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CNS > NRISE 2018 > Flashcards

NRISE 2018 Flashcards

1
Q

Multiple System atrophy

A

Blue Putamen

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2
Q

Effect of dystrophinopathies on sarcoglycans

A

Decreased

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3
Q

Dematiaceous Fungi (Chromomycoses)

A

Pigmented with melanin
Cladophialophora- neurotropic yeast (chromoblastomycosis)
Phaeohyphomyocosis- hyphae

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4
Q

Acute Disseminated Encephalomyelitis (ADEM)

A

Clinical: Acute, monophasic, post-URI, vaccine, M. pneumoniae, or Campylobacter
RX: steroids and IVIG
Path: Peri-venous macrophages and T-cells in white matter, perivenous zones of demyelination

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5
Q

Petechiae in hypothalamus, mammilary bodies and periaqueductal gray matter

A

Wernicke encephelopathy

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6
Q

Choroidal/Uveal melanoma poor prognostic features

A

Epitheloid morphology, mitosis, lymhpocytes, large nucleoli, tumor size, extraoccular extension, ciliary body location > choroid > iris

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7
Q

Variant CJD MRI

A

bilateral, symmetric, pulvinar/posterior thalamus, T2 hyperintenstiy

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8
Q

Sporadic CJD MRI

A

bilateral, symmetric, head of caudate and putamen, T2 hyperintensity

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9
Q

Holoprosencephaly

A

Failure of ventricular cleavage and rotation

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10
Q

Sudden fatal obstructive hydrocephalus

A

Third ventricle colloid cyst

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11
Q

Perinaud’s syndrome

A

Caused by pineal region tumors. Paralysis of upward gaze, Pseudo-Argyll Robertson pupils, convergance retraction nystagmus, eyelid retraction, conjugate down gaze

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12
Q

Wallenberg syndrome

A

Lateral medullary infracts, vertebral artery/PICA occlusion; Most common brain stem stroke
Ipsilateral cerebellars signs and cranial nerve findings
Contralateral loss of pain/temp
Hiccups

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13
Q

ALS

A

corticospinal tract degeneration

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14
Q

Anterograde amnesia

A

Cannot form new memories. Most commonly Alzheimer disease, but any bilateral disruptionof the circuit of Papez

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15
Q

Kernicterus

A

Most common cause is hemolytic disease of the newborn

Criggler Najjar: autosomal recessive inability to conjugate bilirubin

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16
Q

Traumatic/diffuse axonal injury

A

rapid acceleration-deceleration of the head

Petechiae of the parasagita WM, corpus callosum, dorsolateral brainstem

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17
Q

Menke’s desease

A

autosomal recessive, ATP7A, copper transport protein, kinky steely hair.
Copper cannot get out of enterocytes
Low serum copper and ceruloplasmin

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18
Q

Wilson’s disease

A

autosomal recessive, ATP7B, Kayser Fleischer rings, basal ganglia lesions
Copper cant be excreted from hepatocytes
Low serum copper and ceruloplasmin

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19
Q

Encephalomalacia

A

Old damage, typically ischemic

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20
Q

Cystic leukomalacia

A

periventricular WM atrophy w/wo cysts

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21
Q

Status Marmoratus

A

Firm, white basal ganglia from hypermyelination of glial scars, myelinated astrocyte processes

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22
Q

Ulegyria

A

loss of gray matter only in deeper parts of sulci, mkaing them look like mushrooms in cross-section

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23
Q

Porencephaly

A

Total focal loss of cortex and WM, making a hole from surface to ventricle, can be a developmental issue

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24
Q

Familial amyloidotic polyneuropathy

A

Mutations in transthyretin is most common causing sensorimotor neuropathy that starts peripherally and involves autonomic functions
Other forms invovle apolipoprotein A1 or gelsolin and have more sensory neruopathy

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25
Q

Pick bodies

A

Lots in dentate fascia granule neurons and cortical layers II and III (Tau)

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26
Q

Palatal myoclonus

A

Inferior olive lesions, symmetric jerky movements

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27
Q

Cerebral edema peaks at what days post infarct

A

2-5 days

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28
Q

Subdural hematomas frequently develop what as they organize?

A

Extramedullary hematopoiesis

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29
Q

Oligodenodrocyte coiled bodies

A

similar morphology regardless of the tauopathy

composed of 4Rtau, non-specific, little, round blobbies

30
Q

Zebra bodies

A

Mucopolysacchroidoses Fabry dz, Hurler dz, and other lysosomal storage disorders

31
Q

Fingerprint bodies

A

Neuronal ceroid lipofuscinosis

32
Q

Mesial temporal sclerosis/Hipocampal sclerosis

A

Secondary to long standing epilepsy

Loss of neurons, spreading of dentate neurons, gliosis, corpora amylacea, Worst in CA1. Volume loss/atrophy on MRI

33
Q

Multiple System Atrophy

A

Sickle and flame shaped a-synuclein glial cytoplasmic inclusions

34
Q

Area Postrema

A

Nausea and vomiting center, linked to chemical trigger zone for bloodborne toxins, no blood brain barrier (no tight junctions)

