1
Q
Isolated CN3 palsy
A
Think PCOM aneurysm
2
Q
Foetal origin PCA
A
Common vascular variant
- seen in up to 30% of general population.
PCA is feed primarily as an anterior circulation artery (occipital lobe is feed by the ICA).
3
Q
Persistent Trigeminal Artery
A
Persistent fetal connection between the cavernous ICA to the basilar.
“tau sign” on Sagittal MRI
It increases the risk of aneurysm.
4
Q
Anastomotic Vein of Trolard
A
Connects the Superficial Middle Cerebral Vein and the Superior Sagittal Sinus
5
Q
Anastomotic Vein of Labbe
A
Connects the Superficial
Middle Cerebral Vein and
the Transverse Sinus
6
Q
Superficial venous system
A
Superior Cerebral Veins
Superior Anastomotic Vein of Trolard
Inferior Anastomotic Vein of Labbe
Superficial Middle Cerebral Veins
7
Q
Deep venous system
A
Basal Vein of Rosenthal
Vein of Galen
Inferior Petrosal Sinus
8
Q
Basal veins of Rosenthal
A
Deep veins that passes lateral to the midbrain through the
ambient cistern and drains into the vein of Galen. Their course is similar to the PCA.
9
Q
Vein of Galen
A
Big vein (“great”) formed by the union of the two internal cerebral veins.
10
Q
Concha bullosa
A
Common variant where the middle concha is pneumatized
11
Q
Isolated CN6 palsy
A
Think increased ICP
(Increased ICP -> Brain Stem Herniates Interiorly -> CN 6 Gets Stretched)
12
Q
Brain myelation pattern
A
Inferior to Superior, Posterior to Anterior
The brainstem, and posterior limb of the internal capsule are normally myelinated at birth.
13
Q
Brain myelation timeline
A
The subcortical white matter is the last part of the brain to myelinate.
The occipital white matter around 12 months, and the frontal regions finishing around 18 months.
The “terminal zones” of myelination occur in the subcortical frontotemporoparietal regions finishing around 40 months.
14
Q
MRI pituitary birth
A
Ant pit T1 Hyper
(until 2 months old)
Post pit T1 Hyper
15
Q
MRI pituitary adult
A
Ant pit T1 iso, T2 iso
Post pit T1 Hyper, T2 Hypo
16
Q
Sinuses development order
A
1- Maxillary
2- Ethmoid
3- Sphenoid
4- Frontal
Most finished forming by age 15
17
Q
Sinus development ages
(visible on CT)
A
Maxillary - present at birth - 5 months
Ethmoid - present at birth - 1 year
Sphenoid - NOT present at birth - 4 years
Frontal - NOT present at birth - 6 years
18
Q
Dysgenisis / Agenesis of the Corpus Callosum coronal appearance
A
Steer horn
19
Q
Dysgenisis / Agenesis of the Corpus Callosum axial appearance
A
Vertical ventricles
(racing car)
20
Q
Why are the lateral ventricles widely spaced when you have no corpus callosum?
A
“Probst bundles” (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.
21
Q
Dysgenesis / Agenesis of the Corpus Callosum associations
A
Intracranial lipoma, Heterotopias, Schizencephaly, Lissencephaly
22
Q
Intracranial lipoma
A
The most classic association with CC agenesis. Congenital malformations, not true neoplasm.
50% are found in the interhemispheric fissure.
The 2nd most common location is the quadrigeminal cistern (25%).
23
Q
How to see intracranial lipoma
A
Non Fat Sat Tl
(most non-bleeding
things in the brain are not T1 bright).
24
Q
Anencephaly
A
Reduced / Absent cerebrum and cerebellum.
The hindbrain will be present.
25
Iniencephaly defect level
Defect at level of the cervical spine
Deficient occipital bone with defect in the cervical region.
Inion= Back of head/neck
26
Iniencephaly gross findings
Extreme retroflexion of the head.
Enlarged foramen magnum.
Jacked up spines.
Often visceral problems.
27
Anencephaly imaging findings
"Frog Eye" appearance on the coronal plane (due to absent cranial bone/brain with bulging orbits).
28
Anencephaly secondary signs
Antenatal Ultrasound with Polyhydramnios (hard to swallow without a brain)
AFP will be elevated (true with all open neural tube defects)
29
Iniencephaly imaging appearances
"Star Gazing Fetus" - contorted in a way that makes their face turn upward (hyper-extended cervical spine, short neck, and upturned face).
30
Encephalocele (meningoencephalocele)
Brain+ meninges herniate through a defect in the cranium (mostly occipital).
Classically associated with Chiari III
31
Rhombencephalosynapsis
Vermis is absent (failure to form defect) therefore abnormal fusion of the cerebellum
32
Rhombencephalosynapsis imaging appearance
***Transversely oriented single lobed cerebellum***
Small 4th ventricle.
Rounded fastigial point.
Absent primary fissure.
33
Rhombencephalosynapsis associations
Holoprosencephaly Spectrum
34
Joubert syndrome
Vermis is absent (or small) - failure to form defect
35
Joubert syndrome imaging appearance
Molar Tooth appearance of the superior cerebellar peduncles (elongated like the roots of a tooth).
Small cerebellum
Absence of pyramindal decussation
Large 4th ventricle (batwing shaped)
Absent fastigial point
Absent 1ry fissure
36
Joubert syndrome associations
Retinal dysplasia (50%)
Multicystic dysplastic kidneys (30%)
Liver fibrosis (COACH syndrome)
37
Dandy Walker key findings
1. Hypoplasia of the vermis (usually inferior)
2. Hypoplastic vermis is elevated and rotated
3. Dilated cystic 4th ventricle
38
Dandy Walker imaging findings
Non-specific appearance of enlarged posterior fossa CSF space on axial
Cerebellar hemisphere is displaced forward and laterally (overall volume and morphological characteristics preserved)
39
Torcula-Lambdoid inversion
The torcula (confluence of venous sinuses) above the level of the lambdoid suture, secondary to elevation of the tentorium
In Dandy Walker, but not the variant version
40
Dandy Walker association
Hydrocephalus (90%)
Additional CNS malformations (~ 40%)
(agenesis of the corpus callosum, encephaloceles, heterotopia, polymicrogyria, etc ... ).
41
Mega cisterna magna
Focal enlargement of the retrocerebellar CSF space
42
Blake pouch
Sac like cystic protrusion through the foreman of Magendie into the infra/retrocerebellar region
Vermis normally formed but upwardly displaced. Dilated 4th ventricle. Gets hydrocephalus.
43
Variant DWM aka
Hypoplastic rotated vermis
44
Variant DWM
Hypoplastic vermis with dilation of the 4th ventricle.
Vermis is hypoplastic (less severe than DWM). Dilated 4th ventricle. Hypoplastic cerebellar hemispheres. 25% cases get hydrocephalus.
Diagnosis at 18/52 old as vermis not finished forming prior.
45
Holoprosencephaly gross appearance
Cyclops Eyes
Cleft lips / Palates
Pyriform Aperture Stenosis (from nasal process overgrowth)
Solitary Median Maxillary Incisor (MEGA-Incisor)
46
Holoprosencephaly types
Failure to cleave -
Lobar least severe
Semi lobar
Alobar most severe
47
Lobar holoprosencephaly
Mild fusion frontal horns.
Incomplete septum.
Focal areas of incomplete fusion anteriorly (usually the fornix)
48
Semi-Lobar holoprosencephaly
Fused frontal lobes
Back is cleaved, not the front
49
Alobar holoprosencephaly
Zero midline cleavage.
Hemispheres are fused and there is a single midline ventricle.
Imaging - Pancake/cup shape, ball shaped, rim/mono ventricle
50
Arhinencephaly
Minor HPE expression
Midline olfactory bulbs/tracts are absent (can't smell)
51
Lobar holoprosencephaly absent structures
Septum pellucidum
Corpus callosum (partial vs normal)
Normal thalamus
52
Semi-Lobar holoprosencephaly absent structures
Septum pellucidum
Corpus callosum (partial)
Anterior interhemispheric fissure
Anterior falx cerebri
Thalamus is fused (partial or complete)
53
Alobar holoprosencephaly absent structures
Septum pellucidum
Corpus callosum
Interhernispheric fissure
Falx cerebri
Thalamus is fused
54
Ventricle patterns in HPE
Lobar - mild fusion of the frontal horns of the lateral ventricles
S-L - body of the lateral ventricles are 1 chamber. Occipital and temporal horns are partially developed
Alobar - Single ventricle (distinct lateral and third ventricles are absent)
55
Meckel-Gruber Sx
Classic triad:
1. Occipital encephalocoele
2. Multiple renal cysts
3. Polydactyly
Strongly associated with holoprosencephaly
56
de Morsier Sx
Septo optic dysplasia
Absent septum pellucidum and hypoplastic "optic" structures such as the optic chiasma and optic nerves
Associated with schizencephaly
57
Azygous ACA
Associated with septo optic dysplasia and lobar HPE
58
Hemimegalencephaly
Failure to proliferate disorder
Malformation characterized by enlargement (from hamartomatous overgrowth) of all or part/s of one cerebral hemisphere
59
Hemimegalencephaly associations
Polymicrogyria, pachygyria, and heterotopia
60
Hemimegalencephaly imaging findings
BIG Side with BIG Ventricle
"Hamartomatous overgrowth " of all or part of a cerebral hemisphere secondary to differentiation / migration failure.
61
Rasmussen's encephalitis imaging findings
SMALL side with BIG ventricle = Atrophy
The shrunken half is atrophic, resulting in ex-vacuo dilation of the ventricle .
62
Rasmussen's encephalitis
Viral (or autoimmune) disease that destroys half the brain. Age <10 normally
63
Lissencephaly "classic" (type 1)
Smooth surface
Thick cortex
Colpocephaly common
Figure 8 shape (axial) as shallow vertical Sylvian fissures
(undermigration)
64
Lissencephaly "cobblestone" (type 2)
Gray matter nodules (variable size and location) so cobblestoned appearance
Most commonly located adjacent to the Sylvian fissures
(overmigration)
65
Lissencephaly type 2 association
Congenital muscular dystrophy
Retinal detachment
66
Double cortex band heterotopia
Mildest form of lishencephaly
Double cortex appearance
Gyral pattern normal (or mildly simplified)
Subcortical band of heterotrophic gray matter
67
Double cortex band heterotopia association
Seizure disorders
X linked inheritance
68
Periventrical nodular heterotopia
(failed migration)
Nodular grey matter deposition along the ventricle borders
Associated seizure disorders
69
Polymicrogyria
Fine undulating/bumpy cortex, most common adjacent to Sylvian fissure bilaterally. Zika virus.
