Question 509

A Few Extra Tips op Characterization “T1 Bright”

Answer 509

Most tumors are T l dark (or intermediate). Exceptions might include a tumor that has bled (Pituitary apoplexy or hemorrhagic mets). Hemorrhagic mets are classically seen on MR and CT (Melanoma, Renal, Carcinoid / Choriocarcinoma, Thyroid). Tumors with fat will also be Tl bright (Lipoma, Dermoid). Melanin is Tl bright (Melanoma). Lastly think about cholesterol in a colloid cyst.

Question 510

A Few Extra Tips op Characterization “T1 Bright” quick

Answer 510

Fat: Dermoid, Lipoma Melanin: Melanoma Blood: Bleeding Met or Tumor Cholesterol: Colloid Cyst

Question 511

Special Topics - Syndromes NF-1

Answer 511

Optic Nerve Gliomas

Question 512

Special Topics - Syndromes NF-2

Answer 512

MSME: Multiple Schwannomas, Meningiomas, Ependymomas

Question 513

Special Topics - Syndromes VHL

Answer 513

Hemangioblastoma (brain and retina)

Question 514

Special Topics - Syndromes TS

Answer 514

Subependymal Giant Cell Astrocytoma, Cortical Tubers

Question 515

Special Topics - Syndromes Nevoid Basal Cell Syndrome (Gorlin)

Answer 515

Medulloblastoma

Question 516

Special Topics - Syndromes Turcot

Answer 516

GBM, Medulloblastoma, Intestinal Polyposis

Question 517

Special Topics - Syndromes Cowdens- “COLD”

Answer 517

Lhermitte-Duclos (Dysplastic Cerebellar Gangliocytoma)

Question 518

MSME

Answer 518

If you see tumors EVERYWHERE then you are dealing with NF-2. Ironically there are no neurofibromas in neurofibromatosis type 2 (obviously that would make a great distractor). Just remember MSME Multiple Schwannomas, Meningiomas. Ependymomas

Question 519

L h e rm itte -D u c lo s (Dysplastic Cerebellar Gangliocytoma)

Answer 519

This thing is very uncommon, but when you see it you need to have the following thoughts: - Hey! That is Lhermittc Dulcos.... - I guess she has Cowdcns syndrome.... - I guess she has breast CA Next Step? - Mammogram The appearance is classic, with a “tiger stripe” mass, typically contained in one cerebellar hemisphere (occasionally crosses the vermis). It’s not a “cancer”, but actually a hamartoma - which makes sense since Cowdens is a hamartoma syndrome.

Question 520

Brain Tumors - MRS Pearls

Answer 520

As cell walls get broken down NAA (a maker for neuronal viability) will go down, Creatine (marker for cellular metabolism) will go down, and Choline (a maker for cell membrane turnover) will go up. This is why the ratios o f NAA/Cho, Cho/Cr and NAA/Cr get throw around.

Question 521

Brain Tumors - MRS Pearls Other relevant marker changes:

Answer 521

• Lactate may go up. You see this in the scenario o f a high grade tumor outgrowing its blood supply and changing over to anaerobic pathways. • Lipids may go up. You see this in the scenario o f a necrotic tumor. Lipids are associated with necrosis. • Alanine - is associated with meningiomas. • NAA - This is a glioma maker. Non gliomas tend to have little or no NAA.

Question 522

Brain Tumors - MRS Pearls um o r Grade:

Answer 522

``` Higher Grade Tumors will have more cellular destruction, inflammation, and more ischemia / necrosis. Higher Grade Will Have: Less NAA Less Creatine More Lactate More Choline More Lipids Relative to a lower grade tumor. ```

Question 523

Brain Tumors - MRS Pearls R e c u rre n t T um o r vs R ad ia tio n N e c ro s is

Answer 523

``` Recurrent Tumor: Rising choline infers that cell walls are being turned over (something is growing). Mo Choline, Mo Problems Radiation Necrosis: When you think necrosis you should think elevated lipids (found in necrotic tissue) and elevated lactate. You could also reason that NAA, Creatinine, and Choline (makers o f cell integrity, metabolism, and turnover) would also be low - if the tissue in that region was fried like chicken (or bananas - if you enjoy denying your true nature as the apex predator) ```

Question 524

Brain Tumors - MRS Pearls GBM vs Met:

Answer 524

``` Both can look gnarly on conventional MR (big enhancing tumor). The GBM is classically underestimated on brain MRI (if you are ju st looking at the solid enhancing tumor). The surround T2 edema often contains infiltrative mircotumor. By using a multiple voxel analysis (looking at the tumor, and also surrounding tissue) MRS supposedly adds value (allegedly). For the puipose o f multiple choice, elevated Choline in the T2 signal surrounding the tumor = infiltrating glioma (rather than a met) ```

Question 525

Brain Tumors - MRS Pearls Voxel Selection

Answer 525

It is important to choose an area o f interest with enhancing tumor (avoid cystic parts o f the tumor, calcifications, blood, or frank necrosis).

Question 526

Neonatal Infections

Answer 526

Wc are talking about TORCH infections. The first critical thing is that they only really matter in the first two trimesters (doesn’t cause as much harm in the third trimester). Calcifications and microcephaly are basically present in all o f them.

Question 527

Neonatal Infections CMV Trivia

Answer 527

``` Most Common TORCH (3x more common than Toxo - which is the second most common). ```

Question 528

Neonatal Infections CMV Classic Look

Answer 528

It prefers to target the germinal matrix resulting in periventricular tissue necrosis. The result is the most likely test question = Periventricular calcifications. Of the TORCHs CMV has the highest association with polymicrogyria.

Question 529

Neonatal Infections CMV Highest Yield Trivia

Answer 529

``` Most Common TORCH Periventricular Calcifications Polymicrogyria ```

Question 530

Neonatal Infections Toxoplasmosis Trivia

Answer 530

This is the second most common TORCH.

Question 531

Neonatal Infections Toxoplasmosis Classic Look

Answer 531

The calcification pattern is more random, and targets the basal ganglia (like most other TORCH infections). The frequency is increased in the 3rd trimester (but only causes a problem in the first two). Associated with Hydrocephalus

Question 532

Neonatal Infections Toxoplasmosis Highest Yield Trivia

Answer 532

Hydrocephalus, Basal Ganglia Calcifications

Question 533

Neonatal Infections Rubella Trivia

Answer 533

Less common because of vaccines

Question 534

Neonatal Infections Rubella Classic Look

Answer 534

``` Calcifications are less common than in other TORCHs. Focal high T2 signal might be seen in white matter (related to vasculopathy and ischemic injury). ```

Question 535

Neonatal Infections Rubella Highest Yield Trivia

Answer 535

Ischemia. High T2 signal Fewer Calcifications

Question 536

Neonatal Infections HSV Trivia

Answer 536

It’s HSV-2 in | 90% of cases

Question 537

Neonatal Infections HSV Classic Look

Answer 537

Unlike adults, the virus does not primarily target the limbic system but instead prefers the endothelial cells resulting in thrombus and hemorrhagic infarction with resulting encephalomalacia and atrophy

Question 538

Neonatal Infections HSV Highest Yield Trivia

Answer 538

``` Hemorrhagic Infarct, with resulting Bad Encephalomalacia (Hydranencephaly) ```

Question 539

Neonatal Infections HIV Trivia

Answer 539

``` Not a TORCH but does occur during pregnancy, at delivery, or via breast feeding. ```

Question 540

Neonatal Infections HIV Classic Look

Answer 540

``` You may have faint basal ganglia enhancement seen on CT and MRI preceding the appearance of basal ganglia calcification. Brain atrophy pattern favors the Frontal Lobes ```

Question 541

Neonatal Infections HIV Highest Yield Trivia

Answer 541

Brain Atrophy, predominantly in the Frontal Lobes

Question 542

Infections of the Immunosuppressed

Answer 542

The most common opportunistic infection in patients with AIDS is toxo. The most common fungal infection (in people with AIDS) is . Cryptococcus. Two other infections worth talking about are JC . Virus, and CMV.

Question 543

Infections of the Immunosuppressed Gamesmanship

Answer 543

nipple rings = aids | from south africa = aids

Question 544

Infections of the Immunosuppressed HIV Encephalitis

Answer 544

``` The encephalitis that people with AIDS get. This is actually pretty common and affects about 50% of AIDS patients. ``` We are talking about a situation with a CD4 < 200. These tend to spare the subcortical U-Fibers (PML will involve them).

Question 545

Infections of the Immunosuppressed HIV Encephalitis imaging

Answer 545

``` Symmetric increased T2 / FLAIR signal in the deep white matter. T1 will be normal. The lesions will not enhance. There may be associated brain atrophy. ```

Question 546

Infections of the Immunosuppressed Progressive Multifoca l Leukoencephalopathy (PML):

Answer 546

Caused by the JC virus. We are talking about a situation with a CD4 < 50 Will involve subcortical U-fibers

Question 547

Infections of the Immunosuppressed Progressive Multifoca l Leukoencephalopathy (PML): imaging

Answer 547

``` CT will show single or multiple scattered Hypodensitics, with corresponding T1 hypointensity (remember HIV was T1 normal), T2/FLAIR hyperintensities out of proportion to mass effect - buzzword ```

Question 548

Infections of the Immunosuppressed C M V

Answer 548

Think about brain atrophy, periventricular hypodensities (that are T2/FLAIR bright), and thin ependymal enhancement

Question 549

Infections of the Immunosuppressed C ry p to co c cu s

Answer 549

The most common fungal infection in AIDS. The most common presentation is meningitis that involves the base o f the brain (leptomeningeal enhancement). The most likely way this will be shown on a multiple choice exam is dilated perivascular spaces filled with mucoid gelatinous crap (these will not enhance). The second most likely way this will be shown is lesions in the basal ganglia “cryptococcomas” - these are T1 dark, T2 bright, and may ring enhance.

Question 550

Ependymal cells

Answer 550

Ependymal cells are the cells that line the ventricles and central portion o f the spinal cord.

Question 551

Infections of the Immunosuppressed toxo

Answer 551

Most common opportunistic infection in AIDS. Classically we are talking about T1 dark, T2 bright, ring enhancing (when larger than 1 cm) lesions. These guys will NOT show restricted diffusion. Just think “ ring enhancing lesion, with LOTS o f edema

Question 552

Infections of the Immunosuppressed toxo high yeild trivia

Answer 552

Toxo is Thallium Cold, and Lymphoma is Thallium hot

Question 553

Infections of the Immunosuppressed imaging

Answer 553

Tl+C Ring Enhancing T2 Lots of Edema DWI: NO Restriction

Question 554

WTF ?! i thought abscesses restrict diffusion

Answer 554

``` Typical they do. However, atypical infections like Toxo or fungal don’t always follow this rule ```

Question 555

THIS vs THAT toxo and lymphoma

Answer 555

``` toxo: Ring Enhancing Hemorrhage more common after treatment Thallium Cold PET Cold (acts like necrosis) MR Perfusion: Decreased CBV ``` ``` Lymphoma: Ring Enhancing Hemorrhage less common after treatment Thallium HOT PET Hot (acts like a tumor) MR Perfusion: Increased (or Decreased) CBV ```

Question 556

Infections of the Immunosuppressed quick AIDS Encephalitis

Answer 556

Symmetric T2 Bright Spare U Fibers

Question 557

Infections of the Immunosuppressed quick PML

Answer 557

Asymmetric T2 Bright t1 daark involve u fibers

Question 558

Infections of the Immunosuppressed quick CMV

Answer 558

periventricular t2 birght thin pendymal nhancement

Question 559

Infections of the Immunosuppressed quick toxo

Answer 559

ring enhancement plus lots of edema no restricted diffusion thallium cold

Question 560

Infections of the Immunosuppressed quick cryptoccis

Answer 560

dilated perivascular spaces basila meningitis

Question 561

TB M en in g itis

Answer 561

Has a predilection for the basal cisterns (enhancement o f the basilar meninges with minimal nodularity). May have dystrophic calcifications. Enhancement o f the Basilar Meninges + Hydrocephalus = TB *Sarcoid can have a nearly identical appearance. If it looks like TB - but that isn ’t a choice, it’s probably Sarcoid

Question 562

TB M en in g itis complications

Answer 562

Complications include vasculitis which may result in infarct (more common in children). Obstructive hydrocephalus is common

Question 563

HSV - “Herpes” or “The Dirty Herp

Answer 563

``` HSV 1 in adults and HSV 2 in neonates. I mention that because (1) It seems like testable trivia and (2) They actually have different imaging appearances (as previously mentioned, type 1 prefers the limbic system). ```

Question 564

HSV - “Herpes” or “The Dirty Herp imaging

Answer 564

``` Earliest Sign = Restricted Diffusion - related to vasogenic edema. This could be tested by asking “What sequence is more sensitive? ”, with the answer being that diffusion is more sensitive than T2. Blooming on gradient means it’s bleeding (common in adults, rare in neonate form). ```

Question 565

HSV - “Herpes” or “The Dirty Herp THIS vs THAT:

Answer 565

HSV spares the basal ganglia (distinguishes it from MCA stroke).

Question 566

HSV - “Herpes” or “The Dirty Herp” quick

Answer 566

``` For the purpose of a multiple choice test think swollen T2 bright (unilateral or bilateral) medial temporal lobe. ```

Question 567

Lim b ic E n c e p h a litis :

Answer 567

``` Not an infection, but a commonly tested mimic. It is a paraneoplastic syndrome (usually small cell lung cancer), that looks very similar to HSV. This could be asked by showing a classic HSV image, but then saying the HSV titer is negative. The second order question would be to ask for lung cancer screening. ```

Question 568

W e s t Nile

Answer 568

Several viruses characteristically involve the basal ganglia (Japanese Encephalitis, Murray Valley Fever, West Nile...), the only one realistically testable is West Nile

Question 569

W e s t Nile classic look

Answer 569

Classic Look: T2 bright basal ganglia and thalamus, with corresponding restricted diffusion. Hemorrhage is sometimes seen.

Question 570

CJD: C re u tz fe ld t-J a k o b D is e a s e

Answer 570

The imaging features arc variable and can be unilateral, bilateral, symmetric, or asymmetric

Question 571

CJD: C re u tz fe ld t-J a k o b D is e a s e random facts

Answer 571

``` - Characteristic look on EEG the “periodic sharp wave ” (whatever the fuck that is). - “ 14-3-3” protein assay is a CSF test neurologists order. ```

Question 572

CJD: C re u tz fe ld t-J a k o b D is e a s e 3 types

Answer 572

- Sporadic (80-90%), - Variant “Mad Cow” (rare) - Familial (10%).

Question 573

CJD: C re u tz fe ld t-J a k o b D is e a s e dwi

Answer 573

``` DWI Cortical Gyriform Restricted Diffusion- Supposedly diffusion is the most sensitive sign. & the cortex is the most common early site of manifestation. Basal Ganglia may also be involved ```

Question 574

CJD: C re u tz fe ld t-J a k o b D is e a s e hockey stick sign

Answer 574

- Bilateral FLAIR bright dorsal medial thalamus - Described in the variant subtype.

Question 575

CJD: C re u tz fe ld t-J a k o b D is e a s e pulvinar sign

Answer 575

- Bilateral FLAIR bright pulvinar thalamic nuclei (posterior thalamus). - Classic in the variant subtype

Question 576

CJD: C re u tz fe ld t-J a k o b D is e a s e another way to show

Answer 576

Another way to show this (which would be more work for the test writer - and is therefore less likely) would be a series of MRs or CTs showing rapidly progressive atrophy.

Question 577

N e u ro c y s tic e rc o s is

Answer 577

Caused by eating pig shit (or undercooked pork). The bug is tinea solium (pork tapeworm). Trivia: Involvement of the basal cisterns carries the worst outcome.

Question 578

N e u ro c y s tic e rc o s is Most common locations (in descending order):

Answer 578

1- Subarachnoid over the cerebral hemispheres, 2- Basal cisterns, 3- Brain parenchyma, 4- Ventricles

Question 579

N e u ro c y s tic e rc o s is stage 1

Answer 579

Stage I: Vesicular Cyst + Scolex No Enhancement

Question 580

N e u ro c y s tic e rc o s is stage 2

Answer 580

Stage 2: Colloidal CT: Hyperdense Cyst MR: Edema + Enhancement

Question 581

N e u ro c y s tic e rc o s is stage 3

Answer 581

``` Stage 3: Granular CT: Early Calcification MR: Smaller Cysts, Less Edema, Less Enhancement ```

Question 582

N e u ro c y s tic e rc o s is stage 4

Answer 582

``` Stage 4: Calcified / Involution CT: Calcification MR: Blooming on SWI (T2* etc..) ```

Question 583

M e n in g itis and C e re b ra l A b s c es s

Answer 583

You can think of meningitis in 4 main categories: bacterial (acute pyogenic), viral (lymphocytic), chronic (TB or Fungal), and non-infectious (sarcoid).

Question 584

M e n in g itis and C e re b ra l A b s c es s vocab

Answer 584

Leptomeningeal: Pial +Arachnoid Pachymeningcal: Dural

Question 585

M e n in g itis and C e re b ra l A b s c es s Complications include

Answer 585

``` Venous thrombosis, Vasospasm (leading to the stroke), Empyema, Ventriculitis, Hydrocephalus, Abscess ```

Question 586

M e n in g itis and C e re b ra l A b s c es s lumpy and thicker

Answer 586

Fungal and Carcinomatous meningitis tend to be “more lumpy” and “thicker”

Question 587

M e n in g itis and C e re b ra l A b s c es s essentially

Answer 587

``` Essentially, we are talking about thick leptomeningeal enhancement, in the appropriate clinical setting ``` ``` This pattern can be seen with Bacterial Meningitis or Carcinomatous Meningitis ```

Question 588

M e n in g itis and C e re b ra l A b s c es s Leptomeningeal (Pia-Arachnoid) Enhancement

Answer 588

Fills the subarachnoid | spaces & extends into the sulci & cisterns

Question 589

M e n in g itis and C e re b ra l A b s c es s trivia

Answer 589

A very testable piece of trivia is that infants will often get sterile reactive subdurals (much less common in adults).

Question 590

Abscess Facts (trivia)

Answer 590

- DW1 - Restricts - MRS - Lactate High - FDG PET - Increased Metabolic

Question 591

a ch ym e n in g e a l (D u ra l) E n h a n c em e n t

Answer 591

Key Feature: Enhancement does NOT extend into the sulci Seen this with lots of stuff: Intracranial Hypotension, Dural attachment of a Meningioma , Sarcoid, TB, Wegener’s , Fugal Infections. Both Breast and Prostate Cancer can deposit a solitary dural met. Secondary CNS Lymphoma is often extra-axial and can be dural based or fill the subarachnoid space ( “Rim Phoma ”)

Question 592

Empyema

Answer 592

Can be subdural or epidural (just like blood). Follows the same rules as far as crossing dural attachments (epidurals don’t) and crossing the falx (subdurals don’t). Subdurals are more common and have more complications relative to epidurals. The vast majority of subdurals are the sequela of frontal sinusitis. The same is true of epidurals with some sources claiming 2/3 of epidurals are secondary to sinusitis.

Question 593

empyema classic look

Answer 593

T1 bright and restrict diffusion.

Question 594

Tl+C | Subdural Empyema

Answer 594

Dural Enhancement

Question 595

Intraaxial Infections Abscess

Answer 595

A cerebral abscess is a cavity that contains pus, debris, and necrotic tissue. These can develop secondary to to bacterial, fungal, or parasitic infection - most commonly via hematogenous spread. For the purpose of multiple choice, remember to think about right-to-left shunts and pulmonary AVMs. Direct spread (example = sinus) is possible, but just less common because of the dura.

Question 596

Intraaxial Infections Abscess ct

Answer 596

``` Focal area of low density with surrounding low density vasogenic edema. ```

Question 597

Intraaxial Infections Abscess t1+c

Answer 597

Smooth Ring Enhancement with Multiple Lesions - Suggests Abscesses

Question 598

Intraaxial Infections Abscess t2

Answer 598

Multiple Lesions with Vasogenic Edema — this is nonspecific (could be mets)

Question 599

Intraaxial Infections Abscess DWI

Answer 599

``` Typical Abscess (bacteria) will restrict. Remember Atypical (Toxo etc..) doesn’t always restrict ```

Question 600

Intraaxial Infections Cerebritis

Answer 600

is the early form of intra-axial infection, which can lead to Abscess if not treated. The typical look is the vasogenic edema without the well defined central enhancing lesion. There may be spotty restricted diffusion.

Question 601

Intraaxial Infections Ventriculitis

Answer 601

Usually the result of a shunt placement or intrathecal chemo - as discussed on page 51. The ventricle will enhance and you can sometimes see ventricular fluid-fluid levels If septa start to develop you can end up with obstructive patterns of hydrocephalus. The intraventricular extension of abscess is a very serious / ominous “pre-terminal event

Question 602

Intraaxial Infections Multiple Rings Mets vs Abscess

Answer 602

The smooth margin suggests Abscess, but doesn't exclude mets. The difference is that tumor usually starts out as a solid enhancing mass then becomes ring enhancing with necrosis. Also, Abscesses tend to be smaller (usually less than 10mm).

Question 603

Intraaxial Infections Smooth Ring =

Answer 603

Abscess ``` Abscess Rings tend to be thicker on the “Oxygen Side” or "Grey Matter Side" of the Brain - and thinner towards the ventricle. ```

Question 604

Intraaxial Infections Irregular Ring

Answer 604

tumor "Bumpy” or “Shaggy” inner lip of the ring is supposed to suggest necrosis

Question 605

Intraaxial Infections Both Tumor & Abscess will have

Answer 605

vasogenic edema

Question 606

MRl Gamesmanship - Enhancement Patterns

Answer 606

In general, to solve MR puzzles you will need to be able to work through some MR sequences. The trick is to have a list o f things that are T1 bright, T2 bright, Restrict diffusion, and Enhance. Plus you should know the basic enhancement patterns (homogenous, heterogenous, ring, and incomplete ring).

Question 607

STROKE vs TUMOR vs ABSCESS vs MS Plaque T2

Answer 607

For the most part, T2 is not super helpful for lesion characterization - as stroke, tumors, abscess, MS, all have edema.

Question 608

STROKE vs TUMOR vs ABSCESS vs MS Plaque DWI

Answer 608

This is helpful only if they follow the classic rules. Out o f those 4 (stroke, tumors, abscess, MS) the classical diffusion restrictors are: Abscess, and Stroke. Certain hypercellular tumors (classically lymphoma) can restrict, and demyelinating lesions with acute features can restrict

Question 609

STROKE vs TUMOR vs ABSCESS vs MS Plaque Enchancement

Answer 609

In this situation this is probably the most helpful. Out o f those 4 (Tumor, Abscess. MS, and Stroke) each should have a different pattern. • Tumor usually heterogeneous or homogenous if high grade (or none if low grade). Technically ring enhancement can also be seen with Gliomas, and Mets (though I expect this is less likely to be shown on multiple choice). • Abscess will classically have RING pattern. • MS will classically have an INCOMPLETE RING pattern. • Stroke will have cortical ribbon (GYRIFORM) type enhancement in the sub-acute time period (around 1 week).

