Podcast
Questions and Answers
Which cranial nerves are primarily responsible for eye movement?
Which cranial nerves are primarily responsible for eye movement?
What effect would damage to the trochlear nerve have on eye function?
What effect would damage to the trochlear nerve have on eye function?
What visual field defect can occur as a result of glaucoma?
What visual field defect can occur as a result of glaucoma?
What percentage of optic fibers cross at the optic chiasm?
What percentage of optic fibers cross at the optic chiasm?
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Which structure do optic tract fibers synapse with?
Which structure do optic tract fibers synapse with?
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What structure connects the optic nerve to visual processing areas in the brain?
What structure connects the optic nerve to visual processing areas in the brain?
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Which of the following conditions is directly associated with strabismus?
Which of the following conditions is directly associated with strabismus?
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What is the visual defect called when there is a loss of vision in the outer fields of both eyes?
What is the visual defect called when there is a loss of vision in the outer fields of both eyes?
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Which visual field defect is characterized by a loss of vision in one half of the visual field on the same side for both eyes?
Which visual field defect is characterized by a loss of vision in one half of the visual field on the same side for both eyes?
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In the context of visual fields, what condition results when there is vision loss in an area surrounded by normal vision?
In the context of visual fields, what condition results when there is vision loss in an area surrounded by normal vision?
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What is the first step in the regeneration of rhodopsin after activation?
What is the first step in the regeneration of rhodopsin after activation?
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Why are rods less effective in bright light conditions after exposure to darkness?
Why are rods less effective in bright light conditions after exposure to darkness?
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What happens to the pupil when you move from a bright light environment to a darker one?
What happens to the pupil when you move from a bright light environment to a darker one?
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What separates from opsin during the process of rhodopsin activation?
What separates from opsin during the process of rhodopsin activation?
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How does the regeneration process for cones compare to that of rods?
How does the regeneration process for cones compare to that of rods?
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What happens to opsin during the regeneration of rhodopsin?
What happens to opsin during the regeneration of rhodopsin?
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What limits the rods' ability to adapt to rapid changes in light conditions?
What limits the rods' ability to adapt to rapid changes in light conditions?
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What is the term used for the process when trans-retinal is converted back to cis-retinal?
What is the term used for the process when trans-retinal is converted back to cis-retinal?
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What happens to the eyes when the accommodation reflex is activated?
What happens to the eyes when the accommodation reflex is activated?
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Which facial nerve is involved in the accommodation reflex?
Which facial nerve is involved in the accommodation reflex?
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If the visceral component of CN III is damaged, which symptoms might you expect?
If the visceral component of CN III is damaged, which symptoms might you expect?
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What is the role of the Edinger-Westphal nucleus in the accommodation reflex?
What is the role of the Edinger-Westphal nucleus in the accommodation reflex?
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Which type of eye movement occurs when the eyes accommodate for a closer object?
Which type of eye movement occurs when the eyes accommodate for a closer object?
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How does light in one eye affect pupil constriction in both eyes?
How does light in one eye affect pupil constriction in both eyes?
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Which muscle is activated to increase the convexity of the lens during the accommodation reflex?
Which muscle is activated to increase the convexity of the lens during the accommodation reflex?
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Which other cranial nerve pairs with CN III in the pupillary reflex?
Which other cranial nerve pairs with CN III in the pupillary reflex?
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Which cranial nerve is responsible for the action of abduction of the eye?
Which cranial nerve is responsible for the action of abduction of the eye?
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What is the function of the Medial Longitudinal Fasciculus (MLF)?
What is the function of the Medial Longitudinal Fasciculus (MLF)?
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Which part of the brain contains the nucleus of the Abducens nerve?
Which part of the brain contains the nucleus of the Abducens nerve?
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Which reflex allows the eyes to maintain fixation on an object while the head moves?
Which reflex allows the eyes to maintain fixation on an object while the head moves?
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The lateral rectus muscle is primarily innervated by which cranial nerve?