(failure to organise)
Layer 5 gets removed (infection/toxins) after normal migration. With this gone, other more superficial layers overfold and fuse resulting in excessive number of small folds
70
Schizencephaly
Split brain
Cleft (lined with grey matter) connecting the CSF spaces with the ventricular system
Closed lip (20%) or open lip (80%)
30% have non CNS vascular stigmata (eg gastroschisis)
71
Closed lip schizencephaly
20%.
Less common, less severe.
The lip will appear closed without CSF filled cleft.
Grey matter will run across the normally uniform corona radiata
72
Open lip schizencephaly
80%
More common, more severe
CSF-filled cleft (lined with grey matter) extending from the ventricle to the pial surface.
Grey matter lining often nodular looking
73
Schizencephaly associations
Absent septum pellucidum (70%), focally thinned corpus callosum, optic nerve hypoplasia (30%), epilepsy
74
Porencephalic cyst
Brain cleft/hole from a prior ischaemic event resulting in encephalomalacia.
+/- communication with the subarachnoid space.
75
Hydrancephaly
Bilateral ICA occlusion causes massive destruction of both cerebral hemispheres. Only the cerebellum, midbrain, and the falx (usually) remain.
76
Hydrancephaly causes
Herpes is the most classic, but in utero infection with toxo or CMV are also described causes.
77
Open lip schizencephaly vs Porencephalic cyst
OLS - Not normally formed brain. Cleft is lined with grey matter
PC - Normally formed brain. Cleft is NOT lined with grey matter
78
Cortical mantle and falx present
Severe hydrocephalus
79
Cortical mantle present, no falx
Holoprosencephaly - alobar
- anterior falx usually missing in the semi-lobar form
- lobar (mild) subtype should still have the falx
80
No cortical mantle present
Hydranencephaly
81
Cephalocele
Herniation of the cranial contents through a defect in the skull.
82
Meningocele
Herniation sac with CSF and meninges
No brain in herniation sac
83
Meningo-encephalocele
Herniation sac contains CSF, meninges and brain
84
Cystocele
Herniation sac with CSF, meninges, brain and ventricle
85
Myelocele
Herniation sac with spinal cord
86
Type I Chiari
Herniation of 1/both cerebellar tonsils (more than 5mm) below level of basin-opisthion
Associated syrinx (cervical cord)
87
Type II Chiari
Relatively less tonsillar herniation than type I.
Relatively more cerebellar vermian displacement.
88
Type II Chiari classic features
- low lying torcula
- tectal beaking
- hydrocephalus
- clival hypoplasia
89
Type III Chiari
Features of type II
AND
occipital encephalocele (cerebellum +/- brainstem, occipital lobe, 4th ventricle)
90
Type 1.5 Chiari
Features type I and II
Not associated with neural tube defects despite significant downward movement of tonsils and brain stem.
91
Type I Chiari symptoms
1) Occipital headache from pressure of the cerebellar tonsils - worse with sneezing
2) Weakness, spasticity, and loss of proprioception from pressure on the cord
92
Chiari I association
- syrinx of cervical cord
- less so - Klippel-Feil Syndrome (congenital c-spine fusion)
NOT associated with a neural tube defect
93
Chiari II imaging features
- thinned corpus callous
- tectal beak
- clinal hypoplasia
- low lying torcula
- long skinny 4th ventricle
- "towering" cerebellum
- interdigitated cerebral gyro
94
Chiari II association
Lumbar myelomeningocele
Spina bifida
95
Chiari I mechanism/cause
Congenital underdevelopment of posterior fossa -> overcrowding -> downward displacement
OR
Post traumatic deformity ie acquired later in life
96
Chiari II mechanism/cause
Neural tube defect "sucks" the cerebellum downward prior to full development of the cerebellar tonsils
97
Chiari III associations
- syrinx (cervical)
- tethered cord
- hydrocephalus
- agenesis of the corpus callous
Only seen in patients with neural tube defect
98
Mesial temporal sclerosis
Hippocampal volume loss and glosis/scar
Intractable seizures, most common cause of partial complex epilepsy
Cured by surgical removal
Most likely developmental
99
Mesial temporal sclerosis imaging findings
- reduced hippocampal volume (10% loss is bilateral)
- increased T2 signal from gliosis/scar
- loss of normal morphology (loss of normal interdigitations)
- compensatory enlargement of temporal horn of the lateral ventricle
- atrophy of the ipsilateral fornix and maxillary body
- contralateral amygdala enlargement
100
MRI epilepsy protocol
- T1 - superior for cortical thickness, evaluation of grey/white
- FLAIR - superior for cortical/subcortical height signal (gliosis)
- T2*/SWI - superior for blood breakdown products
101
6th nerve palsy
Abducens nerve (cranial nerve VI) is damaged, impairing its ability to control the eye's outward movement (abduction)
102
Obstruction at Foramen of Monro
Colloid cyst
103
Obstruction at cerebral aqueduct
- aqueduct stenosis
- tectal glioma
104
Obstruction of 4th ventricle
- posterior fossa tumour
- cerebellar oedema/bleed
105
Normal pressure hydrocephalus
- urinary incontinence
- confusion
- ataxia
wet wacky wobbly
106
Communicating hydrocephalus
All ventricles are big
Level of obstruction between basal cisterns and arachnoid granulations
CSF can exit all the ventricles
107
Communicating Hydrocephalus +
Elderly + Ataxia
Normal pressure hydrocephalus
108
Communicating Hydrocephalus + Middle Aged + Headache
SHYMA
Syndrome of Hydrocephalus in the Young and Middle-aged Adult
109
Congenital hydrocephalus causes
1. Aqueductal stenosis
2. Neural tube defect - usually Chiari II
3. Arachnoid cysts
4. Dandy-Walker
110
Aqueductal stenosis
Most common cause of congenital obstructive hydrocephalus.
Classically from a web or diaphragm at the aqueduct.
Because of the location you get a "non-communicating" pattern
- dilation of the lateral ventricles and 3rd ventricle
- normal sized 4th ventricle.
Macrocephaly with thinning of the cortical mantle.
111
Aqueductal stenosis treatment
- shunting
- 3rd ventriculostomy
112
Aqueductal stenosis appearance
"sunset eyes" or upward gaze paralysis
113
Bickers Adams Edwards syndrome
A male with "flexed thumbs" - x-linked variant of aqueductal stenosis
114
Arachnoid cysts
Cysts located in the arachnoid space of CSF density, no solid components or abnormal restricted diffusion.
Can block CSF pathway (obstructive)
115
CSF shunt
Proximal tube placed within frontal horn of lateral ventricle anterior to the foreman of Monroe.
Tip usually in peritoneum, though can be placed in pleural space or right atrium
116
Under shunting caused by proximal obstruction
Most common cause = in growth of choroid plexus and particulate debris/blood products.
Can be from catheter migration
117
Undershunting caused by distal obstruction
Pseudocyst (loculated fluid along distal tip)
Catheter migration (more common in children)
118
Overshunting
"slit like ventricles" - meaningless or overshunting (worrying for causing a subdural hygroma or haematoma)
119
CSF shunt infection
Usually within 6 months of placement. Blood cultures negative, fluid should be cultured. Debris within the ventricles (DWI) for diagnosis of ventriculitis.
Let stigmata includes ventricular loculations
120
CSF shunt distal complications
Hydrothorax or ascites
121
Cytotoxic oedema
Intracellular swelling due to malfunction of Na/K pump
Favours grey matter - looks like grey-white matter differentiation loss
Seen with stroke or trauma
122
Vasogenic oedema
Extracellular swelling due to disruption of blood-brain barrier.
Oedema tracking through the white matter
Seen with tumour and infection (or late stage cerebral ischaemia). Improves with steroid.
123
Subfalcine (Cingulate) Herniation
Midline shift
ACA may be compressed, and can result in infarct.
124
Descending Transtentorial (Uncal) Herniation
Uncus and hippocampus herniate through the tentorial incisura.
Effacement of the ipsilateral suprasellar cistern occurs first.
125
Duret Hemorrhages
Perforating basilar artery branches get compressed in uncal herniation.
Located in the midline at the pontomesencephalic junction. Can also affect cerebellar peduncles.
126
Which nerve is affected in uncle herniation
CN 3 gets compressed between the PCA and Superior Cerebellar Artery causing ipsilateral pupil dilation and ptosis
127
Kernohan's Notch/Phenomenon
Uncal herniation - midbrain on the tentorium forms an indentation (notch) and the physical exam finds ipsilateral hemiparesis (false localising sign).
128
Ascending Transtentorial Herniation
Vermis herniates upward through tensorial incisura, often resulting in severe obstructive hydrocephalus.
Think posterior fossa mass
129
Cerebellar Tonsil Herniation
Can be from severe herniation after downward transtentorial herniation.
If in isolation - Chiari (Chiari I= 1 tonsil - 5 mm).
130
Ascending Transtentorial Herniation imaging findings
- The "Smile" of the quadrigeminal cistern will
be flattened or reversed
- "Spinning Top" appearance of the midbrain from bilateral compression along its posterior aspect
- Severe hydrocephalus ( at the level of the aqueduct).
131
Osmotic Demyelination aka
Central Pontine Myelinolysis
132
Osmotic Demyelination
- T2 bright in the central pons (spares periphery)
- Earliest change: restricted diffusion in lower pons
133
Wernicke Encephalopathy on MRI
- T2/FLAIR bright classically seen in medial/dorsal thalamus (around the 3rd ventricle), periaqueductal grey, mamillary bodies, and the tectal plate.
- Enhancement is classic in the mamillary bodies
- MR Spect = Lactate
134
Marchiafava-Bignami
- confusion
- altered gait
- seizures
-muscle rigidity
135
Marchiafava-Bignami acute imaging appearances
- 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
136
Marchiafava-Bignami chronic imaging appearances
Thinned corpus callosum + cystic cavities favouring in the genu and splenium
137
"Sandwich sign"
On sagittal imaging - describes the pattern of preference for central fibers with relative sparing of the dorsal and ventrals fibers of T2 bright signal of CC in acute Marchiafava-Bignami
138
Direct Alcoholic Injury
Brain Atrophy. Particularly the cerebellum
and especially the cerebellar vermis
139
Copper & Manganese Deposition
- 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
140
Methanol Toxicity
Optic nerve atrophy, hemorrhagic putaminal and subcortical white matter necrosis
141
Carbon monoxide imaging
CT Hypodensity / T2 Bright: Globus Pallidus Monoxide
(carbon monoxide causes "globus" warming)
142
Methanol poisoning imaging
T2 Bright: Putaminal - which may be hemorrhagic, and thus CT Hyperdense.
