Pupils, Bino/Accom, Optic Neuropathies Flashcards
What is the afferent pupillary pathway
pupillary fibers bypass the LGN and go to the pretectal nucleus (olivary nuclei) then to the edinger westphal nucleus
What is the efferent (parasympathetic) pupillary pathway?
parasympathetic fibers join CN III and pass through the cavernous sinus, synapsing at ciliary ganglion
Which nerves take parasympathetic signals to the iris sphincter?
short ciliary nerve
What is the sympathetic efferent pupillary pathway?
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
Which nerves take sympathetic signals to the iris dilator?
long ciliary nerves
What is the first thing you should evaluate with anisocoria?
if it is greater in bright or dim light
What is the issue when anisocoria is worse in bright light?
parasympathetic- bigger pupil not constricting
What is the issue when anisocoria is worse in dim light?
sympathetic- smaller pupil not dilating
With parasympathetically driven anisocoria what should you look for in A seg?
sector palsy/damage
Dilute pilo and anisocoria worse in bright conditions (parasympathetic)
if constricts= CN III palsy, if no constriction= pharmacologic dilation
What might an aide’s pupil look like in the slit lamp?
flattened/flaccid pupillary border
What are possible causes of adie’s tonic pupil?
viral infection (zoster), trauma, GCA, neurosyphilis (bilateral)
How do you treat Aides’s?
treat cosmesis with tinted CL, dilute pilo or brimonidine
Horner’s triad
ptosis, miosis, anhydrosis
T/F a horner’s pupil does not dilate with topical cocaine or reversal of aniso with apraclonidine
true
How does cocaine 10% work?
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
How does apraclonidine work?
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
Hydroxyamphetamine (paredrine-Alcon) and Horner’s
dilation occurs with 1st or 2nd order/central/pre-ganglionic… no dilation with 3rd order/post-ganglionic
How does hydroxyamphetamine work?
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
What additional tests may be run with Horner’s?
neoplasia-chest x-ray, stroke MRI/MRA, carotid dissection-doppler
T/F convergence and accommodative issues can give results that mimic each other
true
How to distinguish CI and pseudo CI?
NPC through +1 CI will get worse, pseudo better
Morgan’s norms creation
800 adults, normative data and 1/2 SD
“Group A”
accom amp, PRA, NPC (BI to blur)
“Group B”
NRA, PRC (BO to blur)
Accommodative fatigue
Group A low B high aka low amp/PRA/BI/high NRA, BO
What does accommodative fatigue respond to?
plus or VT
Vergence fatigues
Group B low A high aka low NRA/BO and high amp/PRA/BI
What does vergence fatigue responds to?
VT and possibly prism
What does CN III innervate?
levator palprebrae; SR, IR, MR, IO, presynaptic parasympathetic to iris sphincter
Cranial nerve III palsy presents as
down out and blown
CN III palsy pupil sparing
more likely vascular occlusion than aneurysm
Where are pupillary fibers compared to CN III?
pupillary fibers course outside the nerve and are more affected by compression
What is aberrant regeneration?
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
Incomplete palsy, inferior
internal ophthalmoplegia, medial/inferior recti, inferior oblique paresis … superior rectus and lid not affected
Incomplete palsy, superior
ptosis, superior rectus paresis … superior incomplete palsy is more rare
Incomplete palsy, single muscle paresis
small vessel disease, quite rare
CN III palsy workup
MRI/MRA unless 50+ with pupil spared
What do you do if CN III palsy with pupil spared 50+?
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
What testing might you do with aberrant regeneration?
MRI/MRA
What deviation does a CN IV palsy cause?
slight hypertopia because superior oblique
Where is diplopia worse with CN IV palsy?
gaze opposite side of lesion and head tilt toward side of lesion
What techniques identifies muscle palsy with hypertropia?
Parks 3 step
What is the most common cause of CN IV palsy?
trauma common, ischemia, decompensated phoria
What is the workup of CN IV palsy?
measure vertical fusional amplitudes for decompensated phoria, older patients > 50 years eval BG, BP and cholesterol, younger patients MRI and vascular eval
What diplopia is caused by CN VI palsy?
horizontal diplopia
What causes CN VI palsy in older patients?
ischemia, may complain of pain behind the eye
What are other cause of CN VI palsy?
masses, inflammation, migrane, in response to increase ICP – courses over petrous ridge/pyramid
What is the work up for a CN VI palsy?