The lateral rectus muscle is primarily innervated by which cranial nerve?
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What typically begins the vision loss in macular degeneration?
What typically begins the vision loss in macular degeneration?
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What is the primary focus for prevention of atrophic ARMD?
What is the primary focus for prevention of atrophic ARMD?
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Which type of ARMD is characterized by disordered blood vessels beneath the retina?
Which type of ARMD is characterized by disordered blood vessels beneath the retina?
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What are drusen associated with in atrophic ARMD?
What are drusen associated with in atrophic ARMD?
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Which of these is NOT associated with the etiology of macular degeneration?
Which of these is NOT associated with the etiology of macular degeneration?
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What clinical feature typically appears first in patients with dry ARMD?
What clinical feature typically appears first in patients with dry ARMD?
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Which treatment is more effective for exudative ARMD compared to atrophic ARMD?
Which treatment is more effective for exudative ARMD compared to atrophic ARMD?
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At what age is the incidence of macular degeneration more commonly observed?
At what age is the incidence of macular degeneration more commonly observed?
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In atrophic ARMD, what primarily happens as the retinal pigment epithelium (RPE) atrophies?
In atrophic ARMD, what primarily happens as the retinal pigment epithelium (RPE) atrophies?
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What role does lutein play in relation to macular health?
What role does lutein play in relation to macular health?
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Study Notes
Eye Pathology P1
- Conjunctival and corneal pathologies are covered
- Disorders of the eye appendages are also covered
Outcomes
- Pathophysiological processes underlying eye illnesses are described
- Processes are related to clinical features
- Cataracts, keratitis, blepharitis, conjunctivitis, hypopyon, and chalazion are specific illnesses
Eyelid/Conjunctival anatomy and histology
- Eyelids, conjunctiva, and associated structures are ocular adnexa
- Includes lacrimal apparatus
- Conjunctiva is a mucous membrane covering the inside of eyelids (palpebrae) and anterior sclera
- Palpebrae structure includes skin on outer surface and conjunctiva on inner surface.
- Supported by tarsus (with connective tissue)
- Cilia (eyelashes) associated with sebaceous and sudoriferous glands
- Orbicularis oculi (CN VII) and levator palpebrae muscles (SNS) are beneath the skin.
- Modified sebaceous glands in tarsus known as Meibomian glands contribute to tear film
- Glands of Zeis are small, modified sebaceous glands opening into hair follicles of the eyelid's lashes.
- Glands of Moll are modified sweat glands opening near the base of the lashes
- Zoomed-out view shows the complex sebum-filled tarsal glands emptying into duct at eyelid's edge.
- Conjunctiva is stratified columnar epithelium with goblet cells
- Secretes mucous that contributes to the tear film
- Also includes accessory lacrimal glands that secrete tears, in addition to lymphoid follicles (like lymph nodes).
Orbital septum
- A fascial plane behind the orbicularis oculi
- Separates the eyelid from the orbit
- An important barrier to infection
- Orbital cellulitis is a very dangerous type of cellulitis
- Can result in vision loss, and intracranial infection, and thrombosis of intracranial venous sinuses
Lacrimal glands
- Innervated mostly by CN VII (great petrosal nerve) and sympathetic branches accompanying lacrimal artery
- Puncta connect to the lacrimal sac, and then drains into the inferior meatus
- Accessory lacrimal glands are located in the conjunctiva
Conjunctivitis - overview
- Infectious types include bacterial (Staph aureus, Strep pneumoniae, H. influenzae, M. catarrhalis), Chlamydial, gonococcal
- Infections also includes Viral (adenovirus), Parasitic, fungal (uncommon).
- Immune-mediated types include Allergic, atopic, vernal
- Irritants such as dust, smoke, toxins, or chemicals
- Bacterial conjunctivitis is common, often self-limiting, while Chlamydial and gonococcal infections can cause scarring.
