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Flashcards in Neuro IX Deck (71):
1

Central retinal artery occlusion presentation

acute, painless monocular vision loss.

2

central retinal artery occlusion findings

1) Retina cloudy with attenuated vessels.
2) "cherry-red" spot at fovea (center of macula)

3

central retinal artery occlusion management

Evaluate for embolic source.

4

Embolic sources of central retinal artery occlusion

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

5

retinitis pigmentosa presentation

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

6

retinitis pigmentosa etiology

inherited retinal degeneration.

7

retinitis pigmentosa findings

1) Bone spicule-shaped deposits around macula.

8

retinitis pathophys

retinal edema and necrosis leading to scarring.

9

retinitis causes

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

10

retinitis association

immunosuppression

11

papilledema pathophys

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

12

papilledema fundoscopy findings

Enlarged blind spot + elevated optic disc with blurred margins.

13

Miosis pathway

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

14

pupillary light reflex pathway

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

15

Mydriasis pathway

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.

16

marcus gunn etiology

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

17

Horner syndrome pathophys

lesion of spinal cord above T1 leads to sympathetic denervation.

18

Horner syndrome pathway

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

19

horner syndrome associations

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

20

Superior oblique functions

Abducts, introits, and depresses while adducted

21

ocular motility diagram

FA 488

22

How do you test for SO function?

Have patient look down.

23

How do you test for IO function?

Have patient look up.

24

Pathophys of CN III motor dysfunction

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.

25

Pathophys of CN III PS dysfunction

Fibers on periphery are first affected by compression.

26

Causes of CN III PS dysfunction

1) posterior communicating artery aneurysm
2) uncle herniation

27

CN IV palsy presentation

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).

28

CN VI palsy presentation

Medially directed eye that can't abduct

29

Meyer loop

Inferior retina; loops around inferior horn of lateral ventricle.

30

dorsal optic radiation

Superior retina; takes shortest path via internal capsule.

31

MLF function

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

32

MLF characteristics

highly myelinated.

33

Most common cause of dementia in elderly?

AD

34

ApoE2 and alzhheimers

Decreases risk of sporadic form

35

ApoE4 and alzheimers

increased risk of sporadic form

36

familial forms of AD

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

37

gross findings in AD

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

38

neurofibrillary tangles

intracellular hyperphosphyrlated tau protein = insoluble cytoskeletal elements.

39

what correlates with degree of dementia in AD?

number of neurofibrillary tangles.

40

FTD association

can also have movement disorders + progressive aphasia.

41

FTD pathology

1) hyperphosphorylated tau inclusions
2) ubiquitinated TDP-43

42

lewy bodies found...

primarily in cortex.

43

2nd most common cause of dementia in elderly?

vascular dementia

44

Imaging findings in vascular dementia

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

45

myoclonus type associated with JCD

"startle myoclonus"

46

prions in CJD transform to...

Beta pleated sheet (resistant to proteases)

47

Other causes of dementia

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

48

what happens if you correct hypernatremia too quickly?

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

49

osmotic demyelination presentation

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

50

other common presentation of MS

1) hemiparesis
2) hemisensory symptoms

51

Charcot triad of MS

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

52

CSF findings in mS

1) increased IgG
2) elevated myelin basic protein

53

gold standard for MS diagnosis

MRI

54

Disease modifying therapies for mS

1) beta-interferon
2) glatiramer
3) natalizumab

55

management of acute MS flares

IV steroids

56

treatment for neurogenic bladder in MS

1) catheterization
2) muscarinic antagonists

57

treatment for spasticity in MS?

1) baclofen
2) GABA-B receptor agonists

58

acute inflammatory demyelinating polyradiculopathy pathophys

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

59

Other findings in acute inflammatory demyelinating polyradiculopathy

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

60

acute inflammatory demyelinating polyradiculopathy prognosis

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

61

CSF findings in GBS/acute inflammatory demyelinating polyradiculopathy

Increased CSF protein with normal cell count.

62

Term for CSF findings in GBS

albuminocytologic dissociation

63

potential sequela of GBS

increased protein may cause papilledema

64

GBS pathophys

molecular mimicry. *no definitive link to pathogens though.

65

GBS management

1) Plasmapheresis
2) IVIG

66

Acute disseminated (post infectious) encephalomyelitis pathophys

Multifocal periventricular inflammation and demyelination after infection or vaccination.

67

Acute disseminated (post infectious) encephalomyelitis presentation

Rapidly progressive multifocal neurologic symptoms + altered mental status

68

Other name for CMT...

Hereditary motor and sensory neuropathy.

69

CMT pathophys

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

70

pes cavus

high arch

71

CMT presentation

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