143
PRES (Posterior Reversible Encephalopathy syndrome)
Asymmetric cortical and subcortical white matter oedema (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).
144
Vasogenic oedema pattern in PRES
Bilateral, posterior, mildly asymmetric
145
Post chemo PRES
Nonclassic look compared to hen as spares the occipital lobes.
Targets basal ganglia, brainstem, and cerebellum.
146
Leukoencephalopathy (treatment induced)
Classic look would be centered in the periventricular white matter - bilateral, symmetric, confluent, T2/FLAIR bright changes (history obviously key to the diagnosis).
147
Disseminated necrotizing leukoencephalopathy
Severe white matter changes, which demonstrate ring enhancement , classically seen with leukemia patients undergoing radiation and chemotherapy.
Can be fatal
148
Post radiotherapy change MRI brief
T2 bright areas and atrophy corresponding to the radiation portal
149
Post radiotherapy - acute MRI changes
Days - weeks
Rare
150
Post radiotherapy - early delayed MRI changes
1-6 months
Looks similar to chemo
High T2/FLAIR signal in the periventricular white matter
Usually reversible
151
Post radiotherapy - late delayed MRI changes
6 months
"Mosaic" pattern with high WM signal changes again favoring the deep white matter. Can appear "mass-like" and expansile. Classically sparing of the U-Fibers & Corpus Callosum.
Progressive but usually reversible
152
Radiation-Induced Vascular Malformations: MRI appearance
Blooming on GRE/SWI sequences.
The most classic types are capillary telangiectasias / cavernous malformations.
The most classic scenario is a kid getting whole brain radiation for ALL.
153
Radiation-induced Brain Cancer
* 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
154
Radiation-Induced Vasculopathy: MRI appearance
Strokes and Moya-Moya type of look.
155
Mineralizing Microangiopathy MRI appearance
A delayed finding (2 years) following radiation treatment.
Think calcifications (basal ganglia and subcortical white matter)
156
Heroin lnhalational Leukoencephalopathy
Non specific imaging appearance
Classic -
- symmetric butterfly in the centrum semi ovale
- high signal in the posterior limb of the interior capsule
- high signal in the deep cerebellar white matter
- sparing of the dentate nucleus
157
Classic MS pattern
Pattern favors involvement of the juxtacortical and periventricular regions with lesions that have ovoid and/or fusiform morphology
158
Ovoid/fusiform MS lesion size
A single lesion > 15 mm in size suggests the underlying etiology is not vascular.
159
McDonald Diagnostic Criteria for MS
- lesions disseminated in space (periventricular, juxtacortical, infratentorial, spinal cord) - more than 1 in at least 2 of these locations
- dissemination in time: best shown as a T2 bright lesion that does enhance (active) and a T2 bright lesion that does not enhance (in-active) - lesions are in different phases of the disease and therefore separated by time
160
MS epidemiology
Usually targets women 20-40 (in children there is no gender difference).
Multiple sub-types - relapsing-remitting form being the most common (85% )
Clinical history of "separated by time and space" is critical
161
Classic MS finding
T2/FLAIR oval and periventricular perpendicularly oriented lesions
162
Involvement of the calloso-septal interface
98% specific for MS
163
Children MS appearance
In children the posterior fossa is more commonly involved.
164
MS brain atrophy
Accelerated
165
MS solitary spinal cord involvement
Solitary spinal cord involvement can occur but it is typically seen in addition to brain lesions
166
MS spinal lesion location?
Cervical spine is the most common location in the spine (65%).
Tend to be peripherally located
167
Which MR sequence for MS juxtacortical and periventricular lesions?
FLAIR is more sensitive than T2 in detection of juxtacortical and periventricular plaques.
168
Which MR sequence of infratentorial lesions MS?
T2 is more sensitive than FLAIR for detecting infratentorial lesions
169
MR spectroscopy in MS
Reduced NAA peaks within the plaques.
170
Active vs not active MS MRI
Acute demyelinating plaques should enhance and restrict diffusion
171
Tumor vs MS MRI
A big MS plaque can ring enhance but classically incomplete (like a horseshoe), with a leading demyelinating edge.
172
ADEM
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.
173
Acute Hemorrhagic Leukoencephalitis (Hurst Disease)
This a fulminant form of ADEM with
massive brain swelling and death. The hemorrhagic part is only seen on autopsy (not imaging).
174
Devics (neuromyelitis optica)
Transverse Myelitis + Optic Neuritis.
Lesions in the Cord and the Optic Nerve
175
Marburg Variant
Childhood variant that is fulminant and terrible leading to rapid death. It usually has a febrile prodrome.
"MARBURG!!!" = DEATH
176
Subcortical Arteriosclerotic Encephalopathy (SAE) is AKA?
Binswanger Disease
177
What is SAE?
Multi-infarct dementia that ONLY involves the white matter
Strong association with hypertension, aged >55
178
SAE location
Favors the white matter of the centrum semiovale (white matter superior to the lateral ventricles/ corpus callosum)
Classically spares the subcortical U fibers
179
Genetically transmitted form of SAE
CADASIL
Younger patient with migraines that looks like SAE
180
CADASIL stands for
Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy
181
Most common hereditary stroke disorder
CADASIL
182
CADASIL gene mutation
NOTCH3 mutations on chromosome 19
183
CADASIL classic imaging findings
- 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.
184
Motor strip on PET
On FDG PET the motor strip is always preserved in a degenerative type of dementia
185
Alzheimer Disease classic imaging
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
186
Multi infarct dementia classic imaging
Cortical infarcts and lacunar infarcts are seen on MRI. Brain atrophy (generalized) is usually
advanced for the patients age
187
Dementia with Lewy bodies classic imaging
Mild generalized atrophy without lobar predominance (unlike multi-infarct).
Hippocampi will be normal in
size ( unlike AD)
188
Alzheimers disease FDG pattern
Low posterior temporoparietal uptake -
"headphones" or "ear muffs".
189
Multi infarct dementia FDG pattern
Multiple scattered areas of decreased
activity. No specific lobar predominance.
Can knock out motor strip.
190
Lewy body dementia FDG pattern
Decreased FDG uptake in the lateral occipital cortex
Sparing of the mid posterior cingulate gyrus (Cingulate Island Sign).
191
11C PiB (Pittsburgh compound B)
Amyloid Binding Tracer
192
Picks / Frontotemporal dementia
- earlier onset than AD (40-50s)
- compulsive or inappropriate behaviours
193
Picks imaging appearance
Severe symmetric atrophy of the frontal lobes (milder volume loss in the
temporal lobes).
194
Picks FDG pattern
Low uptake in the frontal and temporal lobes.
195
Fahr Disease (syndrome) is AKA
"Bilateral Striatopallidodentate Calcinosis",
"Primary Familial Brain Calcification"
196
Fahr disease imaging
Extensive calcification in the Basal Ganglia and thalami.
Globus is typically involved first
197
Hallervorden Spatz is AKA
PKAN (pantothenate kinaseassociated
neuropathy)
198
Hallervorden Spatz
Iron in the Globus Pallidus
T2 Dark Globus with central bright area of necrosis "Eye of the Tiger". No enhancement. No Restricted Diffusion.
199
Amyotrophic Lateral Sclerosis
Upper motor neuro loss in the brain and spine. Most people die within 5 years.
200
Amyotrophic Lateral Sclerosis imaging
Does NOT show gross volume loss.
T2/FLAIR tends to be normal (rarely can
be bright in the posterior internal capsule).
201
Cortico-basal Degeneration
Tauopathy
Asymmetric frontoparietal atrophy.
Clinical manifestations like the
"Alien limb phenomenon" - 50% of cases.
202
Huntington Disease
Caudate Atrophy and reduced FDG uptake.
The frontal horns will become enlarged and
outwardly convex (from the atrophy pattern)
203
Leigh disease
Mitochondrial Disorder
Elevated Lactate peak at 1.3 ppm
204
Leigh disease imaging
T2/FLAIR bright lesions in the Brainstem,
Basal Ganglia , and Cerebral Peduncles.
They can restrict, but do NOT enhance.
205
MELAS syndrome
Mitochondrial Disorder
Lactic Acidosis, Seizures, and Strokes
Elevated Lactate "doublet" at 1.3 ppm
206
MELAS syndrome imaging
Atypical strokes in the cortical gray matter with a nonvascular distribution (usually occipital and parietal).
207
Hurler syndrome
Lysosomal Storage Disease / Mucopolysaccharidoses
(1) Macrocephaly with Metopic "beak"
(2) Enlarged Perivascular Spaces
(3) Beaked Inferior L1 Vertebral Body
(2) - Underlying white matter normal - Hurler Holes
208
Parkinson Disease (PD)
Impossible to diagnose on CT or MR alone
Supposedly has mild midbrain volume loss with a "butterfly" pattern
**Sparing of the midbrain and superior cerebellar peduncles.**
209
MultiSystem Atrophy (MSA) vs PD
I-123 MIBG can be used to differentiate PD from MSA, by looking at the cardiac/mediastinal ratio (which is normal in MSA, and abnormal in PD)
210
MSA imaging
Cerebellar Hemisphere / Peduncle Atrophy with a Shrunken Flat Pons & an enlarged 4th ventricle.
211
Hot cross bun sign
MSA
Loss of transverse fibres in pons
212
Progressive Supranuclear Palsy (PSP) is AKA
Steele-Richardson-Olszewski
213
Mickey Mouse sign
Tegmentum atrophy with sparing of the tectum and peduncles
PSP
214
Hummingbird sign
Midbrain volume loss with concave upper surface and relative sparing of the pons
PSP
215
Progressive Supranuclear Palsy (PSP)
Parkinsons disease but Tauopathy
216
Wilsons disease
AR copper metabolism malfunction.
Liver then elsewhere, 95% have "Kayser-Fleischer Rings"
217
Wilsons disease CT
Cortical Atrophy is the most common CT finding (although obviously very non-specific).