35
Q

Nucleus of Solitary Tract

A

Major autonomic nucleus connected to vagus nerve; coordinates nausea and vomiting with area postrema

36
Q

Clear cell Ependymoma

A

More aggresive than usual ependymomas, not infiltrative, look like oligos

37
Q

Ependymoma EM

A

Zipper like intraluminal intercellular junctions and intraluminal microvilli

38
Q

Coat’s Disease

A

exudative retinits or retinal telangiectasis, cholesterol crystals and lipid laden macrophages in the retina and subretinal space due to breakdown of blood-retinal barrier in the endothelial cells and leakage of blood products. Retinal detachment. Clinically mimics retinal detachment

39
Q

Parkinson plus syndromes

A

Multiple system atrophy (MSA)
Progressive suprnuclear palsy (PSP)
Corticobasal degeneration (CBD)

40
Q

Multiple system atrophy

A

wet, wacky and wobbly (like normal pressure hydrocephalus) plus parkinsonism

41
Q

Progressive Supranuclear palsy

A

Vertical gaze palsy and other oculomotor problems, ataxia, emotional outbursts

42
Q

Corticobasal degeneration

A

movement disorders and problems with cortical processing, “alien hand syndrome”, apraxia and aphasia

43
Q

Popcorn or berry circumscribed lesion with dark halo on T2 and bright halo on T1 and SWI

A

Cavernous malformation, halo is due to hemosideran

44
Q

Spinal cord AVM causes a rapidly progressing meylopathy

A

Foix-Alajouanine Syndrome - mechanism unknown, can be fatal

45
Q

Congenital myopathy

A

Nemaline rods forming little dark haystacks in the myofibers

46
Q

Nemaline rods forming little dark haystacks in the myofibers

A

Congenital myopathy

47
Q

Foix-Alajouanine Syndrome

A

Spinal cord AVM causes rapidly progressing myelopathy, can be fatal, mechanism unknown

48
Q

Uncrossed corticospinal/pyramidal tracts, right motor strip controls the right side

A

Trisomy 18/Edwards Syndrome

49
Q

Medulloepithelioma of the eye

A

Kids, arise in the ciliary body, can be benign or malignant, can have heterologouse elements (teratoid medulloepithelioma)

50
Q

Neo/isocortex layers

A

I: Molecular layer- dendrites
II: External granular layer- input from neighboring cortex
III: External pyramidal- projects to neighboring cortex
IV: Internal granular- receives input from thalamus
V: Internal pyramidal- projects to distant structures
VI: Fusiform/multiform- projects to claustum

51
Q

Molecular layer

A

I: dendrites

52
Q

External granular layer

A

II: receives input from neighboring cortex, usually the next gyrus over

53
Q

External pyramidal layer

A

III: Projects to neighboring cortex

54
Q

Internal granular layer

A

IV: Receives input from thalamus

55
Q

Internal pyramidal layer

A

V: Projects to distant structures- spinal cord, striatum, brain stem

56
Q

Fusiform/Multiform

A

VI: Projects to claustrum, wasted space

57
Q

Gross appearance of demyelinating plaques

A

Patches of gray matter within white matter

58
Q

Trans-synaptic degeneration

A

Recieveing neurons die from loss of input signal after the projecting neurons are cut. This is different from Wallerian degeneration

59
Q

Wallerian degeneration

A

Distal portion of the axon dies after being transected

60
Q

Balloned Neurons

A

Tau Positive, Frequent in corticobasal degeneration but also found in progressive supranuclear palsy (PSP) and other neurodegen dx (Alzheimer’s)

61
Q

Topography of the visual cortex

A

Retinotopic, Left VC correlates to left half of retina (right half of the visual field). Retina is upside down and backward of the visula fields

62
Q

Chiari I malformation

A

Cerebellar tonsils protrude through the foramen magnum, usually asymptomatic. Good

63
Q

Chiari II/ Arnold-Chiari Malformation

A

Type 1 (protrusion of cerebellar tonsils through the foramen magnum) + myelomeningocele, can have syringomyelia of cervical cord. BAD

64
Q

Chiari III.

A

Type II (protrusion of cerebellar tonsils + myelomeningocele), and occipital encephalocele. WORST

65
Q

Chiari IV

A

Agenesis or hypoplasia of the cerebellum. Incompatible with life

66
Q

Hypothalamic Hamartoma Symptomatology

A

Gelastic seizures (random laughing fits that are not connected to any stimulus) and sometimes precocious puberty and/or obesity

67
Q

Random laughing fits and percocious puberty and/or obesity

A

Hypothalamic Hamartomas- Gelastic seizures

68
Q

Cysticercosis cause

A

Taenia solium, fecal oral transmission of tapeworm eggs from someone with an intestinal tapeworm, not eating undercooked pork

69
Q

Ecchordosis Physaliphora

A

Notochordal remnant on the anterior brainstem, usually in front of the basilar artery on the pons, usually pea sized, bubbly (like a chordoma) but not growing

70
Q

Notochordal remnant on the anterior brainstem

A

Ecchordosis physaliphora- bubbly usually pea sized on the pons in front of the basilar artery

CNS (17 decks)

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