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Skull & Brain Flashcards

1
Q

By what age do the anterior and mastoid fontanelles typically close?

A

Approx. 2 yrs

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2
Q

By what age do the posterior and sphenoid fontanelles typically close?

A

Approx 1-3 months

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3
Q

What is the weakest part of the skull and what is a complication from fx to this area?

A

Pterion; middle meningeal artery sits right below this area and fx to this area can result in rupture and an epidural hematoma.

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4
Q

By what age does the metopic suture typically fuse and early fusion results in which type of craniosynostosis?

A

Usually fuses by 9 months;

Trigonocephaly.

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5
Q

a) Which foramen does the middle meningeal artery travel through?
b) Which foramen does the mandibular division of CNV travel through?
c) Which foramen does the maxillary division of CNV travel through?

A

a) Foramen spinosum
b) Foramen ovale
c) Foramen rotundum

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6
Q

Which embryological anatomy gives rise to the peripheral nerves, roots and ganglia of the ANS?

A

Neural crest

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7
Q

What are the 5 divisions of the brain after ventral induction?

A 
Prosencephalon (forebrain)
  -- telencephalon
  -- diencephalon
Mesencephalon (midbrain)
Rhombencephalon (hindbrain)
  -- metencephalon
  -- myelencephalon
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8
Q

What are the 6 stages of neurogenesis?

A

1) Dorsal induction
2) Ventral induction
3) Proliferation
4) Migration
5) Organization
6) Myelination

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9
Q

Which embryological division makes up the cerebrum? Which makes up the cerebellum?

A

Cerebrum –> telencephalon

Cerebellum –> metencephalon

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10
Q

List 4 locations where the blood-brain barrier is not continuous.

A

1) Portions of hypothalamus – where hormones enter the systemic circulation
2) Posterior lobe pituitary gland – where ADH and oxytocin are released
3) Pineal gland – pineal secretions
4) Choroid plexus – ependymal cells maintain the blood-CSF barriar

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11
Q

What is the M/C/C and 2nd M/C/C of congenital CNS infection?

A 
1st = CMV
2nd = Toxoplasmosis
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12
Q

Where do CNS toxoplasmosis like to affect?

A
  • basal ganglia
  • parenchyma (peripheral corticomedullary junction)
  • periventricular (sparsely)
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13
Q

Does CNS toxoplasmosis like to calcify?

A

Yes (71%)

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14
Q

What is the enhancing pattern in adult toxoplasmosis?

A

Ring-enhancing

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15
Q

What clinical finding is common to both toxiplasmosis & CMV?

A

chorioretinitis

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16
Q

Which congenital infection has a high risk for miscarriage and birth defects?

A

Rubella

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17
Q

What are the clinical features of CMV?

A
  • chorioretinitis
  • CNS involvement (50%)
  • microencephaly (10%)
  • hepatosplenomegaly (10%)
  • petechial rash (10%)
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18
Q

What are the radiographic findings associated with CNS CMV?

A
  • parenchymal & periventricular Ca++ (50%)
  • Schizencephaly
  • ventricular dilation
  • cerebellar hypoplasia
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19
Q

What % of children will develop CMV if present in their mothers?

A

40%

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20
Q

How do neonates acquire herpes simple infection?

A

Through contact with infected mother’s cervix or vagina during birth.

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21
Q

What is the M/C/C for an epidural abscess?

A

Direct extension from infection in mastoids, paranasal sinuses or calvarium.
Can also be post-surgical.

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22
Q

What is a subdural empyema and how does it form?

A

Purulent collection collected within the potential subdural space by disruption of arachnoid meningeal barrier.

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23
Q

What enhances in a subdural empyema?

A

The granulation tissue that forms over time adjacent to the infection.

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24
Q

What is the M/C/C of a pyogenic brain (cerebral abscess)?

A 
Hematogenous dissemination (33%) from a primary infectious site. 
Eg. AV shunts, cardiac, drug abuse, pulmonary infection, sepsis.
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25
Q

Other than timing (days vs. 1-2 weeks), what is the difference btwn early and late cerebritis?

A

Early: May or may not be detected on CT; patchy enhancement.
Late: Central necrosis (hypodense) in with irregular ring enhancement.

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26
Q

What is the difference btwn the early capsule vs. late capsule stage in a cerebral abscess?

A

Early capsule: well-defined rim enhancing with surrounding vasogenic edema (double rim sign)
Late capsule: thickened capsule

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27
Q

What are the 4 stages of cerebritis?

A

a) Early cerebritis
b) Late cerebritis
c) Early capsule formation
d) Late capsule formation

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28
Q

What is the ddx for ring enhancing lesions?

A 
MAGIC DR:
Mets
Abscess
Glioblastoma multiform
Infarct
Contusion
Demyelinating
Radiation necrosis

(Toxoplasmosis can also present like this.)

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29
Q

What is commonly the cause of death with infectious cerebritis?

A

Herniation of infection into the ventricles (the medial wall of the capsule is often less thick, allowing for easier rupture).

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30
Q

What is the M/C organism to cause stroke from infective endocarditis?

A

Staph aureus

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31
Q

What is the M/C location for a cerebral abscess?

