Neurology- Ophthalmology Flashcards
Conjunctivitis
- Allergic
- Bacterial
- Viral
Allergic—itchy eyes, bilateral.
Bacterial—pus; treat with antibiotics.
Viral—most common, often adenovirus; sparse mucous discharge, swollen preauricular node; selfresolving.
Refractive errors
- Hyperopia
- Myopia
“farsightedness.” Eye too short for refractive power of cornea and lens.
“nearsightedness.” Eye too long for refractive power of cornea and lens
Refractive errors
- Astigmatism
- Presbyopia
Abnormal curvature of cornea different refractive power at different axes. (cilindrical lens correct).
Aging-related impaired accommodation. (reading glasses).
Cataract
- Congenital risk factors
classic galactosemia, galactokinase deficiency, trisomies (13, 18, 21), ToRCHeS infections (eg, rubella),
Marfan syndrome, Alport syndrome, myotonic dystrophy, neurofibromatosis 2.
Aqueous humor pathway
Trabecular outflow (90%) : Schlemm canal
Uveoscleral outflow (10%): drainage into uvea and sclera. (increased by prostaglandin agonist),
Agents that decrease production of Aqueous humor
beta-blockers, alfa-2-agonists, and carbonic anhydrase inhibitors
Glaucoma definition
Optic disc atrophy with characteristic cupping, usually with elevated intraocular pressure (IOP) and progressive peripheral visual field loss if untreated.
Open-angle glaucoma
- Associations
- Primary
- Secondary
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).
Closed- or narrowangle glaucoma
- Primary
- Secondary
Primary—enlargement or anterior movement of lens against central iris.
Secondary—hypoxia from retinal disease induces
vasoproliferation in iris that contracts angle.
Closed- or narrowangle glaucoma
- Chronic closure
- Acute closure
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.
Uveitis
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
Age-related macular degeneration
- Dry (nonexudative, > 80%)
- Wet (exudative, 10–15%)
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
Diabetic retinopathy
- Nonproliferative
- Proliferative
Damaged capillaries leak blood lipids and fluid seep into retina hemorrhages and macular edema.
Chronic hypoxia results in new blood vessel formation with resultant traction on retina. Treatment: peripheral retinal photocoagulation, surgery, anti-VEGF.
Hypertensive retinopathy
- fundoscopy
Flame-shaped retinal hemorrhages, arteriovenous nicking, microaneurysms, macular star (exudate), cotton-wool spots.
*Presence of papilledema requires immediate
lowering of BP.
Retinal vein occlusion
- Etiology
- fundoscopy
Compression from nearby arterial atherosclerosis.
Retinal hemorrhage and venous engorgement (“blood and thunder appearance”), edema in affected area.
Retinal detachment
- Risk factors
- Fundoscopy
- Clinical presentation
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.”
Central retinal artery occlusion
- Presetation
- Fundoscopy
Acute, painless monocular vision loss.
Retina cloudy with attenuated vessels and “cherry-red” spot at fovea. Evaluated for embolic source
Retinitis pigmentosa
- Presentation
- Fundoscopy
Inherited retinal degeneration. Painless, progressive vision loss beginning with night blindness.
Bone spicule-shaped deposits around macula
Retinitis
Retinal edema and necrosis leading to scar. Often viral (CMV, HSV, VZV), but can be bacterial or parasitic. May be associated with immunosuppression.
Pupillary light reflex via
Light in either retina sends a signal via CN II
to pretectal nuclei in midbrain that activates bilateral Edinger- Westphal nuclei; pupils constrict bilaterally.
Mydriasis via
1st neuron: hypothalamus to ciliospinal center of Budge (C8–T2).
2nd neuron: exit at T1 to superior cervical ganglion (travels along cervical sympathetic chain near lung apex, subclavian vessels)
3rd neuron: plexus along internal carotid, through cavernous sinus; enters orbit as long ciliary nerve to pupillary dilator muscles.
Marcus Gunn pupil
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.
Horner syndrome
- Causes of lesions of 1st, 2nd, 3rd neurons
Associated with lesions along the sympathetic chain:
1st neuron: pontine hemorrhage, lateral medullary syndrome, spinal cord lesion above T1.
2nd neuron (stellate ganglion): Pancoast tumor
3rd neuron: carotid dissection (painful)
Ocular motility
CN VI innervates the Lateral Rectus.
CN IV innervates the Superior Oblique.
CN III innervates the Rest
CN III damage
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
CN IV damage
Eye moves upward, (going down stairs, head may tilt in
the opposite direction to compensate). Particularly with contralateral gaze
CN VI damage
Unable to abduct and is displaced medially in primary position of gaze
Visual field defects
- Right anopia
- Bitemporal hemianopia (pituitary lesion, chiasm)
- Left homonymous hemianopia
- Left upper quadrantanopia (right temporal lesion, MCA)
- Left lower quadrantanopia (right parietal lesion, MCA)
- Left hemianopia with macular sparing (PCA infarct)
- Central scotoma (eg, macular degeneration)
Cavernous sinus syndrome
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
Internuclear ophthalmoplegia
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.