- Bacterial conjunctivitis tends to have more purulent discharge and last for less time than a viral conjunctivitis.
- Viral conjunctivitis (common with adenovirus) is extremely infectious and self-limiting; other viruses (herpes virus and varicella virus) can cause it as well.
- Antivirals improve outcomes of herpes and varicella conjunctivitis.
- Symptoms include redness, swelling, and excessive tearing (epiphora)
Inflammation of the conjunctiva
- Bacterial conjunctivitis is common
- Chlamydia and gonorrhea cause significant conjunctival scarring and blindness
- Scarring eradicates goblet cells in the conjunctival fornix causing corneal irritation and scarring
- Bacterial conjunctivitis lasts shorter than viral
Inflammation of the conjunctiva - Viral conjunctivitis
- Extremely common
- Usually caused by adenovirus
- May also be caused by herpes virus and varicella virus
Clinical Features – Infectious Conjunctivitis
- Red eye (conjunctival injection)
- Itchiness sometimes like a foreign body
- Tearing, discharge, and crusting of the lashes (more crusting with bacterial)
- Pre-auricular and/or submandibular lymph nodes, more likely for bacterial infection
- Allergic and atopic conjunctivitis is addressed more when discussing rhinitis and asthma
- Chemosis (conjunctival swelling) is often more pronounced here
Selected types of conjunctivitis
- Gonorrheal and chlamydial conjunctivitis should be treated urgently to avoid damage
- Can lead to corneal ulceration and scarring
- Trachoma, a type of chlamydial infection, is a leading cause of blindness globally
Conjunctivitis findings
- "Bumpies" (follicles) are seen in viral and chlamydial conjunctivitis.
- Papillae are seen in allergic and bacterial conjunctivitis
- Trachoma results in an opaque cornea (basically destroyed)
Blepharitis
- Inflammation of the eyelids
- Causes can be multiple:
- Purulent infection (sty)
- Seborrheic dermatitis, rosacea
- Allergies, drug toxicity, autoimmune disease (Sjogren syndrome)
- Generalized infections (herpes, varicella)
General Clinical Features
- Redness, itching, and irritation of eyelids
- Dry or gritty feeling in the eyes
- Often confused with conjunctivitis, particularly in the elderly
- Untreated blepharitis can lead to conjunctivitis
Infections of the eyelid
- Hordeolum (stye) - purulent bacterial infection of sebaceous or sudoriferous glands; usually caused by Staph aureus
- Small, inflamed, very tender bump on eyelid margin
- Chalazion - granulomatous inflammation is not infectious; involves buildup of lipid products from breakdown of bacteria (or blocked secretions) and penetrates tarsal tissue. Mildly tender bump on eyelid (usually upper eyelid); often treated with heat and massage
- Treated with heat and massage, though antibiotics may be necessary
Keratitis
- Usually caused by HSV-1 (cold sores) or HSV-2 (genital herpes)
- Initial infection is usually not severe; reactivation can cause more severe corneal inflammation.
- Reactivation can occur due to stress, sunlight exposure, or hormonal fluctuations
- Typical symptoms include pain, tearing, and foreign body sensation
HSV Keratitis
- Pathogenesis: causes many intraepithelial ulcerations due to edema below the epithelium
- If chronic, the stroma gets thinned and scarred; edema in stroma and abnormalities in corneal endothelium
- Clinical Symptoms: pain, tearing, foreign-body sensation, red eye; vision loss is possible unless scarring occurs
- Herpes zoster ophthalmicus (HSV-3) causes dermatitis in the dermatomal distribution of CN V1, typically unilateral. Hutchinson’s sign is present if tip of nose involved; involved in ~75% of cases with nasal involvement
The Eye - Part 1b
- Physiology and Neurophysiology
Retina
- Structure and function (last day)
- Retinal cells: Rods and cones (structure and function continued)
- Signal transduction
- Adaptation
- Visual processing
Retina - Bipolar Cells
- Role in processing visual information through receptive field organization
- Mechanism of contributing to lateral inhibition which sharpens signals about contrasts in light and dark areas, enabling fine discrimination
Rod and Cone Bipolar Cells
- Rod bipolar cells are associated with scotopic vision (low light) and are "on-center" cells
- Activated when light falls on the center of their receptive field.