Question 610

STROKE vs TUMOR vs ABSCESS vs MS Plaque Enchancement how many rings

Answer 610

The number of rings can be a helpful strategy. A single ring is more likely to be tumor (around half of mets and 3/4 of gliomas are solitary). Abscess and MS Lesions are almost always (like 75-85%) multiple.

Question 611

STROKE vs TUMOR vs ABSCESS vs MS Plaque Enchancement heterogenous

Answer 611

-Most likely Tumor | higher grade

Question 612

STROKE vs TUMOR vs ABSCESS vs MS Plaque Enchancement ring

Answer 612

-Can be lots of stuff: Abscess and Tumor are both prime suspects

Question 613

STROKE vs TUMOR vs ABSCESS vs MS Plaque Enchancement incomplete ring

Answer 613

-Can be lots of stuff: Abscess and Tumor are both prime suspects

Question 614

STROKE vs TUMOR vs ABSCESS vs MS Plaque Enchancement gyriform

Answer 614

``` -Classic for subacute stroke (can also be seen with P R E S or encephalopathy / encephalitis) ```

Question 615

Parenchymal Contusion

Answer 615

The rough part of the skull base ean scrape the brain as it slides around in a high speed MVA. Typical locations include the anterior temporal lobes and inferior frontal lobes. The concept of coup (site of direct injury) and contre-coup (opposite side of brain along vector of force). Contusion can look like blood with associated edema in the expected regions.

Question 616

Diffuse Axonal Injury/Shear Injury

Answer 616

There are multiple theories on why this happens (different density of white and gray matter etc...) they don’t matter for practical purposes or for multiple choice.

Question 617

Diffuse Axonal Injury/Shear Injury Things Worth Knowing

Answer 617

• Initial Head CT is often normal • Favorite sites of DAI are the posterior corpus callosum, and GM-WM junction in the frontal and temporal lobes • Multiple small T2 bright foci on MRI

Question 618

Diffuse Axonal Injury/Shear Injury DAI Grading

Answer 618

Grade 1 = Grey-White Interface Grade 2 = Corpus Callosum Grade 3 = Brainstem

Question 619

Subarachnoid Hemorrhage

Answer 619

Trauma is the most common cause. FLAIR is the most | sensitive sequence. This is discussed in more later in the chapter.

Question 620

THIS vs THAT: Subdural v s Epidural Epidura l

Answer 620

Classic History: Trauma Patient - with a skull fracture “Bi-convex” or Lenticular can cross micline cannot cross a suture usually arterial can rapidly expand kill you

Question 621

THIS vs THAT: Subdural v s Epidural Sub dural

Answer 621

``` Classic History: Elderly alcoholic with a shriveled up atrophic brain spent the evening with a bottle of “Rotgut - Hobo Tranquilizer” brand whiskey, then fell over stretching & tearing his cortical bridging veins. A week later he seems to be acting progressively more confused. ``` “Bi-concave” Does not cross the midline, may extend into interhemispheric fissure Can cross a suture Usually venous More mass effect than expected for size

Question 622

Subdural quick

Answer 622

``` - Crescent Shape -No Respect For the Sutures ```

Question 623

epidural quick

Answer 623

``` - Lentiform Shape -Skull Fracture -Respect for the Sutures ```

Question 624

How Old is that Blood CT

Answer 624

This is an extremely high yield topic. Maybe the most high yield topic in all o f neuro, with regard to multiple choice. The question can be asked with CT or MRI (MRI more likely). If they do ask the question with CT it’s most likely to be the subacute subdural that is isointense to brain, with loss o f sulci along the margins. They could also show the “swirl sign” - see below.

Question 625

Blood on CT Flyperacute Acute (< 1 hour)

Answer 625

Hypodense

Question 626

Blood on CT Acute (1 hour - 3 days)

Answer 626

Hypodense

Question 627

Blood on CT Subacute (4 days - 3 weeks)

Answer 627

Progressively less dense, eventually becoming isodense to brain. Peripheral rim enhancement may occur with contrast.

Question 628

Blood on CT Chronic (> 3 weeks)

Answer 628

Hypodense

Question 629

Sw irl Sign

Answer 629

This is an ominous sign o f active bleeding. The central low attenuation blood represents hyper-acute non-clotted blood, with surrounding acute clotted blood.

Question 630

Blood Age V ia MR

Answer 630

MRI is more difficult to remember. Some people use the mnemonic “IB, ID, BD, BB, DD” or “ It Be Iddy Biddy, BaBy, Doo-Doo” which I find very irritating. I prefer mnemonics that employ known words (just my opinion). Another one with actual words is “George Washington Bridge” For T1 (Gray, White, Black), and Oreo Cookie for T2 (Black, White, Black).

Question 631

Blood Age V ia MR (c o n tin u e d ):

Answer 631

Another strategy (which is somewhat unconventional) is to actually try and understand the MRI changes (I strongly discourage this). If you insist on trying to understand this I have a 40 min lecture on TitanRadiology.com explaining it (this lecture is also free on my YouTube Channel — google “Prometheus Lionhart Blood Age”).

Question 632

Blood Age V ia MR Hyperacute

Answer 632

24 hours Oxyhemoglobin, Intracellular T l- Iso, T2 Bright

Question 633

Blood Age V ia MR acute

Answer 633

1 -3 days Deoxyhemoglobin, Intracellular T1 - Iso, T2 Dark

Question 634

Blood Age V ia MR Early Subacute

Answer 634

> 3 days Methemoglobin, Intracellular Tl Bright, T2 Dark

Question 635

Blood Age V ia MR Late Subacute

Answer 635

>7 days Methemoglobin, Extracellular Tl Bright, T2 Bright

Question 636

Blood Age V ia MR Chronic

Answer 636

> 14 days Ferritin and Hemosiderin, Extracellular T1/T2 Dark Peripherally, Center may be T2 bright

Question 637

Atraumatic Subarachnoid Hemorrhage

Answer 637

Yes, the most common cause is trauma. A common point o f trivia is that the most sensitive sequence on MRI for acute SAH is FLAIR (because it wo n ’t suppress out - making it hyperintense). Be aware that supplemental oxygen (usually 50-100%) can give you a fake out that looks like SAH on FLAIR.

Question 638

Sequela of SAH

Answer 638

(1) Hydrocephalus - Early (2) Vasospasm - 7-10 days (3) Superficial Siderosis - Late

Question 639

When the blood is real, in the absence o f trauma, there are a few other things to think about

Answer 639

Aneurysm Benign Non-Aneurysm Perimesencephalic hemorrhage Superficial Siderosis

Question 640

Benign Non-Aneurysm Perimesencephalic hemorrhage

Answer 640

This is a well described entity (although not well understood). This is NOT associated with aneurysm (usually - 95%), and may be associated with a venous bleed. *You have to prove that - you need a negative CTA. The location o f the blood - around the midbrain and pons without extension into the lateral Sylvian cisterns or interhemispheric fissures is classic. Just think anterior to the brainstem. Re-bleeding and ischemia are rare- and they do extremely well

Question 641

Superficial Siderosis

Answer 641

``` This is a si^e effect o f repeated episodes o f SAH. I like to think about this as “staining the surface o f the brain with hemosiderin. ” The classic look is curvilinear low signal on gradient coating the surface of the brain. The classic history is sensorineural hearing loss and ataxia. ```

Question 642

P s eu d o -S u b a ra ch n o id H em o rrh a g e

Answer 642

This is a described mimic of SAH that is seen in the setting of diffuse cerebral edema (most commonly anoxic brain injury). Near drowning, or suicide attempt by hanging would be classic clinical vignettes

Question 643

P s eu d o -S u b a ra ch n o id H em o rrh a g e qwhat youre actually seeing

Answer 643

What you are seeing is actually two things at once. (1) You are seeing diffuse edema which lowers the attenuation of the brain (makes it darker). (2) You are seeing compression and collapse of the sub arachnoid spaces which gives them a hyper dense appearance. The combination of these factors gives the suggestions of hyper density in the cerebral sulci, fissures, and cisterns which can mimic SAH (hence the name).

Question 644

THIS vs THAT: Pseudo SAH vs Real SAH

Answer 644

If they give you history that should help (anoxic brain injury vs headache / trauma). The absence of any intraventricular bleeding can suggest pseudo SAH. Lastly density of the Pseudo SAH will be less than 40. Acute blood tends to be around 60-70 HU.

Question 645

Intraparenchymal Hemorrhage

Answer 645

Hypertensive Hemorrhage Amyloid Angiopathy Septic Emboli Other Random Causes

Question 646

Hypertensive Hemorrhage

Answer 646

Common locations arc the basal ganglia, pons, and cerebellum. For the purpose of multiple choice tests, the basal ganglia is the most common location (specifically the putamen). You typically have intraventricular extension of blood.

Question 647

Amyloid Angiopathy

Answer 647

History of an old dialysis patient (or some other history to think Amyloid). The classic look is multiple lobes at different ages with scattered microbleeds on gradient.

Question 648

Septic Emboli

Answer 648

These are seen in certain clinical scenarios (IV drug user, organ transplant, cyanotic heart disease, AIDS patients, people with lung AVMs). The classic look is numerous small foci of restricted diffusion. Septic emboli to the brain result in abscess and mycotic aneurysms (most commonly in the distal MCAs), The location favors the gray-white interface and the basal ganglia. There will be surrounding edema around the tiny abscesses. The classic scenario should be parenchymal bleed in a patient with infection.

Question 649

Other Random Causes of intraparenchymal hemorrhage

Answer 649

These would include AVMs, vasculitis, brain tumors (primary and mets) - these are discussed in greater detail in various sections of the text

Question 650

Intraventricular Hemorrhage

Answer 650

Not as exciting. Just think about trauma, tumor, hypertension, AVMs, and aneurysms - all the usual players.

Question 651

Epidural I Subdural Hemorrhage

Answer 651

Obviously these are usually post-traumatic. Dural AVFs and High Flow AVMs can bleed causing subdurals / subarachnoid hemorrhage. These are discussed further later in the chapter.

Question 652

Stroke

Answer 652

Stroke is a high yield topic. You can broadly categorize stroke into ischemic (80%) and hemorrhagic (20%). It’s critical to remember that stroke is a clinical diagnosis and that imaging findings compliment the diagnosis (and help exclude clinical mimic o f stroke - tumor etc..).

Question 653

Stroke Vascular Territories

Answer 653

Below is a diagram showing the various vascular territories. The junction between these zones is sometimes referred to as a “watershed’. These areas are prone to ischemic injury, especially in the setting o f hypotension or low oxygen states (near drowning or Roger Gracie’s mounted cross choke or a Marcello Garcia high elbow guillotine). ``` aca mca pca lenticulostriate anterior choroidal ```

Question 654

Watershed Ischemia

Answer 654

``` favors the border zones o f different vascular territories (just like the bowel). Border Zone Between AC A and MCA The classic clinical scenario for watershed infarcts would be severe hypotension (shock / CPR / E tc ..), severe carotid stenosis, or a 2009 IBFFJ worlds match up with Roger Gracic. ``` looks up borders betweent he aca, mca, and pca

Question 655

Watershed Ischemia gamesmanship

Answer 655

Watershed Infarcts in a Kid = Moyamoya (Idiopathic supraclinoid ICA vasculo-occlusive disease)

Question 656

Subacute Infarct

Answer 656

Unique that it Enhances but creates NO Mass Effect

Question 657

Stroke Imaging S ign s on CT

Answer 657

``` Dense MCA Sign Insular Ribbon Sign Loss of GM-WM differentiation Mass Effect Enhancement ```

Question 658

Stroke Imaging S ign s on CT Dense MCA SigDn

Answer 658

Intraluminal thrombus is dense, usually in the M1 and/or M2 segments

Question 659

Stroke Imaging S ign s on CT Insular Ribbon Sign

Answer 659

Loss of normal high density insular cortex from cytotoxic edema

Question 660

Stroke Imaging S ign s on CT Loss of GM-WM differentiation

Answer 660

Basal Ganglia / Internal Capsular Region and Subcortical regions

Question 661

Stroke Imaging S ign s on CT Mass Effect

Answer 661

Peaks at 3-5 days

Question 662

Stroke Imaging S ign s on CT Enhancement

Answer 662

Rule of 3s: Starts in 3 days, peaks in 3 weeks, gone by 3 months.

Question 663

Fogging

Answer 663

This is a phase in the evolution of stroke when the infarcted brain looks like normal tissue. This is seen around 2-3 weeks post infarct, as the edema improves.

Question 664

“Fogging” is classically | described with

Answer 664

``` non-contrast CT, but T2 MRI sequences have a similar effect (typically occurring around day 10). In the real world, you could give IV contrast to demarcate the area of infarct or just understand that fogging occurs. ```

Question 665

Artery of Percheron Stroke

Answer 665

Classic V Shaped bilateral infarct o f the paramedian thalami. This can only occur in the setting of the Artery o f Percheron vascular variant. This variant is characterized by a solitary trunk originating from one of the two PCAs to feed the rostral midbrain and both thalami (normally there are several bilateral paramedic arteries originating from the PCAs).

Question 666

Recurrent Artery of | Heubner Stroke

Answer 666

``` Classic Caudate Infarct The Artery of H is a deep branch off the proximal AC A This thing can get “bagged” during the clipping of ACOM artery aneurysm. ```

Question 667

Cardioembolic Stroke:Cardioembolic Stroke:

Answer 667

``` This has the classic pattern of multiple foci of restricted diffusion scattered bilaterally along multiple vascular territories. The clinical history is usually A-Fib or endocarditis. ```

Question 668

Fetal PCOM Stroke Pattern

Answer 668

``` This pattern demonstrates infarcts in both the anterior and posterior circulation of the same hemisphere. This pattern is possible as the variant anatomy with the PCA feeds primarily from the ICA. ```

Question 669

Not Everything That Restricts | is a Stroke

Answer 669

Bacterial Abscess, CJD (cortical), Herpes, Epidermoids, Hypercellular Brain Tumors (Classic is lymphoma), Acute MS lesions, Oxyhemoglobin, and Post Ictal States. Also artifacts (susceptibility and T2 shine through).

Question 670

stroke restricted diffusion

Answer 670

Acute infarcts usually arc bright from about 30 mins after the stroke to about 2 weeks. Restricted diffusion without bright signal on FLAIR should make you think hyperacute (< 6 hours).

Question 671

Stroke enhancement

Answer 671

The rule of 3’s is still useful. Starts day 3, peaks ~ 3 weeks, gone by 3 months

Question 672

Stroke enhancement Diffusion 0-6 hours 6-24 hours 24 hours -1 week

Answer 672

Bright Bright Bright

Question 673

Stroke enhancement FLAIR 0-6 hours 6-24 hours 24 hours -1 week

Answer 673

NOT BRIGHT Bright Bright

Question 674

Stroke enhancement T1 0-6 hours 6-24 hours 24 hours -1 week

Answer 674

Iso Dark Dark, with Bright Cortical Necrosis

Question 675

Stroke enhancement T2 0-6 hours 6-24 hours 24 hours -1 week

Answer 675

Iso Bright Bright

Question 676

H em o rrh a g ic T ra n s fo rm a tio n :

Answer 676

This occurs in about 50% of infarcts, with the typical time period between 6 hours and 4 days. If you got TPA it’s usually within 24 hours of treatment. People break these into (1) tiny specs in the gray matter called "petechial” which is the majority (90%) and (2) full on hematoma - about 10%.

Question 677

H em o rrh a g ic T ra n s fo rm a tio n Who gets it

Answer 677

People on anticoagulation, people who get TPA, people with embolic strokes (especially large ones), people with venous infarcts.

Question 678

Venous Infarct

Answer 678

Not all infarcts are arterial, you can also stroke secondary to venous occlusion (usually the sequelae of dural venous sinus thrombosis or deep cerebral vein thrombosis). In general, venous infarcts arc at higher risk for hemorrhagic transformation. In little babies think dehydration, in older children think about mastoiditis, in adults think about coagulopathies (protein C & S dcf) and oral contraceptives. The most common site of thrombosis is the superior sagittal sinus, with associated infarct occurring 75% of the time

Question 679

Venous thrombosis signs

Answer 679

Venous thrombosis can present as a dense sinus (on non-contrast CT) or “empty delta” (on contrast enhanced CT). Venous infarcts tend to have heterogeneous restricted diffusion. Venous thrombosis can result in vasogenic edema that eventually progresses to stroke and cytotoxic edema.

Question 680

Arterial stroke

Answer 680

Cytotoxic Edema

Question 681

Venous Stroke

Answer 681

Vasogenic Edema + Cytotoxic Edema

Question 682

Stigmata of chronic venous thrombosis

Answer 682

the development of a dural AVF, and/or | increased CSF pressure from impaired drainage.

Question 683

ASPECTS

Answer 683

Alberta Stroke Program Earty CT Score)

Question 684

ASPECTS overview

Answer 684

This was developed to give “providers” a more specific guideline for giving TPA - as an alternative to the previous 1/3 vascular territory rule. The idea being that the greater the vascular territory involved, the worse the clinical outcome (post TPA bleed etc..). The way this works is that you start out with 10 points, and lose points based on findings of acute cytotoxic ischemia to various locations (example: minus 1 for caudate, or lentiform nucleus, or insular ribbon, etc.. etc.. so on and so forth).

Question 685

ASPECTS testable pearls

Answer 685

• This is for MCA ONLY (not other vascular territories) • This is for ACUTE ischemia (don’t subtract points for chronic lacunar infarcts etc..) • A score of 8 or greater has a better chance of a good outcome (score of 7 or less may contraindicate TPA — depending on the institutional policy.

Question 686

CT Perfusion - Crash Course

Answer 686

After an arterial occlusion perfusion pressure is going to be rapidly reduced. Millions of neurons will suddenly cry out in terror then suddenly silenced, unless they are lucky to have arteriolar dilation with capillary recruitment to bring in as much blood to that area of brain as possible. This process is called physiologic auto-regulation and should result in an increase in capillary blood pool. The key point is that you need live neurons (penumbra) to cry out for help. If they cry out and are suddenly silenced (infarct core) you won’t see any auto regulation attempts. This physiology makes up the basis of perfusion for stroke.

Question 687

CT Perfusion - Crash Course parameters

Answer 687

• Cerebral Blood Flow (CBF): Represents instantaneous capillary flow in tissue. • Cerebral Blood Volume (CBV): Describes the blood volume of the cerebral capillaries and venules per cerebral tissue volume. • Mean Transit Time (MIT) = CBV divided by CBF ; it is the average length of time a certain volume of blood is present in the capillary circulation. • Time to Peak (TTP): This is the opposite of CBF. Less flow = Longer Time to reach maximum concentration of contrast.

Question 688

The primary role of perfusion is to distinguish between

Answer 688

``` salvagable brain (penumbra), and dead brain. The penumbra may benefit from therapy. The dead brain will not- "He s Dead Jim ’’ - Dr. McCoy ```

Question 689

Peniumbra

Answer 689

decreased CBF, increased CBV, increased MTT

Question 690

Infarct core

Answer 690

Decreased CBF (alot), Decreased CBV

Question 691

Aneurysm Who gets them

Answer 691

People who smoke, people with polycystic kidney disease, connective tissue disorders (Marfans, Ehlers-Danlos), aortic coarctation, NF, FMD, and AVMs.

Question 692

Aneurysm Where do they occur

Answer 692

They occur at branch points (why do persistent trigeminals get more aneurysms ? - because they have more branch points). They favor the anterior circulation (90%) - with the anterior communicating artery being the most common site. As a piece of random trivia, the basilar is the most common posterior circulation location (PICA origin is the second most common).

Question 693

Aneurysm When do they rupture

Answer 693

Rupture risk is increased with size, a posterior location, history of prior SAH, smoking history, and female gender.

Question 694

Aneurysm Which one did it

Answer 694

A common dilemma is SAFI in the setting of multiple aneurysms. The things that can help you are location of the SAH/Clot, location of the vasospasm, size, and which one is the most irregular Focal out-pouching - "Murphy s tit ”)

Question 695

Dolichoectasia of the | Basilar Artery

Answer 695

``` This refers to a widened elongated twisty appearance of the basilar artery. This is probably the result of chronic hypertension (abnormal vessel remodeling). The height of the bifurcation and the more lateral the position of the vessel (relative to the clivus) the more severe - so says the Smoker criteria. ```

Question 696

Dolichoectasia of the Basilar Artery complications

Answer 696

Complications include: nothing (most have no symptoms), dissection, compression of cranial nerves (hcmi-facial spasm), stroke

Question 697

Aneurysm locations

Answer 697

ACA~ 35% M1/M2 Junction ~ 30% ICA / PComm Junction ~ 30% Basilar Tip ~ 3% PICA - 2%

Question 698

Saccular (Berry):

Answer 698

``` The most common type and the most common cause o f nontraumatic SAH. They are commonly seen at bifurcations. The underlying pathology may be a congenital deficiency o f the internal elastic lamina and tunica media (at branch points). Remember that most are idiopathic (with the associations listed above). They arc multiple 15-20% o f the time. ```

Question 699

Fusiform Aneurysm

Answer 699

Associated with PAN, Connective Tissue Disorders, or Syphilis. These more commonly affect the posterior circulation. May mimic a CPA mass

Question 700

Pseudoaneurysm

Answer 700

Think about this with an irregular (often saccular) arterial out-pouching at a strange / atypical location. You may see focal hematoma next to the vessel on noncontrast.

Question 701

Pseudoaneurysm traumatic

Answer 701

Often distal secondary to | penetrating trauma or adjacent fracture.

