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PATH FINAL > Neuro PATH > Flashcards

Neuro PATH Flashcards

1
Q

Chronic menigitis causes ?

A
  • TB
  • Cryptococcus
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2
Q

Pyogenic meningitis causes by age
Neonate-
Young adult-
Older pts-

A

Neonate
- E-coli
- Group B strep

Young adult
- Neisseria Meningitidis

Older patients
- Strep pneumonia, listeria, H-influenza

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3
Q

Aseptic meningitis causes

A
  • Enterovirus
  • Self limiting
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4
Q

CADASIL
- inheritance ?

A

AD

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5
Q

CADASIL
- affects small, medium or large vessels ?

A
  • Small vessel vasculopathy without stroke risk factors*
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6
Q

CADASIL
- mutation ?

A

NOTCH 3 gene on Chromosome 19

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7
Q

CADASIL small vessel morphology ?

A
  • Fibrotic thickening of basement membrane
  • No atherosclerosis or amyloid deposition
  • Diagnosed with gene testing*
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8
Q

CADASIL affects which part of brain ?

A
  • Basal ganglia (most common) >
  • Paramedian superior frontal lobe**
  • Parietal lobe
  • External capsule*
  • Anterior temporal lobe** (classic)
  • Cerebral cortex and U-fibers spared**
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9
Q

What’s unique about CADASIL infarcts ?

A
  • Infarcts cross arterial territory
  • Less frequently hemorrhage
  • Diagnosed with skin/muscle biopsy**
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10
Q

4 types of vascular malformations ?

A
  • AVM
  • Cavernous malformations
  • Capillary telangiectasia
  • Venous angiomas
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11
Q

of the 4 types of vascular malformations, which type are associated with hemorrhage and development of neurologic symptoms ?

A
  • AVM
  • Cavernous malformations
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12
Q

AVM associated with what mutation ?

A

KRAS oncogene mutation

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13
Q

AVM vs Cavernous malformation

A

AVM
- intervening gliotic tissue
- no intervening capillary
- often have prior hemorrhage
- most common MCA territory posterior* branch
- AD familial form are common (will have multiple)
- High flow (dAVF, pial AVF, then everything else low flow)

Cavernous malformation
- No intervening brain
- Most common in cerebellum > pons > subcortical
- Low flow
- Old hemorrhage as well

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14
Q

Capillary telangiectasia (hemangioma) RF ?

A
  • Radiation*
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15
Q

Sinus Pericranii

A
  • Anomalous communication between intracranial dural venous sinus, extracranial venous
    circulation.
  • Majority congenital.
  • Probable anomalous venous development during late embryogenesis.
  • Incomplete sutural fusion over prominent/abundant diploic or emissary veins.
  • In utero DVS thrombosis*.
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16
Q

Capillary telangectasia

A
  • Cluster of dilated, but histologically normal capillaries. - Thin-walled, endothelial-lined vascular channels, largest channels may represent draining veins.
  • Normal brain interspersed between dilated
    capillaries.
  • No surrounding gliosis, hemorrhage or calcification.
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17
Q

Developmental venous anomaly

A
  • Radially oriented dilated medullary veins.
  • Separated by normal brain.
  • Normal white matter (no gliosis).
  • 20% have mixed histology (CM most common), may hemorrhage.
  • Variant: “Angiographically occult” DVA
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18
Q

Summary of tumor grades

A

Grade 1
- well circumscribed

Grade 2
- Poorly circumscribed

Grade 3
- Mitotic cells and atypia

Grade 4
- Necrosis and angiogenesis

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19
Q

Diffuse Astrocytic and Oligodendroglial Tumours ?

A

IDH Mutant (1p/19q codeletion present)
- Oligodendroglioma (grade 2)

IDH Mutant (1p/19q codeletion absent)
- Diffuse astrocytoma (grade 2)
- Anaplastic astrocytoma (grade 3)

IDH Wild type
- GBM (grade 4)

H3K27M
- Diffuse midline glioma (grade 4)

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20
Q

Ependymal tumors ?

