Cataract
Painless, often bilateral, opacification of lens, often resulting in glare and ↓ vision, especially at night. Acquired risk factors:- ↑ age- smoking- excessive alcohol use- excessive sunlight- prolonged cotricosteroid use- diabetes mellitus- trauma- infection Congenital risk factors: - classic galactosemia- galactokinase deficiency- trisomies (13, 18, 21)- ToRCHeS infections (eg, rubella)- Marfan syndrome- Alport syndrme- myotonic dystrophy- neurofibromatosis 2
Glaucoma
Optic disc atrophy with characteristic cupping (thinning of outer rim of optic nerve head), usually with elevated intraocular pressure (IOP) and progressive peripheral visual field loss. Open-angle glaucoma:Associated with ↑ age, African-American race, family history, more common in US.- Primary – cause unclear.- Secondary – blocked trabecular meshwork from WBCs (eg, uveitis), RBCs (eg, vitreous hemorrhage), retinal elements (eg, retinal detachment). Closed- or narrow-angle glaucoma:- Primary – enlargement or anterior movement of lens against central iris (pupil margin) → obstruction of normal aqueous flow through pupil → fluid builds up behind iris, pushing peripheral iris against cornea and impeding flow through trabecular meshwork.- Secondary – hypoxia from retinal disease (eg, diabetes mellitus, vein occlusion) induces vasoproliferation in iris that contracts angle.Chronic closure – often asymptomatic with damage to optic nerve and peripheral vision.Acute closure – true ophthalmic emergency. ↑ IOP pushes iris forward → angle closes abruptly. Very painful, red eye, sudden vision loss, halos around lights, frontal headache, fixed and mid-dilated pupil. Mydriatic agents (eg, epinephrine) contraindicated.
Open-angle glaucoma
- associated with ↑ age, African-American race, family history Primary: cause unclear Secondary: blocked trabecular meshwork from WBC (eg uveitis), RBC (eg vitreous hemorrhage), retinal elements (eg retinal detachment)
Closed-angle glaucoma
Primary: enlargement or forward movement of lens against central iris --> obstruction of normal aqueous flow through pupil --> fluid builds up behind iris, pushing peripheral iris against cornea and impeding flow through trabecular meshwork Secondary: hypoxia from retinal disease (eg diabetes mellitus, vein occlusion) induces vasoproliferation in iris that contracts angle Chronic closure: often asymptomatic with damage to optic nerve and peripheral vision Acute closure: true ophthalmic emergence. ↑ IOP pushes iris forward --> angle closes abruptly. Very painful, red eye, sudden vision loss, halos around lights, rock-hard eye, frontal headache Do not give epinephrine because of its mydriatic effect
Conjunctivitis
Inflammation of the conjunctiva → red eye Allergic – itchy eyes, bilateral Bacterial – pus; treat with antibiotics Viral – most common, often adenovirus; sparse mucous discharge, swollen preauricular node; self-resolving
Uveitis
Inflammation of uvea, specific name based on location within affected eye. Anterior uveitis: iritisPosterior uveitis: choroiditis and/or retinitis - May have hypopyon (accumulation of pus in anterior chamber) or conjunctival redness. - Associated with systemic inflammatory disorders (eg, sarcoidosis, rheumatoid arthritis, juvenile idiopathic arthritis, HLA-B27-associated conditions).
Age-related macular degeneration
Degeneration of macula (central area of retina).- Most common cause of blindness in individuals >65 in developed countries. Causes distortion (metamorphopsia, detected with Amsler grid) and eventual loss of central vision (scotomas). Dry (nonexudative, >80%): deposition of yellowish extracellular material in between Bruch membrane and retinal pigment epithelium ("drusen") with gradual ↓ in vision.- Drusen contain lipids, vitronectin, proteins.Prevent progression with multivitamin (A, C, E, beta-carotene, zinc) and antioxidant supplements. Wet (exudative, 10-15%): rapid loss of vision due to bleeding 2° to choroidal neovascularization.- Fundusocopy: grayish-green subretinal discoloration with adjacent fluid/hemorrhage, drusen.Treat with anti-VEGF injections (eg, bevacizumab, ranibizumab).
Diabetic retinopathy
Retinal damage due to chronic hyperglycemia.- Most common cause of visual impairment and blindness in patients aged 24-75 in the US. Nonproliferative: damaged capillaries leak blood → lipids and fluid seep into retina → hemorrhages and macular edema.- Hard exudates (lipid deposits in retina)- MicroaneurysmsTreatment: blood sugar control. - Proliferative: chronic hypoxia results in new blood vessel formation (rubeosis iridis) with resultant traction on retina.- Can lead to secondary glaucomaTreatment: peripheral retinal photocoagulation, surgery, anti-VEGF.