A

Frontal & parietal lobe (distribution of MCA)

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32
Q

What is the M/C etiology for meningitis?

What is the 2nd M/C?

A 
1st = hematogenous dissemination from distant infectious focus
2nd = direct geographic extension from sinusitis, otitis or mastoiditis
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33
Q

What is the M/C form of CNS infection?

A

Meningitis

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34
Q

What is the M/C organism to cause acute pyogenic meningitis in a neonate?
In kids?
In adults?
In the elderly?

A 
Neonates = Group B streptococcus
Kids = N. meningitidis
Adults = Strep pneumonia
Elderly = Listeria; Strep pneumonia; N. meningitidis
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35
Q

What is the imaging appearance of meningitis on MRI?

A
  • exudates in the cisterns (do not suppress on FLAIR like CSF)
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36
Q

What is the M/C/C of acute lymphocytic meningitis? What is its prognosis?

A

Viral origin (50-80% enterovirus); benign and self-limiting.

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37
Q

What is the M/C/C for chronic meningitis?

A

Tuberculosis (or granulomatous origin)

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38
Q

In encephalitis, what part of the cerebrum is M/C affected?

A

Gray matter

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39
Q

Herpes varicella zoster virus presents with small vessel vasculitis (and hence CNS involvement) in which pop’n?

A

Immuno-compromised patients (eg. lymphoma, AIDS)

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40
Q

What is the preferred intracranial site for herpes simplex encephalitis?

A

Temporal lobes & insular cortex

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41
Q

Infectious mononucleosis (from an Epstein-Barr virus) has a predilection for which intracranial regions in children?

A

Brain stem & cerebellum

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42
Q

The “giant panda sign” is associated with which condition?

Which MSK condition is it also classically seen in?

A

Japanese encephalitis
(high signal in tegmentum but spares red nucleus and corticospinal tract)

Also seen in Wilson’s disease.

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43
Q

What % of TB cases have CNS involvement?

A

5-10%

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44
Q

What is the M/C form of TB CNS?

What is the 2nd M/C form?

A 
1st = Tuberculous meningitis
2nd = Tuberculoma
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45
Q

Where do tuberculomas M/C like to occur?

A

brain stem

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46
Q

What is the pathomechanism for tuberculous meningitis?

A

Ruptured tuberculoma into the subarachnoid space –> discharges necrotic debris –> causes meningitis

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47
Q

Which granulomatous disease likes to affect the CN7?

A

Sarcoidosis

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48
Q

What CNS locations does sarcoidosis like to involve?

A

Hypothalamus, pituitary stalk, optic nerve and chiasm

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49
Q

What are 2 forms that CNS sarcoidosis can present as?

A

i) Chronic basilar leptomeningitis

ii) Parenchymal sarcoid nodule

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50
Q

A white matter disease (radiologically similar to MS & ADEM) in a patient from the midwest (eg. Minnesota/Wisconsin) who has a “target sign” on their skin, most likely has which condition?

A

Lyme disease

(It is also common in the New England area).

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51
Q

What is the M/C CNS parasitic disease?

A

Cysticercosis (called neurocysticercosis)

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52
Q

What is the classic imaging appearance of an old neurocysticerocsis infection?

A

Cyst with dot sign –> rim enhancing and dot enchancing

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53
Q

What is the M/C opportunistic infection in AIDS patients?

A

Toxoplasmosis

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54
Q

How is amebic meningoencephalitis acquired and manifested in the CNS?

A

Amebic enters nasal cavity and directly extends through the cribiform plate of ethmoid bone to brain.

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55
Q

What is an aka for Progressive Dementia Complex?

A

AIDS Encephalopathy

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56
Q

What are the imaging findings associated with AIDS encephalopathy?

A
  • progressive volume loss
  • bilateral, patchy confluent hypodensities in white matter (T2 periventricular hyperintensity)
  • reduced gray matter
  • no enhancement
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57
Q

What is a major differential for progressive dementia complex (AIDS encephalopathy)?

A

progressive multifocal leukoencephalopathy (PML)

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58
Q

What are other manifestations of HIV/AIDS?

A

a) Vasculopathy
b) HIV/AIDS bone marrow changes (eg. bright disc sign)
c) Benign lymphoepithelial lesions (=non-neoplastic cystic masses that enlarge salivary glands)
- - bilateral M/C
- - Parotid gland M/C
- - Imaging: multiple cysts w/ thin enhancing rim/hyper T2

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59
Q

What is the M/C opportunistic infection in HIV patients?

A

Toxoplasmosis

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60
Q

Sarcoidosis M/C involves which portion of the CNS?

A

meninges

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61
Q

Which cranial nerve is involved in sarcoidosis?

A

CN7 (facial palsy) & CN2 (optic neuritis)

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62
Q

What are the M/C cosmopolitan CNS fungal diseases?

A

a) aspergillosis
b) mucormycosis
c) candida
d) cryptococcus

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63
Q

What are the M/C geographically restricted CNS fungal diseases?

A

a) coccidioidomycosis
b) blastomycosis
c) histoplasmosis

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64
Q

What is the M/C CNS (fungal?) infection?