218
Wilsons disease MRI
T1 and T2 bright BG are the most common initial MR findings (supposedly).
T2 bright dorsal medial thalamus
219
Panda sign
T2 Bright Tegmentum with normal dark red nuclei & substantial nigra
Wilson disease
220
Deep brain stimulator position
Parkinson Disease - 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).
221
The lower the NAA... (MRS)
The higher the grade of tumour (MRS)
222
Reversed Hunters angle (MRS)
Abnormal - tumour?
223
MRS - lipid
Product of brain destruction - necrosis marker.
Elevated in high grade tumours, infarcts, brain abscesses
224
MRS - lactate
Absent when normal.
Brain tumour has outgrown its blood supply and using anaerobic pathway for metabolism. Also elevated in cerebral abscess.
225
MRS - lactate neonates
Normal to be elevated in first hours of life
226
MRS - lipid and lactate
Peaks superimpose. Use intermediate TE (around 140) to cause "inversion" of lactate peak to see it
227
MRS - alanine
Amino acid. Found in meningiomas
228
MRS - NAA
Neuronal marker (neuron viability), usually tallest peak.
Glial tumours have NAA. The higher the tumour grade, the lower the NAA.
229
Super high NAA peak
Canavans
230
MRS - Glutamine (GLX)
Neurotransmitter. Increased with hepatic encephalopathy
231
MRS - Creatinine
Energy motabolism.
Decreased in tumour necrosis
232
MRS - Choline
Cell membrane turnover.
More turnover more choline (so high in high grade tumour, demyelination, inflammation)
233
MRS - myoinositol (mI)
Cell volume regulator and byproduct of glucose metabolism.
234
MRS - myoinositol (mI) elevated in
- low grade gliomas
- Alzheimers
- PML
235
MRS - myoinositol (mI) reduced in
- high grade gliomas
- hepatic encephalopathy
236
Leukodystrophy
Messed up white matter, untreatable, fatal (kids)
237
Adreno Leukodystrophy (ALD) genetics
X linked recessive, male predominant.
238
Adreno Leukodystrophy (ALD) imaging
Parietal occipital predominant.
Extends across the splenium of the corpus callosum.
Can enhance and restrict on FLAIR.
239
Metachromatic leukodystrophy imaging
MOST COMMON
Frontal predominance.
Periventricular and deep white matter - trigroid pattern (stripes of milder disease).
U-fibers are relatively spared.
240
Head size leukodystrophy - normal
- ALD
- Metachromatic
- Pelizaeus-Merzbacher
- Leigh disease
241
Head size leukodystrophy - big
- Alexander disease
- Canavans disease
242
Head size leukodystrophy - small
- Krabbe
243
Alexander disease imaging
Frontal predominance
Also hits cerebellum and middle cerebellar peduncles
Can enhance (FLAIR)
244
Canavan disease imaging
Diffuse bilateral subcortical U fibres.
"Subcortical predominance"
Elevated NAA (MRS)
245
Krabbe imaging
Centrum semiovale and periventricular white matter with parieto-occipital predominance.
High density foci on CT (in the thalamus,
caudate, and deep white matter).
Early sparing of the subcortical U fibres.
246
Pelizaeus-Merzbacher imaging
Typically diffuse "total lack of normal
myelination" with extension to the subcortical U fibres.
Patchy variant is also described as "tigroid" -
although that term is more classic form metachromatic.
No enhancement. No restricted diffusion.
247
Mitochondrial leukodystrophies
More asymmetric and favour the grey matter
(Mitochondrial dysfunction - inability to process O2. Grey matter needs more O2 than white matter.)
248
MELAS
Mitochondrial Encephalomyopathy, Lactic
Acidosis, and Stroke - like episodes.
249
MELAS imaging
Tends to have a parietooccipital distribution.
"Migrating Infarcts"
250
MELAS MRS
Increased Lactate, Decreased NAA.
251
Leigh Disease aka
Also called Subacute Necrotizing Encephalo-Myelopathy
252
Leigh Disease imaging
White matter distribution: Focal areas of subcortical white matter.
Gray matter distribution: Basal ganglia and Periaquaductal Gray
253
Multiple masses (brain tumours)
- multifocal primary from seeding
- mets (50% at solitary)
- syndromes (eg NF2)
254
Signs of extra axial location brain tumour
- 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
255
Why don't things enhance
They don't enhance because of the blood brain barrier
256
Why do things enhance
- they are outside the blood brain barrier (they are extra axial)
- they have disrupted the blood brain barrier
257
Differentiating infection and mets - brain imaging
Infection will restrict on diffusion
258
Most common CNS met in paeds
Neuroblastoma
(BONES DURA ORBIT - not brain)
259
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).
260
Most common morphology brain tumour
"round" or "spherical"
261
Mnemonic for bleeding mets
MRCT
Melanoma
Renal
Carcinoid / Choriocarcinoma
Thyroid
262
Which has more surrounding oedema - brain primary or mets (when similar size)
Mets
263
Most common intra axial mass in an adult
Met
264
Brain tumours that are multifocal from seeding
Medulloblastoma
Ependymoma
GBM
Oligodendroglioma
265
Brain Tumors that Like to be Multifocal
**Mets **
Lymphoma
Multicentric GBM
Gliomatosis Cerebri
266
Brain tumours in syndromes
More likely to be multifocal
267
NF1 brain tumours
Optic gliomas
Astrocytomas
268
NF2 "MSME" brain tumours
Multiple Schwannomas
Meningiomas
Ependymomas
269
Tuberous sclerosis brain tumours
Subependymal tubers
IV Giant cell astrocytomas
270
VHL brain tumours
Hemangioblastomas
271
Cortically based brain tumours
P-DOG
P - pleomorphic xanthoastrocytoma (PXA)
D - dysembryoplastic neuroepithelial tumour (DNET)
O - oligodendroglioma
G - ganglioglioma
272
PXA information
Paeds - age 10-20
Will enhance
Usually no peritumeral T2 signal
Dural tail ***
Cyst with nodule (50%)
Temporal lobe
Frequently invades the leptomeninges
273
DNET information
Paeds - <20
No enhancement
High T2 signal with bright FLAIR rim
"Bubbly" (High T2 signal)
Temporal lobe
Focal cortical dysplasia in 80%
274
Oligodendroglioma
Adult - 40-50s
Can enhance
Calcification common (90%)
"Expands the cortex"
Frontal lobe
1p/19q deletion
275
Ganglioglioma information
Any age
Can enhance
NOT bubbly
Can look like anything
Temporal lobe
Can have overlying bone remodelling
276
Kid with drug resistant seizures
DNET
277
Bright rim sign
Persistent rim of FLAIR signal in DNET
Looks similar to T2 FLAIR
Mismatch of astrocytomas
278
Tumours arising from the ventricular wall and septum pellucidum
- Ependymoma (Paeds)
- Medulloblastoma (Paeds)
- SEGA (Subependymal Giant Cell Astrocytoma) (Paeds)
- Subependymoma (Adult)
- Central Neurocytoma (young adult)
279
Tumours arising from the choroid plexus
- Choroid Plexus Papilloma (paeds in trigone, adults in 4th vent)
- Choroid plexus carcinoma (paeds)
- Xanthogranuloma ("Found" in adults)
280
Ependymoma age
Bimodal - large peak at 6yo and tiny peak 30yo
281
Ependymoma types
- 4th ventricle 70% (FLOOR) - freq extension into foramen of Luschka and Magendie.
TOOTHPASTE
- parenchymal supratentorial 30% - usually big >4cm at presentation
282
Medulloblastoma age
Most occur before 10yo
(small second peak 20-40)
283
Medulloblastoma location
Cerebellar arising from vermis / ROOF of the 4th ventricle -project into 4th ventricle
284
Medulloblastoma imaging appearance
Dense mass on CT
Heterogenous on T1 and T2
Enhances homogenously
Hypercellular and may restrict
Calcify in 20%
285
Zuckerguss
German for sugar icing
For drop mets (medulloblastomas)
Post con brain/spinal cord - leptomeningeal carcinomatosis
Associated with basal cell nevus syndrome and Turcots syndrome
286
Gorlin syndrome
Medulloblastoma and thick dural calcifications
They get basal cell skin ca after radiation and have odontogenic cyst
287
More common - medulloblastoma or ependymoma
Medulloblastoma
288
4th ventricle roof origination tumour
Medulloblastoma
289
4th ventricle floor origination tumour
Ependymoma
290
Brain tumour extends into basal cisterns like toothpaste
Ependymoma
291
Brain tumour enhancement medulloblastoma vs ependymoma
Medulloblastoma - enhances homogenously
Ependymoma - enhances heterogeneously
292
Which calcifies more medulloblastoma vs ependymoma
Medulloblastoma less at 20%
Ependymoma more at 50%
293
Linear "icing like" enhancement of the brain surface
Zuckerguss - associated with medulloblastoma
294
SEGA
Subependymal giant cell astrocytoma
295
SEGA imaging
Arises from lateral wall of ventricle near foramen of Monro.
Often causes hydrocephalus.
Enhances homogeneously.
Can calcify.
296
Subependymoma
Adults
Well circumscribed IV mass most commonly at the foramen of Monro and the 4th ventricle.
Can cause hydrocephalus.
Don't typically enhance.
T2 bright.
297
Central neurocytoma information
Most common IV mass in adult 20-40
SWISS CHEESE
298
Central neurocytoma
SWISS CHEESE - numerous cystic spaces on T2
Calcify a lot
299
Chroroid plexus papilloma/carcinoma demographics
85% <5yo, or adults
Make up 15% of brain tumours in kids <1yo
300
Chroroid plexus papilloma/carcinoma location
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
301
Chroroid plexus papilloma/carcinoma association
Carcinoma association with Li-Fraumeni syndrome (bad p53)
IV mass often making CSF so causes hydrocephalus
302
Chroroid plexus papilloma/carcinoma angiography
Angiography may show enlarged choroidal arteries which shunt blood to the tumor,
303
Chroroid plexus papilloma/carcinoma spread
The tumor is typically solitary but in rare instances you can have CSF dissemination
303
Xanthogranuloma
Benign choroid plexus mass
They restrict on diffusion
304
The most common location of intra ventricular metastasis
The trigone of lateral ventricles (because of the vascular supply of the choroid).
