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Integrative Analysis II > Pupils, Bino/Accom, Optic Neuropathies > Flashcards

Pupils, Bino/Accom, Optic Neuropathies Flashcards

1
Q

What is the afferent pupillary pathway

A

pupillary fibers bypass the LGN and go to the pretectal nucleus (olivary nuclei) then to the edinger westphal nucleus

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2
Q

What is the efferent (parasympathetic) pupillary pathway?

A

parasympathetic fibers join CN III and pass through the cavernous sinus, synapsing at ciliary ganglion

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3
Q

Which nerves take parasympathetic signals to the iris sphincter?

A

short ciliary nerve

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4
Q

What is the sympathetic efferent pupillary pathway?

A

hypothalamus to ciliospinal center of budge C8-T2, preganglionic fibers leave spinal cord over apex of lung under the subclavian artery to synapse at cervical ganglion, sympathetic plexus travels along the internal carotid through the cavernous sinus to long ciliary nerves

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5
Q

Which nerves take sympathetic signals to the iris dilator?

A

long ciliary nerves

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6
Q

What is the first thing you should evaluate with anisocoria?

A

if it is greater in bright or dim light

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7
Q

What is the issue when anisocoria is worse in bright light?

A

parasympathetic- bigger pupil not constricting

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8
Q

What is the issue when anisocoria is worse in dim light?

A

sympathetic- smaller pupil not dilating

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9
Q

With parasympathetically driven anisocoria what should you look for in A seg?

A

sector palsy/damage

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10
Q

Dilute pilo and anisocoria worse in bright conditions (parasympathetic)

A

if constricts= CN III palsy, if no constriction= pharmacologic dilation

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11
Q

What might an aide’s pupil look like in the slit lamp?

A

flattened/flaccid pupillary border

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12
Q

What are possible causes of adie’s tonic pupil?

A

viral infection (zoster), trauma, GCA, neurosyphilis (bilateral)

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13
Q

How do you treat Aides’s?

A

treat cosmesis with tinted CL, dilute pilo or brimonidine

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14
Q

Horner’s triad

A

ptosis, miosis, anhydrosis

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15
Q

T/F a horner’s pupil does not dilate with topical cocaine or reversal of aniso with apraclonidine

A

true

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16
Q

How does cocaine 10% work?

A

blocks reuptake of NE that has been released at the post-ganglionic synaptic terminal. NE will only be released if the complete 3 neuron chain is intact, so if the anisocoria disappears with cocaine it was phsyiologic

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17
Q

How does apraclonidine work?

A

the affected eye will develop super sensitivity to the alpha 1 receptor, so that pupil will dilate more so in response to the highly alpha 1 agonistic apraclonidine. This hypersinsitivity takes 1-3 days to develop

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18
Q

Hydroxyamphetamine (paredrine-Alcon) and Horner’s

A

dilation occurs with 1st or 2nd order/central/pre-ganglionic… no dilation with 3rd order/post-ganglionic

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19
Q

How does hydroxyamphetamine work?

A

acts directly on the receptors so requires an intact 3rd order neuron. Thus if the eye dilates with hydroxy it’s likely a preganglionic lesion, if it does not dilate it’s post ganglionic

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20
Q

What additional tests may be run with Horner’s?

A

neoplasia-chest x-ray, stroke MRI/MRA, carotid dissection-doppler

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21
Q

T/F convergence and accommodative issues can give results that mimic each other

A

true

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22
Q

How to distinguish CI and pseudo CI?

A

NPC through +1 CI will get worse, pseudo better

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23
Q

Morgan’s norms creation

A

800 adults, normative data and 1/2 SD

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24
Q

“Group A”

A

accom amp, PRA, NPC (BI to blur)

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25
Q

“Group B”

A

NRA, PRC (BO to blur)

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26
Q

Accommodative fatigue

A

Group A low B high aka low amp/PRA/BI/high NRA, BO

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27
Q

What does accommodative fatigue respond to?