Question 702

Pseudoaneurysm mycotic

Answer 702

``` Often distal (most commonly in the MCA), with the associated history of endocarditis, meningitis, or thrombophlebitis ```

Question 703

Blister Aneurysm

Answer 703

This is a sneaky little dude (the angio is often negative). It’s broad-based at a non-branch point (supraclinoid ICA is the most common site).

Question 704

Infundibular Widening

Answer 704

Not a true aneurysm, but instead a funnel-shaped enlargement at the origin o f the Posterior Communicating Artery at the junction with the ICA. Thing to know is "not greater than 3 mm. ”

Question 705

AVM A s s o c ia te d | P e d ic le A n eu ry sm :

Answer 705

Aneurysm associated with an AVM. The trivia to know is that it’s found on the artery feeding the AVM (15% of the time). These may be higher risk to bleed than the AVM itself (because they are high flow).

Question 706

Aneurysm Rupture Trivia:

Answer 706

``` • Aneurysm > 10mm have a 1% risk of rupture per year. • Although controversial, 7 mm is often thrown around as a treatment threshold for anterior circulation aneurysms • In general, posterior circulation aneurysms have a higher rate of rupture per mm in size. ```

Question 707

A neury sm S u b typ es S um m a ry

Answer 707

Saccular Branch Points - in the (Berry) Anterior Circulation Fusiform Posterior Circulation Pedicle Aneurysm Artery feeding the AVM Mycotic Distal MCAs ``` Blister Broad Based Non-Branch Aneurysm Point (Supraclinoid ICA) ```

Question 708

M a x im um B le ed in g | - A n e u ry sm L o c a tio n

Answer 708

ACOM Interhemispheric Fissure PCOM Ipsilateral Basal Cistern MCA trifurcation Sylvian fissure Basilar tip intrapeduncular cistern or intraventricular PICA Posterior Fossa or Intraventricular

Question 709

H i g h F l o w | A VM

Answer 709

• Most Common Most Common Type of High Flow • Congenital malformation • Supratentorial location (Usually) • Most common complication = bleeding (3% annual) • Risk increased with: Smaller AVMs (they are under higher pressure), Small Draining Veins (can’t reduce pressure), Perinidal Aneurysm, and Basal Ganglia location . Symptoms: Headache (#1), Seizure (#2)

Question 710

H i g h F l o w A VM imaging

Answer 710

Arterial Component Nidus Draining veins Adjacent brain may be gliotic (T2 bright) and atrophic.

Question 711

Dural AVF

Answer 711

• Flow Rate is Variable (can be high or low flow) • SPINAL AVFs are actually the most common type of AVFs - a helpful hint is the classic clinical history of “gradual onset LE weakness” • Risk of Bleeding - increased with direct cortical venous drainage. • These aren’t congenital (like AVMs) but instead are acquired — classically from dural sinus thrombosis • Symptoms: Tinnitus — especially if the sigmoid sinus is involved

Question 712

Dural AVF imaging

Answer 712

``` • No Nidus • Can be occult on MR1/MRA - need catheter angio if suspicion high ```

Question 713

DVA

Answer 713

• Variation in normal venous drainage • Resection is a bad idea = venous infarct • Associated with cavernous malformations. • They almost never bleed in isolation. If you see evidence of prior bleeding (blooming on gradient) there is probably an associated cavernoma.

Question 714

DVA Imaging

Answer 714

``` • “Caput medusa” or “large tree with multiple small branches” - collection of vessels converging towards an enlarged vein (seen on venous phase only). • Can have a halo of T2 bright gliosis ```

Question 715

Cavernous Malformation (cavernoma, or cavernous angioma)

Answer 715

• Low Flow - WITHOUT intervening normal tissue • Can be induced from radiotherapy • Can ooze some blood, but typically don’t have full-on catastrophic bleeds. Presence of a “fluid-fluid” level suggests recent intralesional hemorrhage • Single or multiple (more common in Hispanics). • Classic gamesmanship is to show you a nearby DVA

Question 716

Cavernous Malformation (cavernoma, or cavernous angioma) imaging

Answer 716

Popcorn like with “Peripheral Rim of Hemosiderin.” Best seen on gradient

Question 717

Capillary | Telangiectasia

Answer 717

• Low Flow - WITH intervening normal tissue • Can also be radiation induced • Usually don’t bleed (thought of as an incidental finding) • Classic Look = Single lesion in the Pons

Question 718

Capillary Telangiectasia imaging

Answer 718

``` • Brush-like” or “Stippled pattern” of enhancement • Best seen on gradient (slow flow and deoxyhemoglobin) ```

Question 719

Mixed vascular malformations

Answer 719

• Wastebasket term, most often used for DVA with AV | shunting or DVAs with telangiectasias

Question 720

Calcification Rapid Review I Summary Pineal Gland

Answer 720

- Common in adults, Rare in kids. If you see calcification in a kid under 7, it could suggest underlying neoplasm. —Germinoma = “Engulfed" Pattern “ 1” —Pineoblastoma & Pineocvtoma: “Expanded” Pattern “2”

Question 721

Calcification Rapid Review I Summary Habenular

Answer 721

Curvilinear structure (solid white arrow) located a few millimeters anterior to the pineal body (open arrow). About 1 in 5 normal adults will have calcification here. The trivia is an increased association with schizophrenia

Question 722

Calcification Rapid Review I Summary Choroid plexus

Answer 722

Common in adults. Remember there is no choroid plexus in the frontal/occipital horn of the lateral ventricles or the cerebral aqueduct.

Question 723

Calcification Rapid Review I Summary Dural Calcifications

Answer 723

Common in adults. If the calcs are bulky and there are a bunch of tooth cysts (Odontogenic keratocysts) think Gorlin Syndrome.

Question 724

Calcification Rapid Review I Summary Basal Ganglia

Answer 724

Very common with age, favors the globus pallidus. If | extensive & symmetrical think Fahr disease

Question 725

Calcification Rapid Review I Summary Tuberous Sclerosis

Answer 725

Calcifications of the subependymal nodules are pathognomonic typically found at the caudothalamic groove and atrium. You can see calcified subcortical tubers - more typical in older patients.

Question 726

Calcification Rapid Review I Summary | Sturge-Weber

Answer 726

Tram track / double-lined gyriform pattern parallel to the cerebral folds. Tuberous Sclerosis - Calcifications of the subependymal nodules are pathognomonic typically found at the caudothalamic groove and atrium. You can see calcified subcortical tubers - more typical in older patients. Etiology = subcortical ischemia secondary to pial angiomatosis.

Question 727

Calcification Rapid Review I Summary Congenital CMV

Answer 727

Periventricular calcifications. | Can also have brain atrophy

Question 728

Calcification Rapid Review I Summary Congenital Toxo

Answer 728

Basal Ganglia Calcifications + | Hydrocephalus,

Question 729

Calcification Rapid Review I Summary Neurocysticercos

Answer 729

Etiology: Eating Mexican pork sandwiches -end-stage will have scattered quiescent calcified cyst remnants.

Question 730

Calcification Rapid Review I Summary Cavernoma Cavernoma

Answer 730

scattered dots or stippled “popcorn” calcification

Question 731

Calcification Rapid Review I Summary AVM

Answer 731

calcifications in the tortuous veins or the nidus

Question 732

Calcification Rapid Review I Summary Brain Tumors can calcify. The ones most people talk about are

Answer 732

Old Elephants Age Gracefully O: Oligodendroglioma - variable, but “ribbon” pattern is most commoon E: Ependymoma (Medulloblastomas can also calcify - just less often) A: Astrocytoma G: Glioblastoma - mural calcified nodule Even though more Oligodendrogliomas calcify, Astrocytoma is still the most common calcified tumor (because there are alot more of them). Craniopharyngioma, Meningioma, Choroid plexus tumors are all known to calcify as well. Osteosarcoma mets famously calcify.

Question 733

Vasospasm

Answer 733

Vessels do not like to be bathed in blood (SAH), it makes them freak out (spasm). The classic timing for this is 4-14 days after SAH (NOT immediately). It usually looks like smooth, long segments o f stenosis. It typically involves multiple vascular territories. It can lead to stroke.

Question 734

Vasospasm Who gets it?

Answer 734

It’s usually in patients with SAH and the more volume o f SAH the greater the risk. In 1980 some neurosurgeon came up with this thing called the Fisher Score, which grades vasospasm risk. The gist o f it is greater than 1 mm in thickness or intraventricular / parenchymal extension is at higher risk

Question 735

Vasospasm Are there Non-SAH causes o f vasospasm?

Answer 735

Yep. Meningitis, PRES, and Migraine Headache.

Question 736

Vasospasm

Answer 736

Vasospasm is a delayed side effect o f SAH. It does NOT occur immediately after a bleed. You see it 4-14 days after SAH.

Question 737

“Crescent Sign”oi Dissection

Answer 737

- it’s the T1 bright intramural blood.

Question 738

Vascular Dissection

Answer 738

Vascular dissection can occur from a variety o f etiologies (usually penetrating trauma, or a trip to the chiropractor). / Penetrating trauma tends to favor the carotids, and blunt trauma tends to favor the * * mm vertebrals. This would be way too easy to show on CT as a flap, so if it’s shown it’s much more • likely to be the T1 bright “crescent sign”, or intramural hematoma.

Question 739

Vasculitis

Answer 739

``` You can have a variety o f causes o f CNS vasculitis. One way to think about it is by clumping it into (a) Primary CNS vasculitis, (b) Secondary CNS vasculitis from infection, or sarcoid, (c) systemic vasculitis with CNS involvement, and (d) CNS vasculitis from a systemic disease ``` ``` They all pretty much look the same with multiple segmental areas o f vessel narrowing, with alternating dilation (“beaded appearance"). You can have focal areas o f vascular occlusion ```

Question 740

PAN is the Most Common systemic vasculitis to involve

Answer 740

the CNS

Question 741

SLE is the Most Common

Answer 741

Collagen Vascular Disease

Question 742

Primary CNS Vasculitis

Answer 742

Primary Angiitis o f the CNS (PACNS)

Question 743

Secondary CNS vasculitis | from infection, or sarcoid

Answer 743

Meningitis (bacterial, TB, Fungal), | Septic, Embolus, Sarcoid,

Question 744

Systemic vasculitis with CNS involvement CNS vasculitis from

Answer 744

PAN, Temporal Arteritis, Wegeners, Takayasu’s,

Question 745

CNS vasculitis from a | Systemic Disease

Answer 745

Cocaine Use, RA, SLE, Lyme’s

Question 746

Moyamoya

Answer 746

This poorly understood entity (originally described in Japan - hence the name), is characterized by progressive non-atherosclerotic stenosis o f the supraclinoid ICA, eventually leading to occlusion. The progressive stenosis results in an enlargement o f the basal perforating arteries.

Question 747

Moyamoya trivia

Answer 747

Buzzword = “P u ff o f Smoke ” - for angiographic appearance Watershed Distribution In a child think sickle cell Other notable associations include: NF, prior radiation, Downs syndrome Bi-Modal Age Distribution (early childhood and middle age) Children Stroke, Adults Bleed

Question 748

Crossed C e re b e lla r D ia s ch is is (CCD

Answer 748

Depressed blood flow and metabolism affecting the cerebellar hemisphere after a contralateral supratentorial insult (infarct, tumor resection, radiation). Creates an Aunt Minnie Appearance

Question 749

Crossed C e re b e lla r D ia s ch is is (CCD mechanism/gamesmanship

Answer 749

When I was a medical student, I had to memorize a bunch o f tiny little tracks and pathways all over the brain, cerebellum, and spine. It (like many things in medical school) made me super angry because it was such a colossal waste o f time. More PhD bullshit, lumped right in with those step 1 ‘‘what chromosome is that on ? ” questions.

Question 750

Crossed C e re b e lla r D ia s ch is is (CCD corticopontine-cerebellar pathway

Answer 750

Redemption for the PhDs has arrived. Apparently, one o f these pathways, the “corticopontine-cerebellar pathway,” is actually important. S orta.... Allegedly, this pathway connects one cerebral hemisphere to the opposite cerebellar hemisphere. If the pathway gets disrupted (by tumor, radiation, e tc ...), then metabolism shuts down in the opposite cerebellum even though there is nothing structurally wrong with it. That is why you get this criss-crossed hypometabolic appearance on FDG-PET. The trick is to show you the FDG-PET picture, and try and get you to say there is a pathology in the cerebellum. There isn ’t! The cerebellum is normal - the problem is in the opposite cerebrum where the pathway starts.

Question 751

NASCET Criteria

Answer 751

The North American Symptomatic Carotid Endarterectomy Trial (NASCET) criteria, are used for carotid stenosis. The rule is: measure the degree o f stenosis using the maximum internal carotid artery stenosis ( “A ”) compared to a parallel (noncurved) segment o f the distal cervical internal carotid artery ("B ”). You then use the formula: [1- A/B] X 100% = % stenosis Carotid endarterectomy (CEA) is often performed for symptomatic patients with > 50% stenosis.

Question 752

LeFort Fracture Buzzwords 1

Answer 752

“The Palate Separated from the Maxilla” or “Floating Palate

Question 753

LeFort Fracture Buzzwords 2

Answer 753

2:“The Maxilla Separated from the Face” or “Pyramidal”

Question 754

LeFort Fracture Buzzwords 3

Answer 754

“The Face Separated from the Cranium”

Question 755

LeFort Fracture E s s en tia l E lem en ts

Answer 755

All three fracture types share the pterygoid process fracture. If the pterygoid process is not involved, you do n ’t have a LeFort. Each has a unique feature (which lends itself easily to multiple choice).

Question 756

LeFort Fracture E s s en tia l E lem en ts 1

Answer 756

* LeFort 1: Lateral Nasal Aperture

Question 757

LeFort Fracture E s s en tia l E lem en ts 2

Answer 757

* LeFort 2: Inferior Orbital Rim and Orbital Floor

Question 758

LeFort Fracture E s s en tia l E lem en ts 3

Answer 758

* LeFort 3: Zygomatic Arch and Lateral Orbital Rim/Wall

Question 759

M u co c e le

Answer 759

If you have a fracture that disrupts the frontal sinus outflow tract (usually nasal-orbital-ethmoid types) you can develop adhesions, which obstruct the sinus and result in mucocele development. The buzzword is “airless, expanded sinus.” They are usually Tl bright, with a thin rim o f enhancement (tumors more often have solid enhancement). The frontal sinus is the most common location - occurring secondary to trauma (as described above).

Question 760

CSF L e ak

Answer 760

Fractures o f the facial bones, sinus walls, and anterior skull base can all lead to CSF leak. The most common fracture site to result in a CSF leak is the anterior skull base. "Recurrent bacterial meningitis ” is a known association with CSF leak.

Question 761

T bone fractures

Answer 761

The traditional way to classify these is longitudinal and transverse, and this is almost certainly how the questions will be written. In the real world that system is old and worthless, as most fractures are complex with components o f both. The real predictive finding o f value is violation o f the otic capsule - as described in more modern papers

Question 762

T bone fractures longitudinal

Answer 762

``` Long Axis of T-Bone More Common More Ossicular Dislocation Less Facial Nerve Damage (around 20%) More Conductive Hearing Loss ```

Question 763

T bone fractures transverse

Answer 763

``` Short Axis of T-Bone Less Common More Vascular Injury (Carotid / Jugular) More Facial Nerve Damage (>30%) More Sensorineural hearing Loss ```

Question 764

Th in g s to K n ow A b o u t F a c ia l F ra c tu re s

Answer 764

• Nasal Bone is the most common fracture • Zygomaticomaxillary Complex Fracture (Tripod) is the most common fracture pattern, and involves the zygoma, inferior orbit, and lateral orbit. • Le-Fort Fractures are both a stupid and a high yield topic in facial trauma - for multiple choice. Floating Palate = 1, Pyramidal = 2, Separated Face = 3 • Transverse vs Longitudinal Temporal Bone Fractures - this classification system is stupid and outdated since most are mixed and otic capsule violation is a way better predictive factor... but this is still extremely high yield

Question 765

TEMPORAL BONE

Answer 765

It would be very easy to get completely carried away with this anatomy and spend the next 20 pages talking about all the little bumps and variants. I’m gonna resist that urge and instead try and give you some basic framework. Then as we go through the various pathologies I ’ll try and give “normal” anatomy comparisons and point out some landmarks that are relevant for pathology. Additionally, I’m gonna do a full anatomy T-Bone talk for RadiologyRonin this year - so if your really want to understand this deeper, that might be helpful

Question 766

TEMPORAL BONE anatomy

Answer 766

At the most basic level you can think about 3 | general locations: External, Middle, and Inner

Question 767

TEMPORAL BONE anatomy The External car

Answer 767

``` is everything superficial to the ear drum (tympanic membrane). ```

Question 768

TEMPORAL BONE anatomy The Inner ear is everything

Answer 768

deep to the medial | wall of the tympanic cavity.

Question 769

TEMPORAL BONE anatomy The Middle ear is

Answer 769

is everything in-between

Question 770

TEMPORAL BONE anatomy The Epitympanum

Answer 770

also called “the attic” is | basically everything above the tip of the scutum

Question 771

TEMPORAL BONE anatomy The Hypotympanum

Answer 771

is everything below the tympanic membrane. This is where the Eustachian tube arises.

Question 772

TEMPORAL BONE anatomy The Mesotympanum

Answer 772

The Mesotympanum is everything in-between | or everything directly behind the ear drum

Question 773

The scutum

Answer 773

is a “shield” like osseous spur formed via the lateral wall of the tympanic cavity. This anatomic land mark is often brought up with discussion of the erosion pattern of Cholesteatomas.

Question 774

Cholesteatoma

Answer 774

The simple way to think about this is “a bunch o f exfoliated skin debris growing in the wrong place.” It creates a big inflammation ball which wrecks the temporal bone and the ossicles. There are two parts to the ear drum, a flimsy whimpy part “Pars Flaccida” , and a tougher part “Pars Tensa.” The flimsy flaccida is at the top, and the tensa is at the bottom. If you “acquire” a hole with some inflammation / infection involving the Pars Flaccida you can end up with this ball o f epithelial crap growing and causing inflammation in the wrong place.

Question 775

Cholesteatoma dwi

Answer 775

restrict

Question 776

Cholesteatoma Pars Flaccida Type

Answer 776

Acquired Types are more common - typically involving the pars flaccida. They grow into Prussak’s Space The Scutum is eroded early (maybe first)- considered a very specific sign o f acquired cholesteatoma The Malleus head is displaced medially The long process o f the incus is the most common segment o f the ossicular chain to be eroded. Fistula to the semi-circular canal most commonly involves the lateral segment

Question 777

Cholesteatoma Pars Tensa Type:

Answer 777

``` •The inner ear structures are involved earlier and more often •This is less common than the Flaccida Type ```

Question 778

P ru s s a k ’s S p a c e and S cu tum Erosion

Answer 778

The membrane is usually too thin to see, but it’s right around there. Remember the flimsy Flacida is at the top and the thicker Tensa is at the bottom. There are two white arrows here. The top arrow is pointing to a space between an ossicle (incus) and the lateral temporal bone. This is called “Prussak’s space” and is the most common location of a Pars Flacida Cholesteatoma. Remember the incus was the most common ossicle eroded. The bottom arrow is pointing to a bony shield shaped bone - “the scutum” which will be the first bone eroded by a pars flaccida.

Question 779

L a b y rin th in e F is tu la (p e rilym p h a tic fis tula

Answer 779

This is a potential complication o f cholesteatoma (or other things - iatrogenic, trauma, e tc ...). What we are talking about here is a bony defect creating an abnormal communication between the normally fluid filled inner ear and normally air filled tympanic cavity. In the case o f cholesteatoma, the lateral semicircular canal (arrows) is most often involved.

Question 780

L a b y rin th in e F is tu la (p e rilym p h a tic fis tula classic history

Answer 780

The classic clinical history is “sudden fluctuating sensorineural hearing loss and vertigo.’

Question 781

L a b y rin th in e F is tu la (p e rilym p h a tic fis tu CT

Answer 781

``` On CT, you want to see the soft tissue density o f the cholesteatoma eating through the otic capsule into the semicircular canal. The presence o f air in the semicircular canal (pneumolabyrinth) is definitive evidence o f a fistula (although it’s not often seen in the real world). ```

Question 782

Otitis Media (OM)

Answer 782

This is a common childhood disease with effusion and infection of the middle ear. It’s more common in children and patients with Down Syndrome because of a more horizontal configuration of the Eustachian tube. It’s defined as chronic if you have fluid persisting for more than six weeks. It can look a lot like a cholesteatoma (soft tissue density in the middle cart

Question 783

Complications of OM Coalescent Mastoiditis

Answer 783

Erosion of the mastoid septae with or | without intramastoid abscess

Question 784

Complications of OM Facial Nerve Palsy

Answer 784

``` Secondary to inflammation of the tympanic segment (more on this later in the chapter). Adjacent inflammation may cause thrombophlebitis or thrombosis of the sinus. This in itself can lead to complications: ```

Question 785

Complications of OM Dural Sinus Thrombosis

Answer 785

``` Venous Infarct: This can occur secondary to dural sinus thrombosis ``` ``` Otitic Hydrocephal us: Lateral sinus thrombosis can alter resorption of CSF and lead to hydrocephalus ```

Question 786

Complications of OM Meningitis, and Labyrinthitis

Answer 786

it can happen

Question 787

L a b y rin th itis O s s ific a n s

Answer 787

• Gamesmanship - "history o f childhood meningitis. ” • You see it in kids (ages 2-18 months). • Classic Appearance on CT - Ossification o f the membranous labyrinth. • They present with sensorineural hearing loss. • Calcification in the cochlea is often considered a contraindication for cochlear implant.

Question 788

WTF is a “membranous labyrinth ” ?

Answer 788

``` The world “Labyrinth” most commonly refers to the timeless 1986 science fiction adventure staring David Bowie as Jareth the Mother Fucking Goblin King. Another less popular use o f the word “Labyrinth” is the anatomical blanket term encompassing the Vestibule, Cochlea, and Semicircular Canals. Under the umbrella o f the “Labyrinth” you can have the bony portion (the series o f canals tunneled out o f the tbone), and the membraneous portion (which is basically the soft tissue lining inside the bony part). You can then further divide the “membranous” portion into the cochlear & vestibular labyrinths. ```

Question 789

Chronic Otitis Media Mastoids: Middle Ear Opacification: For the purpose of multiple choice this could be a hing: Erossions (scutum and ossicular chain): Displacement of the ossicular chain:

Answer 789

Mastoids: poorlypneumatized Middle Ear Opacification:Can completely opacity For the purpose of multiple choice this could be a hing:Thickened mucosa Erossions (scutum and ossicular chain):Rare (< 10%) Displacement of the ossicular chain:NEVEr

Question 790

Cholesteatoma Mastoids: Middle Ear Opacification: For the purpose of multiple choice this could be a hing: Erossions (scutum and ossicular chain): Displacement of the ossicular chain:

Answer 790

Mastoids:poorlypneumatized Middle Ear Opacification:Can completely opacity For the purpose of multiple choice this could be a hing:Non- Dependent Mass Erossions (scutum and ossicular chain):Common (75%) Displacement of the ossicular chain:It can happen

Question 791

L a b y rin th itis

Answer 791

This is an inflammation o f the membranous labyrinth, probably most commonly the result o f a viral respiratory track infection. Acute otomastoiditis can also spread directly to the inner ear (this is usually unilateral). Bacterial meningitis can cause bilateral labyrinthitis.