A
  • Myxopapillary ependymoma : grade 1
  • Ependymoma : grade 2
  • Anaplastic ependymoma : grade 3
  • Subependymoma : grade 1
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21
Q

Choroid Plexus tumours (all enhance a lot)

A
  • Choroid plexus papilloma (grade 1) - kids
  • Atypical choroid plexus papilloma (grade 2)
  • Choroid plexus carcinoma (grade 3) - adults
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22
Q

Neuronal and Mixed Neuronal-Glial Tumours

A

Grade I
- Dysembryoplastic neuroepithelial tumour (DNET)
- Ganglioglioma and gangliocytoma
- Desmoplastic infantile astrocytoma and ganglioglioma
- Dysplastic gangliocytoma of the cerebellum (Lhermitte-Duclos)

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23
Q

Embryonal Tumours

A

All are WHO 4
- Medulloblastoma
- Atypical teratoid/rhabdoid tumour
- CNS neuroblastoma
- CNS ganglioneuroblastoma
- Medulloepithelioma

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24
Q

Arachnoidal Tumours

A

All Meningiomas basically

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25
Q

Craniopharyngioma arises from?

A
  • Rathke pouch remnant
  • Epithelial tumor*
  • Benign grade 1 tumor
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26
Q

Craniopharyngioma clinical presentation

A
  • Growth retardation due to pituitary dysfunction (Growth hormone deficiency)
  • Headache and visual disturbance
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27
Q

Ependymoma epidemiology

A
  • Bi-Modal
  • first peak 1-5 year old (A subtype)
  • second peak mid 30s (B subtype)
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28
Q

Ependymoma arises from ?

A
  • Glial cells of ependymal lining of ventricles / ependymal rests
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29
Q

Ependymoma subtype and prognosis and location ?

A

60% infratentorial - 2 subtypes in the posterior fossa
- Subtype A: Most common, predominately infants, poor prognosis
- Subtype B: Older children and adults, better prognosis

10% spinal

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30
Q

Supratentorial Ependymoma location ?

A
  • Extra-ventricular (most)*
  • if intra-ventricular will be in 3rd ventricle*

supratentorial ependymoma, ZFTA (RELA) fusion-positive (POOR PROGNOSIS)

supratentorial ependymoma, YAP1-MAMLD1 fusion

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31
Q

Ependymoma microscopic ?

A
  • Perivascular Pseduorosettes**
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32
Q

Myxopapillary ependymoma seen, next step ?

A
  • MRI whole spine
  • Benign but up to 50% do have leptomeningeal disease at time of diagnosis so must image neural axis
  • Despite this, excellent prognosis*
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33
Q

GBM associations ?

A
  • NF-1
  • Li-Fraumeni
  • Turcot
  • Ollier
  • Maffuci
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34
Q

Uncal herniation causes:

A
  • Duret Hemorrhages from basilar perforating arteries
  • CN3 compressed between PCA and SCA causing ipsilateral pupil dilatation and ptosis
  • “Kernohan’s Notch”: Ipsilateral hemiparesis. Mid brain compresses tentorium, cerebral peduncle on contralateral.
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35
Q

HTN causes what vessel changes

A

Accelerated atherosclerosis
- larger arteries

Hyaline arteriosclerosis + Hyperplastic
- small arteries
- vulnerable to rupture

Lipohyalinosis –> Charcot buchard microaneurysm
- basal ganglia
- site of rupture

Fibrinoid necrosis
- small vessels

In amyloid angiopathy there is deposition of AB in the walls of medium to small meningeal and cortical vessels - PERIPHERAL rather than central*

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36
Q

Global hypoxic ischemia
- most common site

A
  • Diffuse cortical Grey Matter perirolandic cortex (affected first)
  • Watershed infarcts after hypotensive episodes*
  • Cerebellum (more common in older patients)
  • Diffuse white matter
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37
Q

Meningioma morphology types

A

Rounded “globose”
- well defined dural base
- CSF cleft between tumour and cortex

En plaque
- sheet like over dura
- Hyperostosis*

–> Psamomma bodies

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38
Q

Meningioma genetic mutations

A
  • loss of chromosome 22** (most common)
  • NF2 mutation seen in sporadic (60%) and almost all high grade meningiomas
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39
Q

Define grade II and III Meningioma features

A

Grade II = < 20 mitoses / brain invasion / 3 atypical features*

Grade III = overt malignancy cytology or  20 mitoses / 10 HPF*

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40
Q

Multiple Sclerosis epidemiology

A
  • Female
  • Peak at 35
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41
Q

MS pathophysiology

A
  • Autoimmune attack against myelin sheath
  • EBV associated
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42
Q

MS active vs chronic plaque

A

Active
- Periventricular
- Myelin breakdown with abundant macrophages
- Lyphocytes as perivascular cuffs