A

Cryptococcus

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65
Q

What is the 1st, 2nd and 3rd M/C CNS pathogen?

A 
1st = HIV
2nd = toxoplasmosis
3rd = cryptococcus
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66
Q

Which fungal infection M/C infects the CNS when disseminated?

A

Aspergilosis

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67
Q

What is the clinical findings associated with CNS histoplasmosis infection?

A

Asymptomatic infection

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68
Q

Other than CNS, disseminated blastomycosis likes to involve which other body region?

A

Male genital tract

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69
Q

What is the difference between the locations involved in CNS toxoplasmosis and lymphoma?

A

Toxoplasmosis has a predilection for the basal ganglia and at the corticomedullary junction.
Lymphoma has a predilection for periventricular and subependymal regions.

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70
Q

Which region of the spine is most frequently involved in AIDS-associated myelopathy?

A

Thoracic spine

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71
Q

What is the difference btwn demyelinating and dysmyelinating disorders?

A

Demyelinating = inflammatory component that injures/destroys white matter

Dysmyelinating = intrinsic abnormalities of myelin formation or myelin maintenance (in pediatric/adolescence)

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72
Q

Is MS a primary or secondary demyelinating disease?

A

Primary

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73
Q

What are some secondary demyelinating disease?

A

a) Allergic – ADEM
b) Viral – HIV, encephalitis, progressive multifocal leukoencephalopathy
c) Vascular – Binswanger disease (small vessel dementia)
d) Toxic – alcohol, radiation
e) Traumatic – diffuse axonal injury

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74
Q

Optic neuritis is seen in what % of MS patients?

A

80%

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75
Q

What are 2 positive laboratory tests that are associated with MS?

A 
IgG (70%)
Oligoclonal bands (90%)

(Both are found in CSF)

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76
Q

What are the different clinical courses that can occur in MS and which is the M/C?

A

a) Relapsing remitting (M/C 85%) – exacerbations followed by remissions
b) Secondary progressive – progressive w/out much remission
c) Primary progressive (chronic progressive) – progressive from start
d) Progressive relapsing – progressive disease with clear acute relapses

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77
Q

MS likes to affect which location?

A
  • periventricular (85%)
  • callososeptal interface (50-90%)
  • subcortical U-fibers
  • brain stem
  • spinal cord
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78
Q

What is the imaging appearance of MS in the brain?

A
  • Multiple hyperintense T2 lesions
  • thinned corpus callosum
  • Dawson’s fingers
  • Dot-dash sign
  • Tumefactive (lesions >2cm) –> produce horseshoe-shaped ring enhancement
  • horse-shoe enhancement
  • ONLY enhances early in disease process when its active
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79
Q

What differentiates a tumefactive MS lesion from a tumor?

A

i) Perfusion in tumor increased, not in MS

ii) Veins displaced by neoplasm, they course through MS lesion

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80
Q

What does a MS lesion look like in the spinal cord?

A
  • 90% MS lesions less than 2 VB lengths

- cervical region

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81
Q

What are some imaging differences between MS and ADEM?

A

ADEM

  • favors subcortical & deep white matter regions
  • no Dawson’s fingers
  • cranial nerve enhancement
  • usually at least one large dominant lesion
  • no new lesions on MR 6 months from start of disease
  • more symmetric in appearance
  • DWI may show restriction (MS typically does not OR may show increased diffusion)
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82
Q

Most ADEM patients completely recover after what time period?

A

1-2 months (>50%)

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83
Q

What is the etiology of progressive multifocal leukeoencephalopathy (PML) and what does it specifically affect?

A

JC virus – infects oligodendrocyte

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84
Q

What is the main condition associated with PML?

A

AIDS

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85
Q

What’s an aka for Binswanger disease?

What is the pathology?

A

Subcortical arteriosclerotic encephalopathy

Small vessel dementia –> severe arteriosclerosis of the small vessels causing infarction.

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86
Q

How does Binswanger disease present on imaging?

A

CT: diffuse, symmetrical, hypodense white matter lesions
MR: high signal T2 lesion

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87
Q

What location does Binswanger disease affect?

A
  • subcortical U-fibers (according to radiopedia BUT Neuroreq says these are spared b/c they have dual blood supply!!!)
  • periventricular
  • frontal lobe
  • centrum semiovale
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88
Q

Which condition is radiographically identical to Binswanger disease except it affects the subcortical fibers? (This is according to Neurorequisite)

A

Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopahty (CADASIL)

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89
Q

What are vascular causes for white matter disease?

A
  • Binswanger disease
  • CADASIL
  • Reversible posterior leukoencephalopathy
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90
Q

What are some dysmyelinating disease?

A
  • Alexander disease
  • Krabbe disease
  • Canavan disease
  • X-linked adrenoleukodystrophy
  • Metachromatic leukodystrophy
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91
Q

A glasgow coma scale of which number is considered severe?

A

<8

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92
Q

Which bone and vascular structure is most commonly involved in an epidural hematoma?

A

Temporal (90%)

Middle meningeal artery (90%)

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93
Q

What is the deceiving clinical presentation in 50% of epidural hematoma cases and what is it called?