Question 792

L a b y rin th itis classic look

Answer 792

The cochlea and semicircular canals | will be shown enhancing on Tl post contrast imaging.

Question 793

the F a c ia l N e rv e (CN 7) segments

Answer 793

• Intracranial (“Cisternal”) segment • Meatal (“Canalicular”) segment - the part inside the Internal Auditory Canal “IAC”). • Labyrinthine segment (LS) - from the IAC to geniculate ganglion (GG). • Tympanic segment (TS) - GG to pyramidal eminence • Mastoid segment (MS) - from pyramidal eminence to stylomastoid foramen “SMF” • Extratemporal segment - Distal to the SMF

Question 794

the F a c ia l N e rv e (CN 7) enhancement

Answer 794

``` The facial nerve is unique in that portions of it can enhance normally. The trick is which parts are normal and which parts arc NOT. Normal Enhancement: Tympanic & Mastoid Segments including the Geniculate Ganglia. The Labyrinthine segment can also sometimes. No normal enhancement = Cisternal, Canalicular, or Extratemporal ```

Question 795

the F a c ia l N e rv e (CN 7) IVhat causes abnormal enhancement?

Answer 795

Big one is Bell’s Palsy. Lymes, Ramsay | Hunt, and Cancer can do it too.

Question 796

the F a c ia l N e rv e (CN 7) When do yo u think Cancer

Answer 796

Nodular Enhancement

Question 797

the F a c ia l N e rv e (CN 7) When do yo u damage the facial nerve

Answer 797

T-Bone fracture (transverse > longitudinal).

Question 798

Axial CT- Level of I AC | -the bend at the GG =

Answer 798

anterior genu

Question 799

Axial MR T2 - Cisternal Segment

Answer 799

-CN8 is posterior also | entering the IAC

Question 800

Bells

Answer 800

Etiology is probably viral. Usually a clinical diagnosis. Abnormal enhancement in the Canalicular Segment (in the IAC) is probably the most classic finding.

Question 801

RH

Answer 801

Caused by reactivation varicella zoster virus. Classic rash around ear. CN 5 is usually also involved.

Question 802

O to s c le ro s is (F e n e s tra l and R e tro fe n e s tra l):

Answer 802

A better term would actually be “otospongiosis,” as the bone becomes more lytic (instead of sclerotic). When I say conductive hearing loss in an adult female, you say this

Question 803

Fenestral

Answer 803

This is bony resorption anterior to the oval widow at the fissula ante fenestram. If not addressed, the footplate will fuse to the oval window.

Question 804

Retro-fenestral

Answer 804

This is a more severe form, which has progressed to have demineralization around the cochlea. This form usually has a sensorineural component, and is bilateral and symmetric nearly 100% of the time.

Question 805

to s c le ro s is (F e n e s tra l and R e tro fe n e s tra l): treatment optoins

Answer 805

Early on (if the focus is small) dietary supplementation with Fluoride may be useful. Although this is controversial - may or may not w o rk ... and may or may not be part o f a new world order David Icke Reptilian conspiracy to lower IQs (Alex Jones has the documents). Later on they might try a stapedectomy (partial removal o f the stapes with implantation o f a prosthetic device) or a Cochlear implant

Question 806

S u p e r io r S em ic ir cu la r Canal D e h is c e n c e

Answer 806

This is an Aunt Minnie. It’s supposedly from long standing elevated ICP. The most likely way this will be asked is either (1) what is it? with a picture or (2) “Noise Induced Vertigo” or “Tullio’s Phenomenon.”

Question 807

Pietro Tullio

Answer 807

``` Mad scientist who drilled holes in the semicircular canals of pigeons then observed that they became off balance when he exposed them to loud sounds. He also created a “pigeon rat” like Hugo Simpson did in the 1996 Simpsons Halloween Special. ```

Question 808

Large V e s tib u la r A q u ed u c t S y n d rom e

Answer 808

The vestibular aqueduct is a bony canal that connects the vestibule (inner ear) with the endolymphatic sac. The enlargement of the aqueduct (> 1.5 mm) has an Aunt Minnie appearance. The classic history is progressive sensorineural hearing loss. Supposedly the underlying etiology is a failure of the endolymphatic sac to resorb endolymph, leading to endolymphatic hydrops and dilation.

Question 809

Large V e s tib u la r A q u ed u c t S y n d rom e trivia

Answer 809

«This is the most common cause of congenital sensorineural hearing loss •The finding is often (usually) bilateral, j l v ‘There is an association with cochlear deformity - near 100% 4y r l (absence o f the bony modiolus in more than 90%) •Progressive Sensorineural Hearing Loss (they arc NOT bom deaf)

Question 810

The normaI Vestibular Aqueduct (VA) is | NEVER

Answer 810

larger than the adjacent | Posterior Semicircular Canal (PSCC)

Question 811

Congenital malformations o f the inner ear

Answer 811

Along those lines, we can discuss two disorders on opposite ends o f that severity spectrum with the Michel’s Aplasia being the earliest and most severe, and the Classic Mondini’s Malformation (incomplete partition II) being the latest and least severe

Question 812

Mondini Malformation

Answer 812

Type o f cochlear hypoplasia where the basal turn is normal, but the middle and apical turns fuse into a cystic apex. This is usually written as “only 1.5 turns" - instead o f the normal 2.5. There is an association with an enlarged vestibule, and enlarged vestibular aqueduct. They have sensorineural hearing loss, although high frequency sounds are typically preserved (as the basal turn is normal).

Question 813

Michel’s A p la sia

Answer 813

This is also referred to as complete labyrinthine aplasia or “CLA.” As above, this represents the most severe o f the congenital abnormalities o f the inner ear - with absence o f the cochlea, vestibule, and vestibular aqueduct. No surprise these kids are completely deaf.

Question 814

Michel’s A p la sia associations

Answer 814

Anencephaly, Thalidomide Exposure

Question 815

Michel’s A p la sia gamesmanship

Answer 815

Some people think this looks like labyrinthitis ossificans. Look for the absent vestibular aqueduct to help differentiate.

Question 816

h i s vs THAT: Mondini vs Michel mondine Timing: Severity: Cochlea: Vestibule: Vestibular Aqueduct: Frequency:

Answer 816

Timing:Late (7th Week Severity:Some Preserved High Frequency Hearing Cochlea:Cystic Apex (basilar turn is normal) Vestibule:Sometimes Enlarged (can be normal) Vestibular Aqueduct:Large Frequency:Common (relative to other malformations)

Question 817

h i s vs THAT: Mondini vs Michel michel Timing: Severity: Cochlea: Vestibule: Vestibular Aqueduct: Frequency:

Answer 817

Timing:Early (3rd Week) Severity:Total Deafness Cochlea:Absent Vestibule:Absent Vestibular Aqueduct:Absent Frequency:Rare As Fuck

Question 818

E n d o lym p h a tic S a c Tumor

Answer 818

Rare tumor o f the endolymphatic sac and duct. Although most are sporadic, when you see this tumor you should immediately think Von-Hippel-Lindau.

Question 819

E n d o lym p h a tic S a c Tumor classic look

Answer 819

They almost always have internal amorphous calcifications on CT. There are T2 bright, with intense enhancement. They are very vascular often with flow voids, and tumor blush on angiography.

Question 820

P a r a g a n g liom a

Answer 820

On occasion, paraganglioma o f the jugular fossa (glomus jugulare or jugulotympanic tumors) can invade the occipital bone and adjacent petrous apex

Question 821

P a r a g a n g liom a trivia

Answer 821

»40% o f the time it’s hereditary, and they are multiple. »The most common presenting symptom is hoarseness from vagal nerve compression. A »They are very vascular masses and enhance avidly with a “salt and pepper” appearance on post contrast MRI, with flow voids. *They are FDG avid.

Question 822

Petrous Apex - Anatomic Variations A sym m e tr ic Marrow

Answer 822

Typically the petrous apex contains significant fat, closely following the scalp and orbital fat (T1 and T2 bright). When it’s asymmetric you can have two problems (1) falsely thinking y o u ’ve got an infiltrative process when you d o n ’t, and (2) overlooking a T1 bright thing (cholesterol granuloma) thinking it’s fat. The key is to use STIR or some other fat saturating sequence

Question 823

Petrous Apex - Anatomic Variations C e p h a lo c e le s

Answer 823

A cephalocoele describes a herniation o f CNS content through a defect in the cranium. In the petrous apex they are a slightly different animal. They d o n ’t contain any brain tissue, and simply represent cystic expansion and herniation o f the posterolateral portion o f Meckel’s cave into the superomedial aspect o f the petrous apex. Describing it as a herniation o f Meckel’s Cave would be more accurate. These are usually unilateral and are classically described as “smoothly marginated lohulated cystic expansion o f the petrous apex. ”

Question 824

Petrous Apex - Anatomic Variations Aberrant in te rn a l ca ro tid .

Answer 824

The classic history is pulsatile tinnitus (although other things can cause that). This term is used to describe the situation where the Cl (cervical) segment o f the ICA has involuted/underdeveloped, and middle ear collaterals develop (enlarged caroticotympanic artery) to pick up the slack. The hypertrophied vessel runs through the tympanic cavity and joins the horizontal carotid canal. The ENT exam will show a vascular mass pulsing behind the ear drum (don’t expect them to make it that easy for you). The oldest trick in the book is to try and fool you into calling it a paraganglioma. Look for the connection to the horizontal carotid canal - that is the most classic way to show this. DO NOT BIOPSY !

Question 825

A p ica l P e tr o s itis

Answer 825

Infection o f the petrous apex is a rare complication o f infectious otomastoiditis. It can have some bad complications if it progresses including osteomyelitis o f the skull base, vasospasm o f the ICA (if it involves the carotid canal), subdural empyema, venous sinus thrombosis, temporal lobe stroke, and full on meningitis. In children, it can present as a primary process. In adults it's usually in the setting o f chronic otomastoiditis or recent mastoid surgery

Question 826

G rad en ig o S yn d rom e

Answer 826

This is a complication o f apical petrositis, when Dorello’s canal (CN 6) is involved. They will show you (or tell you) that the patient has a lateral rectus palsy

Question 827

G rad en ig o S yn d rom e classic triad

Answer 827

• Otomastoiditis, • Face pain (trigeminal neuropathy), and • Lateral Rectus Palsy

Question 828

Dorello's Canal

Answer 828

``` The most medial point of the pertrous ridge - between the pontine cistern and cavernous sinus ```

Question 829

Petrous Apex - Inflammatory Lesions C h o le s te r o l Granuloma

Answer 829

The most common primary petrous apex lesion. Mechanism is likely obstruction o f the air cell, with repeated cycles o f hemorrhage and inflammation leading to expansion and bone remodeling. The most common symptom is hearing loss.

Question 830

Petrous Apex - Inflammatory Lesions Choelsteatoma

Answer 830

This is basically an epidermoid (ectopic epithelial tissue). Unlike the ones in the middle ear, these are congenital (not acquired) in the petrous apex. They are typically slow growing, and produce bony changes similar to cholesterol granuloma. The difference is their MRI findings; T l dark. T2 bright, and restricted diffusion

Question 831

C h o le s te r o l Granuloma imaging

Answer 831

``` On CT the margins will be sharply defined. On MRI it’s gonna be T l and T2 bright, with a T2 dark hemosiderin rim, and faint peripheral enhancement ```

Question 832

C h o le s te r o l Granuloma key point

Answer 832

Cholesterol Granuloma = | Tl and T2 Bright.

Question 833

THIS vs THAT: Cholesterol Granuloma Cholesteatoma

Answer 833

Cholesterol Granuloma Cholesteatoma T l Bright Tl Dark T2 Bright T2 Bright Doesn’t Restrict Does Restrict Smooth Expansile Bony Change Smooth Expansile Bony Change

Question 834

R egu la r and N e c r o tiz in g O titis Externa

Answer 834

Otitis Externa - the so called “swimmers ear” is an infection (usually bacterial) o f the external auditory canal. The more testable version Necrotizing Otitis Externa (also called "Malignant" Otitis Externa - for the purpose o f fucking with you) is a more aggressive version seen almost exclusively in diabetics. You are going to see swollen EAC soft tissues, probably with a bunch o f small abscesses, and adjacent bony destruction. They always (95%) have diabetes and the causative agent is always (98%) Pseudomonas

Question 835

E x te rn a l Auditory Canal E x o s t o s is (“Sw im m e r s Ear”)

Answer 835

This is an overgrowth o f tissue in the ear canal, classically seen in Surfers who get repeated bouts o f ear infections. It’s usually bilateral, and when chronic will look like bone. Unlike Necrotizing Otitis, these patients are immunocompetent and non-diabetes (although they are dirty hippie surfers).

Question 836

E x te rn a l Auditory Canal O s te om a

Answer 836

This is a benign bone tumor, maybe best thought o f as an overgrowth o f normal bone. They are usually incidental and unilateral (,remember exostosis was bilateral) occurring near the junction o f cartilage and bone in the ear canal.

Question 837

E x te rn a l Auditory Canal A tr e sia

Answer 837

This is a developmental anomaly where the external auditory canal (secondary crayon storage compartment) doesn’t form. As you might imagine, this results in a hearing deficit (conductive subtype). There may or may not be a mashed up ossicular chain.

Question 838

E x te rn a l Auditory Canal A tr e sia trivia

Answer 838

ENT will want to know: (1) if the tissue covering the normally open ear hole (atretic plate) is soft tissue or bone, and (2) if there is an aberrant course o f the facial nerve.

Question 839

Pagets

Answer 839

This is discussed in great depth in the MSK chapter. Having said that, I want to remind you o f the Paget skull changes. You can have osteolysis as a well-defined large radiolucent region favoring the frontal and occipital bones. Both the inner and outer table are involved.

Question 840

pagets buzzwork

Answer 840

osteolysis circumscripta.

Question 841

pagets skull related complications

Answer 841

* Deafness is the most common complication * Cranial Nerve Paresis * Basilar Invagination -> Hydrocephalus -> Brainstem Compression * Secondary (high grade) osteosarcoma.

Question 842

Fibrous D y sp la s ia

Answer 842

The ground-glass lesion. If you are getting ready to call it Pagets, stop and look at the age. Pagets is typically an older person (8% at 80), whereas fibrous dysplasia is usually in someone less than 30.

Question 843

Fibrous D y sp la s ia findings

Answer 843

• Classically, fibrous dysplasia o f the skull spares the otic capsule • McCune Albright Syndrome - Multifocal fibrous dysplasia, cafe-au-lait spots, and precocious puberty. • The outer table is favored (Pagets tends to favor in the inner table)

Question 844

Sinus D isea se Strategy Intro

Answer 844

You will see C’T and MRI used in the evaluation of sinus disease. It is useful to have some basic ideas as to why one modality might be preferred over the other (for gamesmanship and distractor elimination). CT is typically used for orbital and sinus infections. In particular it is useful to see if the spread of infection involves the anterior 2/3 of the orbit. If you wanted to know if the patient has cavernous sinus involvement, or involvement of the posterior 1/3 (orbital apex) MRI will be superior. CT also has the ability to differentiate common benign disease (inspissated secretion and allergic fungal sinusitis) from the more rare sinus tumors. The trick being that a hyperdense opacified sinus is nearly always benign (tumor will not be dense). In addition to that CT is useful for characterization of anatomical variation (justification of endoscopic nasal surgery for recurrent sinusitis). MRI is going to be more valuable for tumor progression / extension (perineural spread, marrow involvement etc..).

Question 845

- Hyper Dense Sinus

Answer 845

• Blood • Dense (inspissated) Secretions • Fungus

Question 846

Fungal Sinusitis

Answer 846

This comes in two flavors; the good one (allergic) and the bad one (invasive). The chart below will contrast the testable differences:

Question 847

Allergic Fungal Sinusitis

Answer 847

Opacification of multiple sinuses, ususually bilateral favoring the ethmoid and maxillary sinuses. Normal Immune System (Asthma is common) CT: Hyperdense centrally or with layers. Can erode and remodel sinus walls if chronic. MRI: T1-T2 Dark - because of the high protein content / heavy metals. Can mimic an aerated sinus. Inflamed (T2 bright) mucosa which will enhance. The glob of fungus snot will not enhance (thats how you know it is not a tumor).

Question 848

Acute Invasive Fugal Sinusitis

Answer 848

Opacification of multiple sinuses. Stranding / Extension into the fat around the sinuses in the key finding. Immunocompromised - Neutropenic = Aspergillus - Diabetic in DKA = Zygomycetes / Mucor CT: Opacified Sinus with is NOT hyperdense. Fat stranding in the orbit, masticator fat, pre-antral fat, or PPF suggests invasion. This does NOT require bone destruction. MRI: Also can be T1/T2 Dark. However, the mucosa may not enhance (suggesting it is necrotic). The extension of disease out of the sinus will be bright on STIR and enhance.

Question 849

C h r o n ic In f lam m a to r y S in o n a s a l D i s e a s e

Answer 849

This is typically thought of as an inflammation of the paranasal sinuses that lasts at least 12 weeks. The causes arc complex and people write long boring papers about the various cytokines and T-Cell mediation pathways are involved but from the Radiologist’s point of view the issue is primarily anatomical patency of sinus Ostia Infundibular Pa tte rn . O s tiom e a ta l U nit P a tte rn Sinonasal Polyposis P a tte rn .

Question 850

Infundibular | Pa tte rn .

Answer 850

``` The most common pattern. In this pattern, disease is limited to the maxillary sinus and occurs from the obstruction at the ipsilateral ostium / infundibulum (star). ```

Question 851

O s tiom e a ta l U nit P a tte rn

Answer 851

``` Second most common pattern. I’m not going to get into depth on the various subtypes - just think about this as more centered at the middle meatus (star) with disease involving the ipsilateral maxillary, frontal and ethmoid sinuses. The contributors to this pattern involve all the usually suspects (hypertrophied turbinates, anatomic variants - concha bullosa, middle turbinates which curl the wrong way “paradoxical”, and septal deviation). ```

Question 852

Sinonasal Polyposis | P a tte rn .

Answer 852

``` The pattern is characterized by a combination of soft tissue nasal polyps (found throughout the nasal cavity) and variable degrees of sinus opacification. About half the time fluid levels will also be present. A key feature is the bony remodeling and erosion. In particular the “widening of the infiindibula” is the classic description. This erosion and remodeling is important to distinguish between the “expansion” o f the sinus - which is more classic for a mucocele. Testable associations include CF and Aspirin Sensitivity. ```

Question 853

Mu co ce le

Answer 853

This is how I think about these things. You have an obstructed sinus. Maybe you had trauma which fucked the drainage pathway or you’ve got CF and the secretions just clog things up. Mucus continues to accumulate in the sinus, but it can’t clear (because it's obstructed). Over time the sinus become totally filled and then starts to expand circumferentially. Hence the buzzword “expanded airless sinus.” The frontal sinus is the most common location. It won't enhance centrally (it is not a tumor), but the periphery may enhance from the adjacent inflamed mucosa

Question 854

A n tro c h o a n a l Polyp

Answer 854

Seen in young adults (30s-40s), classically presenting with nasal congestion / obstruction symptoms. Arises within the maxillary sinuses and passes through and enlarges the sinus ostium (or accessory ostium).

Question 855

A n tro c h o a n a l Polyp buzzword

Answer 855

“widening of the maxillary ostium/'

Question 856

A n tro c h o a n a l Polyp clasically

Answer 856

Classically, there is no associated bony destruction but instead smooth enlargement o f the sinus. The polyp will extend into the nasopharynx. This thing is basically a monster inflammatory polyp with a thin stalk arising from the maxillary sinus

Question 857

J u v e n ile N a s a l A n g io fib rom a (JN A

Answer 857

Often you can get this one right just from the history - Male teenager with nose bleeds (obstruction is actually a more common symptom in real life, but not so much on multiple choice).

Question 858

J u v e n ile N a s a l A n g io fib rom a (JN A things to know

Answer 858

* Location = Centered on the sphenopalatine foramen * Bone Remodeling (not bone destruction) * Extremely vascular (super enhancing) with intratumoral Flow Voids on MR * Pre-surgical embolization is common (via internal maxillary & ascending pharyngeal artery)

Question 859

In v e r te d P ap illom a :

Answer 859

This uncommon tumor has distinctive imaging features (which therefore make it testable). The classic location is the lateral wall of the nasal cavity - most frequently related to the middle turbinate. Impaired maxillary drainage is expected.

Question 860

In v e r te d P ap illom a : thinkgs to know

Answer 860

* A focal hyperostosis tends to occur at the tumor origin. * Another high yield pearl is that 10% harbor a squamous cell CA. * MRI “cerebriform pattern” - which sorta looks like brain on T1 and T2.

Question 861

E s th e s io n e u ro b la s tom a :

Answer 861

This is a neuroblastoma o f olfactory cells so it’s gonna start at the cribiform plate. It classically has a dumbbell appearance with growth up into the skull and growth down into the sinuses, with a waist at the plate. There are often cysts in the mass. There is a bi-modal age distribution

Question 862

E s th e s io n e u ro b la s tom a : things to know

Answer 862

•Dumbbell shape with wasting at the cribiform plate is classic .Intracranial posterior cyst is a “diagnostic” look ‘Octreotide scan will be positive - since it is o f neural crest origin

Question 863

S q u am o u s C e ll I SNUC

Answer 863

Squamous cell is the most common head and neck cancer. The maxillary antrum is the most common location. It's highly cellular, and therefore low on T2. Relative to other sinus masses it enhances less. SNUC (the undifferentiated squamer), is the monster steroided-up version o f a regular squamous cell. They are massive and seen more in the ethmoids

Question 864

Epistaxis (Nose Bleeds

Answer 864

This is usually idiopathic, although it can be iatrogenic (picking it too much - or not enough). They could get sneaky and work this into a case of HHT (hereditary hemorrhagic telangiectasia). The most common location is the anterior septal area (Kiesselbach plexus) - these tend to be easy to compress manually. The posterior ones are less common (5%) but tend to be the ones that “bleed like stink" (need angio). Most cases are given a trial o f nasal packing. When that fails, the N-IR team is activated.

Question 865

Epistaxis (Nose Bleeds what to know

Answer 865

The main supply to the posterior nose is the sphenopalatine artery (terminal internal maxillary artery) and tends to be the first line target. Watch out for the variant anastomosis between the ECA and ophthalmic artery (you don’t want to embolize the eye).

Question 866

Nasal Septal Perforation

Answer 866

Typically involves the anterior septal cartilaginous area.

Question 867

Nasal Septal Perforation causes

Answer 867

• Surgery - Old school Septoplasty techniques - essentially resecting the thing (Killian submucous resection) • Cocaine use (> 3 months) • Too much nose picking (or perhaps not picking it enough) • Granulomatosis with polyangiitis (Wegener granulomatosis) — Triad o f renal masses, sinus mucosal thickening and nasal septal erosion, disease, and cavitary lung nodules / fibrosis. cANCA positive. • Syphilis - affects the bony septum (most everything else effect the cartilaginous regions).

Question 868

S ia lo lith ia s is

Answer 868

Stones in the salivary ducts. The testable trivia includes: (1) Most commonly in the submandibular gland duct (wharton’s), (2) can lead to an infected gland “sialoadenitis”, and (3) chronic obstruction can lead to gland fatty atrophy.

Question 869

salivary gland ducst

Answer 869

``` Submandibular = Wharton Parotid = Stenson Sublingual = Rivinus ```

Question 870

Odontogenic In fe c tio n

Answer 870

These can be dental or periodontal in origin. If I were writing a question about this topic I would ask three things. The first would be that infection is more common from an extracted tooth than an abscess involving an intact tooth. ``` The second would be that the attachment of the mylohyoid muscle to the mylohyoid ridge dictates the spread of infection to the sublingual and submandibular spaces. Above the mylohyoid line (anterior mandibular teeth) goes to the sublingual space, and below the mylohyoid line (second and third molars) goes to the submandibular space. ``` The third thing I would ask would be that an odontogenic abscess is the most common masticator space “mass” in an adult.

