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STEP > Neuro IX > Flashcards

Neuro IX Flashcards

1
Q

Central retinal artery occlusion presentation

A

acute, painless monocular vision loss.

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2
Q

central retinal artery occlusion findings

A

1) Retina cloudy with attenuated vessels.

2) “cherry-red” spot at fovea (center of macula)

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3
Q

central retinal artery occlusion management

A

Evaluate for embolic source.

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4
Q

Embolic sources of central retinal artery occlusion

A

1) carotid artery atherosclerosis
2) cardiac vegetations
3) PFO

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5
Q

retinitis pigmentosa presentation

A

Painless, progressive vision loss beginning with night blindness (rods affected first)

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6
Q

retinitis pigmentosa etiology

A

inherited retinal degeneration.

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7
Q

retinitis pigmentosa findings

A

1) Bone spicule-shaped deposits around macula.

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8
Q

retinitis pathophys

A

retinal edema and necrosis leading to scarring.

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9
Q

retinitis causes

A

1) often viral (CMV, HSV, VZV)
2) bacterial
3) parasitic

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10
Q

retinitis association

A

immunosuppression

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11
Q

papilledema pathophys

A

Optic disc swelling (usually bilateral) due to increased ICP.

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12
Q

papilledema fundoscopy findings

A

Enlarged blind spot + elevated optic disc with blurred margins.

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13
Q

Miosis pathway

A

1st neuron: Edinger-Westphal nucleus to ciliary ganglion via CN III.
2nd neuron: short ciliary nerves to pupillary sphincter muscles.

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14
Q

pupillary light reflex pathway

A

Light in either retina sends a signal via CN II to pretectal nuclei in midbrain that activates bilateral Edinger-Westphal nuclei; pupils contract bilaterally.

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15
Q

Mydriasis pathway

A

1st neuron: hypothalamus to ciliospinal center of Budge (C8-T2)
2nd neuron: exit at T1 to superior cervical ganglion (travels along cervical sympathetic chain near lung apex, subclavian vessels)
3rd neuron: plexus along internal carotid, through cavernous sinus; enters orbit as long ciliary nerve to pupillary dilator muscles. Sympathetic fibers also innervate smooth muscle of eyelids (minor retractors) and sweat glands of forehead and face.

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16
Q

marcus gunn etiology

A

Due to optic nerve damage or severe retinal injury. Decreased bilateral pupillary constriction when light is shone in affected eye relative to unaffected eye.

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17
Q

Horner syndrome pathophys

A

lesion of spinal cord above T1 leads to sympathetic denervation.

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18
Q

Horner syndrome pathway

A

1st order neuron from hypothalamus to synapse in lateral horn
2nd order neuron from lateral horn to superior cervical ganglion
3rd order neuron from superior cervical ganglion to various sympathetic innervations.
***look at all landmarks

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19
Q

horner syndrome associations

A

1) pan coast tumor
2) Brown-Sequard
3) late-stage syringomyelia.

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20
Q

Superior oblique functions

A

Abducts, introits, and depresses while adducted

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21
Q

ocular motility diagram

A

FA 488

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22
Q

How do you test for SO function?

A

Have patient look down.

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23
Q

How do you test for IO function?

A

Have patient look up.

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24
Q

Pathophys of CN III motor dysfunction

A

Due primarily to vascular disease (DM: glucose –> sorbitol) due to decreased diffusion of oxygen and nutrients to the interior fibers from compromised vasculature residing on outside of nerve.

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25
Q

Pathophys of CN III PS dysfunction

A

Fibers on periphery are first affected by compression.

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26
Q

Causes of CN III PS dysfunction

A

1) posterior communicating artery aneurysm

2) uncle herniation

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27
Q

CN IV palsy presentation

A

1) eyes move upward, particularly with contralateral gaze
2) head tilt toward side of lesions (problems going down stairs, may present with compensatory head tilt in opposite direction).

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28
Q

CN VI palsy presentation

A

Medially directed eye that can’t abduct

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29
Q

Meyer loop

A

Inferior retina; loops around inferior horn of lateral ventricle.

30
Q

dorsal optic radiation

A

Superior retina; takes shortest path via internal capsule.

31
Q

MLF function

A

crosstalk between CN VI and CN III, allowing eyes to move in same horizontal direction.

