5 Pupils + Ptosis Flashcards by Dyllan Nye

Palpebral fissure measurement and ptosis requirement:

12-15mm normally

Upper marginal reflex (reflex to up. Lid) <2mm or asymmetry of 2mm

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Muscles in upper lid opening:

Levator primary superioris, supplied by sup. Division of oculomotor nerve (CV 3)
Modified by mullers; sympathetic smooth muscle (arousal/excitement
Orbicularis oculi / frontalis muscle (facial nerve, CV 7)

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LPS function assessment:

Lid difference in upgaze and downgaze while holding eyebrow (frontalis involvement
Fatigue assessed by 60s upgaze

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Causes of ptosis:

Disinsertion of LPS (most common)
Myasthenia gravis / Graves (muscular)
Horners (sympathetic)
CN3 palsy
Globe retraction / eyelid swelling
Fatigue/trauma

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Disinsertion of LPS:

Lid dehiscence/aponeurotic ptosis
LPS tendon less from tarsal from rubbing, CLs, trauma/surgery
Low lid, high crease, normal range of motion
Treated with LPS shortening

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Myathenia gravis:

Autoimmune against acetylcholine receptors of striated muscle.
Fatigue, facial weakness, ptosis (LPS weak)/diplopia.
Cognan’s lid twitch (upper lid overshoot on upgaze)
Curtaining/enhanced ptosis (contralateral drooping/elevation)

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Curtaining/enhanced ptosis:

Curtining, manual potoc elevation lowers normal
Enhances ptosis, manual normal elevation lowers potic moreso
Herings law of equal innervation to paired yoke muscles (potic processes less of the same innervation)

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Causes of anisocoria:

Physiological (aysymetric inhibition of edinger-westphal)
Horners 
CN3 palsy
Adies tonic pupil
Pharmacological
Pupil damage
Acute angle glaucoma

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Mitochondrial myopathy in ptosis:

Mitochondrial dysfunction leads to fatigue of EOMs

Bilateral ptosis, ophthalmoplegia (weak motility)

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CN3 palsy:

Lesion to CN3, often unilateral
Ptosis, mydriasis (depending on cause), down and out turn, headache.
Aberrant regeneration > miosis

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Pupil-involving/sparing CN3 palsy:

Involving, mass/aneurysm/trauma causing compression and ischemia of parasympathetic fibres
Sparing, diabetes/hypertension > ischemia of nerve trunk, sparing outer fibres

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CN3 palsy lesion site and cause:

Subarachnoid (trauma/aneurysm)
SO fiss./cavernous sinus (trauma/tumor)
Orbit (trauma)
Full lesion (multiple sclerosis)
Superior division lesion -> no LPS innervation
Inferior division -> only lat rectus and sup. Oblique have innervation (CN6)

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Pseudoptosis

Ptosis appearance unrelated to lid function
Dermatochalasia most common
CN 7 facial palsy (brow muscle loss)

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Para/sympathetic iris path for miosis/mydriasis

Parasympathetic > miosis via sphincter muscle

Sympathetic > mydriasis via dilator muscle

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Parasympathetic pathway for iris

Afferent: Optic nerve > split at chiasm > optic track > split before LGN > sup. Colliculus > pretectal nuclei (processed) > both edinger-westphal nuclei.
Efferent: Edinger-westphal nuclei > CN 3 > ciliary ganglion > iris sphincter

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Sympathetic pathway for iris:

1st neuron: hypothalamus > spinal cord > ciliospinal centre
2nd neuron: ciliospinal > lung apex > superior cervical ganglion (jaw)
3rd neuron: superior cervical g. > internal carotid > cavernous sinus > CN 6 (abducens) > CN 5 V1 (nasociliary div. Of ophthalmic) > long ciliary nerves > iris dilator
Also innervate mullers / facial

Third nerve eye innervation:

Oculomotor nerve has somatic voluntary, and automatic fibers
Somatic: LPS, SR/MR (adducts)/IR/IO (elevates when adducted)
Automatic: sphincter pupillae / ciliary

Tonic pupil/ Adie’s

Post ganglionic parasympathetic denervation,
Poor light constriction, good convergence constriction
Worm like redilation/constriction from partial denervation
Initially dilated pupil, long term mitotic pupil (abberant nerve regeneration)
Mainly young women

Pharmacological drugs that effect pupil:

Mydriasis: Scopolamine (motion sickness), ipratropium (asthma), nasal spray, antiperspirant, jimson weed/herbals
Miosis: pilocarpine (IOP decrease/Glauc.), prostglandins (IOP decrease/glauc.), opioids, clondine (Glauc.), insectisides

Pilocarpine pharmacology and DDX

Muscarinic agonist for neuromuscular junction of sphincter, upregulates receptor number > hypersensitivity > constriction.
Dilute pilocarpine (0.5-0.15%) > tonic pupil constriction
Pilocarpine  (1-2%)  > no constriction in pharmacogically induced

Horners testing with cocaine:

Cocaine hydrochloride (10%), blocks norepinephrine reuptake in presynaptic terminal 
Horners: 2 cocaine doses 5 mins apart. Normal redilation 45-60 mins, horners will fail to dilate from lack of norepinephrine relaease. Expect light anisocoria

Horners testing with apraclondine:

Apraclondine (0.5-1%), A-adrenergic receptor agoinist.
40mins Horners will have abnormal lid raise, pupil dilate, normal eye remain unchanged.
requires denervation hypersensitivity, as its Stronger effect on a-2 recepters downregulate noradrenaline (resulting in no effect on normal eye)
Less reliable until 7 days (adrenergic sensitivity development), not usable <2 years, more available than cocaine (used in IOP reduction)

Horners syndrome testing/signs:

Unilateral miosis, ptosis, anhidrosis. Congenital iris heterochromia (lack of sympathetic for melanocyte development)
Dilation lag of mitotic pupil in dark (5-10s dark)
Anisocoria greater at 5s and lesser at 15s
No abnormal light/near constriction

Horners lesion localization

1% hydroxyamphetamine, ^norepinephrine release at neuromuscular junction for bilateral dilation.
First/second order neuron > no dilation
>48h following cocaine/apraclondine, hard to obtain

Horners causes by lesion location:

First order: hypothalmic/brainstem/spinal cord lesion Second order: lung/sympathetic tumor, thyroid lesion Third order: carotid artery damage, cavernous sinus lesion

Trigeminal autonomic cephalalgias:

Cluster headaches, resulting in ptosis | Requires neurology consultation

Anisocoria testing when greater in dark:

Small pupil anisocoria. Apraclonidine / cocaine: No/residual dilation > physiologic Potic dilation > horners > hyrodyamphetaime/MRI

Anisicoria testing when greater in light

Large pupil anisocoria Motility/ptosis abnormal > CN3 palsy > MRI/CTA Full motility/no ptosis + worm constriction > tonic pupil Full motility/no ptosis > dilute pilocarpine > tonic on constriction Dilute pilo. Non-constriction > non-dilute > constriction in third nerve palsy / pharmacologic / trauma

Symptoms of horners syndrome:

``` Ipsilateral anhidrosis of face Miosis in dark 2mm partial ptosis (muller denervation) Partial lower lid raise Accommodative excess/blur (sympathetic loss to ciliary) Red eye Heterochromia ```

Advantages of apraclondine over cocaine in pharmacologic testing of horners:

``` Available commercially Longer shelf life No stigma Does not require normal second pupil May have false negatives in recent horners ```

Miosis in horners:

``` Loss of sympathetic dilator muscle innervation, constrictor unopposed Immediate darkness provides notable anisicoria Dilation lag (Mydriasis after 15s) occurs from passive dilator force ```

Ptosis in horners

Loss of sympathetic mullers innervation, <2mm ptosis | Lower lid elevation may occur from sympathetic innervated mullers analogue

Horners first order neuron causes:

Stroke (wallenberg) brain/thalamus tumour myelin diseases (MS) Spinal cord lesion (tetraplegia/bilateral horners)

Horners second order neuron causes

Lung tumor (pancoast) Neck trauma / surgery Carotid/aortic aneurysm

Horners third order neuron causes:

Internal carotid dissection (nerves surrounding artery strain under artery expansion) Cavernous sinus mass/aneurysm Cluster headache/pain Related to sixth nerve pals and HZO

Sphincter pupillae muscle:

Miosis from pupillary zone of iris via smooth muscle Innervated by post-ganglionic parasympathetic fibres from ciliary ganglion Post-g. Fibres travel with CN 3 then with short fibres of ophthalmic trigeminal

Dilator pupillae muscle

Mydriasis from iris root via myoepithelium, continuous with outer pigmented epithelium of ciliary Innervated by postganglionic fibres from superior cervical g. Travelling with long ciliary nerves of ophthalmic trigeminal