Question 871

Sublingual | Space

Answer 871

-Above the Mylohyoid Line | (Anterior Mandibular Teeth

Question 872

Submandibular | Space

Answer 872

-Below the Mylohyoid Line | 2nd and 3rd Molars

Question 873

L u dw ig ’s Angina:

Answer 873

This is a super aggressive cellulitis in the floor o f the | mouth. If they show it, there will be gas everywhere

Question 874

L u dw ig ’s Angina: trivia

Answer 874

most cases start with an odontogenic infection

Question 875

Torus Palatinus

Answer 875

``` This is a normal variant that looks scary. Because it looks scary some multiple choice writer may try and trick you into calling it cancer. It’s just a bony exostosis that comes off the hard palate in the midline. Classic History. “Grandma’s dentures won’t stay in.” ```

Question 876

O s te o n e c ro s is of | th e M a n d ib le

Answer 876

``` The trivia is most likely gonna be etiology. Just remember it is related to prior radiation, licking a radium paint brush, or bisphosphonate treatment. ```

Question 877

Ranula

Answer 877

``` This is a mucous retention cyst. They are typically lateral. There are two testable pieces o f trivia to know: (1) They arise from the sublingual gland / space. and (2) Use the word “plunging” once it’s under the mylohyoid muscle. ```

Question 878

T h y ro g lo s s a l D u c t C y s t

Answer 878

This can occur anywhere between the foramen cecum (the base o f the tongue) and the thyroid gland. They are usually found in the midline. It looks like a thin-walled cyst. Further discussion in the endocrine & peds chapters.

Question 879

Floor of Mouth Dermoid I Epidermoid

Answer 879

There isn’t a lot o f trivia about these other than the buzzword and what they classically look like. The buzzword is “sack of marbles” - fluid sack with globules o f fat. They are typically midline. Further discussion in the peds chapter.

Question 880

Head and neck cancer

Answer 880

Squamous cell is going to be the most common cancer o f the mouth (and head and neck). In an older person think drinker and smoker. In a younger person think HPV. HPV related SCCs tend to be present with large necrotic level 2a nodes (don’t call it a branchial cleft cyst!).

Question 881

Head and neck cancer trivia

Answer 881

Classic Scenario = Young adult with new level 1/ neck mass = HPV related SCC.

Question 882

lesions of the Jaw

Answer 882

There are a BUNCH o f these and they all look pretty similar. Lesions in the jaw are broadly grouped into either odontogenic (from a tooth) or non-odontogenic (not from a tooth). The non-odontogenic stuff you see in the mandible is the same kind o f stuff you see in other bones (ABCs, Simple Bone Cysts, Osteomyelitis, Myeloma / Plasmacytoma e tc ...). I think if a test writer is going to show a jaw lesion - they probably are going to go for odontogenic type. Obviously your answer choices will help you decide what they are going for. The other tip is that odontogenic lesions are usually associated with a tooth. Pe ria p ic a l Cyst (R a d ic u la r Cys t) D en tig e ro u s Cyst (F o llic u la r Cyst) K e ra to g e n ic O d o n to g en ic T um or Am e lo b la s tom a Odontoma

Question 883

Pe ria p ic a l Cyst (R a d ic u la r Cys t)

Answer 883

This is the most common type o f odontogenic cyst. They are typically the result o f inflammation from dental caries (less commonly trauma). The inflammatory process results in a cystic degeneration around the periodontal ligament.

Question 884

e ria p ic a l Cyst (R a d ic u la r Cys t) things to know

Answer 884

‘Located at the apex o f a non-vital tooth ‘ Round with a Well Corticated Border • Usually < 2 cm

Question 885

D en tig e ro u s Cyst (F o llic u la r Cyst)

Answer 885

This is a cyst that forms around the crown o f an un-erupted tooth. It’s best thought o f as a developmental cyst (peri-apicals are acquired). These things like to displace and resorb adjacent teeth - usually in an apical direction. This is the kind o f cyst that will displace a tooth into the condylar regions o f the mandible or into the floor o f the orbit.

Question 886

D en tig e ro u s Cyst (F o llic u la r Cyst) things to know

Answer 886

‘ Located at the crown o f an un-erupted tooth | • Tend to displace the tooth

Question 887

K e ra to g e n ic O d o n to g en ic T um o

Answer 887

(Odontogenic Keratocyst) - Unlike the prior two lesions (which were basically fluid collections) this is an actual tumor. They tend to occur at the mandibular ramus or body. Although they can be uni-locular the classic look is multi-locular ( “daughter cysts ”) and th at’s how I would expect them to look on the test.

Question 888

K e ra to g e n ic O d o n to g en ic T um o things to know

Answer 888

* Body / Ramus Mandible * They typically grow along the length o f the bone * Without significant cortical expansion * May have daughter cysts * When multiple think Gorlin Syndrome

Question 889

Am e lo b la s tom a

Answer 889

(Adamantinoma o f the jaw) - This is another tumor (locally aggressive). The appearance is variable but for the purpose o f multiple choice I would expect the most classic look - multi-cystic with solid components and expansion o f the mandible. Out o f the four I’ve discussed, this will be the most aggressive-looking one. If they show you a really aggressive-looking lesion, especially if it has multiple “soap bubbles” - you should consider this.

Question 890

Am e lo b la s tom a things to know

Answer 890

* Hallmark = Extensive Tooth Root Absorption * Mandibular Expansion * Solid component (shown on MR or CT) favors the Dx o f Ameloblastoma * About 5% arise from Dentigerous Cysts

Question 891

Odontoma

Answer 891

This is the easy one to pick out because it’s most likely to be shown in it’s mature solid form (they start out lucent). It’s actually the most common odontogenic tumor o f the mandible. It’s basically a “tooth hamartoma.”

Question 892

Odontoma what to know

Answer 892

• Radiodense with a lucent rim

Question 893

Suprahyoid neck

Answer 893

The suprahyoid neck is usually taught by using a “spaces” method. This is actually the best way to learn it. What space is it? What is in that space? What pathology can occur as the result o f what normal structures are there? Example: lymph nodes are there - thus you can get lymphoma or a met.

Question 894

Parotid Space

Answer 894

``` The parotid space is basically the parotid gland, and portions o f the facial nerve. You can 't see the facial nerve, but you can see the retromandibular vein (which runs ju st medial to the facial nerve). Another thing to know is that the parotid is the only salivary gland to have lymph nodes, so pathology involving the gland itself, and anything lymphatic related, is fair game. ```

Question 895

Parotid Space contains

Answer 895

- The Parotid Gland - Cranial Nerve 7 (Facial) - Retro-mandibular Vein

Question 896

Parotid Space Pathology

Answer 896

Pleomorphic A denoma (benign m ixed tum o r) Warthins M u coepide rm oid C a rc in om a Lymphoma Sjo gren s Benign L ym p h o e p ith e lia l D is e ase A c u te P a ro titis

Question 897

Pleomorphic A denoma (benign m ixed tum o r)

Answer 897

This is the most common major (and minor) salivary gland tumor. It occurs most commonly in the parotid, but can also occur in the submandibular or sublingual glands. 90% o f these tumors occur in the superficial lobe. They are commonly T2 bright, with a rim o f low signal. They have a small malignant potential and are treated surgically.

Question 898

Pleomorphic A denoma (benign m ixed tum o r) superficial vs deep

Answer 898

Involvement o f the superficial (lateral to the facial nerve) or deep (medial to the facial nerve) lobe is critical to the surgical approach. A line is drawn connecting the lateral surface o f the posterior belly o f the digastric muscle and the lateral surface o f the mandibular ascending ramus to separate superficial from deep

Question 899

Pleomorphic A denoma (benign m ixed tum o r) resection

Answer 899

Apparently, if you resect these like a clown you can spill them, and they will have a massive, ugly recurrence.

Question 900

Major Salivary Glands:

Answer 900

* Parotid * Submandibular * Sublingual

Question 901

Minor Salivary Glands

Answer 901

• Literally 100s of unnamed | minor glands

Question 902

Warthins

Answer 902

This is the second most common benign tumor. This one ONLY occurs in the parotid gland. This one is usually cystic, in a male, bilateral (15%), and in a smoker. As a point o f total trivia, this tumor takes up pertechnetate (it’s basically the only tumor in the parotid to do i t , ignoring the ultra rare parotid oncocytoma).

Question 903

M u coepide rm oid C a rc in om a

Answer 903

This is the most common malignant tumor of minor salivary glands. The general rule is - the smaller the gland, the more common the malignant tumors; the bigger the gland, the more common the benign tumors. There is a variable appearance based on the histologic grade. There is an association with radiation.

Question 904

Adenoid Cys tic C a rc in om a

Answer 904

This is another malignant salivary gland tumor, which favors minor glands but can be seen in the parotid. The number one thing to know is perineural spread. This tumor likes perineural spread.

Question 905

When I say adenoid cystic, you say

Answer 905

perineural spread

Question 906

Adenoid Cys tic C a rc in om a Pearl

Answer 906

I used to think that perineurial tumor spread would widen a neural foramen (foramen ovale for example). It’s still m ight... but it’s been my experience that a nerve sheath tumor (schwannoma) is much more likely to do that. Let’s ju st say for the purpose o f multiple choice that neural foramina widening is a schwannoma - unless there is overwhelming evidence to the contrary

Question 907

Lymphoma (parotid)

Answer 907

Because the parotid has lymph nodes (it’s the only salivary gland that does), you can get lymphoma in the parotid (primary or secondary). If you see it and it’s bilateral, you should think Sjogrens. Sjogrens patients have a big risk (like lOOOx) o f parotid lymphoma. Like lymphoma is elsewhere in the body, the appearance is variable. You might see bilateral homogeneous masses. For the purposes o f the exam, just knowing you can get it in the parotid (primary or secondary) and the relationship with Sjogrens is probably all you need.

Question 908

Sjo gren s

Answer 908

Autoimmune lymphocyte-induced destruction o f the gland. “Dry Eyes and Dry Mouth.” Typically seen in women in their 60s. Increased risk (like lOOOx) risk o f non-Hodgkins MALT type lymphoma. There is a honeycombed appearance o f the gland.

Question 909

Benign L ym p h o e p ith e lia l D is e ase :

Answer 909

You have bilateral mixed solid and cystic lesions with diffusely enlarged parotid glands. This is seen in HIV. The condition is painless (unlike parotitis - which can enlarge the glands).

Question 910

A c u te P a ro titis :

Answer 910

Obstruction o f flow o f secretions is the most common cause. They will likely show you a stone (or stones) in Stensen’s duct, which will be dilated. The stones are calcium phosphate. Post infectious parotitis is usually bacterial. Mumps would be the most common viral cause. As a point o f trivia, sialography is contraindicated in the acute setting.

Question 911

Parapharyngeal Space overview

Answer 911

``` Also referred to as the “pre-styloid” parapharyngeal space - for the purpose of fucking with you. The primary utility o f the space is when it is displaced (discussed below). ```

Question 912

Parapharyngeal Space spread

Answer 912

``` Mets and infections can spread directly in a vertical direction through this space (squamous cell cancer from tonsils, tongue, and larynx). ```

Question 913

Parapharyngeal Space cystic mass

Answer 913

``` A cystic mass in this location could be an atypical 2nd Branchial Cleft Cyst (but is more likely a necrotic lymph node). ```

Question 914

Parapharyngeal Space borders

Answer 914

``` The parapharyngeal space is bordered on four sides by different spaces. If you have a mass dead in the middle, it can be challenging to tell where it’s coming from. Using the displacement o f fat, you can help problem solve. Much more important than that, this lends itself very well to multiple choice. ```

Question 915

Parapharyngeal Fat (PPF) Displacement

Answer 915

Carotid Space = Anterior Displacement Parotid Space = Medial Displacement ``` Masticator Space = Posterior Medial Displacement ``` ``` Superficial Mucosal Space = Lateral Displacement ```

Question 916

The parapharyngeal | space is primarily a

Answer 916

ball of fat with a few branches of the trigeminal nerves, and the pterygoid veins

Question 917

Carotid Space overview

Answer 917

The carotid space is also sometimes called the “post styloid” or “retro-styloid’' parapharyngeal space — for the purpose of fucking with you. ``` Although it is worth noting that this space is commonly involved in secondary spread of aggressive multi-spatial disease - such as infectious path (necrotizing otitis external) or malignant spread (nasopharyngeal, squamous cell etc..). Metastatic squamous cell is what you should think for nodal disease in this region ```

Question 918

Carotid Space 3 classic tumors

Answer 918

1) Paraganglioma (2) Schwannoma (3) Ncurofibroma

Question 919

Carotid Space contains

Answer 919

``` " Carotid artery ■ Jugular vein ■ Portions o f CN 9, CN 10, CN 11 ■ Internal jugular chain lymph node ```

Question 920

Carotid Space | paraganglioma

Answer 920

There are three different ones worth knowing about - based on location. The imaging features are the same. They are hypervascular (intense tumor blush), with a “Salt and Pepper” appearance on MRI from the flow voids. They can be multiple and bilateral in familial conditions (10% bilateral, 10% malignant, etc.). ,n In-octreotide accumulates in these tumors (receptors for somatostatin).

Question 921

Carotid Space schwannoma

Answer 921

Most commonly in this location we are talking about vagal nerve (CN 10), but if the lesion is pretty high up near the skull base it could also be involving CN 9, 11, or even 12. The typical MR appearance is an oval mass, heterogenous (cystic and sold parts) with heterogenous bright signal on T2. These things enhance a ton (at least the solid parts anyway). They enhance so much you might even think they were vascular. Ironically, schwannomas are considered hypo vascular lesions and the only reason they enhance is because o f extravascular leakage (and poor venous drainage).

Question 922

Carotid Space neruofibroma

Answer 922

These are less common than the schwannoma. About 10% o f the time they are related to NF-1 (in which case you should expect them to be bilateral and multiple). In contrast to schwannomas they tend to be more homogenous, and demonstrate the classic target sign on T2 with decreased central signal.

Question 923

Carotid Space paraganglioma Carotid Body Tumor

Answer 923

Carotid Bifurcation (Splaving ICA and EC A)

Question 924

Carotid Space paraganglioma Glomus Jugulare

Answer 924

Skull Base (often with destruction o f jugular fo ram en ) Middle Ear Floor Destroyed = Glomus Jugulare

Question 925

Carotid Space paraganglioma Glomus Vagale

Answer 925

Above Carotid Bifurcation, but below the Jugular Foramen

Question 926

Carotid Space paraganglioma Glomus Tympanicum

Answer 926

``` Confined to the middle ear. Buzzword is “overlying the cochlear promontory. ” Middle Ear Floor Intact = Glomus Tympanum ```

Question 927

Carotid space Surgical Planning Trivia

Answer 927

``` • Distance of Skull Base ( > 1 cm = Neck Dissection) • Degree of Vascularity (might need preembolization) • Relationship to the Carotid (Don’t Fuck with Big Red) ```

Question 928

Neurofibroma quick

Answer 928

``` Mildly Heterogenous Enhancement T2: Target Sign (bright rim, dark middle) NF-1 Association ```

Question 929

Schwannoma quick

Answer 929

``` Although they enhance intensely they are not vascular on Angio T2: Moderate to High Signal - Heterogenous NF-2 Association ```

Question 930

Paraganglioma quick

Answer 930

``` Hypervascular (tumor blush on angio) T2: Light Bulb Bright with Salt and Pepper (flow voids) ' "In-Octreotide avid ```

Question 931

Lemierre’s Syndrome

Answer 931

This is a thrombophlebitis of the jugular veins with septic emboli in the lung. It’s found in the setting of oropharyngeal infection (pharyngitis, tonsillitis, peritonsillar abscess) or recent ENT surgery. Buzzword bacteria = “Fusobacterium Necrophorum”

Question 932

Grisel’s Syndrome

Answer 932

Torticollis with atlanto-axial joint inflammation seen in H&N surgery or retropharyngeal abscess

Question 933

Pleomorphic A denoma (benign m ixed tum o r)

Answer 933

This is the most common major (and minor) salivary gland tumor. It occurs most commonly in the parotid, but can also occur in the submandibular or sublingual glands. 90% o f these tumors occur in the superficial lobe. They are commonly T2 bright, with a rim o f low signal. They have a small malignant potential and are treated surgically.

Question 934

Pleomorphic A denoma (benign m ixed tum o r) superficial vs deep

Answer 934

Involvement o f the superficial (lateral to the facial nerve) or deep (medial to the facial nerve) lobe is critical to the surgical approach. A line is drawn connecting the lateral surface o f the posterior belly o f the digastric muscle and the lateral surface o f the mandibular ascending ramus to separate superficial from deep

Question 935

Pleomorphic A denoma (benign m ixed tum o r) resection

Answer 935

Apparently, if you resect these like a clown you can spill them, and they will have a massive, ugly recurrence.

Question 936

Major Salivary Glands:

Answer 936

* Parotid * Submandibular * Sublingual

Question 937

Minor Salivary Glands

Answer 937

• Literally 100s of unnamed | minor glands

Question 938

Warthins

Answer 938

This is the second most common benign tumor. This one ONLY occurs in the parotid gland. This one is usually cystic, in a male, bilateral (15%), and in a smoker. As a point o f total trivia, this tumor takes up pertechnetate (it’s basically the only tumor in the parotid to do i t , ignoring the ultra rare parotid oncocytoma).

Question 939

M u coepide rm oid C a rc in om a

Answer 939

This is the most common malignant tumor of minor salivary glands. The general rule is - the smaller the gland, the more common the malignant tumors; the bigger the gland, the more common the benign tumors. There is a variable appearance based on the histologic grade. There is an association with radiation.

Question 940

Adenoid Cys tic C a rc in om a

Answer 940

This is another malignant salivary gland tumor, which favors minor glands but can be seen in the parotid. The number one thing to know is perineural spread. This tumor likes perineural spread.

Question 941

N e rv e S h e a th Tumo rs Masticator Space

Answer 941

Since you have a nerve, you can have a schwannoma or neurofibroma of V3. Remember the schwannoma is more likely to cause the foramina expansion vs perineural tumor spread.

Question 942

Adenoid Cys tic C a rc in om a Pearl

Answer 942

I used to think that perineurial tumor spread would widen a neural foramen (foramen ovale for example). It’s still m ight... but it’s been my experience that a nerve sheath tumor (schwannoma) is much more likely to do that. Let’s ju st say for the purpose o f multiple choice that neural foramina widening is a schwannoma - unless there is overwhelming evidence to the contrary

Question 943

Lymphoma (parotid)

Answer 943

Because the parotid has lymph nodes (it’s the only salivary gland that does), you can get lymphoma in the parotid (primary or secondary). If you see it and it’s bilateral, you should think Sjogrens. Sjogrens patients have a big risk (like lOOOx) o f parotid lymphoma. Like lymphoma is elsewhere in the body, the appearance is variable. You might see bilateral homogeneous masses. For the purposes o f the exam, just knowing you can get it in the parotid (primary or secondary) and the relationship with Sjogrens is probably all you need.

Question 944

Sjo gren s

Answer 944

Autoimmune lymphocyte-induced destruction o f the gland. “Dry Eyes and Dry Mouth.” Typically seen in women in their 60s. Increased risk (like lOOOx) risk o f non-Hodgkins MALT type lymphoma. There is a honeycombed appearance o f the gland.

Question 945

Benign L ym p h o e p ith e lia l D is e ase :

Answer 945

You have bilateral mixed solid and cystic lesions with diffusely enlarged parotid glands. This is seen in HIV. The condition is painless (unlike parotitis - which can enlarge the glands).

Question 946

A c u te P a ro titis :

Answer 946

Obstruction o f flow o f secretions is the most common cause. They will likely show you a stone (or stones) in Stensen’s duct, which will be dilated. The stones are calcium phosphate. Post infectious parotitis is usually bacterial. Mumps would be the most common viral cause. As a point o f trivia, sialography is contraindicated in the acute setting.