A

Lucid interval = brief loss of consciousness followed by asymptomatic period then onset of coma and/or neuro deficit.

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94
Q

Which extraaxial hematoma is M/C?

2nd M/C?

A

Subarachnoid hemorrhage

Subdural hematoma

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95
Q

Which vessels are affected in a subdural hematoma?

A

Bridging veins

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96
Q

What are the 2 subtypes of subdural hematomas?

A

a) Simple = w/out brain parenchymal injury

b) Complicated = w/ brain parenchymal injury (poorer prognosis)

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97
Q

Subdural effusion is usually a complication of which condition?

A

Meningitis (eg. hx of prior infection)

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98
Q

Subdural empyema is usually secondary to which condition(s)?

A

Sinusitis or mastoiditis

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99
Q

What are some non-traumatic causes of sudural hematoma?

A
  • aneurysm
  • amyloid
  • Menkes disease
  • post-shunt coagulopathy
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100
Q

What is a non-traumatic cause for epidural hematoma?

A

Post-operative

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101
Q

What is a subdural hygroma and what is its etiology?

A

Fluid collection with similar characteristics as CSF (but has more protein).
Etiology:
a) Tear in arachnoid membrane causing of leaking of CSF.
b) Chronic degradation of subdural hematoma

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102
Q

What is the M/C/C of intracranial subarachnoid hemorrhage?

A

Trauma

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103
Q

What is the M/C/C of a non-traumatic intracranial subarachnoid hemorrhage?

A

Ruptured basilar aneurysm (80%)

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104
Q

What is the M/C intraaxial injury?

A

Hemorrhagic contusion

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105
Q

Which lobe is most commonly involved in a hemorrhagic contusion?

A

Temporal lobe (50%)

106
Q

A pneumatocele can form in which type of brain injuries?

A

Penetrating/lacerating injuries

107
Q

What is the 2nd M/C brain parenchymal traumatic lesion?

A

Diffuse Axonal Injury

108
Q

Which locations in the brain does diffuse axonal injuries M/C affect?

A
  • Gray-white junctions (frontal & temporal lobes)
  • Corpus callosum
  • Internal capsule
109
Q

What are the 2 subtypes of diffuse axonal injuries and which one is more common?

A

i) Hemorrhagic

ii) Non-hemorrhagic (M/C 80%)

110
Q

Which condition is considered as the extreme end case of diffuse axonal injury?

A

Diffuse vascular injury –> numberous small parenchymal hemorrhages (most die within minutes to hrs)

111
Q

List the 5 types of herniation syndromes.

A

1) Inferior tonsillar and cerebellar herniation
2) Superior vermian herniation (upward herniation)
3) Temporal lobe/uncal herniation
4) Central transtentorial herniation (inferior herniation)
5) Subfalcine herniation

112
Q

What are two types of scalp injuries?

A

a) Cephalohematoma
- - subperiosteal blood collections that elevate the periosteum
- - extradural equivalent of intracranial epidural hematoma
- - does not cross sutures

b) Subgaleal hematoma
- - subaponeurotic collection
- - blood collects under aponeurosis of occipitofrontalis mm
- - crosses sutures

113
Q

What is the M/C type of skull fx?

114
Q

Linear vs. depressed skull fx: which requires high energy and which requires low?

A

Linear –> low

Depressed –> high

115
Q

What is a rare complication seen in children under 3 yrs of age with skull fx?

A

Leptomeningeal cyst (aka. growing fx)

116
Q

What is an orbital blow-out fx?

A

Fracture of orbital wall & decompression of orbital contents.

117
Q

What is the risk associated with lamina papyracea fx?

A

Since it is the medial wall btw the orbit and ethmoid sinus - a fx can cause subcutaneous emphysema of the eyelids OR entrapment of medial rectus mm.

118
Q

What is an orbital blow-in fx?

A

Direct blow of maxillary sinus causing elevation of orbital floor into orbit.

119
Q

What are the 3 components of a tripod fx?

A

i) fx of lateral wall of orbit
ii) fx of inferior orbital rim/floor
iii) fx of zygomatic arch

120
Q

What is the M/C extra-axial neoplasm of brain?

A

Meningioma

121
Q

Intraventricular meningiomas M/C occur in which ventricle?

A

Left lateral ventral

122
Q

Multiple meningiomas are associated with which phakomatosis?

123
Q

What is the 2nd M/C extraaxial tumor in adults?

A

Schwannomas

124
Q

Which nerves are M/C affected by schwannomas?

A
  • CN8
  • CN7
  • CN5 (2nd division)
125
Q

There are 3 types of schwannomas: cellular, plexiform and melanotic. Melanotic schwannomas are associated with which condition 50% of the time?

A

Carney complex

126
Q

What feature about meningiomas makes it a ddx to schwannomas?

A

Meningiomas can track along nerves.

127
Q

Neurofibromas have a predilection for which nerves?

A

Peripheral nerves > spinal nerves > cranial nerves

128
Q

True or false: neurofibromas are associated with both NF-1 & NF-2.

A

False - not associated with NF-2.

129
Q

What is a neuroma?

A

POST-TRAUMATIC proliferation of nerve cells (not a true neoplasm).