Retinal vein occlusion
Blockage of central or branch retinal vein due to compression from nearby arterial atherosclerosis. Etiology:- Atherosclerosis, hypertension, diabetes mellitus- Hypercoagulable states: Polycythemia vera, sickle cell disease, oral contraceptive use- Glaucoma (increased intraocular pressure can compress the vein) - Retinal hemorrhage ("flame-shaped") and venous engorgement ("blood and thunder appearance"), edema in affected area.
Retinal detachment
Separation of neurosensory layer of retina (photoreceptor layer with rods and cones) from outermost pigmented epithelium (normally shields excess light, supports retina) → degeneration of photoreceptors → vision loss. Etiology:- Retinal breaks- Diabetic traction as a result of neovascularization of retina- Inflammatory effusions- Trauma- Tumor growth - Visualized on fundoscopy as crinkling of retinal tissue and changes in vessel direction. - Breaks are more common in patients with high myopia and/or history of head trauma. - Often preceded by posterior vitrous detachment ("flashes" and "floaters") and eventual monocular loss of vision like a "curtain drawn down."- "Floaters" = Floating blood cells from vitreous hemorrhage- "Flashes" (photopsia) = Caused by traction on the retina - Surgical emergency.
Central retinal artery occlusion
Acute, painless monocular vision loss. - Retina cloudy with attenuated vessels and "cherry-red" spot at fovea (center of macula)- Grayish-white discoloration of entire retina - Evaluate for embolic source (eg, carotid artery atherosclerosis, cardiac vegetations, patent foramen ovale). Ophthalmologic emergency:- Eyeball massage- Carbogen therapy, decrease intraocular pressure
Retinitis pigmentosa
Inherited retinal degeneration. Frequently mutation in the rhodopsin gene. - Early onset (5-30 years) - Painless, progressive vision loss beginning with night blindness (rods affected first). - Bone spicule-shaped deposits around macula.
Retinitis
Retinal edema and necrosis leading to scar. - Often viral (HSV, CMV, VZV), but can be bacterial or parasitic. - May be associated with immunosuppression. - CMV retinitis is associated with a high rate of retinal detachment.- Fundoscopy: "pizza pie" appearance (retinal hemorrhages, fluffy/granular white opacities around retinal vessels resembling cotton wool spots, retinal detachment)
Horner syndrome
Sympathetic denervation of face →:- Ptosis (drooping of eyelid: superior tarsal muscle)- Anhidrosis (absence of sweating) and flushing of affected side- Miosis (pupil constriction) Associated with lesions along the sympathetic chain:- 1st neuron: pontine hemorrhage, lateral medullary syndrome, spinal cord lesion above T1 (eg, Brown-Séquard syndrome, late-stage syringomyelia) - 2nd neuron (stellate ganglion): Pancoast tumor- 3rd neuron: carotid dissection (painful)
CN III damage
CN III has both motor (central) and parasympathetic (peripheral) components. Common causes include:- Ischemia → pupil sparing- Uncal herniation → coma- PCA aneurysm → sudden-onset headache- Cavernous sinus thrombosis → proptosis, involvement of CNs IV, V1/V2, VI- Midbrain stroke → contralateral hemiplegia Motor output to extraocular muscles – affected primarily by vascular disease (eg, diabetes mellitus: glucose → sorbitol) due to ↓ diffusion of oxygen and nutrients to the interior fibers from compromised vasculature that resides on outside of nerve. Signs: ptosis, "down and out" gaze Parasympathetic output – fibers on the periphery are 1st affected by compression (eg, PCom aneurysm, uncal herniation).Signs: diminished or absent pupillary light reflex, "blown pupil" (mydriasis) often with "down-and-out" gaze
Internuclear opthalmoplegia
Medial longitudinal fasciculus (MLF): pair of tracts that allows for crosstalk between CN VI and CN III nuclei. Coordinates both eyes to move in same horizontal direction. Highly myelinated. Lesions may be unilateral or bilateral (latter classically seen in multiple sclerosis). Lesion in MLF = internuclear ophthalmoplegia (INO), a conjugate horizontal gaze palsy. Lack of communication such that when CN VI nucleus activates ipsilateral lateral rectus, contralateral CN III nucleus does not stimulate medial rectus to fire. Abducting eye gets nystagmus (CN VI overfires to stimulate CN III). Convergence normal. Directional term (eg, right INO, left INO) refers to which eye is paralyzed.
CN IV damage
Eye moves upward, particularly with contralateral gaze. Problems going down stairs, may present with compensatory head tilt in the opposite direction.