Question 947

Parapharyngeal Space overview

Answer 947

``` Also referred to as the “pre-styloid” parapharyngeal space - for the purpose of fucking with you. The primary utility o f the space is when it is displaced (discussed below). ```

Question 948

Parapharyngeal Space spread

Answer 948

``` Mets and infections can spread directly in a vertical direction through this space (squamous cell cancer from tonsils, tongue, and larynx). ```

Question 949

Parapharyngeal Space cystic mass

Answer 949

``` A cystic mass in this location could be an atypical 2nd Branchial Cleft Cyst (but is more likely a necrotic lymph node). ```

Question 950

Parapharyngeal Space borders

Answer 950

``` The parapharyngeal space is bordered on four sides by different spaces. If you have a mass dead in the middle, it can be challenging to tell where it’s coming from. Using the displacement o f fat, you can help problem solve. Much more important than that, this lends itself very well to multiple choice. ```

Question 951

Parapharyngeal Fat (PPF) Displacement

Answer 951

Carotid Space = Anterior Displacement Parotid Space = Medial Displacement ``` Masticator Space = Posterior Medial Displacement ``` ``` Superficial Mucosal Space = Lateral Displacement ```

Question 952

The parapharyngeal | space is primarily a

Answer 952

ball of fat with a few branches of the trigeminal nerves, and the pterygoid veins

Question 953

Carotid Space overview

Answer 953

The carotid space is also sometimes called the “post styloid” or “retro-styloid’' parapharyngeal space — for the purpose of fucking with you. ``` Although it is worth noting that this space is commonly involved in secondary spread of aggressive multi-spatial disease - such as infectious path (necrotizing otitis external) or malignant spread (nasopharyngeal, squamous cell etc..). Metastatic squamous cell is what you should think for nodal disease in this region ```

Question 954

Carotid Space 3 classic tumors

Answer 954

1) Paraganglioma (2) Schwannoma (3) Ncurofibroma

Question 955

Carotid Space contains

Answer 955

``` " Carotid artery ■ Jugular vein ■ Portions o f CN 9, CN 10, CN 11 ■ Internal jugular chain lymph node ```

Question 956

Carotid Space | paraganglioma

Answer 956

There are three different ones worth knowing about - based on location. The imaging features are the same. They are hypervascular (intense tumor blush), with a “Salt and Pepper” appearance on MRI from the flow voids. They can be multiple and bilateral in familial conditions (10% bilateral, 10% malignant, etc.). ,n In-octreotide accumulates in these tumors (receptors for somatostatin).

Question 957

Carotid Space schwannoma

Answer 957

Most commonly in this location we are talking about vagal nerve (CN 10), but if the lesion is pretty high up near the skull base it could also be involving CN 9, 11, or even 12. The typical MR appearance is an oval mass, heterogenous (cystic and sold parts) with heterogenous bright signal on T2. These things enhance a ton (at least the solid parts anyway). They enhance so much you might even think they were vascular. Ironically, schwannomas are considered hypo vascular lesions and the only reason they enhance is because o f extravascular leakage (and poor venous drainage).

Question 958

Carotid Space neruofibroma

Answer 958

These are less common than the schwannoma. About 10% o f the time they are related to NF-1 (in which case you should expect them to be bilateral and multiple). In contrast to schwannomas they tend to be more homogenous, and demonstrate the classic target sign on T2 with decreased central signal.

Question 959

Carotid Space paraganglioma Carotid Body Tumor

Answer 959

Carotid Bifurcation (Splaving ICA and EC A)

Question 960

Carotid Space paraganglioma Glomus Jugulare

Answer 960

Skull Base (often with destruction o f jugular fo ram en ) Middle Ear Floor Destroyed = Glomus Jugulare

Question 961

Carotid Space paraganglioma Glomus Vagale

Answer 961

Above Carotid Bifurcation, but below the Jugular Foramen

Question 962

V o c a l Cord P a ra ly s is buzzword

Answer 962

“Hoarseness” - If you see “Hoarseness” in the question header, you need to dkjpO think recurrent laryngeal nerve compression in the AP Window - either from a mass/node or aortic path. *Hoarseness is also a classic Laryngeal CA buzzword (so look there too).

Question 963

Carotid space Surgical Planning Trivia

Answer 963

``` • Distance of Skull Base ( > 1 cm = Neck Dissection) • Degree of Vascularity (might need preembolization) • Relationship to the Carotid (Don’t Fuck with Big Red) ```

Question 964

Neurofibroma quick

Answer 964

``` Mildly Heterogenous Enhancement T2: Target Sign (bright rim, dark middle) NF-1 Association ```

Question 965

Schwannoma quick

Answer 965

``` Although they enhance intensely they are not vascular on Angio T2: Moderate to High Signal - Heterogenous NF-2 Association ```

Question 966

Paraganglioma quick

Answer 966

``` Hypervascular (tumor blush on angio) T2: Light Bulb Bright with Salt and Pepper (flow voids) ' "In-Octreotide avid ```

Question 967

Lemierre’s Syndrome

Answer 967

This is a thrombophlebitis of the jugular veins with septic emboli in the lung. It’s found in the setting of oropharyngeal infection (pharyngitis, tonsillitis, peritonsillar abscess) or recent ENT surgery. Buzzword bacteria = “Fusobacterium Necrophorum”

Question 968

Grisel’s Syndrome

Answer 968

Torticollis with atlanto-axial joint inflammation seen in H&N surgery or retropharyngeal abscess

Question 969

Masticator Space

Answer 969

As the name implies this space contains the muscles o f mastication (masticator, temporalis, medial and lateral pterygoids). Additionally, you have the angle and ramus of the mandible, plus the inferior alveolar nerve (branch o f V3). A trick to be aware o f is that the space extends superiorly along the side o f the skull via the temporalis muscle. So, aggressive neoplasm or infection may ride right up there

Question 970

Masticator Space lesions displace

Answer 970

the Parapharyngeal Fat | POSTERIOR and MEDIAL

Question 971

Masticator Space: key point

Answer 971

Congenital Stuff and Aggressive Infection/ Cancer tends to be Trans- Spatial.

Question 972

Masticator Space ddx

Answer 972

O d o n to g en ic In fe c tio n S a rcom a s C av e rnou s H em a n g iom a s P e rin e u ra l S p re ad N e rv e S h e a th Tumo rs

Question 973

O d o n to g en ic In fe c tio n Masticator Space

Answer 973

In an adult, this is the most common cause of a masticator space mass. If you see a mass here, the next move should be to look at the mandible on bone windows. Just in general, you should be on the look out for spread via the pterygopalatine fossa to the orbital apex and cavernous sinus. The relationship with the mylohyoid makes for good trivia - as discussed above.

Question 974

S a rcom a s Masticator Space

Answer 974

In kids, you can run into nasty angry masses like Rhabdomyosarcomas, from the bone of the mandible (chondrosarcoma favors the TMJ

Question 975

C av e rnou s H em a n g iom a s Masticator Space

Answer 975

These can also occur, and are given away by the presence of phlcboliths. Venous or lymphatic malformations may involve multiple compartments / spaces.

Question 976

P e rin e u ra l S p re ad Masticator Space

Answer 976

You can have perineural spread from a head and neck primary along V3. When I say ''perineural spread” you should think two things: ( 1) Adenoid Cystic Carcinoma of the minor salivary gland (2) Melanoma

Question 977

N e rv e S h e a th Tumo rs Masticator Space

Answer 977

Since you have a nerve, you can have a schwannoma or neurofibroma of V3. Remember the schwannoma is more likely to cause the foramina expansion vs perineural tumor spread.

Question 978

Retropharyngeal Space / Danger Space

Answer 978

The retropharyngeal space has some complex anatomy. Simplified, this is a midline space, deep to the oral & nasal pharynx. The retropharyngeal space has an anterior “true” space which extends caudal to around C6-C7, and a more posterior “danger space” - which is dangerous because it listens to rap music and plays first person shooter video games - plus it extends into the mediastinum - so you could potentially dump pus, or cancer, right into the mediastinum

Question 979

Infectious behind this deep cervical fascia (the Prevertebral Space)

Answer 979

are different than the ones | discussed below in that they are not spread from the neck but instead the spine/disc (osteomyelitis

Question 980

Retropharyngeal Space / Danger Space In fe c tio n

Answer 980

Involvement o f the retropharyngeal space most often occurs from spread from the tonsillar tissue. You are going to have centrally low density tissue and stranding in the space. You should evaluate for spread o f infection into the mediastinum. ``` Don 'I Forget: Delays are often critical for differentiate phlegmon and drainable abscess ```

Question 981

Retropharyngeal Space / Danger Space N e c ro tic N ode s

Answer 981

``` (nodes o f Rouviere) - These things are located in the lateral retropharyngeal region. In kids you can see suppurative infection in these, but around age 4 they start to regress - so adults are actually much less to get infection in this region. Now, you can still get mets (squamous cell, papillary thyroid, etc..). Lymphoma can involve these nodes as well - but won’t be necrotic until treated. ```

Question 982

SCC and infrahyoid neck

Answer 982

When you are talking about head and neck cancer, you are talking about squamous cell cancer. Now, this is a big complex topic and requires a fellowship to truly understand / get good at. Obviously, the purpose o f this book is to prepare you for multiple choice test questions not teach you practical radiology. If you want to actually learn about head and neck cancer in a practical sense you can try and find a copy o f Hamsberger’s original

Question 983

Lymph node anatomy testable trivia

Answer 983

Anterior Belly o f Digastric separates 1A from 1B Stylohyoid muscle (posterior submandibular gland) separates 1B from 2A Jugular Vein (Spina! Accessory Nerve) separates 2A from 2B *see below Vertical borders: 2-3 = Lower Hyoid 3-4= lower cricoid

Question 984

Lymph node anatomy 2A

Answer 984

Anterior, Medial, Lateral or Abutting the Posterior Internal Jugular

Question 985

Lymph node anatomy 2B

Answer 985

Posterior to the Internal Jugular, with a clear fat plane between node and IJ

Question 986

Floor o f th e M outh SCC

Answer 986

touched on this once already. Just remember smoker/drinker in an old person. HPV in a young person. Necrotic level 2 nodes can be a presentation (not a branchial cleft cyst).

Question 987

N a s o p h a ryn g e a l SCC:

Answer 987

``` This is more common in Asians and has a bi-modal distribution: • group 1 (15-30) typically Chinese • group 2 (> 40). Involvement o f the parapharyngeal space results in worse prognosis (compared to nasal cavity or oropharynx invasion). ```

Question 988

Fossa of Rosenmuller

Answer 988

The FOR is the MOST COMMON location for | Nasopharyngeal Cancer

Question 989

``` See a Unilateral Mastoid Effusion or See a Pathologic Retropharyngeal Node ```

Answer 989

Look at the FOR “Earliest Sign ” o f nasopharyngeal SCC is the effacement o f the fat within the FOR.

Question 990

“Earliest Sign ” o f nasopharyngeal SCC is | the

Answer 990

“Earliest Sign ” o f nasopharyngeal SCC is | the effacement o f the fat within the FOR.

Question 991

See a Pathologic Retropharyngeal or Supraclavicular Node

Answer 991

Look at the Clivus About 30% o f the patients with nasopharyngeal tumors have skull base erosion. (MR1 ^ CT for skull base invasion) Nodal mets are present in 90% o f nasopharyngeal tumors, with the retropharyngeal nodes usually the first involved.

Question 992

Nek anatomy page 153

Answer 992

go there now pictures on phone from 7/15/21

Question 993

L a ry n g o c e le

Answer 993

When the laryngeal “saccule” dilates with air you call it a laryngocele. If it is filled with fluid you still might call it a larygocele (but if saccular cyst is a choice - consider that). If it is filled with fluid and air you still might call it a larygocele (but it laryngopyocele is a choice — and you have any hint of infection - consider that

Question 994

L a ry n g o c e le what is a saccule

Answer 994

The “saccule” is the appendix of the laryngeal ventricle (a blind ending sac that extends anterior and upwards). It’s usually closed or minimally filled with fluid (you don’t typically see it in normal adults).

Question 995

L a ry n g o c e le why does a saccule dilate

Answer 995

Usually because it’s obstructed (ballvalve mechanics at the neck of the saccule), and the testable point is that 15% of the time that obstruction is a tumor. You can also see them in forceful blowers (trumpet players, glass blowers) — well maybe, this depends on what you read. Simply read the mind of the question writer to know if they are on team trumpet player laryngocele.

Question 996

L a ry n g o c e le : internal vs external

Answer 996

ointernal vs external version of this (based on containment of violation of the thyrohyoid membrane).

Question 997

V o c a l Cord P a ra ly s is

Answer 997

The involved side will have an expanded ventricle (it’s the opposite side with a cancer). If you see it on the left, a good “next step” question would be to look at the chest (for recurrent laryngeal nerve involvement at the AP window).

Question 998

V o c a l Cord P a ra ly s is buzzword

Answer 998

“Hoarseness” - If you see “Hoarseness” in the question header, you need to dkjpO think recurrent laryngeal nerve compression in the AP Window - either from a mass/node or aortic path. *Hoarseness is also a classic Laryngeal CA buzzword (so look there too).

Question 999

■gG4- Orbit Lymphocytic Hypophysitis:

Answer 999

``` This is histologically the same thing as orbital pseudotumor but instead involves the cavernous sinus. It is painful (just like pseudotumor), and presents with multiple cranial nerve palsies. It responds to steroids (just like pseudotumor). ```

Question 1000

laryngeal Cancer Risk Factors

Answer 1000

``` Smoking, Alcohol, Radiation, Laryngeal Keratosis, HPV, GERD, & Blasphemy against the correct religion (false religions are safe to talk shit about). ```

Question 1001

laryngeal Cancer role

Answer 1001

The role of the Radiologist is not to make the primary cancer diagnosis here, but to assist in staging. Laryngeal cancers are subdivided into (a) supraglottic, (b) glottic, and (c) subglottic types. “Transglottic” would refer to an aggressive cancer that crosses the laryngeal ventricle.

Question 1002

laryngeal Cancer Supra-Glottic

Answer 1002

-More Aggressive -Early Lymph Node Mets -They do n ’t get hoarseness

Question 1003

laryngeal Cancer Supra-Glottic: Epiglottic Centered

Answer 1003

-Anterior -Likes to Invade the Pre- Epigolttic Space /Fat (which is rich in lymphatics

Question 1004

laryngeal Cancer Supra-Glottic: False Cord / Fold Centered

Answer 1004

-Posterior Lateral -Likes to Invade the Para- Glottic Space /Fat (which communicates superiorly with the Pre-Epiglottic Space

Question 1005

laryngeal Cancer Glottic

Answer 1005

-Most Common -Best Outcome -Grow Slowly -Metastatic Disease is Late

Question 1006

laryngeal Cancer Sub-Glottic

Answer 1006

-Least Common -Often small compared to nodal burden -Bilateral nodal disease & mediastinal extension

Question 1007

laryngeal Cancer Paraglottic space involvement makes the tumor

Answer 1007

T3 and "transglottic: ” *Best seen in coronals.

Question 1008

laryngeal Cancer Fixation of the cords indicates at least a

Answer 1008

``` T3 tumor - this is best assessed with a scope but can be suspected with disease in the cricoarytenoid joint. ```

Question 1009

laryngeal cancer Invasion of the cricoid cartilage

Answer 1009

``` is a contraindication to all types of laryngeal conservation surgery (cricoid cartilage is necessary for postoperative stability of the vocal cords). ```

Question 1010

Laryngeal cancer The only reliable sign of cricoid invasion is

Answer 1010

tumor on both sides of the cartilage (irregular sclerotic cartilage can be normal).

Question 1011

Retinob la stoma

Answer 1011

This is the most common primary malignancy o f the globe. If you see calcification in the globe of a child - this is the answer.

Question 1012

Retinob la stoma globe size

Answer 1012

The globe should be normal in size (or bigger), where Coats’ is usually smaller. It’s usually seen before age 3 (rare after age 6). The trivia is gonna be where else it occurs. They can be bilateral (both eyes - 30%), trilateral (both eyes and the pineal gland), and quadrilateral (both eyes, pineal, and suprasellar).

Question 1013

Retinob la stoma step 1

Answer 1013

The step 1 question is RB suppressor gene (chromosome 13 — “unlucky 13”). That’s the same chromosome osteosarcoma patients have issues with and why these guys are at increased risk o f facial osteosarcoma after radiation

Question 1014

C o a ts ’ D is e a s e

Answer 1014

The cause o f this is retinal telangiectasia which results in leaky blood and subretinal exudate. It can lead to retinal detachment. It’s seen in young boys and typically unilateral. The key detail is that it is NOT CALCIFIED (retinoblastoma is).

Question 1015

C o a ts ’ D is e a s e imaging

Answer 1015

CT - Dense T1 - Hyper T2 - Hyper

Question 1016

Coats disease has a smaller globe. Retinoblastoma has a

Answer 1016

normal sized globe.

Question 1017

P e rs is te n t H y p e rp la s tic P rim a ry V itre o u s (PH P V ) -

Answer 1017

This is a failure o f the embryonic ocular blood supply to regress. It can lead to retinal detachment. The classic look is a small eye (microphthalmia) with increased density of the vitreous. No calcification

Question 1018

Retinal Detachment

Answer 1018

This can occur secondary to PHPV or Coats. It can also be caused by trauma, sickle cell, or just old age. The imaging finding is a “V” or “Y” shaped appearance due to lifted up retinal leaves and subretinal fluid.

Question 1019

Globe Size Comparison | - A Strategy’ for Eliminating Distractors

Answer 1019

``` Retinoblastoma - Normal Size * PH P V - Small Size (Normal Birth Age) Toxocariasis - Normal Size * Retinopathy o f Prematurity - Bilateral Small Coats’ - Smaller Size ```

Question 1020

Orbit Melanoma

Answer 1020

This is the most common intra-occular lesion in an adult. If you see an enhancing soft tissue mass in the back o f an adult’s eye this is the answer.

Question 1021

Melanoma questions

Answer 1021

(1) show a picture - what is it?, (2) ask what the most common intra-occular lesion in an adult is? (3) ask the buzzword "collar button sh a p ed ’’ ? - which is related to Bruch’s membrane, (4) strong predilection for liver mets - next step Liver MR.

Question 1022

O p tic N e rv e Glioma

Answer 1022

These almost always (90%) occur under the age o f 20. You see expansion / enlargement o f the entire nerve. If they are bilateral you think about NF-1. They are most often WHO grade 1 Pilocytic Astrocytomas. If they are sporadic they can be GBMs and absolutely destroy you.

Question 1023

O p tic N e rv e S h e a th M en in g iom a

Answer 1023

The buzzword is "tram-track” calcifications. Another buzzword is “doughnut” appearance, with circumferential enhancement around the optic nerve.

Question 1024

Dermoid optic

Answer 1024

This is the most common benign congenital orbital mass. It’s usually superior and lateral, arising from the frontozygomatic suture, and presenting in the first 10 years o f life. It’s gonna have fat in it (like

Question 1025

Rhabdomyosarcoma orbital

Answer 1025

Most common extra-occular orbital malignancy in children (dermoid is most common benign orbital mass in child). Favors the superior-medial orbit and classically has bone destruction. Just think “bulky orbital mass in a 7 year old.” When they do occur - 40% o f the time it’s in the head and neck - and then most commonly it’s in the orbit. It’s still rare as hell.

Question 1026

Stenosis sagittal view

Answer 1026

vertebral body / spinal canal < 0.85

Question 1027

M e ta s ta tic N eu ro b la s tom a

Answer 1027

This has a very classic appearance of “Raccoon Eyes” on | physical exam.

Question 1028

M e ta s ta tic N eu ro b la s tom a classic location

Answer 1028

The classic location is periorbital tumor infiltration with associated proptosis. Don’t forget a basilar skull fracture can also cause Raccoon Eyes... so clinical correlation is advised. Neuroblastoma mets tend to be more

Question 1029

M e ta s ta tic N eu ro b la s tom a Worth mentioning

Answer 1029

Another thing worth mentioning is the bony involvement of the greater wing of the sphenoid. Neuroblastoma is gonna be bilateral. Ewings favors this location also - but will be unilateral.

Question 1030

M e ta s ta tic Scirrhous (fibrosing) | B re a s t C a n c e r -

Answer 1030

This is classic gamesmanship here. The important point to know is that unlike primary orbital tumors that are going to cause proptosis, classically the breast cancer met causes a desmoplastic reaction and enophthalmos (posterior displacement o f the globe).

Question 1031

M e ta s ta tic Scirrhous (fibrosing) B re a s t C a n c e r - Trivia

Answer 1031

Trivia: Mets are actually more common to the eye | relative to the orbit (like 8x more common).

Question 1032

Infiltrative retrobulbar mass + | enophthalmos

Answer 1032

scirrhous carcinoma | of the breast

Question 1033

■gG4- Orbit Orbital Pseudotumor

Answer 1033

``` This is one of those IgG4 idiopathic inflammatory conditions that involves the extraoccular muscles. It looks like an expanded muscle. The things to remember are that this thing is painful, unilateral, it most commonly involves the lateral rectus and it does NOT spare the myotendinous insertions. Remember that Graves does not cause pain, and does spare the myotendinous insertions. It gets better with steroids. It’s classically T2 dark. ```

Question 1034

■gG4- Orbit Tolosa Hunt Syndrome

Answer 1034

``` This is histologically the same thing as orbital pseudotumor but instead involves the cavernous sinus. It is painful (just like pseudotumor), and presents with multiple cranial nerve palsies. It responds to steroids (just like pseudotumor). ```

Question 1035

■gG4- Orbit Lymphocytic Hypophysitis:

Answer 1035

``` This is histologically the same thing as orbital pseudotumor but instead involves the cavernous sinus. It is painful (just like pseudotumor), and presents with multiple cranial nerve palsies. It responds to steroids (just like pseudotumor). ```

Question 1036

Thyroid Orbitopathy

Answer 1036

This is seen in 1 /4th o f the Graves cases and is the most common cause o f exophthalmos. The antibodies that activate TSH receptors also activate orbital fibroblasts and adipocytes.

Question 1037

Thyroid Orbitopathy things to know

Answer 1037

``` Things to know: Risk of compressive optic neuropathy • Enlargement o f ONLY MUSCLE BELLY (spares tendon) - different than pseudo tumor NOT Painful - different than pseudo tumor Order of Involvement: IR > MR > SR > LR > SO/IO Inferior, Middle, Superior, Lateral, Oblique ```

Question 1038

Thyroid Orbitopathy spares

Answer 1038

tendon insertion

Question 1039

Orbital Vascular Malformations Lymphangioma

Answer 1039

``` These arc actually a mix of venous and lymphatic malfonnations. They arc illdefined and lack a capsule. The usual distribution is infiltrative (multi-spatial), involving, preseptal, post-septal, extraconal, and intraconal locations. Fluid-Fluid levels are the most classic finding , with regard to multiple choice. Do NOT distend with provocative maneuvers (valsalva). ```

Question 1040

Orbital Vascular Malformations Varix

Answer 1040

``` These occur secondary to weakness in the post-capillary venous wall (gives you massive dilation of the valvclcss orbital veins). Most likely question is going to pertain to the fact that they distend with provocative maneuvers (valsalva, hanging head, etc...). Another piece of trivia is that they are the most common cause o f spontaneous orbital hemorrhage. They can thrombose and present with pain. ```

Question 1041

Orbital Vascular Malformations Carotid-Cavernous Fistula

Answer 1041

``` These come in two flavors: (1) Direct - which is secondary to trauma, and (2) Indirect - which just occurs randomly in post menopausal women. The direct kind is a communication between the intracavemous ICA and cavernous sinus. The indirect kind is usually a dural shunt between meningeal branches of the ECA and the Cavernous Sinus. Buzzword: Pulsatile Exophthalmos *although this can also be a buzzword fo r NF-1 in the setting o f sphenoid wing dysplasia. ```

Question 1042

Intraconal | Space

Answer 1042

is the space inside the rectus muscle pyramid.

