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Neuroradiology > Miscellaneous > Flashcards

Miscellaneous Flashcards

1
Q

Which 3 organ systems does TS affect?

A

Cortical and subependymal tubers
AMLs
Cardiac rhabdomyomas

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2
Q

List key neurologic findings in TS

A

Cortical/subcortical tubers
Subependymal hamartomas - may enhance but this does not help distinguish from SEGA
White matter change (i.e. radial bands)

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3
Q

Causes of T1 shortening (hyperintense)

A 
Fat
Proteinaceous substance
Gad
Blood (both intra and extracellular methemoglobin, and slowly flowing blood)
Melanin
Minerals (copper, iron, Mg)
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4
Q

Causes of T2 shortening (hypointense)

A

Most blood (except hyper acute and extracellular methemoglobin)
Calcification
Fibrous lesion
Highly cellular tumours (i.e. lymphoma, medulloblastoma)
Vascular flow void
Mucin (unlike in the pelvis where these lesions are T2 bright)

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5
Q

DDx periventricular enhancement

A
  • Primary CNS lymphoma
  • Infectious ependymitis (usu CMV) - thin linear enhancement along margins of ventricles
  • Primary glial tumour
  • MS
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6
Q

DDx gyriform enhancement

A
  • Herpes encephalitis (medial temp lobes and cingulate gyrus) or cerebritis
  • Subacute infarct - luxury reperfusion or cortical laminar necrosis, occurs 1week-months after (can also see enhancement after thrombolysis or thrombectomy)
  • Seizures, migraines
  • PRES
  • Neoplastic
  • Drugs toxicity (chemo or immunosuppressants)
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7
Q

DDx dural/pachymeningeal enhancement

A
  • Intracranial hypotension (thick/ linear enhancement, sagging of tonsils)
  • Post-op
  • Post LP
  • Meningeal neoplasm (i.e. meningioma), mets from breast and prostate ca
  • Granulomatous disease (sarcoid, TB, fungal disease) - typically in basal meninges
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8
Q

DDx leptomeningeal enhancement

A
  • Meningitis (viral, bacterial, fungal)
  • Leptomeningeal carcinomatosis (see below list)
  • CNS neoplasms - MOCLEGG (medullo, oligo, choroid plexus tumor, lymphoma, ependymoma, GBM, germinoma)
  • Mets - lymphoma, breast cancer
  • Viral encephalitis - CN enhancement
  • Slow vascular flow (i.e. Moya moya)
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9
Q

Which CN does not traverse the cavernous sinus?

A

V3 (mandibular) - exits inferiorly from Meckels cave through foramen ovale

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10
Q

Which CN does not exit via the superior orbital fissure?

A

V2 (maxillary) - exits via foramen rotundum

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11
Q

Where does CN6 travel?

A

Enters petrous portion of temp bone and travels via Dorello’s canal and along medial venous sinusoids

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12
Q

Clinical and imaging findings pseudo tumour cerebri

A

Headache, visual changes, increased ICP

Empty sella, expansion Meckel’s cave, optic disc edema and stenosis of the sigmoid and transverse sinuses

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13
Q

List the segments of the ICA
Key branches of C4 (2)
Key branches of C6 (2)
Key branches of C7 (4)

A

Cervical
Petrous
Lacerum
Cavernous - meningohypophyseal trunk (pituitary, tent, and dura of clivus) and inferolateral trunk (CNs 3-6)
Clinoid
Supraclinoid - ophthalmic artery (significance of aneurysms above versus below this point), superior hypophyseal artery
Communicating - P-comm, ACA, MCA, ant choroidal

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14
Q

What does recurrent artery of Heubner supply?

A

Caudate head, anterior limb internal capsule

Branch off ACA

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15
Q

What do medial lenticulostriate arteries supply?

A

Medial basal ganglia (from ACA)

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16
Q

What do lateral lenticulostriate arteries supply?

A

Lateral BG, including lateral putamen, external capsule, and posterior limb internal capsule (from MCA)

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17
Q

What does artery of Percheron supply? where does this originate?

A

Dom thalamic perforator supplying ventromedial thalami bilaterally and rostral midbrain (bil thalamic infarcts)
Arises from P1

18
Q

What does anterior choroidal artery supply?