130
Q

What is the M/C primary tumor to produce dural mets in an adult?
What is the 2nd?

A

M/C = Breast

2nd M/C = lymphoma

131
Q

What is the primary tumor to cause mets to brain in children?

A

Adrenal neuroblastomas & leukemia

132
Q

Choroid plexus papillomas occur M/C in which location in children? In adults?

A 
Children = lateral ventricle
Adults = 4th ventricle
133
Q

Choroid plexus papillomas are M/C in which age pop’n?

A

Children (80%)

134
Q

What is the etiology of a choroid plexus papilloma?

A

Simian virus 40 (also responsible for ependymomas)

135
Q

The heterogenous enhancement pattern of choroid plexus papillomas is d/t what features of the tumor?

A

i) Hemorrhage

ii) Calcification

136
Q

Choroid plexus hemangiomas are associated with which phakomatosis?

A

Sturge-Weber

137
Q

What are some common choroid plexus neoplasms?

A
  • Meningioma
  • Metastases
  • Ependymoma
  • Medulloblastoma
  • Choroid plexus papilloma
  • Hemangioma (Sturge-Weber)
  • Lymphoma
  • Choroid plexus carcinoma
138
Q

Epidermoids like to occur more commonly extradural or intradurally?

A

Extradural (9:1)

139
Q

What are the imaging differences between epidermoid cyst and arachnoid cyst?

A

Epidermoid Cyst:

  • can calcify
  • cyst insinuates btwn blood vessels
  • no contrast uptake
  • bright FLAIR
  • bright DWI

Arachnoid Cyst:

  • no calcification
  • blood vessels deviated
  • may uptake contrast but delayed
  • dark FLAIR
  • dark DWI
140
Q

What are 2 imaging differences between dermoid cyst and epidermoid cyst?

A

i) Dermoids occur midline (epidermoid don’t)

ii) Dermoids have heterogenous signal intensities

141
Q

What are 2 common locations for intracranial teratoma?

A

i) Pineal region

ii) Suprasellar region

142
Q

Intracranial lipomas have an association with which other intracranial congenital anomaly?

A

Agenesis of corpus callosum

143
Q

List some of the common extra-axial intracranial tumors.

A
  • Metastasis
  • Meningioma
  • Schwannoma
  • Neurofibroma
  • Choroid plexus tumors
  • Epidermoid cyst
  • Dermoid cyst
  • Lipoma
144
Q

Juvenile pilocytic astrocytoma has an association with which phakomatosis?

A

NF-1 (15-20%)

145
Q

The solid form of pilocytic astrocytoma is more likely to be seen in which age pop’n? The cystic form is likely to be seen in which age pop’n?

A

Solid – adults

Cystic – children (60-80%)

146
Q

Tuberous sclerosis is commonly associated with which condition that occurs at the foramen of Monro?

A

Subependymal Giant Cell Tumor

147
Q

What is the M/C astrocytoma in adults?

A

Glioblastoma multiform

148
Q

List 3 corpus callosum neoplasms?

A

i) GBM
ii) Mets
iii) Lymphoma

149
Q

What is the prognosis of a medulloblastoma?

A

Very malignant

150
Q

Medulloblastomas like to occur where within the cerebellum?

151
Q

Cerebral neuroblastomas are now known as?

A

Supratentorial PNET

152
Q

True or false: PNETs can calcify.

A

True - calcify in 50-70%

153
Q

True or false: Medulloblastomas can calcify.

A

True - calcify 10-20%

154
Q

What are the common intracranial locations for an ependymoma?

A
  • midline lesion
  • 4th ventricle
  • intraparenchymal (20%)
155
Q

What is the M/C location for an ependymoma in the spinal cord?

A

Filum terminale

156
Q

Which CNS location has the best prognosis for an ependymoma? Which has the worst?

A 
Best = Filum terminale
Worst = Posterior fossa
157
Q

What are the CT imaging features of ependymoma?

A
  • hypo/isodense
  • punctate calcification (40-50%)
  • mild enhancement
  • hydrocephalus (if involving 4th ventricle)
158
Q

Subependymomas are associated almost exclusively with which condition?

A

Tuberous sclerosis

159
Q

Gangliogliomas M/C involves which intracranial lobe?

A

Temporal lobe

160
Q

Central neurocytomas are commonly found in this/these intracranial location(s).

A
  • 3rd ventricles

- lateral ventricles

161
Q

What are the imaging features of a central neurocytoma?

A
  • calcify
  • can be cystic
  • heterogenous MR appearance (b/c hemorrhage frequently)
162
Q

Oligodendrogliomas M/C affects which intracranial location?

What age group does it affect?

A

Cortical involvement

In adults

163
Q

What is the main imaging feature of oligodendrogliomas?

A

Calcification (40-80%)

164
Q

What is the M/C primary infratentorial, intraparenchymal tumor in an adult?

A

Hemangioblastoma

Overall, it is mets and vestibular schwannomas

165
Q

What is the classic imaging feature of a hemangioblastoma?

A

Cystic mass with a solid mural nodule inside

166
Q

What is the enhancement pattern of hemangioblastoma?

