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Clinical Neuroscience 2 > Clinical- 7 > Flashcards

Clinical- 7 Flashcards

1
Q

Review the eye anatomy

A

on yer own ya filthy animal

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2
Q

What is diplopia?

A

double vision

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3
Q

What causes diplopia?

A

misalignment of the eyes

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4
Q

What is opthalmoplegia?

A

When the extraocular muscle fxn is disrupted

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5
Q

How is the derp in opthalmoplegia?

A

You derp to the opposite direction because of unopposed action of the other muscles

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6
Q

What is ptosis?

A

droopy eyelid

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7
Q

What are the 2 causes for ptosis?

A

damage to either III (LPS) or symapathetics (sup tarsal)

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8
Q

Quick fire eye lesions/conditions/Sx: I will say a Sx and you tell me where the lesion is. Ready?

Total blindness of L eye

A

L optic n lesion

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9
Q

Bitemporal hemianopia

A

pituitary tumor/ optic chiasm lesion

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10
Q

L nasal hemianopia

A

calcified internal carotid

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11
Q

central scotoma

A

optic or retrobulbar neuritis

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12
Q

L homonymous hemianopia (2)

A

R optic tract lesion OR complete lesoion of the R optic radiation

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13
Q

L homonymous hemianopia + macular sparing

A

R PCA occlusion

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14
Q

L homonymous inferior quadrantanopia

A

R parietal lobe lesion

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15
Q

L homonymous supeiror quadrantanopia

A

R temporal lobe lesion

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16
Q

What is papilledema?

A

optic disk swelling due to increased intracranial pressure

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17
Q

What are the clinical features of papilledema?

A

almost always bilateral, typically doenst impair vision, no eye pain, assocaited w/just ↑ ICP Sx.

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18
Q

What happens in early papilledema?

A

retinal veins engorged; spontaneous venous pulsations absent; disk hyperemic (increased blood flow); linear hemorrhages at the disk borders; disk margins blurred

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19
Q

What happens in fully developed papilledema?

A

optic disk is elevated above the plane of the retina; blood vessels crossing the border of the disk are obscured

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20
Q

Papilledema- etiologies

A
  • Intracranial mass (urgent evaluation!)
  • Meningitis
  • Venous sinus thrombosis, subarachnoid hemorrhage
  • Polycythemia, endocrinopathy, hypervitaminosis A
  • Pseudotumor cerebri (idiopathic intracranial hypertension)
  • Congenital cyanotic heart disease
  • Spinal cord tumor
  • Guillan-Barre
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21
Q

What is the pathway for the pupillary light response?

A

light –> II –> optic tracts –> pretectal N. –> stimualtion of BOTH EWN –> PANS to ciliary gang –> ciliary m contraction

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22
Q

What are the 4 things to cause nonreactive pupils?

A

o local disease of the iris (trauma, iritis, glaucoma)
o oculomotor nerve compression (tumor, aneurysm)
o administration of a mydriatic agent
o optic nerve disorders (neuritis, M.S.)

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23
Q

What is light-near dissociation?

A

impaired reactivity to light but accomodation is fine.

24
Q

What causes light-near dissociation?

A

neurosyphilis, diabetes, optic n disorders, tumors compressing the tectum

25
Argyll-Robertson- Sx
bilateral, small pupils and irregular and unequal
26
Argyll-Robertson- response
pupils will accomodate but wont react to light. no change with pilocarpine.
27
Argyll-Roberston- differential
neurosyphilis, diabetes, pineal region tumors, MS
28
Tonic/Adies- appearance
unilateral or bilateral, tonic pupil is larger
29
Adies- response
sluggish to react, reacts with pilocarpine, accommodation is less affected
30
Adies- differential
holmes-adies (benign, often familial disorder, women more affected), ocular trauma, ANS neuropathy, degeneration of the ciliary gang
31
Horners- Sx
unilateral small pupil, ptosis
32
Horners- response
normal reponse to lgiht
33
Relative Afferent/Marcus Gunn- reactivity
1 pupil constricts less in response to direct illumination (kinda like IL optic n dmg)
34
What are the common etiologies of III palsy?
vasculopathy > aneurysm > trauma > neoplasm
35
What are the common eitologies for IV palsy?
trauma > vasculopathy > neoplasm > aneurysm
36
What are common etiologies for VI palsy?
neoplasm > vasculopathy > trauma > aneurysm
37
Where is the lesion to cause internuclear opthalmoplegia (INO)?
a lesion of the MLF
38
What happens if you lesion the MLF?
Since it connects III and IV, a lesion causes the uncoupleig movements where IV tell cant tell III to contract the MR muscle to move both eyes to 1 side
39
True or false: INO can be oveercome by caloric stimulation
FALSE
40
What is the most common cause of INO in young adults, where its usually bilateral?
MS
41
What is the most common cause of INO in the elderly, where it's usually unilatereal involvement?
Brainstem strokes
42
Amaurosis fugax- clinical presentaiton
unilateral transient loss of vision over 1-5 mins
43
Amaurosis fugax- etiology
emboli from atherosclerotic lesion of the carotid bifurcation
44
Amaurosis fugax- complications
risk for subsequent hemispheric infarction
45
Amaurosis fugax- prognosis
endarterectomy+ ASA is the bestestest
46
Optic neuritis- Sx
unilateral impairment of visual acuity over hours-days. eye tenderness/pain. central scotoma. disk swelling. impaired constriction
47
Optic neuritis- etiology
demyelination. viral infection maybe. toxins maybe
48
Optic neuritis- associated problems
hyperintense lesions are seen in the brain in 50-70% of pts. many develop MS
49
Optic neuritis- prognosis
in acute demyelinating optic neuritis, visual acuity improves by 2-3 weeks with return to normal or near-normal vision
50
Anterior Ischemic Optic Neuropathy (AION)- Sx
sudden, painless, monocular vision loss. altitudinal visual defect common. disk swelling. have peripapillary hemorrhages.
51
AION- etiology
atherosclerotic in origin, will have a smaller than normal disk
52
AION- prognosis
in 25% of pts, the other eye is affected in 2-4 years. Tx is UNsuccessful after the swelling resolves. usually optic atrophy.
53
Giant cell arteritis (GCA)- sx
artritic infarction is the most devatating complication, sudden and total vision loss, disk is pale and swollen, increased ESR and CRP, accompanied by feer, malaise, night sweats, weight loss and headahce.
54
GCA- age group
70-80
55
GCA- Dx
bilateral temporal artery biopsy, icnrease in ESR
56
GCA- Tx
corticosteroids to preserve vision

Clinical Neuroscience 2 (16 decks)

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