Neurology- Ophthalmology

Question 1

Conjunctivitis

• Allergic
• Bacterial
• Viral

Answer 1

Allergic—itchy eyes, bilateral.

Bacterial—pus; treat with antibiotics.

Viral—most common, often adenovirus; sparse mucous discharge, swollen preauricular node; selfresolving.

Question 2

Refractive errors

• Hyperopia
• Myopia

Answer 2

“farsightedness.” Eye too short for refractive power of cornea and lens.

“nearsightedness.” Eye too long for refractive power of cornea and lens

Question 3

Refractive errors

• Astigmatism
• Presbyopia

Answer 3

Abnormal curvature of cornea Ž different refractive power at different axes. (cilindrical lens correct).

Aging-related impaired accommodation. (reading glasses).

Question 4

Cataract

- Congenital risk factors

Answer 4

classic galactosemia, galactokinase deficiency, trisomies (13, 18, 21), ToRCHeS infections (eg, rubella),
Marfan syndrome, Alport syndrome, myotonic dystrophy, neurofibromatosis 2.

Question 5

Aqueous humor pathway

Answer 5

Trabecular outflow (90%) : Schlemm canal

Uveoscleral outflow (10%): drainage into uvea and sclera. (increased by prostaglandin agonist),

Question 6

Agents that decrease production of Aqueous humor

Answer 6

beta-blockers, alfa-2-agonists, and carbonic anhydrase inhibitors

Question 7

Glaucoma definition

Answer 7

Optic disc atrophy with characteristic cupping, usually with elevated intraocular pressure (IOP) and progressive peripheral visual field loss if untreated.

Question 8

Open-angle glaucoma

• Associations
• Primary
• Secondary

Answer 8

Associated with age, African-American race, family history. Painless.

Primary—cause unclear.

Secondary—blocked trabecular meshwork from WBCs (eg, uveitis), RBCs (eg, vitreous hemorrhage), retinal elements (eg, retinal detachment).

Question 9

Closed- or narrowangle glaucoma

• Primary
• Secondary

Answer 9

Primary—enlargement or anterior movement of lens against central iris.

Secondary—hypoxia from retinal disease induces
vasoproliferation in iris that contracts angle.

Question 10

Closed- or narrowangle glaucoma

• Chronic closure
• Acute closure

Answer 10

asymptomatic with damage to optic nerve and peripheral vision.

emergency. Very painful, red eye, sudden vision loss, halos around lights, frontal headache, fixed and
mid‑dilated pupil.

Question 11

Uveitis

Answer 11

Anterior uveitis: iritis; posterior uveitis: choroiditis and/or retinitis

May have hypopyon (accumulation of pus in anterior
chamber ) or conjunctival redness. Associated with systemic inflammatory disorders

Question 12

Age-related macular degeneration

• Dry (nonexudative, > 80%)
• Wet (exudative, 10–15%)

Answer 12

Deposition of yellowish extracellular material in between Bruch membrane and retinal pigment epithelium (“Drusen”). Vitamins and antioxidants

Rapid loss of vision due to bleeding 2° to choroidal
neovascularization. Treat with anti-VEGF

Question 13

Diabetic retinopathy

• Nonproliferative
• Proliferative

Answer 13

Damaged capillaries leak blood Ž lipids and fluid seep into retina Ž hemorrhages and macular edema.

Chronic hypoxia results in new blood vessel formation with resultant traction on retina. Treatment: peripheral retinal photocoagulation, surgery, anti-VEGF.

Question 14

Hypertensive retinopathy

- fundoscopy

Answer 14

Flame-shaped retinal hemorrhages, arteriovenous nicking, microaneurysms, macular star (exudate), cotton-wool spots.

*Presence of papilledema requires immediate
lowering of BP.

Question 15

Retinal vein occlusion

• Etiology
• fundoscopy

Answer 15

Compression from nearby arterial atherosclerosis.

Retinal hemorrhage and venous engorgement (“blood and thunder appearance”), edema in affected area.