32
Q

MLF characteristics

A

highly myelinated.

33
Q

Most common cause of dementia in elderly?

A

AD

34
Q

ApoE2 and alzhheimers

A

Decreases risk of sporadic form

35
Q

ApoE4 and alzheimers

A

increased risk of sporadic form

36
Q

familial forms of AD

A

1) APP
2) presenilin-1
3) presenilin-2

37
Q

gross findings in AD

A

1) widespread cortical atrophy
2) narrowing of gyro
3) widening of sulci

38
Q

neurofibrillary tangles

A

intracellular hyperphosphyrlated tau protein = insoluble cytoskeletal elements.

39
Q

what correlates with degree of dementia in AD?

A

number of neurofibrillary tangles.

40
Q

FTD association

A

can also have movement disorders + progressive aphasia.

41
Q

FTD pathology

A

1) hyperphosphorylated tau inclusions

2) ubiquitinated TDP-43

42
Q

lewy bodies found…

A

primarily in cortex.

43
Q

2nd most common cause of dementia in elderly?

A

vascular dementia

44
Q

Imaging findings in vascular dementia

A

MRI or CT shows multiple cortical and/or subcortical infarcts.

45
Q

myoclonus type associated with JCD

A

“startle myoclonus”

46
Q

prions in CJD transform to…

A

Beta pleated sheet (resistant to proteases)

47
Q

Other causes of dementia

A

1) syphilis
2) HIV
3) *hypothyroidism
4) B1 deficiency
5) B3 deficiency
6) B12 deficiency
7) Wilson disease
8) NPH

48
Q

what happens if you correct hypernatremia too quickly?

A

cerebral edema/herniation (from high to low, your brain will blow)

49
Q

osmotic demyelination presentation

A

1) paralysis
2) dysarthria
3) dysphagia
4) diplopia
5) loss of consciousness

50
Q

other common presentation of MS

A

1) hemiparesis

2) hemisensory symptoms

51
Q

Charcot triad of MS

A

SIN
Scanning speech
Intention tremor (also incontinence, and INO)
Nystagmus

52
Q

CSF findings in mS

A

1) increased IgG

2) elevated myelin basic protein

53
Q

gold standard for MS diagnosis

A

MRI

54
Q

Disease modifying therapies for mS

A

1) beta-interferon
2) glatiramer
3) natalizumab

55
Q

management of acute MS flares

A

IV steroids

56
Q

treatment for neurogenic bladder in MS

A

1) catheterization

2) muscarinic antagonists

57
Q

treatment for spasticity in MS?

A

1) baclofen

2) GABA-B receptor agonists

58
Q

acute inflammatory demyelinating polyradiculopathy pathophys

A

Most common subtype of GBS. Destroys Schwann cells leading to inflammation and demyelination of peripheral nerves and motor fibers.

59
Q

Other findings in acute inflammatory demyelinating polyradiculopathy

A

1) facial paralysis (up to 50%)
2) ANS dysregulation –> cardiac irregularities, HTN, hypotension
3) sensory abnormalities

60
Q

acute inflammatory demyelinating polyradiculopathy prognosis

A

Almost all patients survive. Majority recover completely after weeks to months.

61
Q

CSF findings in GBS/acute inflammatory demyelinating polyradiculopathy

A

Increased CSF protein with normal cell count.

62
Q

Term for CSF findings in GBS

A

albuminocytologic dissociation

63
Q

potential sequela of GBS

A

increased protein may cause papilledema

64
Q

GBS pathophys

A

molecular mimicry. *no definitive link to pathogens though.

65
Q

GBS management

A

1) Plasmapheresis

2) IVIG

66
Q

Acute disseminated (post infectious) encephalomyelitis pathophys

A

Multifocal periventricular inflammation and demyelination after infection or vaccination.

67
Q

Acute disseminated (post infectious) encephalomyelitis presentation

A

Rapidly progressive multifocal neurologic symptoms + altered mental status

68
Q

Other name for CMT…

A

Hereditary motor and sensory neuropathy.

69
Q

CMT pathophys

A

Defective production of proteins involved in the structure and function of peripheral nerves or the myelin sheath.

70
Q

pes cavus

A

high arch

71
Q

CMT presentation

A

1) pes Casus
2) lower extremity weakness
3) sensory deficits

STEP (85 decks)

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