A

plus or VT

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28
Q

Vergence fatigues

A

Group B low A high aka low NRA/BO and high amp/PRA/BI

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29
Q

What does vergence fatigue responds to?

A

VT and possibly prism

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30
Q

What does CN III innervate?

A

levator palprebrae; SR, IR, MR, IO, presynaptic parasympathetic to iris sphincter

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31
Q

Cranial nerve III palsy presents as

A

down out and blown

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32
Q

CN III palsy pupil sparing

A

more likely vascular occlusion than aneurysm

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33
Q

Where are pupillary fibers compared to CN III?

A

pupillary fibers course outside the nerve and are more affected by compression

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34
Q

What is aberrant regeneration?

A

most common after recovery from acute CN III palsy… lid retraction on down gaze (pseudo von graef), lid elevation or pupil constriction on adduction, unilateral globe retraction on up or down gaze

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35
Q

Incomplete palsy, inferior

A

internal ophthalmoplegia, medial/inferior recti, inferior oblique paresis … superior rectus and lid not affected

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36
Q

Incomplete palsy, superior

A

ptosis, superior rectus paresis … superior incomplete palsy is more rare

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37
Q

Incomplete palsy, single muscle paresis

A

small vessel disease, quite rare

38
Q

CN III palsy workup

A

MRI/MRA unless 50+ with pupil spared

39
Q

What do you do if CN III palsy with pupil spared 50+?

A

observe 5-7 days, MRI/MRA if pupil becomes involved, if no pupil watch BP, BG, chol, etc F/U in 6 weeks … also consider GCA

40
Q

What testing might you do with aberrant regeneration?

A

MRI/MRA

41
Q

What deviation does a CN IV palsy cause?

A

slight hypertopia because superior oblique

42
Q

Where is diplopia worse with CN IV palsy?

A

gaze opposite side of lesion and head tilt toward side of lesion

43
Q

What techniques identifies muscle palsy with hypertropia?

A

Parks 3 step

44
Q

What is the most common cause of CN IV palsy?

A

trauma common, ischemia, decompensated phoria

45
Q

What is the workup of CN IV palsy?

A

measure vertical fusional amplitudes for decompensated phoria, older patients > 50 years eval BG, BP and cholesterol, younger patients MRI and vascular eval

46
Q

What diplopia is caused by CN VI palsy?

A

horizontal diplopia

47
Q

What causes CN VI palsy in older patients?

A

ischemia, may complain of pain behind the eye

48
Q

What are other cause of CN VI palsy?

A

masses, inflammation, migrane, in response to increase ICP – courses over petrous ridge/pyramid

49
Q

What is the work up for a CN VI palsy?

A

kids with recent flu symptoms- monitor, adults under 50 MRI, adults over 50 check BP, BG, cholesterol, patients who are monitored and get worse or don’t resolve in 3 months MRI

50
Q

3 diseases to the optic nerve

A

optic neuritis, papilledema, anterior ischemic optic neuropathy

51
Q

Optic neuritis

A

unilateral inflammation to the ON

52
Q

Causes of optic neuritis

A

MS, childhood infections, meningitis, granulomatous inflammations

53
Q

S/S of optic neuritis

A

rapid vision loss, pain on EOMs, color vision changes, focal neurologic symptoms, worsened symptoms with exercise (uhthoff sign)

54
Q

How does optic neuritis affect vision?

A

peak vision loss (mild-severe) at 1-2 weeks, resolution in 5 weeks, color desaturation, VF defects

55
Q

How does color vision change in optic neuritis?

A

blue-yellow desaturation in acute and red green in late stages

56
Q

What VF defects may be present for optic neuritis?

A

general depression, defects respecting horizontal midline, central, centrocecal

57
Q

What is the workup for optic neuritis?

A

MRI of brain and orbit w/ contrast, consider blood work (CBC, RPR, FTA-ABS, lyme titer, ESR, ACE, chest x-ray)

58
Q

What did the ONTT find?