305
Most common ca to met to IV brain
Lung, then renal (there are less renal ca compared to lung)
306
Colloid cyst information
Found almost exclusively in the anterior part of the 3rd ventricle behind the foramen of Monro.
Can cause sudden death via acute onset
hydrocephalus.
307
Colloid cyst appearance
Depends on what they are made of
- cholesterol will be T1 bright, T2 dark.
- no cholesterol T2 bright.
The trick is a round well circumscribed mass in the anterior 3rd ventricle.
Hyperdense on CT
308
Intraventricular meningiomas
Can occur in an intraventricular location, most commonly (80%) at the trigone of the lateral ventricles (slightly more on the left).
309
Cerebellar pontine angle brain tumours
1. Vestibular Schwannoma 75%
2. Meningioma 10%,
3. Epidermoid 5%.
The rest are uncommon.
310
Bilateral vestibular schwannoma
NF2
311
Vestibular schwannoma enhancement
Enhances strongly but more heterogenous than meningiomas.
312
Ice cream cone IAC
Vestibular schwannoma
May widen the porus acousticus resulting in a "trumpet shaped" IAC. "Ice Cream Cone IAC. "
313
Most common location of a meningioma
is over the cerebral convexity.
314
Meningioma on nuclear imaging
Meningiomas take up octreotide and Tc-MDP on Nuclear Medicine tests
315
CPA tumour invasion - schwannoma vs meningioma
Schwannoma invades IAC, meningioma doesnt usually
316
CPA tumours enhancement - schwannoma vs meningioma
Schwannoma enhance less homogeneously, meningioma enhances homogenously
317
Epidermoid tumour information
Can be congenital or acquired (after trauma, classically after LP in spine)
Usually off midline
318
Epidermoid tumour imaging
Follow CSF density and intensity on CT and MRI
Bright on FLAIR
Restrict diffusion
319
Dermoid cyst information
4x less common than epidermoid
More common in kids/young adults
Usually midline and found in the 3rd decade
Associated with NF2
320
Dermoid cyst on imaging
They contain lipoid material and are usually hypotenuse on CT and very bright on T1
321
Most common location for a dermoid cyst
is the suprasellar cistern (posterior fossa is no 2)
322
Headache, seizure, "Chemical Meningitis"
Ruptured dermoid cyst
323
Ruptured dermoid cyst brain imaging
Fat droplets (typically shown as low density on CT, or High Signal on Tl) floating in the ventricles and/or subarachnoid space.
324
Fat droplets (typically shown as low density on CT, or High Signal on Tl) floating in the ventricles and/or subarachnoid space.
Ruptured dermoid cyst brain
325
Dermoid vs Epidermoid
The easy way to think of this is that the Epidermoid behaves like CSF, and the Dermoid behaves like fat.
326
IAC Lipoma
Uncommon - basically the only reason you get a T1 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.
327
Arachnoid Cyst
Common benign lesion
They are increased in frequency in mucopolysaccharidoses (as are perivascular spaces).
328
Arachnoid cyst location
Located within the subarachnoid space and contains CSF.
329
Arachnoid cyst imaging
They are dark on FLAIR (like CSF), and will NOT restrict diffusion.
330
330
How can you tell an epidermoid: from an arachnoid cyst?
The epidermoid restricts, the arachnoid cyst does NOT.
331
AT/RT tumour
Atypical teratoma/Rhabdoid tumour
332
AT/RT demographic
Highly malignant tumour (WHO IV)
Rarely occur in patients >6yo
Ave age 2yo
333
AT/RT location
Can occur in supra and infratentorial locations (most common in the cerebellum)
334
AT/RT appearance
Large, with necrosis, often in posterior fossa
Can have calcification
335
Juvenile Pilocytic Astrocytoma (JPA)
Cyst with a nodule in a kid
WHO grade I
Posterior fossa, or optic chiasm
336
Enhancement of the cystic wall (in a tumour)
JPA can have (50%), haemangioblastoma won't
337
Posterior fossa cyst with a nodule - Paeds
JPA
338
Posterior fossa cyst with a nodule - Adult
Haemangioblastoma
339
Haemangioblastoma associted conditions
- Von Hippel Lindau
- Polycythaemia
340
Multiple haemangioblastoma
Think VHL
341
Haemangioblastoma information
Slow growing, indolent, vascular tumour
Hydrocephalus from mass effect
342
Haemangioblastoma location
90% in cerebellum
343
Haemangioblastoma appearance
Cyst with nodule
70% flow voids along periphery of cyst
344
DPG
Diffuse Pontine Glioma
345
DPG age
Paeds, 3-10yo
346
DPG location
Pons most commonly (usually a high grade fibrillary glioma)
347
DPG imaging
T2 bright with subtle or no enhancement
4th ventricle will be flattened
348
Most common primary brain tumour in adults
Astrocytoma
349
Ribbon pattern of calcification classic for ...
Oligodendroglioma
350
Astrocytoma grades
1 - Subependymal Giant Cell Astrocytomas or Pilocytic Astrocytoma
2 - Diffuse
3 - Anapaestic
4 - GBM
351
Grade 1 Astrocytoma
- Subependymal Giant Cell Astrocytomas
- Pilocytic Astrocytoma
352
Grade 2 Astrocytoma
Diffuse
353
Grade 3 Astrocytoma
Anaplastic
354
Subependymal Giant Cell Astrocytomas
-lntraventricular mass near the foramen of
Monro in a young patient with tuberous
sclerosis.
-Can cause obstructive hydrocephalus
355
Grade 4 Astrocytoma
GBM
356
Pilocytic Astrocytoma
- Cyst with nodule in the posterior fossa of a
kid
357
G2 Astrocytoma imaging
White Matter is preferred
NO ENHANCEMENT
T2 Bright - FLAIR lso (mismatch sign)
358
G3 Astrocytoma imaging
White Matter is preferred
Mild ENHANCEMENT
T2 Bright - FLAIR lso (mismatch sign)
359
G4 Astrocytoma imaging
White matter is preferred
Can cross the midline
Ring enhancement (can be diffuse heterogenous)
T2 and FLAIR bright
360
G4 Astrocytoma associated syndromes
GBM -
- NF1
- Turcot
- Li Fraumeni syndrome
361
Mismatch sign
T2/FLAIR Mismatch: Seen with G2 and G3 astrocytoma
T2 tumor has high signal with surrounding vasogenic edema.
On FLAIR the tumor signal become isointense.
362
Gliomatosis Cerebri
A diffuse glioma with extensive infiltration
It involves at least 3 lobes and is often bilateral.
363
Gliomatosis Cerebri imaging appearance
- mild blurring of the gray-white differentiation on CT
- extensive T2 hyperintensity and little mass effect on MR
- it's low grade, so it doesn't typically enhance.
364
The most common supratentorial mass.
Mets
365
Melanoma mets T1
melanoma can be T1 bright even if it doesn't bleed.
366
Mets that like to bleed in the brain
CT-MR
Choriocarcinoma / Carcinoid
Thyroid
Melanoma
Renal
367
Primary CNS Lymphoma
End stage AIDS patients, and those post-transplant. EB virus plays a role.
Most common type is Non-Hodgkin B cell.
368
Thallium Positive on SPECT
Primary CNS Lymphoma
369
Thin, smooth, linear periventricular/ependymal enhancement pattern
Ependymitis
Classic example - CMV
370
Thick irregular periventricular/ependymal enhancement pattern
Lymphoma
371
Desmoplastic Infantile Ganglioma
- large cystic tumors that like to involve the superficial cerebral cortex and leptomeninges.
372
DIG location
- ALWAYS arise in the supratentorial location
- usually involve more than one lobe (frontal
and parietal most commonly)
373
DIG presentation age
usually present before the first birthday.
374
"rapidly increasing head circumference."
DIG
375
376
Chordoma
Locally aggressive tumor that originates from the notochord.
377
Chordomas are midline
- either in the clivus, vertebral bodies (especially C2), or Sacrum.
378
Chordoma most common locations
1. Sacrum
2. Clivus
379
Chondrosarcoma
Nearly always lateral to midline (chordoma is midline).
T2 bright
Have the classic "arcs and rings" matrix of a chondrosarcoma (on CT)
380
Hemangiopericytoma
A soft tissue sarcoma that can mimic an aggressive meningioma because they both enhance homogeneously
They won't calcify or cause hyperostosis , but will invade the skull.
381
The most common met to the dura is from
breast cancer
382
80% of mets will be situated at the
grey white matter junction
383
Pituitary adenoma MR
80% are T1 dark and T2 bright.
They take up contrast more slowly than normal brain parenchyma.
Next step= Dynamic contrast enhanced MR.
384
Most common tumor of the sella
Pituitary adenoma
385
Macroadenoma
Pituitary adenoma >1cm
386
Functional pituitary adenoma
Prolactin secreting (especially women)
387
Microadenoma
Pituitary adenoma <1cm
388
Pituitary Apoplexy
Hemorrhage or Infarction of the pituitary, usually into an enlarged gland ( either from pregnancy or a macroadenoma).
389
Pituitary apoplexy MRI
T1 bright (remember adenoma is usually Tl dark).
390
Rathke Cleft Cyst
Usually incidental, rarely symptomatic
Cleft usually between the anterior and posterior pituitary.
391
Rathke Cleft Cyst MR
Variable on T1 and T2, but are usually
very bright on T2. They do NOT enhance.
392
Craniopharyngioma
(a) Papillary - 10% (adults)
(b) Adamantinomatous - 90%.
393
Craniopharyngioma - papillary
Solid, no calcification
Recur less frequently as encapsulated
Strongly enhance
Occur along the infundibulum
394
Craniopharyngioma - adamantinomatous
Calcified
Recur more
"MACHINERY OIL"
395
Craniopharyngioma - adamantinomatous MR appearance
* Tl Bright
* T2 Bright
* CT I GRE = Calcifications
* Enhance Strongly (in the solid parts)
396
Hypothalamic Hamartoma
hamartoma of the tuber cinereum (part
of the hypothalamus located between the mammillary bodies and the optic chiasm).
397
Hypothalamic Hamartoma MR
* Tl Iso
* T2 Iso
* Do NOT enhance.
398
Hypothalamic Hamartoma classic history
Gelastic Seizures
(although precocious puberty is actually more common).
399
Pineal region tumour presentation
Vertical gaze palsy
(dorsal Parinaud syndrome)
400
Pineal region tumours
Germinoma
Pineoblastoma
Pineocytoma
Pineal cyst
401
Germinoma sellar region
Most common pineal region tumour
Seen almost exclusively in boys
Precocious puberty may occur from secretion of hCG.