Question 1043

Extraconal | Space

Answer 1043

is the space outside the rectus muscle pyramid

Question 1044

Pre-SeptalI Post-Septal Cellulitis

Answer 1044

As above, location of orbital infections are described by their relationship to the orbital septum. The testable trivia is probably (1) that the orbital septum originates from the periosteum of the orbit and inserts in the palpebral tissue along the tarsal plate, (2) that pre-septal infections usually start in adjacent structures (likely teeth and the face), (3) post-septal infections are usually from paranasal sinusitis, and (4) pre-septal infections are treated medically, post septal is surgical

Question 1045

Pre-SeptalI Post-Septal Cellulitis trivia

Answer 1045

Periorbital abscess can cause thrombosis of the ophthalmic veins or cavernous sinus (in extreme examples infection — usually aspergillosis — can even cause a cavemous-carotid fistula).

Question 1046

Dacryocystitis

Answer 1046

This is inflammation and dilation of the lacrimal sac. It has an Aunt Minnie look, with a well circumscribed, round rim enhancing lesion centered in the lacrimal fossa. The etiology is typically obstruction followed by bacterial infection (staph and strep). Usually this is diagnosed clinically unless there is an associated peri-orbital cellulitis in which can CT is needed to exclude post septal infection (treated surgically) from simple dacryocystitis (treated non-surgically).

Question 1047

Orbital Subperiosteal Abscess

Answer 1047

If you get inflammation under the periosteum it can progress to abscess formation. This is usually associated with ethmoid sinusitis. This also has a very classic look

Question 1048

Optic Neuritis:

Answer 1048

There will be enhancement of the optic nerve, without enlargement of the nerve/ sheath complex. Usually (70%) unilateral, and painful. You will often see intracranial or spinal cord demyelination - in the setting o f Devics (neuromyelitis optica). 50% of patient’s with acute optic neuritis will develop MS

Question 1049

If the optic nerve is enlarged, think

Answer 1049

glioma... then think NF-1.

Question 1050

Papilledema:

Answer 1050

This is really an eye exam thing. | Having said that you can sometimes see dilation/ swelling o f the optic nerve sheath.

Question 1051

Drusen

Answer 1051

Mineralization at the optic disc. Supposedly there is an association with age-related maculopathy

Question 1052

NOT Legit Indications for Fluoro Guided LP — all o f which I ’ve heard:

Answer 1052

• “The patient is crazy” • “The patient is crazy & violent” • “The patient is crazy, violent, and has high viral load HIV.... and Hep C” • “The patient recently escaped a locked mental institution for the extremely violent and criminally insane, has both HIV and Hep C. He spits like a camel and has really terrible body odor.”

Question 1053

``` Ectopia Lentis (lens dislocation) ```

Answer 1053

Causes include Trauma, Marfans, and Homocystinuria

Question 1054

Coloboma

Answer 1054

This is a focal discontinuity o f the globe (failure o f the choroid fissure to close). They are usually posterior. If you see a unilateral one - think sporadic. If you see bilateral ones - think CHARGE (coloboma, heart, GU, ears).

Question 1055

Cord Blood Supply

Answer 1055

There is an anterior blood supply and a posterior blood supply to the cord. These guys get taken out with different clinical syndromes

Question 1056

Anterior spinaI artery

Answer 1056

arises bilaterally as two small branches at the level o f the termination of the vertebral arteries. These two arteries join around the level o f the foramen magnum.

Question 1057

Artery o f Adamkiewicz

Answer 1057

This is the most notable Anterior reinforcer o f the anterior spinal artery. In 75% of people it comes off the left side of the aorta between T8 and Ti l . It supplies the lower 2/3 of the cord. This thing can get covered with the placement of an endovascular stent graft for aneurysm or dissection repair leading to spine infarct.

Question 1058

Posterior Spinal Artery

Answer 1058

Paired arteries which arise either from the vertebral arteries or the posterior inferior cerebellar artery. Unlike anterior spinal artery this one is somewhat * discontinuous and reinforced by\ multiple segmental or radiculopial branches.

Question 1059

Conus Medullaris

Answer 1059

This is the terminal end of the spinal cord. It usually terminates at around L I. Below the inferior endplate of the L2 / L3 body should make you think tethered cord (especially if shown in a multiple choice setting).

Question 1060

Epidural Fat

Answer 1060

The epidural fat is not evenly distributed. The epidural space in the cervical cord is predominantly filled with venous plexus (as opposed to fat). In the lumbar spine there is fat both anterior and posterior to the cord. "Epidural Lipomatosis ” = is a hypertrophy of this fat that only occurs with patients on steroids (“on corticosteroids” would be a huge clue).

Question 1061

Stenos is

Answer 1061

Stenos is : Spinal stenosis can be congenital (associated with short pedicles) or be acquired. The Torg-Pavlov ratio can be used to call it (cervical canal diameter to vertebral body width < 0.85). Symptomatic stenosis is more common in the cervical spine (versus the thoracic spine or lumbar spine). You can get some congenital stenosis in the lumbar spine from short pedicles, but it’s generally not symptomatic until middle age

Question 1062

Stenosis sagittal view

Answer 1062

vertebral body / spinal canal < 0.85

Question 1063

Spondylosis Deformans

Answer 1063

``` This is probably part of “normal aging” “Degenerative Change” or spine osteoarthritis. This is more rim / margin centered. Process is characterized by osteophyte formation. ```

Question 1064

Intervertebral Osteochondrosis

Answer 1064

Pathologic (but not necessarily symptomatic “Deteriorated Disc” - This process is more centered in the disc space favoring the nucleus pulposus & vertebral body endplates.

Question 1065

Osteophytes:

Answer 1065

``` • More horizontal / oblique with a “claw” like appearance. • Formed also the vertebral margin. . Seen in “DJD” / Spondylosis ```

Question 1066

Syndesmophytes:

Answer 1066

``` • More vertical symmetric, and thinner • Represent ossification of the annulus fibrosis. • Seen in Ankylosing Spondylitis. ```

Question 1067

En d p la te Changes: Commonly referred to as “Modic Changes types

Answer 1067

Type 1 “Edema” T1 Dark, T2 Bright Type 2 “ Fat” T1 Bright, T2 Bright Type 3 “Scar” T1 Dark, T2 Dark

Question 1068

En d p la te Changes: Commonly referred to as “Modic Changes overview

Answer 1068

There is a progression in the MRI signal characteristics that makes sense if you think about it. You start out with degenerative changes causing irritation / inflammation so there is edema (T2 bright). This progresses to chronic inflammation which leads to some fatty change - just like in the bowel o f an IBD patient - causing T1 bright signal. Finally, the whole thing gets burned out and fibrotic and it’s T1 and T2 dark. As a prominent factoid, Type 1 changes look a lot like Osteomyelitis (clinical correlation is recommended).

Question 1069

A n n u la r Fissure:

Answer 1069

``` As the disc ages, it tends to dry out making it more friable and easily tom. “Tears” in the annulus (which are present in pretty much every degenerated disc) aren’t called “tears” but instead “fissures". People who write the papers on this stuff make a big fucking deal about that - with the idea being that “tear” implies pathology. Fissuring can be asymptomatic and part of the aging process. Even though fissures are present in basically every degenerated disc you don’t always see them on MRI. What you do see (some of the time) is a fluid signal gap in the annulus - which has been given the official vocabulary word “High Intensity Zone,” and anything with official vocabulary nomenclature should be respected as possible multiple choice fodder. ```

Question 1070

A n n u la r Fissure: know this

Answer 1070

•Annular fissures may be a source of pain (radial pain fibers - trigger “discogenic pain”) but are also seen as incidentals. »Fissures are found in all degenerative discs but are not all fissures are visualized as HIZs. »Discography is more sensitive to fissures relative to MRI. but still not 100% sensitive. *Also, Dude, “Tear” is not the preferred nomenclature - “Fissure.”

Question 1071

Schm orl Node: | Intravertebral Herniation

Answer 1071

``` This is a herniation of disc material through a defect in the vertebral body endplate into the actual marrow. Common - like 75% of people have them. Classic look is to favor the inferior endplate of the lower thoracic / upper lumbar spine. When they are acute they can have edema on T2 and be dark on Tl - mimicking osteomyelitis. Chronic versions will have a sclerotic rim. ```

Question 1072

S c h e u e rm a n n ’s

Answer 1072

``` This is multiple levels (at least 3) of wedged vertebral bodies with associated Schmorl’s nodes — Most classically the thoracic spine of a teenager, resulting in kyphotic deformity (40 degrees in thoracic or 30 degrees in thoracolumbar). 25% of patients have scoliosis ```

Question 1073

Limbus | V e r te b ra

Answer 1073

``` This is a fracture mimic that is the result of herniated disc material between the nonfused apophysis and adjacent vertebral body. ```

Question 1074

Disc Nomenclature Herniation

Answer 1074

This is the approved verbiage for the displacement of LESS THAN 25% of disc material beyond the limits of the disc space.

Question 1075

E x te n s io n T e a rd ro p list

Answer 1075

Distraction Injury Stable in flexion (unstable in extension) Hyperextension Classic History “Hitfrom behind

Question 1076

Disc Nomenclature Protrusion (subtype of herniation)

Answer 1076

``` Term used when the distance between the edge of the disc herniation is less than the distance between the edges of the base (base wider than herniation ```

Question 1077

Disc Nomenclature Extrusion (subtype of herniation)

Answer 1077

``` Term used when the edges of the disc are greater than the distance of the base (neck narrower than herniation). ```

Question 1078

Disc Nomenclature Sequestration

Answer 1078

Free (broken off) | disc fragment

Question 1079

Disc Nomenclature Localization Cranial Caudal Plane

Answer 1079

Disc Level Suprapedicle Level -Pedicle Level - Infrapedicle Level

Question 1080

Disc Nomenclature Localization Axial Plane

Answer 1080

``` Extra Foraminal Foraminal *Often symptomatic because o f the relationship to the Dorsal Root Ganglia Sub Articular *Most Common Location Central ```

Question 1081

Which Nerve is CompressedP

Answer 1081

There are 31 pairs o f spinal nerves, with each pair corresponding to the adjacent vertebra - the notable exception being the “C8” nerve. Cervical disc herniations are less common than lumbar ones. The question is most likely to take place in the lumbar spine (the same spot most disc herniations occur). In fact more than 90% o f herniations occur at L4-L5, and L5-S1

Question 1082

A foraminal disc will smash the

Answer 1082

exiting nerve

Question 1083

a central or subarticular disc will smash

Answer 1083

the descending nerve

Question 1084

LP / Myelogram Technique Absolute Contraindications

Answer 1084

* Increased intracranial pressure or obstructed CSF flow * Bleeding diathesis (hvpocoagulabilitv) * Myelogram Specific — Iodinated contrast allergy

Question 1085

LP / Myelogram Technique | Prior to the LP A CR-ASNR recommendations

Answer 1085

``` STOP Coumadin 4-5 days STOP Plavix for 7 days Hold LMW Heparin for 12 hours Hold Heparin for 2-4 hours - document normal PTT Aspirin and NSAIDs are fine (not contraindicated) ```

Question 1086

LP / Myelogram Technique Relative Contraindications

Answer 1086

(vary per institution): • Overlying infection, hematoma, or scarring • Myelogram Specific - Recent myelogram (< 1 week) • Myelogram Specific - History o f seizures

Question 1087

Legit Indications for Fluoro Guided LP:

Answer 1087

• Advanced degenerative spondylosis, • Post-surgical changes, • Patient is so fat (“a person of size”), when Dracula sucked his/her blood, he got diabetes. • Myelogram Specific - MRI contraindication • Myelogram Specific - Geriatric Professor Emeritus of Neurosurgery wants it, and it is better than doing the pneumoencephalogram he originally ordered.

Question 1088

NOT Legit Indications for Fluoro Guided LP — all o f which I ’ve heard:

Answer 1088

• “The patient is crazy” • “The patient is crazy & violent” • “The patient is crazy, violent, and has high viral load HIV.... and Hep C” • “The patient recently escaped a locked mental institution for the extremely violent and criminally insane, has both HIV and Hep C. He spits like a camel and has really terrible body odor.”

Question 1089

LP / Myelogram Technique technical overview

Answer 1089

``` L2-L3 or L3-L4 are common entry points. A potential trick would be to show you imaging with a low lying conus (usually that thing stops at L1-L2). Remember you need to be below the conus - so you might need to adjust down, depending on how low it is ``` ``` Target the inlerlaminar space, just off of midline. . Always aspirate before you inject anything. ``` ``` The needle will naturally steer toward the sharper side and away from the bevel. So, if you are directing the needle, you’ll want the bevel side opposite the direction you are attempting to steer. ``` Myelogram Specific - Contrast should flow freely away from the needle tip, gradually filling the thecal sac. The outlining of the cauda equina is another promising sign that you did it right. If contrast pools at the needle tip or along the posterior or lateral thecal sac without free-flow, a subdural injection or injection in the fat around the thecal sac should be suspected.

Question 1090

Technical Strategies to Reduce the Incidence of Post Dural Puncture Headache (PDPH):

Answer 1090

' Use a small needle (25 G), especially for epidural pain injections or myelography. You might have to use a 22G for a diagnostic LP or you are going to struggle to get enough fluid for a sample, and your opening pressures may not be accurate. 1 Non-cutting “atraumatic” needle (diamond shaped tip) reduce incidence o f PDPH Replace the stylet before you withdraw the needle. This isn’t just for the 1 in a million chance that you suck a nerve root up in the needle. This has also been shown to reduce incidence o f PDPH

Question 1091

Technical Strategies to Reduce the Incidence of Post Dural Puncture Headache (PDPH): Direction o f the bevel: This actually matters

Answer 1091

You want to run the bevel parallel with the fibers to push them apart, not cut them perpendicular is wrong you are going to cut those fibers. Coming in at a crazy angle is not ideal for same reason

Question 1092

Blood Patch Overview

Answer 1092

Even a miniscule defect within the thecal sac post LP can allow leakage of spinal fluid resulting in intracranial hypotension and the dreaded chronic/ debilitating post dural puncture_headache. Classic PDPHs are bilateral, better laying down, and worse sitting up. They are also worse with coughing, sneezing, or straining to push out a large turd (from chronic opioid abuse). The procedure involves injecting between 3-20cc of the patients own blood into the epidural space near the original puncture site with the hope of sealing the hole

Question 1093

Blood Patch bulletts

Answer 1093

``` . Most PDPHs start 24 hours after the puncture (between 24-48 hours) - larger leaks can present earlier. . Most people will wait 72 hours after the headache begins (“conservative therapy”) prior to attempting the patch. . Most people will try at least twice before calling neurosurgery to sew to hole you carved out of the dura (you fucking psycho) • Severe atypical symptoms should prompt a CT (to exclude a subdural from severe hypotension). ```

Question 1094

“Fa iled B a c k S u rg e ry S yn d rom e ” (FBSS)

Answer 1094

Another entity invented by NEJM to take down the surgical subspecialties. Per the NEJM these greedy surgeons generally go from a non-indicated spine surgery, to a non-indicated leg amputation, to a non-indicated tonsillectomy on an innocent child. Text books will define it as recurrent or residual low back pain in the patient after disk surgery. This occurs about 40% of the time (probably more), since most back surgery is not indicated and done on inappropriate candidates. Causes of FBSS are grouped into early and late for the purpose of multiple choice test question writing:

Question 1095

Complications of Spine Surgery Recurrent Residual Disk

Answer 1095

Will lack enhancement (unlike a scar - which will enhance on delays)

Question 1096

Complications of Spine Surgery Epidural Fibrosis

Answer 1096

Scar, that is usually posterior, and enhances homogeneously

Question 1097

Complications of Spine Surgery Arachnoiditis

Answer 1097

Buzzwords are “clumped nerve roots ” and “empty thecal sac ”, Enhancement for 6 weeks post op is considered normal. After 6 weeks may be infectious or inflammatory.

Question 1098

Complications of Spine Surgery 12,000 Square Foot Mansion Syndrome

Answer 1098

As spine surgeons perform more and more unnecessary surgeries they need something to spend all that money on.

Question 1099

THIS v.s THAT: Sca r v.v Residual Disc

Answer 1099

Tl Pre Contrast they will look the same... like a bunch of mushy crap. Tl Post Contrast the disc will still look like mushy crap, but the scar will enhance

Question 1100

Conjoined N e rv e Roots

Answer 1100

Two adjacent nerve roots sharing an enlarged common sleeve - at a point during their exit from the thecal sac. This can be a source of FBSS if it is the source of pain instead of a disc. Alternatively it could be misidentified as a disc preoperatively. In both cases, the Radiologist will be cast in the roll of “Scapegoat” during the malpractice suit.

Question 1101

Odontoid F ra c tu re C la s s ific a tio n type 1

Answer 1101

(rare) ``` Fracture at upper part of Odontoid (related to avulsion o f the alar ligament) May be Stable ```

Question 1102

Odontoid F ra c tu re C la s s ific a tio n type 2

Answer 1102

most common ``` Fracture at the base (high nonunion rate) Unstable ```

Question 1103

Odontoid F ra c tu re C la s s ific a tio n Type 3

Answer 1103

best prognosis for healing ``` Fracture through dens into the body ofC2. Unstable ```

Question 1104

J e ffe rs o n F ra c tu re

Answer 1104

This is an axial loading injury (jumping into a shallow pool) - with the blow typically to the top of the head. The anterior and posterior arches blow out laterally. • About 30% will also have a C2 Fracture • Neurologic (cord) damage is rare, because all the force is directed into the bones. Could be shown on a plain film open mouth odontoid view. Remember the C 1 lateral masses shouldn’t slide off laterally.

Question 1105

Os Od o n to id eum I Os T e rm in a le

Answer 1105

These variants can mimic a type 1 Odontoid fracture. In both cases, you have an ossicle located at the position of the odontoid tip (the orthotopic position). The primary difference is that with an Os Odontoideum the base of the dens is usually hypoplastic

Question 1106

Anterior Cord Syndrome (The Really Bad One):

Answer 1106

The anterior portion of the cord is jacked. Motor function and anterior column sensations (pain and temperature) are history. The dorsal column sensations (proprioception and vibration) are still intact. This is the reason FLEXION injuries are so bad.

Question 1107

H an gm a n ’s F ra c tu re

Answer 1107

Seen most commonly when the chin hits the dashboard in an MVA (“direct blow to the face”). The fracture is through the bilateral pars at C2 (or the pedicles - which is less likely). You will have anterior subluxation of C2 on C3 (> 2mm). Cord damage is actually uncommon with these, as the acquired pars defect allows for canal widening. There is often an associated fracture of the anterior inferior comer at C2 - from avulsion of the anterior longitudinal ligament. Traction is contraindicated.

Question 1108

Flex ion Te a rdrop overview

Answer 1108

This represents a teardrop shaped fracture fragment at the anterior-inferior vertebral body. Flexion injury is bad because it is associated with anterior cord syndrome (85% o f patients have deficits). This is an unstable fracture, associated with posterior subluxation of the vertebral body.

Question 1109

Flex ion Te a rdrop list

Answer 1109

Impaction Injury Extremelv Unstable Hyperflexion Classic History: “Ran into wall

Question 1110

E x te n s io n T e a rd ro p overview

Answer 1110

Another anterior inferior teardrop shaped fragment with avulsion o f the anterior longitudinal ligament. This is less serious than the flexion type

Question 1111

E x te n s io n T e a rd ro p list

Answer 1111

Distraction Injury Stable in flexion (unstable in extension) Hyperextension Classic History “Hitfrom behind

Question 1112

C la y -S h o v e le r’s F ra c tu re

Answer 1112

This is an avulsion injury o f a lower cervical / upper thoracic spinous process (usually C7). It is the result o f a forceful hyperflexion movement (like shoveling). The “ghost sign” describes a double spinous process at C6-C7 on AP radiograph.

Question 1113

C h an c e F ra c tu re

Answer 1113

These are flexion-distraction fractures that are classically associated with a lap-band seatbelt. There are 3 column (unstable) fractures. Most commonly seen at the upper lumbar levels & thoracolumbar junction. High association with solid organ trauma

Question 1114

F a c e t D is lo c a tio n unilaterl

Answer 1114

If you have unilateral locked facet (usually from hyperflexion and rotation) the superior facet slides over the inferior facet and gets locked. The unilateral is a stable injury. You will have the inverted hamburger sign on axial imaging on the dislocated side.

Question 1115

F a c e t D is lo c a tio n bilateral

Answer 1115

This is the result o f severe hyperflexion You are going to have disruption o f the posterior ligament complex. When this is full on, you are going to have the dislocated vertebra displaced forward one - h a lf the AP diameter o f the vertebral body. This is highly unstable, and strongly associated with cord injury.

Question 1116

F a c e t D is lo c a tio n | bilateral

Answer 1116

This is a spectrum: Subluxed facets -> Perched -> Locked.

Question 1117

A tla n to a x ia l In s ta b ility

Answer 1117

The articulation between Cl and C2 allows for lateral movement (shaking your head no). The transverse cruciform ligament straps the dens to the anterior arch o f C l . The distance between the anterior arch and dens shouldn’t be more than 5 mm. The thing to know is the association with Down syndrome and juvenile RA. Rotary subluxation can occur in children without a fracture, with the kid stuck in a “cock-robin” position - which looks like torticollis. Actually differentiating from torticollis is difficult and may require dynamic maneuvers on the scanner. This never, ever, ever happens in the absence o f a fracture in an adult (who doesn’t have Downs or RA). Having said that, people over call this all the time in adults who have their heads turned in the scanner.

Question 1118

Pars In te ra r tic u la r is D e fe c t (S po ndy lo ly sis or A d u lt Is thm ic S p o n d y lo lis th e s is )

Answer 1118

the adult version. Defects in the pars interarticuaris are usually caused by repetitive micro-trauma (related to hyper-extension). It is nearly always at L5-S1 (90%). Pain is typically a L5 radiculopathy caused by foraminal stenosis at L5 -S1. The term “pseudo-disc” is sometimes used to describe the deformed annular fibers seen in the setting o f a related anterolithesis (forward slippage).

Question 1119

Instability trauma overview

Answer 1119

For the purpose of multiple choice you will see the words “stable ” or “unstable ” associated with specific fracture types. There are also some radiologic “definitions” of instability which seem to vary depending on who you ask. In general, if you have acute segmental kyphosis greater than 11 degrees, acute anterolisthesis greater than 3-4 mm, or gross motion on flexion / extension imaging it is probably an unstable fracture. You will also hear people talk about a “power ratio” for occipitocervical instability, and a spinal column theory for the thoracolumbar injury.