A

Striking enhancement of the mural nodule.

No enhancement of the cyst.

167
Q

Hemangioblastoma is associated with which phakomatosis?

A

Von Hippel-Lindau (aka retinalcerebellar hemangioblastoma)

168
Q

Which other condition is a risk factor for the development of lymphoma?

A

AIDS survivors (dysfunction of suppressor T-cells)

169
Q

What are the imaging features of lymphoma on MR?

A
  • T2/FLAIR - LOW!!!
  • Ring enhancement
  • ependymal enhancement
170
Q

What is the nuc med (thallium) features of lymphoma? Of toxoplasmosis?

A 
Lymphoma = avid uptake
Toxoplasmosis = no activity!
171
Q

Which pituitary adenoma is more common?

A

Microadenoma

172
Q

Which pituitary adenoma secretes hormones?

A

Microadenoma

173
Q

What is the cause of an empty sella sign?

A
  • normal variant
  • intracranial pressure
  • hypopituitary
174
Q

What is the M/C pituitary mass?

175
Q

What is unique about craniopharyngiomas?

A

Calcification (90%)

176
Q

What are two subtypes of craniopharyngioma and which one is M/C?

A

i) Cystic adamentinomatous (M/C)
- in children

ii) Papillary
- solid form
- in adults

177
Q

What is the M/C pineal tumor of germ cell origin?

A

Germinoma (aka Seminoma) - 60%

178
Q

Which gender is germinomas commonly seen in?

A

Males (33:1)

179
Q

What is the 2nd M/C neoplasm of the pineal region?

180
Q

What is unique about choriocarcinomas?

A

They like to hemmorrhage and have a bad prognosis.

181
Q

What are tumors of pineal cell origin? Which has the most aggressive qualities and which has the least?

A
  • Pineoblastoma (most aggressive)
  • Pineocytoma
  • Pineal Cyst (least aggressive)
182
Q

How does a pineal cyst present on FLAIR?

A

Suppresses on FLAIR

183
Q

What is the M/C location for an epidermoid cyst?

A

Cerebellopontine angle (50%)

184
Q

What is M/C: dermoid cyst or epidermoid cyst?

A

Epidermoid cyst

185
Q

What are the imaging characteristics of a dermoid cysts?

A

Follows fat characteristics on CT and T1. Lesion is unilocular, cystic & midline.

186
Q

What is the age pop’n and symptomology of an arachnoid cyst?

A

Children (75%) & usually asymptomatic.

187
Q

What are the enhancement differences between arachnoid and epidermoid cyst?

A

Epidermoid cyst – may have peripheral enhancement

Arachnoid cyst – no enhancement

188
Q

What are the 3 M/C locations for an arachnoid cyst?

A

i) Middle cranial fossa (50-60%)
ii) Suprasellar (10%)
iii) Cerebellopontine angle (10%)

189
Q

The inability to move gaze up and down due to a tumor in the pineal region (causing compression of the tectal plate) is termed what?

A

Parinaud syndrome

190
Q

True or false: Rathke cleft cysts calcify often.

A

False – uncommon

191
Q

What is the unique characteristic of a Rathke cleft cyst?

A

Cystic appearance with a nodule inside.

192
Q

Colloid cysts are mostly high on T1 because…

A

They are high in protein.

193
Q

List some intradural-extramedullary tumors.

A
  1. Schwannoma
  2. Meningioma
  3. Metastasis
  4. Neurofibroma
  5. Ependymoma
  6. Lipma
  7. Epidermoid cyst
  8. Arachnoid cyst
194
Q

Where is the M/C location for a neuroenteric cyst?

A 
Posterior fossa (75%)
-- anterior to pontomedullary junction
195
Q

What are the MR imaging characteristics of a neuroenteric cyst?

A
  • T1 & T2 hyperintense

- does not enhance

196
Q

What is the M/C/C for acute strokes?

What is the 2nd M/C/C?

A

1st = Thromboembolic infarcts/ischemia (80%)

2nd = Primary spontaneous hemorrhage (15%)

197
Q

What is the difference btwn ischemia and infarction?

A

Ischemia = viable tissue although inadequate blood flow to maintain normal cellular function

Infarction = frank cell death

198
Q

What is the M/C location for atherosclerotic disease?

A 
1st = carotid bifurcation
2nd = cavernous internal carotid artery
199
Q

What is the M/C intracranial occluded vessel?

A

Middle cerebral artery

200
Q

What is crossed cerebellar diaschisis in pCT?

A

Incidental finding – contralateral cerebellum shows hypoperfusion with reduced CBF from MCA infarcts.

201
Q

At what sites do hypertensive hemorrhage M/C occur?

A

Basal ganglia (80%)
Pontine (10%)
Cerebellar (10%)

202
Q

What is the underlying etiology of hypertensive hemorrhage?

A

Charcot-Bouchard aneurysm

thromboses/hemorrhages/infarcts of small vessels

203
Q

What are the radiographic findings associated with cerebral embolic ischemia?

A
  • Hyperdense artery

- Loss of gray-white matter differentiation

204
Q

What are the imaging features of chronic ischemic infarct?