402
Germinoma suprasellar region
Usually in girls
403
Germinoma imaging findings
Mass containing fat and calcification with variable contrast enhancement.
It is heterogeneous on T1 and T2 (because
of its mixed components).
404
Pineoblastoma
Highly invasive
Associated with retinoblastoma ("trilateral")
405
Pineoblastoma imaging findings
Heterogenous and enhance vividly
406
Pineocytoma
Rare in childhood
Well circumscribed and non invasive
Tend to be more solid, and the solid components typically enhance
407
Pineal cyst
Incidental finding
Can have thin enhancement
Calcifications occur in 25%
408
"Supratentorial tumour with restriction"
1. Abscess
2. Lymphoma
409
"CP angle tumour?"
Epidermoid
410
"Tumour crossing the midline"
1. GBM
2. Lymphoma
- radiation necrosis
- MS plaque in corpus callosum
- meningioma of falx simulating a midline cross
411
"Tumour with calcification"
- oligodendrogliomas calcify 90% of the time by CT
- astrocytomas calcify 20% of the time
Astro is very common, oligo is not.
So probs still astro in real life.
412
Tumours on T1 images
Most are T1 dark (or intermediate)
Exceptions
- tumour that has bled (CT-MR)
- tumour with fat (lipoma, dermoid)
- melanin (melanoma)
- cholesterol in colloid cyst
413
If you see tumours everywhere is brain?
NF2
414
NF1 tumour association
optic nerve glioma
415
NF2 tumour association
MSME;
Multiple Schwannomas
Meningiomas
Ependymomas
416
VHL tumour association
Haemangioblastoma (brain and retina)
417
TS tumour association
Subependymal Giant Cell Astrocytoma
Cortical Tubers
418
Nevoid Basal Cell Syndrome (Gorlin) tumour association
Medulloblastoma
419
Turcot syndrome tumour association
GBM
Medulloblastoma
Intestinal polyposis
420
Cowdens- "COLD" tumour association
Lhermitte-Duclos (Dysplastic Cerebellar Gangliocytoma)
421
MSME
NF2!!!
Multiple Schwannomas,
Meningiomas,
Ependymomas
422
"tiger stripe" mass
Lhermitte Dulcos
Typically contained in one cerebellar hemisphere ( occasionally crosses the vermis).
Actually a hamartoma (Cowdens is hamartoma condition)
423
As cell walls get broken down, NAA...
will go down (neuronal viability)
424
As cell walls get broken down, creatinine...
will go down (cellular metabolism)
425
As cell walls get broken down, choline...
will go up (cell membrane turnover)
426
Higher grade tumour will have (NAA CREAT LACT CHOL LIPID)
Less NAA
Less creatinine
More lactate
More choline
More lipids
(relative to low grade tumour)
427
Radiation necrosis lipids and lactate
Both raised (necrotic tissue)
428
Elevated choline in the T2 signal surrounding a brain tumour?
Infiltrating glioma
429
Most common TORCH?
CMV
3x more common than toxo which is 2nd
430
CMV classic look
Targets the germinal matrix resulting in periventricular tissue necrosis.
*Periventricular calcification*
431
Which TORCH has highest association with polymicrogyria
CMV
432
Toxoplasmosis classic look
Random calcification pattern, targets the basal ganglia
Associated with hydrocephalus
433
Rubella classic look
Calcifications are less common than in other TORCHs.
Focal high T2 signal might be seen in white matter (related to vasculopathy and ischemic injury).
434
HSV classic look paeds
Hemorrhagic Infarct, with resulting Bad Encephalomalacia and atrophy (Hydranencephaly)
435
HIV paeds classic look
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.
436
The most common opportunistic infection in patients with AIDS is
Toxoplasmosis
437
The most common fungal infection (in people with AIDS)
Cryptococcus
438
HIV encephalitis MRI
Symmetric increased T2 / FLAIR signal in the deep white matter. Normal T1.
The lesions will not enhance.
There may be associated brain atrophy.
439
HIV encephalitis CD4 count
<200
440
HIV encephalitis subcortical U fibres
are spared
441
HIV encephalitis T1
Normal
442
HIV encephalitis lesions
Do not enhance
443
Progressive Multifocal Leukoencephalopathy (PML) is caused by
JC virus
444
Progressive Multifocal Leukoencephalopathy (PML) has a CD4 count of
<50
445
Progressive Multifocal Leukoencephalopathy (PML) on CT
Single or multiple scattered hypodensities,
446
PML on MRI
Single or multiple scattered T1 hypointensity
T2/FLAIR hyperintensities out of proportion to mass effect - buzzword
447
PML subcortical U fibres
Involved
448
CMV in HIV
Brain atrophy
Periventricular hypodensities (that are T2/FLAIR bright)
Thin ependymal enhancement
449
Cryptococcus common presentation
Meningitis that involves the base of the brain (leptomeningeal enhancement)
450
Dilated perivascular spaces filled with mucoid gelatinous material (these will not enhance).
Crytococcus
451
Cryptoccomas on MRI
Lesions in the basal ganglia that are T1 dark, T2 bright, and may ring enhance
452
Most common opportunistic infection in AIDS.
Toxoplasmosis
453
Toxoplasmosis MRI
T1 dark, T2 bright, ring enhancing (when larger than 1 cm) lesions.
These guys will NOT show restricted diffusion.
454
"ring enhancing lesion, with LOTS of edema."
Toxoplasmosis
455
Toxo is Thallium ...
Cold
456
Lymphoma is Thallium...
Hot
457
PET appearance of Toxo
Cold (acts like necrosis)
458
PET appearance of Lymphoma
Hot (acts like a tumour)
459
MR Perfusion Toxo
Decreased CBV
460
MR Perfusion Lymphoma
Increased (or decreased) CBV
461
TB meningitis
Predilection for the basal cisterns
(enhancement of the basilar meninges
with minimal nodularity).
May have dystrophic calcifications
462
TB meningitis complications
Vasculitis which may result in infarct (more common in children).
Obstructive hydrocephalus is common.
463
Enhancement of the Basilar Meninges + Hydrocephalus =
TB
464
Earliest sign of HSV on MRI
Restricted Diffusion - related to vasogenic edema.
465
Blooming on gradient in HSV
means it's bleeding
( common in adults, rare in neonate form).
466
Swollen T2 bright (unilateral or bilateral) medial temporal lobe
HSV - Herpes
467
HSV spares the ...
basal ganglia
468
Limbic encephalitis
Paraneoplastic syndrome (usually small cell lung cancer), that looks very similar to HSV.
469
HSV image, but the HSV titer is negative?
Lung cancer screening - worried re limbic encephalitis
470
Classic West Nile imaging
T2 bright basal ganglia and thalamus, with corresponding restricted diffusion.
Hemorrhage is sometimes seen.
471
CJD 3 types
- Sporadic (80-90%),
- Variant "Mad Cow" (rare)
- Familial (10%).
472
CJD 3 features
1. DWI Cortical Gyriform Restricted Diffusion
2. Hockey stick sign
3. Pulvinar sign
473
Hockey Stick Sign:
- Bilateral FLAIR bright dorsal medial thalamus
- Described in the variant subtype.
474
Pulvinar Sign:
- Bilateral FLAIR bright pulvinar thalamic nuclei (posterior thalamus).
- Classic in the variant subtype.
475
CJD DWI
Cortical pyriform 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.
476
A series of MRs or CTs showing rapidly progressive atrophy ...
CJD
477
Most common locations (in descending order) Neurocysticercosis
1- Subarachnoid over the cerebral hemispheres,
2- Basal cisterns,
3- Brain parenchyma,
4- Ventricles
478
Neurocysticercosis bug
tinea solium (pork tapeworm)
479
Neurocysticercosis involving the basal cisterns
Carries the worst outcome
480
Neurocysticercosis stages
1. Vesicular
2. Colloidal
3. Granular
4. Calcified/involution
481
Stage 1 Neurocysticercosis
Cyst + Scolex
No Enhancement
482
Stage 2 Neurocysticercosis
CT: Hyperdense Cyst
MR: Edema + Enhancement
483
Stage 3 Neurocysticercosis
CT: Early Calcification
MR: Smaller Cysts,
Less Edema,
Less Enhancement
484
Stage 4 Neurocysticercosis
CT: Calcification
MR: Blooming on SWI
(T2* etc .. )
485
Vascular Neurocysticercosis
Stage 1
486
Colloidal Neurocysticercosis
Stage 2
487
Granular Neurocysticercosis
Stage 3
488
Calcified/Involution Neurocysticercosis
Stage 4
489
Meningitis 4 categories
1. Bacterial (acute pyogenic)
2. Viral (lymphocytic)
3. Chronic (TB or fungal)
4. Non infectious (sarcoid)
490
Leptomeningeal means ...
Pial +Arachnoid
491
Pachymeningeal means ...
Dural
492
Leptomeningeal (Pia-Arachnoid) Enhancement:
Fills the subarachnoid spaces & extends into the sulci & cisterns.
493
Meningitis complications
Venous thrombosis,
Vasospasm (leading to the stroke),
Empyema,
Ventriculitis,
Hydrocephalus,
Abscess
494
Leptomeningeal enhancement seen with ....
Bacterial meningitis
Carcinomatous meningitis
495
Infants with meningitis also often get...
Sterile reactive subdurals
496
Abscess Facts (trivia)
- DWI - Restricts
- MRS - Lactate High
- FDG PET - Increased Metabolic
497
Pachymeningeal (Dural) Enhancement
Enhancement does NOT extend into the sulci
498
Pachymeningeal (Dural) Enhancement seen with ....
Intracranial Hypotension
Dural attachment of a Meningioma
Sarcoid
TB
Wegener's
Fungal Infections.
499
"Rim Phoma "
Secondary CNS Lymphoma is often extra-axial and can be dural based or fill the subarachnoid space
500
Empyema
Can be subdural (won't cross falx) or epidural (won't cross dural attachment)
Subdurals are more common and have more complications that epidural
501
Empyema
Sequela of frontal sinusitis (vast majority of subdurals, 2/3 of epidurals)
502
Empyema MRI
T1 bright and restrict diffusion
Dural enhancement
503
Abscess CT
Focal area of low density with surrounding low density vasogenic oedema.