Question 1120

Instability definition

Answer 1120

ou will read different definitions of “instability” as it relates to spinal trauma. The one I prefer is something along the lines of “lost capacity to withstand even a normal physiologic load without: potential damage to the spinal cord, nerve roots, or developing an incapacitating deformity that forces one to seek employment in a cathedral bell tower. ”

Question 1121

Occipitocervical Instability

Answer 1121

``` This can be traumatic (in which case the patient rarely lives because they rip their brainstem in half), or congenital (classically seen with Down Syndrome). Two popular methods for evaluating this: ```

Question 1122

Occipitocervical Instability powers ratio

Answer 1122

``` = C-D: A-B Ratio is greater than 1.0 = Ligamentous Instability ```

Question 1123

Transverse Myelitis

Answer 1123

This is a focal inflammation of the cord. The causes are numerous (infectious, post vaccination - classic rabies, SLE, Sjogren’s, Paraneoplastic, AV-malformations). You typically have at least 2/3 of the cross sectional area of the cord involved, and focal enlargement of the cord. Splitters will use the terms “Acute partial” for lesions less than two segments, and “acute complete” for lesions more than two segments. The factoid to know is that the “Acute partials” are at higher risk for developing MS.

Question 1124

Denis 3 Spinal Column Concept

Answer 1124

Most often you will see this idea applied to thoracolumbar spinal fractures, although technically it has some validity in the lower cervical segments as well. The idea is to divide the vertebral column into 3 vertical parallel columns , with instability suggested when all 3 or 2 contiguous columns (anterior and middle column or middle and posterior column) arc disrupted.

Question 1125

Denis 3 Spinal Column Concept anterior

Answer 1125

``` • Anterior Longitudinal Ligament • Anterior 2/3 Vertebral Body ```

Question 1126

Denis 3 Spinal Column Concept middle

Answer 1126

``` • Posterior Longitudinal Ligament • Posterior 1/3 Vertebral Body ```

Question 1127

Denis 3 Spinal Column Concept posterior

Answer 1127

``` • Posterior Ligaments • Pedicles, Facets, Lamina, Spinous Process ```

Question 1128

When Does a “Trauma” Indicate Imaging P Canadian C-Spine Rule

Answer 1128

``` Age >65 years • Paresthesias in extremities • Dangerous mechanism • Fall >3 ft or 5 stairs • Axial load to the head (empty swimming pool diving, piano fell on head - while chasing a road runner High Speed MVA, • Pedestrian vs Car • Hulk Smash ```

Question 1129

When Does a “Trauma” Indicate Imaging P Nexus Criteria:

Answer 1129

``` focal neurological deficie Nexus Criteria: Midline spinal tenderness Altered level o f consciousness Intoxication (you c an ’t clear a drunk guys/girls c-spine while they are Distracting injury ```

Question 1130

Unstable

Answer 1130

Vertebral Overriding > 3mm (“Subluxation”) Angulation > 11 Degrees Flexion Tear Drop Bilateral Facet Dislocation “Double-Locked” Odontoid Fracture Type 2 and 3 (most sources will say Type 2 & 3 or deploy the word “usually”, but for sure if there is lateral displacement) Two Contiguous Thoracolumbar Columns (anterior & middle or middle & posterior) Three Thoracolumbar Columns (Chance Fracture, Etc...) Jefferson Fracture Flangman Fracture Atlanto-Occipital and Atlanto-Axial Dislocations

Question 1131

Stable

Answer 1131

Extension Tear Drop (At least in Flexion) Unilateral Facet Dislocation Odontoid Fracture Type 1 I (usually stable - flex/extension films still usually done \ to exclude atlantooccipital instability ) | Isolated Single Thoracolumbar Column Fracture Clay Shoveler's Fracture Transverse Process Fracture

Question 1132

Named Spine Fractures quick Jefferson

Answer 1132

Burst Fracture of Cl Axial Loading

Question 1133

Named Spine Fractures quick Hangman

Answer 1133

Bilateral Pedicle or Pars Fracture of C2 Hyperextension

Question 1134

Named Spine Fractures quick Teardrop

Answer 1134

Can be flexion or extension Flexion (more common

Question 1135

Named Spine Fractures quick Clay-Shoveler’s

Answer 1135

Avulsion of spinous process at C7 or T1 Hyperflexion

Question 1136

Named Spine Fractures quick Chance

Answer 1136

Horizontal Fracture through thoracolumbar spine “Seatbelt

Question 1137

most important factor for outcome is the presence o f a | hemorrhagic spinal cord injury

Answer 1137

they do bad

Question 1138

Spinal Cord Syndromes Central Cord

Answer 1138

``` Old lady with spondylosis or young person with bad extension injury. Upper Extremity Deficit is worse than lower (corticospinal tracts are lateral in lower extremity) ```

Question 1139

Spinal Cord Syndromes Anterior Cord

Answer 1139

Flexion Injury Immediate Paralysis

Question 1140

Spinal Cord Syndromes Brown Sequard

Answer 1140

Rotation injury or penetrating trauma One side motor, other side sensory deficits

Question 1141

Spinal Cord Syndromes Posterior Cord

Answer 1141

Uncommon - but sometimes seen with hyperextension Proprioception gone

Question 1142

Anterior Cord Syndrome (The Really Bad One):

Answer 1142

The anterior portion of the cord is jacked. Motor function and anterior column sensations (pain and temperature) are history. The dorsal column sensations (proprioception and vibration) are still intact. This is the reason FLEXION injuries are so bad.

Question 1143

Spinal AVM / AVFs overview

Answer 1143

There are 4 types. Type 1 is by far the most common (85%). It is a Dural AVF; the result o f a fistula between the dorsal radiculomedullary arteries and radiculomedullary vein / coronal sinus - with the dural nerve sleeve. It is acquired and seen in older patients who present with progressive radiculomyelopathy. The most common location is the thoracic spine. If anyone asks, the “gold standard for diagnosis is angiography” , although CTA or MRA will get the job done. You will have T2 high signal in the central cord (which will be swollen), with serpentine perimedullary flow voids (which are usually dorsal).

Question 1144

Spinal AVM / AVFs type 1

Answer 1144

Most Common Type (85%). Dural AVF - with a single coiled vessel

Question 1145

Spinal AVM / AVFs type 2

Answer 1145

Intramedullary Nidus from anterior spinal artery or posterior spinal artery. Can have aneurysms, and can bleed. Most common presentation is SAH. Associated with HHT and KTS (other vascular syndromes).

Question 1146

Spinal AVM / AVFs type 3

Answer 1146

Juvenile, very rare, often complex and with a terrible prognosis

Question 1147

Spinal AVM / AVFs type 4

Answer 1147

Intradural perimedullary with subtypes depending on single vs multiple arterial supply. These tend to occur near the conus.

Question 1148

Foix A la jo u an in e Syndrome

Answer 1148

This is a congestive myelopathy associated with a Dural AVF. The classic history is a 45 year old male with lower extremity weakness and sensory deficits. You have increased T2 signal (either at the conus or lower thoracic spine), with associated prominent vessels (flow voids). The underlying pathophysiology is venous hypertension - secondary to the vascular malformation.

Question 1149

Foix A la jo u an in e Syndrome key finding

Answer 1149

The vascular malformation flow voids are - punctate, serpiginous, and serpentine. They are NOT blob like - sorta like what you see with CSF pulsation signal loss. Swollen High Signal Cord with Serpentine flow voids along the surface of cord

Question 1150

Syrinx

Answer 1150

Also known as “a hole in the cord”. People use the word “syrinx” for all those fancy French / Latin words (hydromyelia, syringomyelia, hydrosyringomyelia, syringohydromyelia, syringobulbia etc. . They usually do this because they don’t know what those words mean.

Question 1151

Syrinx simple version

Answer 1151

• Hydromyelia = Lined by ependyma. • Syringomyelia = NOT lined by ependyma These is zero difference clinically - which is why everyone just says “syrinx.” The distinction is strictly academic (i.e. multiple choice trivia).

Question 1152

Syrinx acquired vs congenital

Answer 1152

Most (90%) cord dilations (healthy and sick ones) are congenital, and associated with Chiari I and II, as well as Dandy-Walker, Klippel-Feil, and Myelomeningoceles. The other 10% are acquired either by trauma, tumor, or vascular insufficiency.

Question 1153

Syrinx clinical practice

Answer 1153

normal cord I call it “central cord dilation” or “benign central cord dilation.” If there is the same thing but the cord around the dilation looks “sick” - grayish / high signal, or the cord is atrophic, then I use the word “myelopathy” or “myelopathic changes.” Myelopathy is a word for a diseased cord - usually from disc/osteophyte compression. Although, you can have myelopathy for any number of neoplastic, post traumatic, or inflammatory processes.

Question 1154

Spinal Cord In fa rc t:

Answer 1154

Cord infarct / ischemia can have a variety o f causes. The most common cause is “ idiopathic,” although I ’d expect the most common multiple choice scenario to revolve around treating an aneurysm with a stent graft, or embolizing a bronchial artery. Impairment involving the anterior spinal artery distribution is most common. With anterior spinal artery involvement you are going to have central cord / anterior horn cell high signal on T2 (because gray matter is more vulnerable to ischemia).

Question 1155

The “owl’s eye” sign

Answer 1155

o f anterior spinal cord infarct is a buzzword

Question 1156

Spinal Cord In fa rc t: length

Answer 1156

It’s usually a long segment, (more than 2 vertebral body segments). Diffusion using single shot fast spin echo or line scan can be used with high sensitivity (to compensate for artifacts from spinal fluid movement).

Question 1157

.Demyelinating (T2 / FLAIR Hyperintense cord

Answer 1157

Broadly you can think of cord pathology in 5 categories: Demyelinating, Tumor, Vascular, Inflammatory, and Infectious. In the real world, the answer is almost always MS - which is by far the most common cause. The other three things it could be are Neuromyelitis Optica (NMO), acute disseminating encephalomyelitis (ADEM) or Transverse Myelitis (TM).

Question 1158

MS in the Cord

Answer 1158

"Multiple lesions, over space and time.” The lesions in the spine are typically short segment (< 2 vertebral segments), usually only affect half / part of the cord. The cervical cord is the most common location. There are usually lesions in the brain, if you have lesions in the cord (isolated cord lesions occur about 10% of the time). The lesions can enhance when acute - but this is less common than in the brain. You can sometimes see cord atrophy if the lesion burden is large.

Question 1159

Transverse Myelitis

Answer 1159

This is a focal inflammation of the cord. The causes are numerous (infectious, post vaccination - classic rabies, SLE, Sjogren’s, Paraneoplastic, AV-malformations). You typically have at least 2/3 of the cross sectional area of the cord involved, and focal enlargement of the cord. Splitters will use the terms “Acute partial” for lesions less than two segments, and “acute complete” for lesions more than two segments. The factoid to know is that the “Acute partials” are at higher risk for developing MS.

Question 1160

ADEM in the cord

Answer 1160

As described in the brain section, this is usually seen after a viral illness or infection typically in a child or young adult. The lesions favor the dorsal white matter (but can involve grey matter). As a pearl, the presence of cranial nerve enhancement is suggestive of ADEM. The step 1 trivia, is that the “anti-MOG IgG” test is positive in 50% of cases. Just like MS there are usually brain lesions (although ADEM lesions can occur in the basal ganglia and pons - which is unusual in MS).

Question 1161

NMO (Neuromyelitis Optica): in the cord

Answer 1161

This is also sometimes called Devics. It can be monophasic or relapsing, and favors the optic nerves and cervical cord. Tends to be longer segment than MS, and involve the full transverse diameter of the cord (mild swelling). Brain lesions can occur (more commonly in Asians) and are usually periventricular. If any PhDs ask, the reason the periventricular location occurs is that the antibody (NMO IgG) attacks the Aquaporin 4 channels - which are found in highest concentration around the ventricles.

Question 1162

Subacute Combined Degeneration

Answer 1162

This is a fancy way of describing the effects of a Vitamin B12 deficiency. The classic look is bilateral, symmetrically increased T2 signal in the dorsal columns, without enhancement. The appearance has been described as an “inverted V sign.” The signal change typically begins in the upper thoracic region with ascending or descending progression.

Question 1163

HIV Vacuolar Myelopathy:

Answer 1163

This is the most common cause of spinal cord dysfunction in untreated AIDS. Key word there is “untreated” - this is a late finding. Atrophy is the most common finding (thoracic is most common). The T2 high signal will be very similar to B12 (subacute combined degeneration) - symmetrically involving the posterior columns. It can only be shown 2 ways - (a) by telling you the patient has AIDS or risk factors such as unprotected anal sex at a truck stop with a man “bear” with a thick mustache while sharing IV drug needles, (b) not including B 12 as an answer choice.

Question 1164

MS cord maging

Answer 1164

Lesions favor the white matter of the cervical region. | They tend to be random and asymmetric

Question 1165

“Owl’s Eye”

Answer 1165

-Classic for Ischemia (Anterior) -Also seen in Polio

Question 1166

-Ischemia big

Answer 1166

- More extensive anterior involvement. -Also seen in NMO, TM, or MS

Question 1167

``` Vitamin B12 (SCD) HIV ```

Answer 1167

Posterior. Can look | like an inverted “V”

Question 1168

MS cord quick

Answer 1168

``` Usually Short Segment Usually Part of the Cord Not swollen, or Less Swollen Can Enhance/ Restrict when Acute ```

Question 1169

tm cord quick

Answer 1169

``` Usually Long Segment Usually involves both sides of the cord Expanded, Swollen Cord Can Enhance ```

Question 1170

nmo cord quick

Answer 1170

``` Usually Long Segment Usually involves both sides of the cord Optic Nerves Involved ```

Question 1171

adem cord quick

Answer 1171

Not swollen, or | Less Swollen

Question 1172

infarct cord quick

Answer 1172

Usually Long Segment Restricted Diffusion

Question 1173

tumor cord quick

Answer 1173

Expanded, | Swollen Cord Can Enhance

Question 1174

A ra c h n o id itis cord

Answer 1174

This is a general term for inflammation o f the subarachnoid space. It can be infectious but can also be post-surgical. It actually occurs about 10-15% o f the time after spine surgery, and can be a source of persistent pain / failed back.

Question 1175

A ra c h n o id itis cord Empty Thecal Sa c S ig n

Answer 1175

Nerve roots are adherent peripherally, giving the appearance o f an empty sac.

Question 1176

A ra c h n o id itis cord Central Nerve Ro o t Clumping

Answer 1176

This can range in severity from a few nerves clumping together, to all o f them fused into a single central scarred band.

Question 1177

G u illa in B a rre S yndrom e (GBS)

Answer 1177

Also known as “Acute inflammatory demyelinating polyneuropathy” (AIDP). One o f those weird auto-immune disorders that causes ascending flaccid paralysis. The step 1 trivia was Campylobacter, but you can also see it after surgery, or in patients with lymphoma or SLE.

Question 1178

G u illa in B a rre S yndrom e (GBS) thing to know

Answer 1178

The thing to know is enhancement of the nerve roots o f the cauda equina.

Question 1179

G u illa in B a rre S yndrom e (GBS) trivia

Answer 1179

Other pieces o f trivia that are less likely to be asked are that the facial nerve is the most common cranial nerve affected, and that the anterior spinal roots enhance more than the posterior ones

Question 1180

Chronic In flam m a to ry D em y lin a tin g P o lyn eu ro p a th y (CIDP)

Answer 1180

``` The chronic counterpart to GBS. Clinically this has a gradual and protracted weakness (GBS improves in 8 weeks, CIDP does not). The buzzword is thickened, enhancing, “onion bulb” nerve roots. “Dreadlocks,” “Locs,” “Jata" some people call them. ```

Question 1181

CIDP =

Answer 1181

Diffuse Thickening o f the Nerve Roots

Question 1182

Tumor overview

Answer 1182

The classic teaching with spinal cord tumors is to first describe the location o f the tumor, as either (1) Intramedullary, (2) Extramedullary Intradural, or (3) Extradural. This is often easier said than done. Differentials are based on the location.

Question 1183

Tumor Intramedullary ddx

Answer 1183

A stro cy tom a , E p en d ym om a , H em a n g io b la stom a

Question 1184

Tumor Extramedullary Intradural ddx

Answer 1184

S chw an n om a , M en in g iom a , N e u ro fib rom a , Drop Mets

Question 1185

Tumor Extradural ddx

Answer 1185

``` Disc D ise a se (most common) B o n e T um o rs, Mets, L ym p h om a ```

Question 1186

Cord Intramedullary: A s tro c y tom a

Answer 1186

This is the most common intramedullary tumor in peds. It favors the upper thoracic spine. There will be fusiform dilation o f the cord over multiple segments. They are eccentric, dark on T l, bright on T2, and they enhance. They may be associated with rostral or caudal cysts which are usually benign syrinx(es).

Question 1187

Cord Intramedullary: Astrocytoma list

Answer 1187

Most common in child Eccentric Heterogenous Enhancement

Question 1188

Cord Intramedullary: Ependymoma list

Answer 1188

``` Most common in Adults Central Homogenous Enhancement More Often Hemorrhagic ```

Question 1189

Cord Intramedullary: Epend ymoma

Answer 1189

This is the most common primary cord tumor o f the lower spinal cord and conus / filum terminale. You can see them in the cervical cord as well. This is the most common intramedullary mass in adults. The “myxopapillary form” is exclusively found in the conus /filum locations. They can be hemorrhagic, and have a dark cap on T2. They have tumoral cysts about % o f the time. They are a typically long segment (averaging 4 segments).

Question 1190

Cord Intramedullary: Epend ymoma Myxopapillary

Answer 1190

Most commonly located in the Lumbar spine (conus/filum location)

Question 1191

Cord Intramedullary: H em a n g io b la s tom a

Answer 1191

These are associated with Von Hippel Lindau (30%). The thoracic level is favored (second most common is cervical). The classic look is a wide cord with considerable edema. Adjacent serpinginous draining meningeal varicosities can be seen.

Question 1192

Cord Intramedullary: In tram e d u lla ry M e ts

Answer 1192

This is very very rare, but when it does happen it is usually lung (70%).

Question 1193

Cord Extramedullary Intradural S chw an n om a

Answer 1193

This is the most common tumor to occur in the Extramedullary Intradural location. They are benign, usually solitary, usually arise from the dorsal nerve roots. They can be multiple in the setting o f NF-2 and the Carney Complex. The appearance is variable, but the classic look is a dumbbell with the skinny handle being the intraforaminal component. They are T1 dark, T2 bright, and will enhance. They look a lot like neurofibromas. If they have central necrosis or hemorrhage, that favors a schwannoma.

Question 1194

Cord Extramedullary Intradural S chw an n om a list

Answer 1194

Does NOT envelop the adjacent nerve root Solitary Multiple makes you think NF-2 Cystic change / Hemorrhage

Question 1195

Cord Extramedullary Intradural N eu ro fib rom a

Answer 1195

This is another benign nerve tumor (composed o f all parts o f the nerve: nerve + sheath), that is also usually solitary. There are two flavors: solitary and plexiform. The plexiform is a multilevel bulky nerve enlargement that is pathognomonic for NF-1. Their lifetime risk for malignant degeneration is around 5-10%. Think about malignant degeneration in the setting o f rapid growth. They look a lot like schwannomas. If they have a hyperintense T2 rim with a central area o f low signal - “target sign” that makes you favor neurofibroma.

Question 1196

Cord Extramedullary Intradural N e u ro fib rom a list

Answer 1196

Does envelop the adjacent nerve root (usually a dorsal sensory root) Solitary Associated with NF -1 (even when single) T2 bright rim, T2 dark center “target sign” Plexiform = Pathognomonic for NF-1

Question 1197

Cord Extramedullary Intradural M enin gioma

Answer 1197

These guys adhere to but do not originate from the dura. They are more common in women (70%). They favor the posterior lateral thoracic spine, and the anterior cervical spine. They enhance brightly and homogeneously. They are often T1 iso to hypo, and slightly T2 bright. They can have calcifications.

Question 1198

Cord Extramedullary Intradural Drop Mets

Answer 1198

Medulloblastoma is the most common primary tumor to drop. Breast cancer is the most common systemic tumor to drop (followed by lung and melanoma). The cancer may coat the cord or nerve root, leading to a fine layer o f enhancement (“zuckerguss”).

Question 1199

Cord Extradural V e r te b ra l H em a n g iom a

Answer 1199

These are very common - seen in about 10% o f the population. They classically have thickened trabeculae appearing as parallel linear densities “jail bar” or “corduroy” appearance. In the vertebral body they are T1 and T2 bright, although the extraosseuous components typically lack fat and are isointense on T 1 .

Question 1200

Cord Extradural | Os teoid O s teom a :

Answer 1200

This is also covered in the MSK. chapter, but as a brief review focusing on the spine, they love to involve the posterior elements (75%), and are rare after age 30. They tend to have a nidus and surrounding sclerosis. The nidus is T2 bright and will enhance. The classic story is night pain, improved with aspirin. Radiofrequency ablation can treat them (under certain conditions).

Question 1201

Cord Extradural | O s te o b la s tom a :

Answer 1201

This is similar to an Osteoid osteoma but larger than 1.5 cm. Again, very often in the posterior elements - usually o f the cervical spine.

Question 1202

Cord Extradural A n e u ry sm a l Bone Cyst

Answer 1202

These guys are also covered in the MSK chapter. They also like the posterior elements and are usually seen in the first two decades o f life. They are expansile (as the name implies) and can have multiple fluid levels on T2. They can get big and look aggressive.

Question 1203

Cord Extradural G ian t Cell Tumor

Answer 1203

These guys are also covered in the MSK chapter. These are common in the sacrum, although rare anywhere else in the spine. You do n ’t see them in young kids. If they show this, it’s going to be a lytic expansile lesion in the sacrum with no rim of sclerosis

Question 1204

Cord Extradural Chordoma

Answer 1204

This is most common in the sacrum (they will want you to say clivus - that is actually number 2). The thing to know is that a vertebral primary tends to be more aggressive / malignant than its counter parts in the clivus or sacrum. The classic story in the vertebral column is “involvement o f two or more adjacent vertebral bodies with the intervening disc. ” Most are very T2 bright

Question 1205

Cord Extradural Leu k em ia

Answer 1205

They love to show it in the spine. You have loss o f the normal fatty marrow - so it’s going to be homogeneously dark on T1. More on this in the MSK chapter

Question 1206

Cord Extradural M e ts

Answer 1206

The classic offenders are prostate, breast, lung, lymphoma, and myeloma. Think multiple lesions with low T1 signal. Cortical breakthrough or adjacent paravertebral components are also helpful

Question 1207

V e r t e b r a P la n a :

Answer 1207

The pancake flat vertebral body. Just say Eosinophilic Granuloma in a ^ 3 kid (could be neuroblastoma met), and Mets / Myeloma in an adult.

Question 1208

VHL Associations

Answer 1208

``` • Pheochromocytoma •CNS Hemangioblastoma (cerebellum 75%, spine 25%) •Endolymphatic Sac Tumor •Pancreatic Cysts •Pancreatic Islet Cell Tumors •Clear Cell RCC ```