A
  • well demarcated lesion
  • low density (similar to CSF)
  • negative mass effect w/ widened sulci
205
Q

What are the imaging features of a subacute ischemic infarct?

A
  • hypodense but still hyper to CSF

- mass effect of adjacent sulci

206
Q

When the M1 branch of the middle cerebral artery is affected with an embolism, what cerebral areas are particularly affected?

A
  • basal ganglia

- insular cortex

207
Q

“CT Fogging” following an ischemic infarct is typically seen after what time frame?

208
Q

What is a lacunar infarction?

A

An infarct that becomes cystic and is produced by occlusion of a small “end” artery (usually no collateral supply).

209
Q

90% of berry aneurysms occur in which circulation?

A

Anterior circulation:

  • Anterior cerebral artery/Anterior communicating artery (30-40%)
  • Internal carotid artery/Posterior communicating artery (30%)
  • Middle cerebral artery bifurcation (20-30%)
210
Q

85% of AVM like to occur where in the CNS?

A

Supratentorial

211
Q

Where is the M/C location in the CNS for capillary telangiectasia?

A

Everything midbrain down:

  • pons
  • medulla
  • spinal cord
212
Q

Capillary telangiectasia is commonly seen in which phakomatosis?

A

Osler-Weber-Rendu

213
Q

Capillary telangiectasia has what type of enhancement pattern?

A

Brush-like

214
Q

Which granulomatous condition is characterized by necrotizing inflammation of small and medium sized arteries + allergic angiitis + eosinophilic lung disease?

A

Churg-Strauss

215
Q

Which multisystem disease is characterized by necrotizing inflammation of small and medium sized arteries?

A

Polyarteritis nodosa

216
Q

List the congenital conditions that develop d/t dorsal induction abnormalities.

A
  • Ancencephaly
  • Cephalocele
  • Encephlocele
  • Meningocele
  • Chiari Malformation
217
Q

List the congenital conditions that develop from ventral induction abnormalities.

A
  • Holoprosencephaly
  • Dandy-Walker
  • de Morsier syndrome
218
Q

List the congenital conditions that develop from neuronal proliferation abnormalities.

A
  • NF
  • Sturge Weber (encephalotrigeminal angiomatosis)
  • Tuberous sclerosis
  • Von Hipple Lindau (retinocerebellar hemangioblastoma)
  • Porencephaly
  • Hydranencephaly
219
Q

List the congenital conditions that develop from neuronal migration abnormalities.

A
  • Lissencephaly (agyria)
  • Pachygyria
  • Polymicrogyria
  • Schizencephaly
  • Heterotrophia
  • Corpus callosum agensis
220
Q

Craniosynostosis of the sagittal suture results in:

A

Dolichocephaly/scaphocephaly

221
Q

Craniosynostosis of the coronal suture results in:

A

Brachycephaly

222
Q

Craniosynostosis of the lambdoid suture results in:

A

Turricephaly/Oxicephaly/Acrocephay

223
Q

Craniosynostosis of the metopic suture results in:

A

Trigonocephaly

224
Q

Craniosynostosis of any unilateral suture results in:

A

Plagiocephaly

225
Q

Failure of closure of the cephalic end of the neural tube results in:

A

Anencephaly

226
Q

What is the prognosis of anencephaly?

A

Fetuses aborted or die shortly after birth.

227
Q

Definition:

i) Cephalocele
ii) Encephalocele
iii) Meningocele
iv) Myelomeningocele

A

Cephalocele = herniation of brain contents through a skull defect

Encephalocele = herniation of brain & meningeal contents through a skull defect

Meningocele = defect of the posterior vertebral column with herniation of the meninges

Myelomeningocele = defect of the posterior vertebral column with herniation of the meninges + spinal cord

228
Q

What is the underlying etiology of Chiari Malformations?

A
  • Underdevelopment of posterior fossa

- CSF and posterior cranial fossa volumes are decreased

229
Q

What are some associated conditions with Chiari Malformation I?

A
  • Syringomyelia (20-73%)

- Klippel-Feil, short clivus, odontoid/C1 abnormalities

230
Q

What is the definition of a Chirai II Malformation?

A 
Inferior herniation of:
 -- cerebellar tonsils
 -- vermis
 -- 4th ventricle
 -- brainstem 
Myelomeningocele + tethered cord (~100%)
231
Q

What are some associated findings seen with Chiari II Malformation?

A
  • syringomyelia (50%)
  • cervicomedullary kinking
  • hydrocephalus
  • beaked tectum
  • agenesis of corpus callosum
232
Q

What is the characteristic finding associated with Chiari Malformation III?

A

High cervcial or occipital encephalocele

233
Q

What is the one lesion in which the splenium and posterior portions of the corpus callosum can form but the anterior corpus callosum is absent?

A

Holoprosencephaly

234
Q

What are the 3 subtypes of holoprosencephaly? List them from least severe to most severe.

A

i) Lobar (minor form)
- - falx cerebri incomplete
- - normal separation of cerebral hemispheres and lateral ventricles

ii) Semilobar
- - partial development falx
- - basal ganglia & thalami fused

iii) Alobar (severe form)
- - no separation of most midline structures

235
Q

Which conditions are associated with holoprosencephaly?