504
Abscess T1 + C
Smooth Ring enhancement with multiple lesions - Suggests Abscesses
505
Abscess T2
Multiple Lesions with Vasogenic oedema - this is nonspecific (could be mets)
506
Abscess DWI
Typical Abscess (bacteria) will restrict.
Remember Atypical (Toxo etc .. ) doesn't
always restrict
507
Abscess vs tumour on CT
Hypercellular tumor (classic
example would be lymphoma) will be
hyper dense instead on low density like an abscess
508
Multiple rings mets vs abscess
Smooth margin - suggests abscess
Size - abscess tend to be smaller <10mm
Enhancement - tumour starts out solid then becomes ring enhancing with necrosis
509
Smooth ring
Abscess Rings tend to be thicker on the "Oxygen Side" or "Grey Matter Side" of the Brain - and thinner towards the ventricle.
510
Irregular ring
"Bumpy" or "Shaggy" inner lip of the ring is supposed to suggest necrosis and therefore tumour
511
Cerebritis
Early form of intra-axial infection, which can lead to Abscess if not treated.
512
Cerebritis on imaging
Vasogenic oedema without the well defined central enhancing lesion.
There may be spotty restricted diffusion.
513
Ventriculitis
Usually the result of a shunt placement or intrathecal chemo
514
Ventriculitis imaging
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".
515
DWI restricting pathology
**Abscess and stroke**
Certain hypercellular tumours (lymphoma)
Demyelinating lesions with acute features
516
Tumour enhancement MRI
Usually heterogeneous or homogenous if high grade ( or none if low grade).
Technically ring enhancement can also be seen with Gliomas, and Mets
517
Abscess enhancement MRI
classically have RING pattern.
518
MS enhancement pattern
classically have an INCOMPLETE RING pattern
519
Stroke enhancement pattern
Cortical ribbon (GYRIFORM) type enhancement in the sub-acute time period (around 1 week).
520
Heterogenous enhancement
Most likely Tumor
(higher grade)
521
Ring enhancement
Can be lots of stuff: Abscess and tumour are both prime suspects
522
Incomplete ring enhancement
Classic for demyelinating lesion
523
Gyriform enhancement
Classic for subacute stroke (can also be seen with PRES or encephalopathy/
encephalitis)
524
Parenchymal Contusion
Can look like blood with associated oedema in expected location
525
Parenchymal contusion typical location
Anterior temporal lobe and inferior frontal lobe
526
Diffuse axonal injury/shear injury CT and MRI
- initial head CT normal
- Multiple small T2 bright foci on MR
527
DAI - favourite sites
- posterior corpus callosum and GW-WM junction in the frontal and temporal lobes
528
DAI grading
Grade 1 - Grey-white interface
Grade 2 - Corpus callosum
Grade 3 - Brainstem
529
DAI of brainstem - grade?
3
530
DAI of corpus callosum - grade?
2
531
DAI of GW interface - grade?
1
532
SAH most common cause
Trauma
533
SAH most sensitive sequence?
FLAIR
534
Subdural appearance
Crescent shape
Crosses sutures
535
Epidural appearance
Lentiform shape
Assoc skull fracture - doesn't cross sutures
536
Epidural shape
Biconvex or lenticular
537
Subdural shape
Biconcave
538
Crossing midline - epidural vs subdural
Epidural can cross the midline
Subdural does not cross midline, may extend into interhemispheric fissure
539
Crossing sutures - epidural vs subdural
Epidural - cannot cross a suture
Subdural - can cross a suture
540
Bleed type - epidural vs subdural
Epidural - usually arterial
Subdural - usually venous
541
Swirl Sign
Sign of active bleeding.
The central low attenuation blood represents hyper-acute non-clotted blood, with surrounding acute clotted blood.
542
Hyperacute Acute ( < 1 hour) blood on CT
Hypodense
543
Acute (1 hour- 3 days) blood on CT
Hyperdense
544
Subacute ( 4 days - 3 weeks) blood on CT
Progressively less dense, eventually becoming isodense to brain.
Peripheral rim enhancement may occur with contrast.
545
Chronic (> 3 weeks) blood on CT
Hypodense
546
Hypodense blood on CT
Hyperacute/acute
Chronic
547
Hyperdense blood on CT
Acute
548
Isodense blood on CT
Subacute
549
What time is hyper acute blood on CT
<1 hour
550
What time is acute blood on CT
1 hour - 3 days
551
What time is subacute blood on CT
4 days - 3 weeks
552
What time is chronic blood on CT
>3 weeks
553
Blood on CT with peripheral rim enhancement (post contrast)
Subacute bleed - 4 days to 3 weeks
554
IB ID BD BB DD
It Be
Iddy Biddy
BaBy
DooDoo
555
George Washington Bridge
Oreo Cookie
T1 - Gray White Black
T2 - Black White Black
556
Hyperacute blood MRI
T1- Iso, T2 Bright
557
Acute blood MRI
T1 - Iso, T2 Dark
558
Early subacute blood MRI
T1 bright
T2 dark
559
Late subacute blood MRI
T1 bright
T2 bright
560
Chronic blood MRI
T1/T2 dark peripherally, centre may be T2 bright
561
Sequela of SAH
(1) Hydrocephalus - Early
(2) Vasospasm - 7-10 days
(3) Superficial Siderosis - Late
562
SAH cause in absence of trauma
- aneurysm
- benign non-aneurysm perimesencephalic haemorrhage
- superficial siderosis
563
Benign Non-Aneurysm Perimesencephalic hemorrhage association
Not assoc with aneurysm
May be associated with venous bleed
(need a negative CTA)
564
Benign Non-Aneurysm Perimesencephalic hemorrhage location
Around the midbrain and pons without extension into the lateral Sylvian cisterns or interhemispheric fissures is classic
ANTERIOR TO THE BRAINSTEM
565
Side effect of repeated episodes of SAH
Superficial siderosis
566
Superficial siderosis
Side effect of repeated episodes of SAH
567
Superficial siderosis appearance
Curvilinear low signal on gradient coating the surface of the brain.
568
Superficial siderosis history
Sensorineural hearing loss and ataxia
569
Pseudo-Subarachnoid Hemorrhage
Mimic of SAH that is seen in the setting of diffuse cerebral oedema
570
Density of the Pseudo SAH will be
less than 40
571
572
Acute blood tends to be around ..... HU.
60-70
573
Hypertensive haemorrhage common locations
Basal ganglia (most, esp putamen), pons, cerebellum
574
Interparenchymal haemorrhage types
- Hypertensive haemorrhage
- Amyloid angiopathy
- Septic emboli
AVMs, vasculitis, brain tumours (primary and mets)
575
Amyloid angiopathy haemorrhages
Multiple lobes at different ages with scattered microbleeds on gradient.
576
Septic emboli clinical scenario
IVDU, organ transplant, AIDS, lung AVMs, cyanotic heart disease
577
Septic emboli appearance
Numerous small foci of restricted diffusion.
Surrounding edema around the tiny
abscesses
578
Septic emboli complications
Septic emboli to the brain result in abscess and mycotic aneurysms (most commonly in the distal MCAs)
579
Septic emboli location
Location favors the gray-white interface and the basal ganglia.
580
Intraventricular haemorrhage causes
Trauma, tumour, htn, AVMs, aneurysms
581
Classic clinical scenario for watershed
infarcts ...
Severe hypotension (shock/ CPR/ Etc ..) Severe carotid stenosis
582
Watershed Infarcts in a Kid =
Moyamoya
583
Dense MCA Sign
Intraluminal thrombus is dense, usually in the M1 and/or M2 segments
584
Subacute Infarct uniqueness -
Enhances but creates NO Mass Effect
584
Loss of GM-WM differentiation
Basal Ganglia / Internal Capsular Region and Subcortical regions
584
Insular Ribbon Sign
Loss of normal high density insular cortex from cytotoxic edema
585
Enhancement in stroke CT
Starts in 3 days
Peaks in 3 weeks
Gone by 3 months
586
Artery of Percheron Stroke
V Shaped bilateral infarct of the paramedian thalami
(Artery of Percheron vascular variant)
587
Recurrent Artery of Heubner Stroke
Classic Caudate Infarct
The Artery of H is a deep branch off the proximal ACA
This thing can get "bagged" during the clipping of ACOM arte1y aneurysm.
588
Fetal PCOM Stroke Pattern
Infarcts in both the anterior and posterior circulation of the same hemisphere.
Variant anatomy with the PCA feeds primarily from the ICA.
589
Cardioembolic Stroke
Classic pattern of multiple foci of restricted diffusion scattered bilaterally along multiple vascular territories.
The clinical history is usually A-Fib or endocarditis.
590
Restricted diffusion without bright signal on FLAIR - which timing of stroke?
Hyperacute (< 6 hours).
591
Stroke MRI 0-6hrs
T1 iso
T2 iso
Diffusion Bright
FLAIR NOT BRIGHT
592
Stroke MRI 6-24hrs
T1 Dark
T2 Bright
Diffusion Bright
FLAIR Bright
593
Stroke MRI 24hrs - 1 week
T1 Dark (with bright cortical necrosis)
T2 Bright
Diffusion Bright
FLAIR Bright
594
When does hemorrhagic transformation of stroke typically occur
Between 6 hours and 4 days
595
Who typically gets haemorrhage transformation of stroke?
Pt on anticoagulant
Pt who got TPA
Pt with embolic stroke
People with venous infarct
596
Predictors of haemorrhagic transformation in patients getting TPA
- Multiple Strokes,
- Proximal MCA occlusion,
- Greater than 1/3 of the MCA territory,
- Greater than 6 hours since onset "delayed recanalization"
- Absent collateral flow
597
Venous infarct causes in babies, older children, and adults -
In little babies think dehydration
In older children - mastoiditis
In adults think about coagulopathies (protein C & S def) and oral contraceptives.
598
The most common site of venous thrombosis is -
the superior sagittal sinus, with associated infarct occurring 75% of the time.
599
Venous thrombosis signs on CT
Dense sinus ( on non-contrast CT) or "empty delta" ( on contrast enhanced CT).
600
Venous infarcts diffusion imaging
Tend to have heterogeneous restricted diffusion.
601
Arterial stroke - type of oedema?
Cytotoxic oedema
602
Venous Stroke - type of oedema?
Vasogenic oedema+ Cytotoxic oedema
603
Stigmata of chronic venous thrombosis include -
The development of a dural AVF, and/or increased CSF pressure from impaired drainage.