A

treat optic neuritis with steroids in MS speeds visual recovery but eventual outcome is unchanged. DO NOT use oral steroids because they increase recurrence

59
Q

What are you looking for in a MRI for MS?

A

demyelinated lesions, track like lesions

60
Q

Papilledema

A

bilateral swollen optic nerves secondary to increased intracranial pressure (from mass, heme, pseudotumor)

61
Q

What does papilledema cause?

A

bilateral vision decrease with changes in posture, HA, diplopia, nausea/vomiting, VF defects

62
Q

Signs of true ONH edema

A

disc heme, loss of SVP, Paton’s lines, obscured vessels at ONH, loss of cup

63
Q

What testing is necessary for papilledema?

A

color vision, desaturation if asymmetric, MRI of brain and orbit w/ contrast, MRV, then LP

64
Q

Pseudotumor cerebri

A

increased intracranial pressure in the absence of neurologic conditions

65
Q

Associated factors of pseudotumor

A

females, overweight, under 40, contraceptives, pregnancy

66
Q

Tx of pseudotumor

A

serial LP, oral CAI, weigh loss

67
Q

How to monitor pseudotumor

A

in conjunction with PCP monitor for blood dyscrasias and monitor with regular VF and DFE

68
Q

Anterior ischemic optic neruopathy

A

sudden unilateral loss of vision

69
Q

What are clinical signs of AION

A

APD common, VF defect (altitudinal), color vision defect, unilateral swollen ONH

70
Q

Arteritic

A

associated with inflammation to vascular tissue, poor blood flow to ONH

71
Q

Non-arteritic

A

association with vascular factors yielding poor blood flow to ONH

72
Q

Arteritic AION

A

usually older than 55, associated with jaw or temporal pain, sore joints

73
Q

What is the workup for arteritic AION?

A

Emergency ESR and CRP

74
Q

Norms for ESR

A

male: age/2
female: age+10/2

75
Q

Treatment of AAION

A

systemic steroids, IV pulse dose then orals

76
Q

Non-arteritic AION

A

patient may be younger that AAION with common vascular risk factors, altitudinal defect

77
Q

What are vascular risk factors for NAION?

A

HTN, arterioschlerosis, hyperlipidemia, sleep apnea

78
Q

Treatment of NAION?

A

monitor ocular health with DFE and HVF

79
Q

Differentials for unilateral disc edema

A

ischemic optic neuropathy, optic neuritis, papillitis, papillophlebitis, Leber’s, orbital disease

80
Q

Normal ESR

A

men age/2; women age+10/2 (mm/hr)

81
Q

Normal CRP

A

<10 mg/L

82
Q

What might you see on GCA IVFA?

A

choroidal filling defect

83
Q

What OTC drops can lead to pharmacologic mydriasis

A

get the red out aka decongestant

84
Q

Is the ptosis in Horner’s from a 3rd cranial nerve palsy?

A

no, from sympathetic disruption to Muller’s… 1-2 mm ptosis

85
Q

Causes of Horner’s

A

lung (pancoast) tumor, thyroid disease, orbital disease, trauma or surgery invovleing neck/upper spine/chest, aortic aneurysm, carotid dissection, brainstem stroke

86
Q

With hydroxyamphetamine how do you localize the problem?

A

pre-yes dilation post-no

87
Q

Optic disc edema on early FAF

A

hyper fluorescence due to diffuse leakage

88
Q

Optic disc drusen on FAF

A

defined hyper fluorescence

89
Q

papilledema on OCT

A

upward projection of bruch’s, lazy V

90
Q

Topamax treats///

A

epilepsy, migraine, bipolar disorder, trigeminal neuralgia, cluster headaches, alcohol dependence, weak CAI effect with appetite suppression aka IIH

91
Q

What should you consider with the med benztropine?

A

anticholinergic properties like atropine aka cycloplegia and mydriasis

Integrative Analysis II (5 decks)

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