- Cone bipolar cells are associated with photopic vision (bright light), also "on-center"
- Activated when light hits their center, and center is brighter than the surrounding receptive field
Receptive Field Organization
- Receptive field of bipolar cells has a center-surround organization
- On-center fields stimulated if center is brighter than surround, off-center is reverse
- Antagonistic relationship enhances contrast and edge detection, improving visual acuity
- On-center stimulated inhibits the off-center, and vice versa
Adaptation
- In the dark, rhodopsin needs regeneration before cells respond again
- Trans retinal separates from opsin to be regenerated
- Slow process; similar but faster for cones, as cones are effective at adapting to rapid changes
- Slow regeneration limits rods' ability to function well in bright conditions after exposure to darkness
Visual Processing
- Bipolar cells start processing visual signals at retina
- Other retinal cells involved in visual processing include horizontal cells, and amacrine cells.
- Horizontal cells sharpen contrasts; amacrine cells detect changes in vision (movement, on/off lights)
Visual Processing
- Ultimately, visual signals from rods and cones are transmitted to the brain by ganglion cell axons
- How would increasing light intensity affect the receptor potential?
- What about the action potential?
- How does the brain register increased light intensity?
Outline - Neurophysiology
- Optic nerve
- Brain: Visual processing
- Cranial nerves (general review)
- Oculomotor nerve
- Trochlear nerve
- Abducens nerve
Objectives
- Describe structure/pathways of optic nerve and brain, accommodation/pupillary reflexes
- Given basic pathophysiology, predict resulting visual defects
- Predict anatomical region affected by a visual field defect
- Describe fundamental concepts of visual perception
Objectives
- How damage to somatic motor component of oculomotor nerve would contribute to strabismus
- Role of oculomotor, trochlear nerves with respect to intorsion/extorsion of eye
- Describe interactions of nerves to mediate vestibulo-ocular reflex
- Damage to abducens nerve would contribute to strabismus, decreased depth perception, diplopia
Optic Nerve
- Formed by axons
- Exits back of eyeball and creates the optic nerve
- 50% of fibers cross at the optic chiasm (anatomically located) and join contralateral fibers
- Formed optic tract after chiasm
- Synapses in thalamus (lateral geniculate body)
- Leaves thalamus as optic radiations
- Synapses in visual cortex (occipital lobe)
Predicting visual defects
- Diagram shows trace of nerve fibers from lesion to visual fields
- Areas eye cannot see are colored black in a visual field diagram
Visual Field Diagrams
- Fibers from part of eye that are spared in hemianopsia
- Name the condition (e.g., bitemporal hemianopsia)
- Visual field diagrams of central scotoma from macular degeneration and end stage glaucoma
Outline - Neurophysiology
- Optic nerve
- Brain: visual processing
- Cranial nerves (general review)
- Oculomotor nerve
- Trochlear nerve
- Abducens nerve
Role of the brain in vision
- Scenario: Burning finger on hot stove (ouch!)
- Primary visual cortex registers shape and color
- Secondary visual cortex recognizes color and shape
- Primary somatosensory cortex registers finger is hot
- Secondary somatosensory cortex recognizes how hot finger is
- Parietal-occipito-temporal association cortex combines visual and tactile info
Pathologies of vision: brain
- Visual cortex may ignore images from bad eye if visual defect.
- How to treat it?
- Lesions in primary visual cortex results in cortical blindness; review visual field defects
Pathologies of vision: brain
- Lesions in secondary visual cortex lead to: movement agnosia; inability to identify common objects; inability to copy drawings; color agnosia; seeing in grey-scale.