604
Venous thrombosis can result in ...
Vasogenic oedema that eventually progresses to stroke and cytotoxic oedema.
605
ASPECTS stands for
Alberta Stroke Program Early CT Score
606
ASPECTS is used for
a guideline for giving TPA in MCA strokes
607
How does ASPECTS work
You start out with 10 points, and lose points based on findings of acute cytotoxic ischemia to various locations eg caudate, insular ribbon etc
608
Which region stroke is ASPECTS used for
MCA
609
ASPECTS score with a good outcome
8 or more
610
The primary role of perfusion is -
To distinguish between salvagable brain (penumbra), and dead brain.
611
Who gets aneurysms
Smokers,
People with PKD,
Connective tissue disorders
(Marfans, Ehlers-Danlos),
Aortic coarctation,
NF,
FMD,
and AVMs.
612
Dolichoectasia of the Basilar Artery
A widened elongated twisty appearance of the basilar artery.
This is probably the result of chronic hypertension (abnormal vessel remodeling).
613
Dolichoectasia of the Basilar Artery complications
- nothing (most common)
- dissection
- compression of cranial
nerves (hemi-facial spasm)
- stroke (brainstem)
- hydrocephalus.
614
Where do aneurysms occur
Branch points
Favor anterior circulation (90%)
615
Most common site for aneurysm
Anterior communicating artery
(90% are anterior circulation)
616
The most common posterior circulation aneurysm location
The basilar
(PICA = no 2)
617
Rupture risk of a aneurysm increases with
- size
- posterior location
- hx of prev SAH
- smoker
- female
618
Most common shape of aneurysm
Berry
619
Most common cause of non traumatic SAH
Berry aneurysm
620
Underlying pathology of berry aneurysm
Congenital deficiency of internal elastic lamina and tunica media (at branch points)
Most are idiopathic
621
Fusiform Aneurysm - Associated with
PAN, Connective Tissue Disorders, or Syphilis.
622
Fusiform Aneurysm more commonly affect
the posterior circulation.
623
Fusiform Aneurysm may mimic
a CPA mass.
624
Pseudoaneurysm
An irregular (often saccular) arterial out-pouching at a strange / atypical location.
You may see focal hematoma next to the vessel on noncontrast.
- traumatic or mycotic
625
Traumatic pseudoaneurysm
Often distal secondary to penetrating trauma or adjacent fracture.
626
Mycotic pseudoaneurysm
Often distal (most commonly in the MCA), with the associated history of endocarditis, meningitis, or thrombophlebitis.
627
Blister Aneurysm
Broad-based at a non-branch point (supraclinoid ICA is the most common site).
(the angio is often negative)
628
Infundibular Widening
Not a true aneurysm - a funnel-shaped enlargement at the origin of the PCA at the junction with the ICA.
Thing to know is "not greater than 3 mm."
629
Aneurysm > 10mm
have a 1% risk of rupture per year.
630
Most common site for mycotic aneurysm
Distal MCA
631
Most common site for blister aneurysm
Broad Based Non-Branch Point (Supraclinoid ICA)
632
Most common site for pedicle aneurysm
Artery feeding the AVM
633
Most common site for fusiform aneurysm
Posterior circulation
634
Most common site for saccular aneurysm
Branch points in anterior circulation
635
Maximum bleeding - aneurysm location - ACOM
Interhemispheric fissure
636
Maximum bleeding - aneurysm location - PCOM
Ipsilateral basal cistern
637
Maximum bleeding - aneurysm location - MCA trifurcation
Sylvian fissure
638
Maximum bleeding - aneurysm location - Basilar tip
Interpeduncular cistern
Intraventricular
639
Maximum bleeding - aneurysm location - PICA
Posterior Fossa
Intraventricular
640
High flow AVM
Arterial component
NIDUS
Draining veins
Adjacent brain may be gliotic (T2 bright) and atrophic
641
Dural AVM
No nidus
Can be occult on MRI/MRA (catheter angio!)
642
"Caput medusa"
DVA
643
"large tree with multiple small branches"
DVA
644
Most Common Type of High Flow Congenital malformation
High flow AVM
645
Location of high flow AVM
Supratentorial (usually)
646
Most common complication of AVM
Bleeding (3% annual)
647
Risk of bleeding in AVMs increased with
Smaller AVMs (under higher pressure)
Small draining veins (can't reduce pressure)
Perinidal aneurysm
Basal ganglia location
648
AVM symptoms
Headache (no 1)
Seizure (no 2)
649
Dural AVF flow rate
Variable - can be high or low flow
650
Most common type of AVF
Spinal AVF
651
Risk of bleeding in dural AVF increases with
Direct cortical venous drainage
652
Dural AVFs aren't congenital
Acquired - classically from dural sinus thrombosis
653
Symptoms of dural AVF
Tinnitus (especially if sigmoid sinus involved)
654
Variation in normal venous drainage
DVA
655
Complication of resecting a DVA
Venous infarct
656
DVA is associated with...
cavernous malformations
657
DVA with evidence of prior bleeding (blooming on gradient)
Probably an associated cavernoma
658
DVA on MRI
Can have a halo of T2 bright gliosis
659
"Popcorn like" with "peripheral rim of haemosiderin"
Cavernous malformation
660
Cavernous malformation is best seen on
Gradient
661
Cavernous malformation - high or low flow
Low (WITHOUT intervening normal tissue)
662
Cavernous malformation AKA
Cavernoma
Cavernous angioma
663
Cavernous malformation can be induced from
Radiotherapy
664
Presence of fluid-fluid level
Recent intralesional bleed in a cavernous malformation
665
DVA
Developmental venous anomaly
666
Capillary Telangiectasia high or low flow
Low (WITH intervening normal tissue)
667
Capillary Telangiectasia can be induced with
Radiation
668
Classic look of Capillary Telangiectasia
Single lesion in the pons
Brush like of "stippled pattern" of enhancement
669
Capillary Telangiectasia best seen on
Gradient (slow flow and deoxyhaemoglobin)
670
Pineal Gland calcification
Common in adults, Rare in kids.
If you see calcification in a kid under 7, it could suggest underlying neoplasm.
671
Pineal Gland calcification "engulfed"
Germinoma = "Engulfed" Pattern "1"
672
Pineal Gland calcification "expanded"
Pineoblastoma & Pineocytoma: "Expanded" Pattern "2"
673
Habenular calcification
Curvilinear structure located a few
millimeters anterior to the pineal body.
About 1 in 5 normal adults will have calcification here.
674
Habenular calcification associated with
increased association with schizophrenia.
675
Choroid plexus calcification
Common in adults.
(Remember there is no choroid plexus in the frontal/occipital horn of the lateral ventricles or the cerebral aqueduct.)
676
Dural Calcifications
Common in adults.
If the calcs are bulky and there are a bunch of tooth cysts (Odontogenic keratocysts) think Gorlin Syndrome.
677
Sturge-Weber
Tram track / double-lined gyriform pattern parallel to the cerebral folds.
677
Basal Ganglia calcification
Very common with age, favours the globus pallidus.
If extensive & symmetrical think Fahr disease.
678
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.
679
Congenital CMV
Periventricular calcifications.
Can also have brain atrophy
680
Congenital Toxo
Basal Ganglia Calcifications + Hydrocephalus,
681
Neurocysticercosis - Etiology
Eating Mexican pork sandwiches
682
Sturge Weber - Etiology
Subcortical ischemia secondary to pial angiomatosis.
683
Neurocysticercosis end stage
End-stage will have scattered quiescent
calcified cyst remnants.
684
Scattered dots or stippled "popcorn" calcification
Cavernoma
685
Cavernoma calcification
Scattered dots or stippled "popcorn" calcification
686
Calcifications in the tortuous veins or the nidus
AVM calcification
687
AVM calcification
Calcifications in the tortuous veins or the nidus
688
Brain tumours that calcify
Old Elephants Age Gracefully
O: Oligodendroglioma - variable, but "ribbon" pattern is most common
E: Ependymoma (Medulloblastomas can also calcify - just less often)
A: Astrocytoma
G: Glioblastoma - mural calcified nodule
689
Most common calcified tumour
Astrocytoma as theres more of them
690
Mets that famously calcify
Osteosarcoma
691
When does vasospasm occur after SAH
4-14 days
692
What does vasospasm look like
smooth, long segments of stenosis
693
Vasospasm typically involves -
multiple vascular territories
694
What can vasospasm lead to
Stroke
695
Who gets vasospasm
Patients with SAH
The more volume of SAH the greater the
risk.
696
Are there Non-SAH causes of vasospasm?
Meningitis, PRES, and Migraine Headache.
697
Causes of vascular dissection
Penetrating trauma (tends to be carotids)
Blunt trauma (tends to be vertebrals)
698
T1 bright "crescent sign"
Vascular dissection - T1 bright intramural blood
699
Primary CNS Vasculitis cause
Primary Angiitis of the CNS (PA CNS)
700
Secondary CNS vasculitis cause
From infection, or sarcoid
Meningitis (bacterial, TB, Fungal), Septic, Embolus, Sarcoid,
701
Systemic vasculitis with CNS involvement causes
PAN, Temporal Arteritis, Wegeners, Takayasu's,
702
CNS vasculitis from a Systemic Disease causes
Cocaine Use, RA, SLE, Lyme's
703
Vasculitis appearance
Multiple segmental areas of vessel narrowing, with alternating dilation ("beaded appearance").
You can have focal areas of vascular occlusion.
704
Most common systemic vasculitis to involve the CNS
PAN
705
Most common collagen vascular disease
SLE
706
Puff of smoke
Moyamoya angiographic appearance
707
Progressive non-atherosclerotic stenosis of the supraclinoid ICA, eventually leading to occlusion.
Moyamoya
708
Moyamoya is -
Progressive non-atherosclerotic stenosis of the supraclinoid ICA, eventually leading to occlusion.
709
Distribution of Moyamoya
Watershed
710
Moyamoya in a child then think -
Sickle cell disease
711
Moyamoya associations
Sickle cell
NF
Prior radiation
Downs syndrome
712
Moyamoya age distribution
Bimodal - early childhood and middle age
713
Complications of Moyamoya
Children - stroke
Adults - bleed
714
Crossed Cerebellar Diaschisis (CCD):
Depressed blood flow and metabolism affecting the cerebellar hemisphere after a contralateral supratentorial insult (infarct, tumor resection, radiation).
715