Miosis
Constriction, parasympathetic 1st neuron: Edinger-Westphal nucleus to ciliary ganglion via CN III 2nd neuron: short ciliary nerves to pupillary sphincter muscles
Mydriasis
Dilation, sympathetic 1st neuron: hypothalamus to ciliospinal center of Budge (C8-T2) 2nd neuron: exit at T1 to superior cervical ganlion (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
Auditory physiology
Outer ear: Visible portion of ear (pinna), includes auditory canal and tympanic membrane. Transfers sound waves via vibration of tympanic membrane. Middle ear: Air-filled space with the three ossicles (malleus, incus, stapes). Ossicles conduct and amplify sound from tympanic membrane to inner ear. Inner ear: Snail-shaped, fluid-filled cochlea. Contains basilar membrane that vibrates 2° to sound waves. Vibrations transduced via specialized hair cells → auditory nerve signalling → brain stem.Each frequency leads to vibration at specific location on basilar membrane (tonotopy):- Low frequency heard at apex near helicotrema (wide and flexible).- High frequency heard best at base of cochlea (thin and rigid).
Diagnosing hearing loss
Conductive hearing loss:Rinne: Abnormal (bone > air)Weber: Localizes to affected ear. Sensorineural hearing loss:Rinne: Normal (air > bone)Weber: Localizes to unaffected ear.
Types of hearing loss
Noise-induced hearing loss: Damage to stereociliated cells in the organ of Corti. Loss of high-frequency hearing first. Sudden extremely loud noises can produce hearing loss due to tympanic membrane rupture. Presbycusis: Aging-related progressive bilateral/symmetric sensorineural hearing loss (often of higher frequencies) due to destruction of hair cells at the cochlear base (preserved low-frequency hearing at apex).
Cholesteatoma
Overgrowth of desquamated keratin debris within the middle ear space.Form a round, pearly mass behind the tympanic membrane in the middle ear. Primary cholesteatomas: Result of chronic negative pressure in the middle ear causing retraction pockets in the tympanic membrane that become cystic. As the squamous cell debris accumulates, a cholesteatoma is formed.Secondary cholesteatomas: Occur after squamous epithelium migrates or is implanted in the middle ear. May erode ossicles, mastoid air cells → conductive hearing loss. Often presents with painless otorrhea.If a mass grows sufficiently large, it can erode into the vestibular apparatus or facial nerve, causing vertigo or facial palsies.
Vertigo
Sensation of spinning while actually stationary. Subtype of "dizziness," but distinct from "lightheadedness." Peripheral vertigo: More common. Inner ear etiology (eg, semicircular canal debris, vestibular nerve infection, Ménière disease [triad: sensorineural hearing loss, vertigo, tinnitus], benign paroxysmal positional vertigo). - Treatment: antihistamines, anticholinergics, antiemetics; low-salt diet ± diuretics (Ménière disease), Epley maneuver (BPPV). Central vertigo: Brain stem or cerebellar lesion (eg, stroke affecting vestibular nuclei or posterior fossa tumor). - Findings: directional or purely vertical nystagmus, skew deviation, diplopia, dysmetria. Positional testing → immediate nystagmus in any direction; may change directions. Focal neurologic findings.
Refractive errors
Hyperopia: Also known as "farsightedness." Eye too short for refractive power of cornea and lens → light focused behind retina. Correct with convex (converging) lenses. Myopia: Also known as "nearsightedness." Eye too long for refractie power of cornea and lens → light focused in front of retina. Correct with concave (diverging) lens. Astigmatism: Abnormal curvature of cornea → different refractive power at different axes. Correct with cylindrical lens. Presbyopia: Aging-related impaired accommodation (focusing on near objects), primarily due to ↓ lens elasticity, changes in lens curvature, ↓ strength of the ciliary muscle. Patients often need "reading glasses" (magnifiers").
Papilledema
Optic disc swelling (usually bilateral) due to ↑ ICP (eg, 2° to mass effect). Etiology:- Hypertensive emergency- Idiopathic intracranial hypertension (eg, pseudotumor cerebri)- Intracranial tumores (eg, medulloblastoma)- Hydrocephalus - Enlarged blind spot and elevated optic disc with blurred margins. Fundoscopy: edematous, poorly defined, prominent disc; radial hemorrhage around the disc margin Increased intracranial pressure is transmitted through the CSF in the subarachnoid space, which is continuous with the optic nerve sheath. This buildup of pressure compresses the optic nerves externally, which in turn impairs axoplasmic flow within the optic nervs, causing bilateral optic disc edema (papilledema).