A

Last branch of ICA; supplies hippocampus, optic chasm, posterior limb of internal capsule

19
Q

Most common persistent carotid-basilar connection

A

Persistent Trigeminal artery
Courses adjacent to trigeminal nerve
Trident or tau sign on angiography
Can connect to basilar artery (type I) or superior cerebellar artery (type 2)

20
Q

Presentation, RF and imaging findings RCVS

A

Thunderclap headache, usu occipital, recurrent
Middle aged women
RFs: pregnancy/eclampsia, drugs, other
Imaging: vascular spasm, convexity subarachnoid hemorrhage, lobar hemorrhage, watershed infarct, vasogenic edema
DSA: smooth tapered narrowing of larger vessels, dilated segments (beading)

CT done to rule out aneurysmal cause of bleed (bc CT can be normal in RCVS too)

21
Q

Most common location of hypertensive hemorrhage

A

BG, thalami, cerebellum (can also see microhemorrhages in the brainstem)

22
Q

Most common location of cerebral amyloid angiopathy

A

Lobar and cortical, involving parietal and occipital lobes

Microhemorrhages also in cortex

23
Q

Imaging findings moya moya

A
  • ICA (supraclinoid) +/- PCA stenosis
  • Concentric narrowing, no enhancement (differentiates this from other causes of vasculitis)
  • Extensive pial collaterals (Ivy sign)
  • Watershed infarcts
  • ‘Puff of smoke’ sign on angiography
24
Q

Imaging findings hepatic encephalopathy

A

Mg deposition - T1 hyperintense signal in globus pallidus and substantia nigra

DDx T1 shortening in BG = Lonely Wilson’s Trip to Hawaii (Liver disease, Wilson’s, TPN, Hyperglycemia)

25
Q

Imaging findings severe hypoglycemia

A

Bilateral, asymmetric T2 prolongation and diffusion restriction in gray matter (cortex, hippocampus, BG)
Ddx: HIE
HH-NKT (non-ketotic hyperglycemia hemichorea) - involves one side of BG, produces hemichoria and hemiballimus on contralateral side

26
Q

Imaging findings severe HIE

A

Affect grey matter (cortex, hippocampus, BG)
Diffuse edema with effacement of CSF spaces
Reversal sign
White cerebellum sign
ddx: severe hypoglycemia
Earliest findings on DWI

27
Q

Imaging findings methanol poisoning

A

Optic neuritis

Increased T2 signal/restricted diffusion in PUTAMEN (may have bright T2 signal if hemorrhage ensues)

28
Q

Imaging findings CO poisoning

A

Increased T2 signal/restricted diffusion in GLOBUS PALLIDUS

29
Q

Imaging findings Wilson’s disease

A

Increased T2 signal in BG and thalamus

Panda sign in midbrain

30
Q

DDx: disease involving putamen or BG

A
  • mitochondrial disease (leigh)
  • toxic encephalopathies (CO, methanol, CN)
  • metabolic (Wilson’s, hypoglycemia)
  • HIE
  • infection (CJD)
31
Q

Name the segments of the facial nerve

A

Intracranial/cisternal segment
Meatal/Cannicular (within IAC)
Labyrinthine (IAC to geniculate ganglion)
Tympanic (geniculate ganglion to pyramidal eminence)
Mastoid (pyramidal eminence to stylomastoid foramen)
Extratemporal

32
Q

Most common tumour associated with NF2

A

Vestibular schwanommas

33
Q

Imaging findings neurosarcoidosis

A
  • Leptomeningeal enhancement (including hypothalamus/pituitary and cranial nerves, usu basal skull)
  • Pachymeningeal enhancement
  • Parenchymal involvement (extending along perivascular spaces, periventricular lesions)
34
Q

Scimitar shaped sacrum

A

Anterior sacral meningocele
Rare, present later in life
Associated with sacral agenesis
Risk of rupture - bacterial meningitis

35
Q

What things cause increased signal in CSF spaces on FLAIR?

A
  • Poor CSF suppression/artifact
  • Supplemental oxygen
  • Blood
  • Pus
  • Tumour (leptomeningeal disease)
  • Slow blood flow cortical arteries (stroke)
  • Meningeal collateral (moya moya)
  • Ruptured dermoid
36
Q

Neurosarcoid findings

A

“Great mimicker”

  • Basal cistern leptomeningeal enhancement
  • Parenchymal enhancing lesions
  • Cranial nerve involvement
  • Optic nerve enhancement
  • Suprasellar/pituitary involvement

History is key! (can look like TB, leptomeningeal carcinoma, meningitis etc)

37
Q

Holoprosencephaly subtypes and findings

A

Lobar - partial fusion frontal horns ventricles (absent SP, CC +/- azygous ACA)
Semi-lobar - complete fusion frontal lobes (posterior brain is cleaved)
Alobar - pancake brain, monoventricle (other midline facial anomalies

38
Q

Variants of holoprosencephaly

A

Arhinencephaly - absent olfactory bulbs (Kallman syndrome), minor HPE expression

Meckel-Gruber - encephalocele, renal cysts, polydactyly

Septo-optic dysplasia - absent SP, optic nerve hypoplasia, pituitary abnormalities, azygous ACA
50% have schizencephaly!

39
Q

Most common cause of temporal lobe epilepsy

A

Mesial temporal sclerosis

#2 tumours in temporal lobe - most commonly ganglioglioma, #3 cortical dysplasia

40
Q

Most significant RF for development of CNS neoplasm

A

Radiation

-most commonly meningioma

Neuroradiology (15 decks)

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