Chronic
- Marked loss of Myelin and Oligodendrocytes
- Astrogliosis**
- No perivascular inflammation

43
Q

MS Macroscopy

A
  • Firmer than surrounding white matter due to sclerosis
44
Q

Clinical presentation, Inclusions, Genetic for:
Prion disease
Alzheimer
FTLD
Parkinson
PSP
Corticobasal degeneration (CBD)
MSA
Huntington
ALS
SBMA

A

Prion
- Rapid progerss dementia

Alzheimer
- AB (plaques)
- tau (tangles)
- Trisome 21, PS-1, PS-2, APP

FTLD
- Behavioural, Language change
- Tau*
- TDP-43*

Parkinson
- a-synuclein
- tau
- Lewy bodies

PSP
- Parkinson + abnormal eye movement
- tau

Corticobasal degeneration (CBD)
- Parkinson + asymmetric movement disorder
- tau

MSA
- Parkinson + cerebellar ataxia + autoimmune failure**
- a-synuclein

Huntington
- AD
- Hyperkinetic movement (Chorea)
- HTT gene**

ALS
- weakness with upper and lower motor neuron signs
- SOD1
- TDP43
- FUS

SBMA
- Lower motor neuron weakness and low androgen
- Androgen receptor

45
Q

Huntington
- Inheritance
- Gene
- Image

A
  • AD
  • HTT gene with tri-nucleotide repeat
  • loss of GABAergic neurones at BG
  • Atrophy caudate head and putamen + box-like frontal horn
46
Q

MSA
- inheritance
- gene

A
  • Sporadic
  • Parkinson + cerebellar ataxia + autoimmune failure**
  • a-synuclein
47
Q

Oligodendroglioma macroscopic appearance

A
  • Cystic degeneration, Calcification, Hemorrhage common
  • Remodelling of adjacent bone
  • Supratentorial (adult)
  • Posterior fossa and spinal cord (children)
  • Fried egg appearance of tumor cells
  • Chicken wire pattern of microvasculature
48
Q

Pituitary adenoma epidemiology

A
  • peak 35-60
  • 15% found on autopsy*
  • most are non-functional microadenomas*

–> Pituitary carcinoma is rare, <1% of all pituitary tumours. Mostly functional. Differ from adenomas due to the presence of distant metastases.

49
Q

Least common pituitary hormonal abnormality

A
  • TSH (1%)
50
Q

Pituitary adenoma RF

A
  • MEN-1
51
Q

Pituitary adenoma aetiology

A
  • due to Mutation of G-protein
  • Sporadic (most)
52
Q

Pituitary adenoma macroscopic appearance

A
  • Cyst, necrosis and hemorrhage in large adenomas
  • Calcifications in Prolactinomas*
53
Q

HSV-1 affects who ?

A
  • adults and young children
  • Accounts for 90% of Herpes simplex encephalitis
54
Q

HSV-2 affects who ?

A
  • neonates and immunocompromised
55
Q

CMV, HIV, JCV afects who ?

A
  • Immunocompromised
56
Q

HSV encephalitis brain imaging feature ?

A
  • Medial temporal lobe*
  • Spares basal ganglia
  • restricted diffusion (earliest sign, most sensitive)

Limbic encephalitis looks similar**

57
Q

Limbic encephalitis imaging feature ?

A

(if they say HSV titer is negative..then its this)
- Paraneoplastic syndrome from small cell lung ca*
- Looks like HSV encephalitis on imaging:
- Medial temporal lobe* (same as HSV encephalitis)
- Spares basal ganglia

58
Q

Microscopic finding of HSV encephalitis

A
  • Cowdry Bodies**
  • Perivascular inflammation
59
Q

HIV encephalitis is a chronic or acute inflammation ?

A
  • Chronic inflammation
  • Associated with microglial nodules**
  • Aseptic meningitis occur after seroconversion
60
Q

PML preferentially infects what type of brain cells ?

A
  • Oligodendrocytes*
  • leads to demyelination*
61
Q

What are causes of Basal meningitis ?

A
  • Cryptococcus
  • TB
  • Sarcoidosis
62
Q

SAE association

A
  • HTN (strong association)**
63
Q

SAE imaging ?

