Pupillary, Eyelid, and Facial Abnormalities Flashcards

1
Q

Pupil size during sleep (and why)?

A

small/miotic, 2/2 loss of cortical inputs that inhibit the Edinger-Westphal nucleus

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2
Q

Pupil size after generalized tonic clonic seizure?

A

mydriatic

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3
Q

Pupil size w/ pontine hemorrhage?

A

miotic (“pinpoint pons”)

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4
Q

What is a tadpole pupil?

A

focal spasm of iris dilator muscle that causes peaking of the pupil and lasts a few minutes. Most are benign but a small percentage harbor an underlying sympathetic lesion, so Horner’s testing should be done

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5
Q

What is midbrain corectopia?

A

eccentric or oval pupils caused by rostral midbrain disease, presumably from incomplete damage to pupillary fibers causing selective inhibition of iris sphincter tone

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6
Q

Describe the pupillary light reflex pathway

A

light–>ipsilateral optic nerve–>decussation of nasal retinal fibers leading to bilateral optic tract signal–>pupillary fibers leave optic tract in brachium of superior colliculus just anterior to LGN and synapse at pretectal nucleus–>interneuron to Edinger-Westphal nucleus (part of CNIII complex in midbrain)–>parasympathetics travel on medial superficial surfaceon CNIII–>join inferior div. of CNIII–>synapse at ciliary ganglion in orbital apex–>post-ganglionic fibers join posterior ciliary nerves to innervate iris sphincter muscle

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7
Q

Describe the sympathetic pathway innervating the iris dilator muscle

A

First order neuron: from hypothalamus through brain stem and spinal cord to C8-T2 area synapsing at center of Budge-Waller.

Second order neuron: from center of Budge-Waller fibers join sympathetic chain and pass by subclavian artery and apex of lung before heading raustrally and synapsing at superior cervical ganglion near bifurcation of common carotid

Third order neuron: travels along ICA, then join CN VI and then nasociliary branch of V1 briefly before passing through BUT NOT SYNAPSING at the ciliary ganglion in the orbital apex, then continuing as long ciliary nerve to innervate the iris dilator muscle

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8
Q

Cut-off for physiologic anisocoria?

A

1 mm difference or less

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9
Q

DDx anisocoria greater in dark

A

Abnormal pupil is not dilating: mechanical (synechiae), pharmacologic (miotic), Horner syndrome

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10
Q

Describe the pharmacologic approach to diagnosing Horner’s

A

Anisocoria greater in dark: try cocaine or apraclonidine testing first to diagnose Horner’s.

  • Cocaine blocks the reuptake or norepinephrine at the neuromuscular junction, causing dilation of the normal eye but having no effect on the Horner’s eye. Place 2 drops of 4% or 10% in each ayee and reasses at 45vminutes.
  • Apraclonidine is an alpha-2 agonist with weak alpha-1 activity. Horner’s eyes become supersensitive to alpha-1 stimulation within days (or rarely hours) of damage. Apraclonidine thus reverses anisocoria when applied bilaterally. This is CONTRAINDICATED in children <1 due to risk of CNS depression and respiratory arrest
  • PE (direct testing will dilate a Horner’s eye but not a mechanically restricted eye (synechiae)

Once a Horner’s is diagnosed, hydroxyamphetamine can be applied to localize the lesion. This drug increases the release of NE from an intact presnyaptic terminal, and will only dilate eyes that have an intact 3rd order neuron (i.e. dilation means first or second order neuron damage, no dilation means 3rd order neuron damage)

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11
Q

General findings in Horner syndrome? Findings associated with 1st, 2nd, and 3rd order Horner’s respectively? Congenital?

A

Ptosis (Muller’s muscle), miosis, ipsilateral anhidrosis (just forehead if 3rd order neuron, whole face if 1st/2nd)

1st: ataxia, nystagmus, hemisensory deficit (medullary lesion)
2nd: cough, hemoptysis, arm pain, neck swelling (Pancoast tumor)
3rd: If isolated, usually benign. Can have diplopia or facial numbness (travels briefly w/ CN VI and V1). Pain (to temple or orbit) suggests carotid artery dissection

Congenital: iris heterochromia (affected iris is LIGHTER). Usually caused by birth trauma to brachial plexus. Nontraumatic Horner’s in infants/kids warrants head, neck, and chest imaging to look for neuroblastoma arising from sympathetic chain

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12
Q

Algorithm and DDx for anisocoria greater in light?