A
  • fetal alcohol syndrome
  • maternal diabetes
  • trisomy 13, 15, 18
236
Q

The presence of probst bundle signifies what underlying abnormality?

A

Agenesis of corpus callosum

237
Q

What are the imaging features of callosal agenesis (including named signs)?

A
  • Racing car sign
  • Moose head sign (colpocephaly)
  • pointed, crescent-shaped frontal horns
  • high riding & enlarged 3rd ventricle
238
Q

Malformations associated with callosal dysgenesis:

A

i) Chiari 2 malformation
ii) Dandy-Walker spectrum
iii) Holoprosencephaly
iv) Schizencephaly
v) Septo-optic dysplasia

239
Q

What are the 4 classic imaging features of Dandy-Walker malformation?

A

i) Large cystic, ballooned 4th ventricle
ii) Hydrocephalus
iii) Torcular-lambdoid inversion
iv) Inferior vermian hypoplasia or aplasia

240
Q

What is the cause of a patient’s symptomatology in Dandy-Walker syndrome?

A

Usually from concomitant supratentorial anomalies (eg. agenesis of corpus callosum, holoprosencepahly etc.)

Few clinical sx are from cerebellar abnormality.

241
Q

Which multisystem syndrome is associated with Dandy-Walker malformation?

A 
PHACES syndrome
P = posterior fossa malformation
H = hemangiomas
A = arterial anomalies
C = cardiac defects
E = eye abnormalities
S = sternal defects
242
Q

What are the features/associated conditions of de Morsier syndrome (septo-optic dysplasia)?

A
  • small hypoplastic optic nerves & small optic chiasm

Associated conditions:

  • absent septum pellucidum (64%)
  • pituitary gland hypoplasia (60%) –> diabetes insipidus
  • schizencephaly & neuronal migrational disorders may co-exist (50%)
243
Q

List 6 associated MSK syndromes seen with de Morsier syndrome? (Hint: 4 of them are endocrinological)

A

a. Apert syndrome
b. Carpenter syndrome
c. Diabetes insipidus (hypothalamic-pituitary dysfunction seen in most)
d. Rickets
e. Hyperthyroidism
f. Hypophosphatasia

244
Q

What is the gyral pattern in microcephaly?

A

Simplified & shallow sulci; may be excessive and small or few and small.

245
Q

What is megalencephaly?

A
  • Enlargement of cerebral hemispheres (may be uni or bilateral).
  • White & gray matter volume increased
  • Ipsilateral side may show polymicrogyria or agyria
246
Q

Hemimegalencephaly can be associated with which conditions/syndromes?

A

i) Beckwith-Wiedemann syndrome
ii) NF-1
iii) Proteus syndrome
iv) Tuberous sclerosis
v) Klippel-Trenaunay-Weber syndrome

247
Q

Pseudoarthrosis of the tibia and fibula in children is M/C seen in which condition?

248
Q

Plexiform neurofibroma is commonly seen affecting which cranial nerve?

249
Q

What is the 2nd M/C site for a schwannoma?

250
Q

Which nerve roots (sensory vs. motor) is more likely to be affected in NF-2.

251
Q

Tubers seen in tuberous sclerosis are likely to be found where intracranially and what are their imaging features?

A

Cortical and subcortical
High T2
Frequently calcify
Does not enhance

252
Q

Nodules/hamartomas seen in tuberous sclerosis are likely to be seen where intracranially and what are their imaging features?

A

Periventricular/subependymal
High T1/T2
Frequently calcify
May or may not enhance

253
Q

Which white matter lesion is seen on MR in tuberous sclerosis?

A

Radial bands (linear bands radiating from the periventricular white matter to the subcortical region)

254
Q

Which benign ventricular tumor is seen exclusively in 5-15% of patients with tuberous sclerosis?

A

Subependymal giant cell astrocytoma

255
Q

What are the imaging features of a subependymal giant cell astrocytoma?

A
  • Enhances uniformly and avidly.
  • Calcify but at a lower rate compared to tuberous sclerosis
  • Heterogeneous signal intensity on MRI
  • Hydrocephalus
256
Q

What are some other associated findings seen with tuberous sclerosis (abdominal or thoracic)?

A
  • Renal angiomyolipomas
  • Pheochromocytomas
  • Cardiac rhabdomyomas
  • Renal cell carcinoma
257
Q

What is the aka for Sturge-Weber?

A

Encephalotrigeminal angiomatosis

258
Q

What is a characteristic clinical feature of Sturge-Weber?

A

Port wine stain (eg. nevus flammeus) in distribution of trigeminal nerve

259
Q

What is the characteristic CT finding seen in Sturge-Weber? MRI finding?

A 
CT = tram track (cortical calcification)
MRI = pia enhancement + ocular enhancement (50%)
260
Q

Which CNS tumor is commonly seen in Von Hippel-Lindau disease and where does it commonly occur?

A

Hemangioblastomas (80%) in cerebellum (80%)

261
Q

Hemangioblastomas of the spine most commonly appear in single or multiples?

A

Single (80%) > Multiple (20%)

Neuroradiology (7 decks)

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