A

(looks like CADASIL)
- ONLY involves white matter
- Centrum semiovale white matter*
- Fronto-temporal horn (classic)
- Spares U-fibers
- Seen in >55yo

64
Q

Alzheimer vs Vascular dementia vs Lewy body dementia
- imaging features

A

Alzheimer
- hippocampal, temporal lobe atrophy
- FDG posterior temporoparietal uptake (ear muff)

Vascular Dementia
- Cortical infarcts
- Lacunar infarcts
- Generalized brain atrophy

Lewy body dementia
- Generalized atrophy
- a-synuclein*
- clinically like Parkinsons, but dementia comes before parkinsonism
- Visual hallucinations**

65
Q

MELAS features

A

(MELAS)
- Mitochondria disorder
- Lactic Acidosis
- Seizures
- Strokes (in non-vascular distribution)
- normal WM

66
Q

Adrenal Leukodystrophy (ALD)
- Imaging ?
- F or M more common

A
  • Parietal occipital predominance
  • Crosses splenium of Corpus Callosum
  • MALE predominance
  • can Enhance, restrict
67
Q

Metachromatic
- Imaging ?

A
  • Frontal lobe
  • Periventricular Tigroid
  • Spares U-fibers
  • Most common leukodystrophy*
68
Q

Multifocal brain tumors from seeding ?

A
  • Medulloblastoma
  • GBM
  • Oligodendroglioma
  • Ependymoma
69
Q

Germinoma of pineal gland*
- epidemiology

A
  • Exclusively in BOYS
  • the MOST COMMON pineal gland tumor
70
Q

Germinoma pineal gland labs ?

A
  • high bHCG
71
Q

Pineoblastoma resembles what other tumors ?

A

Small round blue cell tumor, pNET of the pineal gland. WHO grade-4 highly aggressive tumor.

Resembles:
- Medulloblastoma (pineoblastoma also highly aggressive and often seeds)
- Retinoblastoma

72
Q

Pineoblastoma epidemiology

A
  • girls (c.f. germinoma is boys)
73
Q

Pineoblastoma association ?

A
  • Retinoblastoma (5% with retinoblastoma gets pineoblastoma)
74
Q

Pineoblastoma labs

A
  • Homer Wright rosettes and Flexner-Wintersteiner rosettes
  • synaptophysin: positive
  • chromogranin-A
  • neurone-specific enolase: positive
75
Q

Pineocytoma epidemiology ?

A
  • Adult
  • RARE in childhood (c.f. pineoblastoma and germinoma)
  • non-invasive, well circumscribed (c.f. pineoblastoma)
76
Q

Most common neonatal brain infection ?

A
  • CMV (3x more common than toxo)
  • Polymicrogyria (highest association amongst TORCH)
77
Q

What trimesters does TORCH infection matter most ?

A
  • only matter in the first two trimesters (doesn’t cause much harm in third)
77
Q

Calcification pattern of CMV vs Toxo

A
  • CMV (periventricular)
  • Toxo (Basal ganglia with hydrocephalus)
78
Q

Most common opportunistic infection in AIDS ?

A

Toxoplasmosis

79
Q

CJD 3 types ?

A
  • Sporadic (90%)
  • Variant “mad cow” (rare)
  • Familial (10%)
80
Q

CJD imaging

A

Restricted diffusion most sensitive sign
- Cortex (most common early site)
- Basal ganglia
- Progressive brain atrophy**

Hockey stick (variant)
- FLAIR dorsal medial thalamus

Pulvinar sign (variant)
- FLAIR pulvinar thalamic

81
Q

Things that involve corpus callosum

A
  • Tumor: Lymphoma (most classic), GBM
  • Post Treatment: Radiation Necrosis
  • Demyelination; Big Tumefactive MS Plaque, Marchiafava-Bignami
  • Infection: Progressive Multifocal Leukoencephalopathy (PML)
  • Trauma: Diffuse Axonal Injury
  • Weird Shit: transient lesions of the splenium of the corpus callosum - cytotoxic stuff often from seizure medications (oval spot in the splenium)
82
Q

Bilateral thalamic stroke differentials

A
  • Artery of Percheron (arise from PCA)
  • Tip of basilar occlusion
  • Bilateral internal cerebral vein thrombosis
83
Q

Caudate infarct which artery affected

A
  • Recurrent artery of Heubner stroke (from ACA, can be due to clipping of ACOM aneurysm)
84
Q

Infarct in Anterior and Posterior circulation of the same hemisphere

A
  • Fetal PCOM stroke
85
Q

Fusiform aneurysm association and site

A

Association:
- PAN
- Syphilis
- Marfans, Ehlers Danlos

Location:
- Posterior circulation

86
Q

2 types of paraganglioma and locations

A

Parasympathetic paragangliomas
- Carotid body paraganglioma (most common - 40-60%)
- Jugular Paraganglioma (invades occipital and petrous apex)
- Jugulotympanic paraganglioma (erodes middle ear)
- Tympanic paraganglioma (doesnt erode middle ear)