A

Abnormal pupil will not constrict: CN III palsy, Adie’s tonic pupil, pharmacologic, mechanical (traumatic mydriasis).

  1. 125% pilocarpine to both eyes
    - Dilated eye constricts: Adie’s (supersensitive to parasympathetic innervation)
    - Does not constrict: Try 1% pilo to both eyes

1% pilo

  • Does not constrict: pharmacologic or traumatic
  • Constricts: CN III palsy
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13
Q

Findings and mechanism for Adie’s tonic pupil? Other causes of tonic pupil?

A

Mydriasis, can be segmental. In chronic cases, can have miosis. + light-near dissociation. 70% female, 80% unilateral. Holmes-Adie syndrome also has diminished deep tendon reflexes and orthostatic hypotension. Caused by idiopathic damage to ciliary ganglion or short ciliary nerves.

DDx tonic pupil aslo includes neurosyphilis, diabetes, chronic alcoholism, dysautonomias, amyloidosis, sarcoidosis, Miller-Fisher, Charcot-Marie-Tooth.

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14
Q

What is benign episodic pupillary mydriasis?

A

Episodic pupillary mydriasis lasting from minutes to hours in otherwise healthy people w/ h/o headaches. May be accompanied by headache and mild blurring of vision. Each episode is self-limiting and not is associated with systemic disease

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15
Q

What is Marcus Gunn jaw-winking syndrome? Which muscles and cranial nerves are involved?

A

synkinetic eyelid movement associated with jaw movement, can be seen in ptosis patients. External pterygoid (CN V): jaw protrusion, mandibular movement to opposite side, and mouth opening are associated with eyelid elevation. Internal pterygoid (also CN V): jaw clenching leads to eyelid elevation

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16
Q

Which law explains unilateral eyelid retraction in a patient with contralateral ptosis?

A

Hering’s law of equal innervation

17
Q

Most common cause of eyelid retraction in adults?

A

TED

18
Q

What is Collier’s sign?

A

eyelid retraction in dorsal midbrain syndrome

19
Q

Management of Bell’s palsy?

A

If seen w/in 72 hours, 7-10 day course of steroids, +/- antivirals. If progresses for more than 3 weeks or if no improvement by 3 months, consider alternative etiology. Treat corneal exposure with lubrication/moisture chambers/tarsorraphy/botox/gold weight

20
Q

Painful vesicles in auditory canal or tympanic membrane and ipsilateral facial palsy?

A

Ramsay Hunt syndrome (Zoster involving facial nerve)

21
Q

What is Miller Fisher syndrome? Lab test?

A

Guillain-Barre variant with ataxia, areflexia, and ophthalmoplegia. serum anti-GQ1b IgG antibodies

22
Q

most common causes of bilateral facial nerve palsies?

A

sarcoidosis, basilar meningitis, or Guillain-Barre.

23
Q

DDx for recurrent unilateral facial nerve palsies?

A

idiopathic (most common), diabetes, Lyme, Mekersson-Rosenthal syndrome (recurrent uni- or bi-lateral facial nerve paralysis with facial swelling and furrowing of tongue)

24
Q

Progressive CN 7 palsy?

A

Tumor: compressive - brainstem, cerebellopontine, parotid; or infiltrative: meningeal carcinomatosis

25
Q

distinguishing feature of essential blepharospasm v other facial twitches? Presumed site of dysfunction?

A

bilaterality; basal ganglia

26
Q

cause of hemifacial spasm

A

compression of facial nerve root; usually by abbarrant vessel but can be from tumor, so imaging is warranted

27
Q

facial myokymia v hemifacial spasm

A

both unilateral; facial myokymia has fibrillary or undulating contraction of muscles (as opposed to tonic spasm) and is usually caused by pontine glioma in kids and MS in adults