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
3 diseases to the optic nerve
optic neuritis, papilledema, anterior ischemic optic neuropathy
Optic neuritis
unilateral inflammation to the ON
Causes of optic neuritis
MS, childhood infections, meningitis, granulomatous inflammations
S/S of optic neuritis
rapid vision loss, pain on EOMs, color vision changes, focal neurologic symptoms, worsened symptoms with exercise (uhthoff sign)
How does optic neuritis affect vision?
peak vision loss (mild-severe) at 1-2 weeks, resolution in 5 weeks, color desaturation, VF defects
How does color vision change in optic neuritis?
blue-yellow desaturation in acute and red green in late stages
What VF defects may be present for optic neuritis?
general depression, defects respecting horizontal midline, central, centrocecal
What is the workup for optic neuritis?
MRI of brain and orbit w/ contrast, consider blood work (CBC, RPR, FTA-ABS, lyme titer, ESR, ACE, chest x-ray)
What did the ONTT find?
treat optic neuritis with steroids in MS speeds visual recovery but eventual outcome is unchanged. DO NOT use oral steroids because they increase recurrence
What are you looking for in a MRI for MS?
demyelinated lesions, track like lesions
Papilledema
bilateral swollen optic nerves secondary to increased intracranial pressure (from mass, heme, pseudotumor)
What does papilledema cause?
bilateral vision decrease with changes in posture, HA, diplopia, nausea/vomiting, VF defects
Signs of true ONH edema
disc heme, loss of SVP, Paton’s lines, obscured vessels at ONH, loss of cup
What testing is necessary for papilledema?
color vision, desaturation if asymmetric, MRI of brain and orbit w/ contrast, MRV, then LP
Pseudotumor cerebri
increased intracranial pressure in the absence of neurologic conditions
Associated factors of pseudotumor
females, overweight, under 40, contraceptives, pregnancy
Tx of pseudotumor
serial LP, oral CAI, weigh loss
How to monitor pseudotumor
in conjunction with PCP monitor for blood dyscrasias and monitor with regular VF and DFE
Anterior ischemic optic neruopathy
sudden unilateral loss of vision
What are clinical signs of AION
APD common, VF defect (altitudinal), color vision defect, unilateral swollen ONH
Arteritic
associated with inflammation to vascular tissue, poor blood flow to ONH
Non-arteritic
association with vascular factors yielding poor blood flow to ONH
Arteritic AION
usually older than 55, associated with jaw or temporal pain, sore joints
What is the workup for arteritic AION?
Emergency ESR and CRP
Norms for ESR
male: age/2
female: age+10/2
Treatment of AAION
systemic steroids, IV pulse dose then orals
Non-arteritic AION
patient may be younger that AAION with common vascular risk factors, altitudinal defect
What are vascular risk factors for NAION?
HTN, arterioschlerosis, hyperlipidemia, sleep apnea
Treatment of NAION?
monitor ocular health with DFE and HVF
Differentials for unilateral disc edema
ischemic optic neuropathy, optic neuritis, papillitis, papillophlebitis, Leber’s, orbital disease
Normal ESR
men age/2; women age+10/2 (mm/hr)
Normal CRP
<10 mg/L
What might you see on GCA IVFA?
choroidal filling defect
What OTC drops can lead to pharmacologic mydriasis
get the red out aka decongestant
Is the ptosis in Horner’s from a 3rd cranial nerve palsy?
no, from sympathetic disruption to Muller’s… 1-2 mm ptosis
Causes of Horner’s
lung (pancoast) tumor, thyroid disease, orbital disease, trauma or surgery invovleing neck/upper spine/chest, aortic aneurysm, carotid dissection, brainstem stroke
With hydroxyamphetamine how do you localize the problem?
pre-yes dilation post-no
Optic disc edema on early FAF
hyper fluorescence due to diffuse leakage
Optic disc drusen on FAF
defined hyper fluorescence
papilledema on OCT
upward projection of bruch’s, lazy V
Topamax treats///
epilepsy, migraine, bipolar disorder, trigeminal neuralgia, cluster headaches, alcohol dependence, weak CAI effect with appetite suppression aka IIH
What should you consider with the med benztropine?
anticholinergic properties like atropine aka cycloplegia and mydriasis