Sympathetic paraganglioma
- Intra-adrenal: Pheochromocytoma (most common)
- extra-adrenal: organ of Zuckerkandl, bladder, mediastinum

87
Q

Jugular Paraganglioma
- Epidemiology
- Clinical presentation
- Imaging

A

Epi
- 40% hereditary*

Presentation
- Hoarseness from vagal nerve compression (most common)

Imaging
- Can erode middle ear, petrous apex, occipital bone
- Salt and pepper
- FDG-avid

88
Q

Cholesterol Granuloma
- imaging ?

A
  • most common petroud apex lesion with smooth bony expansile lesion
  • T1 and T2 bright
  • T2 dark hemosiderin rim and faint peripheral enhancement
  • slow growing one can watch and wait, fast growing needs surgery
89
Q

Cholesteatoma in petrous apex
- congenital or acquired ?
- how to tell from cholesterol granuloma

A
  • these are Congenital (c.f. middle ear cholesteatoma is acquired)
  • slow growing with similar bony changes to Cholesterol Granuloma
  • T1 dark, T2 bright with restricted diffusion* (c.f. Cholesterol granuloma is T1, T2 bright, No restricted diffusion)
90
Q

Malignant “Necrotizing” Otitis externa
- Causing agent ?
- Risk factor ?

A

Causative agent
- Pseudomonas (always)

Risk factor
- Diabetics* (always)

Swollen EAC soft tissue with small abscesses and bony erosion

91
Q

phthisis bulbi causes

A

IMage: Shrunken, crenated appearance of the left globe with associated calcification

Cause
- chronic end-stage condition due to severe ocular insults
- Traumatic injury
- Infection, or radiation.

92
Q

What is LEAST LIKELY to be associated with enlarged nerves of the cauda equina?

Dejerine-Sottas
Hereditary sensory motor neuropathy
Guillain-Barre syndrome
Metastatic adenocarcinoma

A

Guillain-Barre typically shows diffuse cauda equina enhancement, but does not enlarge the nerves.

  • Chronic demyelinating polyneuropathies such as
  • Dejerine-Sottas and HSMN will enlarge the nerves of the cauda equina.
  • Leptomeningeal metastases will also enlarge the roots in a nodular pattern.
93
Q

Saccular aneurysm in how many % population ? how many % multiple

A

2% of populatoin
- 90% are found near major branch points in anterior circulation.
- 10% posterior

Up to 30% multiple

94
Q

Features of intracranial hypertension

A
  • papilloedema: flattening of the posterior sclera (~80%)
  • Prominent subarachnoid space around the optic nerves
  • Tortuous optic nerves
  • Empty sella
  • Enlarged Meckel cave
  • Slit like ventricle
95
Q

Optic neuritis bilateral

A
  • NMO (devics)
96
Q

ischemic optic neuropathy in Vasculitis can look like ?

A

Optic neuritis

97
Q

Rectus pseudotumor or thyroid disease show tendons sparing

A

Pseudotumor
- Involves unilateral rectus muscle most common
- involves tendons
- will see peri-orbital oedema (if dont seen, then dealing with real tumor)

98
Q

JNA most common arterial supply

A

Internal maxillary artery of the external carotid artery

99
Q

Craniocynosotosis associations

A
  • Apert syndrome
  • Crouzon syndrome
  • Carpenter syndrome
  • Choanal atresia
100
Q

What are some conditions that are associated with BBB disruption besides Infarct, Tumor, Infection ?

A
  • Temporal lobe epilepsy (TLE)
  • Posterior reversible encephalopathy syndrome (PRES)
  • Hypoxia, ischaemia and infarction, tumour
  • Inflammatory conditions, e.g. meningitis, trauma, intracranial irradiation, multiple sclerosis,
    progressive multifocal leukoencephalopathy: the JC virus can cross the BBB.
101
Q

Examples of Communicative hydrocephalus ?

A
  • meningitis, haermorrhage, overproduction of CSF
102
Q

Which vascular malformation has NO normal intervening brain tissue ?

A

Cavernous haemoangioma

103
Q

Which vascular malformation angiographically occult ?

A

DVA

PATH FINAL (10 decks)

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