Question 16

Retinal detachment

• Risk factors
• Fundoscopy
• Clinical presentation

Answer 16

2° to retinal breaks, diabetic traction, inflammatory
effusions.

Visualized on fundoscopy as crinkling of retinal tissue and changes in vessel direction.

Often preceded by posterior vitreous detachment (“flashes” and “floaters”) and eventual monocular loss of vision like a “curtain drawn down.”

Question 17

Central retinal artery occlusion

• Presetation
• Fundoscopy

Answer 17

Acute, painless monocular vision loss.

Retina cloudy with attenuated vessels and “cherry-red” spot at fovea. Evaluated for embolic source

Question 18

Retinitis pigmentosa

• Presentation
• Fundoscopy

Answer 18

Inherited retinal degeneration. Painless, progressive vision loss beginning with night blindness.

Bone spicule-shaped deposits around macula

Question 19

Retinitis

Answer 19

Retinal edema and necrosis leading to scar. Often viral (CMV, HSV, VZV), but can be bacterial or parasitic. May be associated with immunosuppression.

Question 20

Pupillary light reflex via

Answer 20

Light in either retina sends a signal via CN II

to pretectal nuclei in midbrain that activates bilateral Edinger- Westphal nuclei; pupils constrict bilaterally.

Question 21

Mydriasis via

Answer 21

ƒƒ 1st neuron: hypothalamus to ciliospinal center of Budge (C8–T2).

ƒƒ 2nd neuron: exit at T1 to superior cervical ganglion (travels along cervical sympathetic chain near lung apex, subclavian vessels)

ƒƒ 3rd neuron: plexus along internal carotid, through cavernous sinus; enters orbit as long ciliary nerve to pupillary dilator muscles.

Question 22

Marcus Gunn pupil

Answer 22

When the light to the affected eye, both pupils dilate instead of constrict due to impaired conduction of light signal along the injured optic nerve.

Question 23

Horner syndrome

- Causes of lesions of 1st, 2nd, 3rd neurons

Answer 23

Associated with lesions along the sympathetic chain:

ƒƒ 1st neuron: pontine hemorrhage, lateral medullary syndrome, spinal cord lesion above T1.
ƒƒ 2nd neuron (stellate ganglion): Pancoast tumor
ƒƒ 3rd neuron: carotid dissection (painful)

Question 24

Ocular motility

Answer 24

CN VI innervates the Lateral Rectus.
CN IV innervates the Superior Oblique.
CN III innervates the Rest

Question 25

CN III damage

Answer 25

Motor output to extraocular muscles—affected primarily by vascular disease. Signs: ptosis, “down and out” gaze.

Parasympathetic output—fibers on the periphery are first affected by compression. Signs: diminished or absent pupillary light reflex, “blown pupil” often with “down-and-out” gaze

Question 26

CN IV damage

Answer 26

Eye moves upward, (going down stairs, head may tilt in

the opposite direction to compensate). Particularly with contralateral gaze

Question 27

CN VI damage

Answer 27

Unable to abduct and is displaced medially in primary position of gaze

Question 28

Visual field defects

Answer 28

1. Right anopia
2. Bitemporal hemianopia (pituitary lesion, chiasm)
3. Left homonymous hemianopia
4. Left upper quadrantanopia (right temporal lesion, MCA)
5. Left lower quadrantanopia (right parietal lesion, MCA)
6. Left hemianopia with macular sparing (PCA infarct)
7. Central scotoma (eg, macular degeneration)

Question 29

Cavernous sinus syndrome

Answer 29

CNs III, IV, V1, VI, and V2 plus postganglionic sympathetic pupillary fibers en route to orbit all pass through cavernous sinus.

Presents with variable ophthalmoplegia, decrease corneal sensation, Horner syndrome and occasional decreased maxillary sensation

Question 30

Internuclear ophthalmoplegia

Answer 30

Lesion in MLF: a conjugate horizontal gaze palsy

When CN VI nucleus activates ipsilateral lateral rectus,
contralateral CN III nucleus does not stimulate medial rectus to contract. Abducting eye gets nystagmus.

*INO = Ipsilateral adduction failure, Nystagmus
Opposite.