Pupillary control
Miosis: Constriction, parasympathetic- 1st neuron: Edinger-Westphal nucleus to ciliary ganglion via CN III- 2nd neuron: short ciliary nerves to sphincter pupillae muscles (M3) Pupillary light reflex:- Light in either retina sends signal via CN II to pretectal nuclei in midbrain that activates bilateral Edinger-Westphal nuclei; pupils constrict bilaterally (direct and consensual reflex).- Result: illumination of 1 eye results in bilateral pupillary constriction. Mydriasis: Dilation, sympathetic- 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 (α1). Sympathetic fibers also innervate smooth muscle of eyelids (minor retractors) and sweat glands of forehead and face.
Marcus Gunn pupil
= Relative afferent pupillary defect When the light shines into a normal eye, constriction of the ipsilateral (direct reflex) and contralateral eye (consensual reflex) is observed. When the light is then swung to the affected eye, both pupils dilate instead of ocnstrict due to impaired conduction of light signal along the injured optic nerve. Tested with "swinging flashlight test."
Cavernous sinus
Collection of venous sinuses on either side of pituitary. Blood from eye and superficial cortex → cavernous sinus → internal jugular vein. CNs III, IV, V1, VI, and occasionally V2 plus postganglionic sympathetic pupillary fibres en route to orbit all pass through cavernous sinus. Cavernous portion of internal carotid artery is also here. Cavernous sinus syndrome – presents with variable ophthalmoplegia, ↓ corneal sensation, Horner syndrome and occasional decreased maxillary sensation. 2° to pituitary tumor mass effect, carotid-cavernous fistula, or cavernous sinus thrombosis related to infection. CN VI is most susceptible to injury.
Aqueous humor pathway
Produced by nonpigmented epithelium on ciliary body (↓ by β-blockers, α2-agonists, and carbonic anhydrase inhibitors). Trabecular outflow (90%): Drainage through trabecular meshwork → canal of Schlemm → episcleral vasculature (↑ with M3 agonist). Uveoscleral outflow (10%): Drainage into uvea and sclera (↑ with prostaglandin agonists).
Hypertensive retinopathy
Retinal damage due to chronic uncontrolled HTN. - Flame-shaped retinal hemorrhages- Arteriovenous nicking (the arteriole's thick arteriosclerotic wall compresses the vein where it crosses, so that the vein forms an hourglass shape around the arteriole)- Microaneurysms- Macular star (exudate)- Cotton-wool spots - Presence of papilledema requires immediate lowering of BP. - Associated with ↑ risk of stroke, CAD, kidney disease.
Ocular motility
CN VI innervates the lateral rectus:CN IV innervated the superior oblique.CN III innervates the rest. The strongest action of the superior oblique is depression when the eye is adducted. The further the eye is abducted, the more the superior oblique acts to intort the eye toward the nose.
Argyll Robertson pupil
- No direct or consensual light reflex - Accomodation-convergence intact - Seen in neurosyphilis, diabetes
Visual field defects
1. Right anopia (optic nerve)2. Bitemporal hemianopia (pituitary lesion, optic chiasm)3. Left homonymous hemianopia (optic tract)4. Left upper quadrantanopia (Meyer loop, right temporal lesion, MCA)5. Left lower quadrantanopia (Dorsal optic radiation, right parietal lesion, MCA)6. Left hemianopia with macular sparing (Calcarine fissue, if PCA infarct)7. Central scotoma (eg, macular degeneration) Meyer loop – lower retina → upper quadrantanopia; loops around inferior horn of lateral ventricle.Dorsal optic radiation – superior retina → lower quadrantanopia; takes shortest path via internal capsule.
Ménière disease
Cause: Increased pressure & volume of endolymph due to impaired resorption of endolymphatic fluid. Features:Traid: Vertigo, hearing loss, tinnitus- Ear fullness/pain- Episodes last minutes to hours- Sensorineural, low-frequency hearing loss- Horizontal nystagmus Treatment: Low-sodium diet, avoid caffeine/alcohol/stress, betahistine
Benign paroxysmal positional vertigo
Disease of the inner ear caused by small particles (otoliths) dislodging and migrating within the endolymphatic fluid into one of the semicircular canals. Features:- Brief episodes brought on by head movement- Lasts several seconds, but <1 minute- Common triggers: rolling in bed, lying down quickly,- No auditory symptoms Diagnostics:- Dix-Hallpike test Therapy: Epley repositioning maneuver
Vestibular neuritis (labyrinthitis)
Acute unilateral vestibulopathy due to inflammation of vestibular nerve (viral or postviral). Features:- Single episode that can last days- Severe vertigo with falling towards the affected side- No hearing loss Diagnostics:- Head thrush test ⊕ (patient unable to maintain visual fixation)- MRI Treatment: Bed rest, corticosteroids, antiemetic treatment