Outline - Neurophysiology
- Optic nerve
- Brain: visual processing
- Cranial nerves (general review)
- Oculomotor nerve
- Trochlear nerve
- Abducens nerve
Review Table
- Muscle, nerve, and action are tabulated for eye muscles and nerves
Memory help: Review at home
- Divide cranial nerves into 3 equal groups (based on number)
- Label from midbrain to medulla
- Exceptions; optic and olfactory nerve, are not found in brainstem
- Trigeminal nerve runs through all 3 brainstem portions
Oculomotor (III)
- Nuclei are found in midbrain
- Motor innervation to all eye muscles (except lateral rectus)
- Action: down and abduct, and innervation to levator palpebrae superioris
- Edinger-Westphal nucleus (EDW) is parasympathetic innervation to pupillary sphincter (miosis)
- Action and location of ciliary muscle
Oculomotor (III): Somatic
- Weakness in eye muscle is opthalmoplegia
- Symptoms from somatic damage to CN III
- Rationale for symptoms
Oculomotor (III): Visceral
- If CN III’s visceral component damaged... what additional signs or symptoms?
- Rationale/hint; think “accommodation”
Oculomotor (III) - Reflexes
- Accommodation reflex (CN II and III)
- Convergence of eyes, activation of CN III
- Increased convexity of lens, activation of CN III
- Constriction of pupil, activation of CN III (All use the EDW nucleus)
Oculomotor (III) - Reflexes
- Pupillary reflex from CN I & CN III
- Light in one eye causes constriction in both pupils
Oculomotor (III) - Reflexes
- Accommodation and pupillary reflexes utilize EDW nucleus
- Damage to pretectal area affects pupil constriction to light and accomodation
Trochlear (IV)
- Nucleus found in midbrain
- Muscle innervated; contralateral superior oblique
- Action: eye down and abducted; additional action: intorsion(rotation of eye towards the nose)
Trochlear (IV)
- If trochlear nucleus (right side) is damaged
- Affected eye is (R/L)
- Muscle will be compromised
- Affected eye will rotate towards ear or nose
Outline - Neurophysiology
- Optic nerve
- Brain: Visual processing
- Cranial nerves (general review)
- Oculomotor nerve
- Trochlear nerve
- Abducens nerve
Abducens (VI)
- Nucleus found in pons
- Muscle: lateral rectus
- Action: Abduction
- Mediate lateral gaze
- Coordinated to reticular formation (PPRF)
- Involves 3 extra-ocular nucleus (CNIII, IV, VI) connected by a tract (MLF)
Abducens (VI)
- Vestibulo-ocular reflex, along with CN III and IV
- Allowing eyes to remain fixed on an object even when head moves
- Movement picked up by vestibular apparatus, sent to PPRF
- Extra-ocular muscles run through the MLF
Abducens (VI)
- Damage to left abducens nucleus.
- Right eye is fine; CN III innervates medial rectus and allows adduction. Left eye deviates medially/ will not abduct
- Clinical considerations: decreased depth and diplopia
Eye part 3 – Eye Pathologies
- BMS 200
Cataracts
- Opacity of lens, common, reversible cause of blindness
- Cortical is radial or spoke-like opacity in anterior or posterior cortex
- Nuclear sclerosis is yellow-brown discolouration of central lens
- Posterior subcapsular is next to posterior capsule
Cataracts
- Caused by changes within the lens, often by aging,
- Systemic diseases and medications (e.g., diabetes, Wilson's disease, hypocalcemia, steroid use),
- Diseases affecting eye locally (trauma, radiation, uveitis) cause cataracts.
- Gradual painless, progressive decrease in visual acuity (VA)
- Glaucoma, monocular diplopia, halos, increased myopia if nuclear sclerosis
Cataracts – Clinical features
- Gradual, painless, progressive decrease in VA
- Glare, dimness, halos around lights, monocular diplopia (double vision)
- Second sight phenomenon: patient more myopic than previously noted
- Visible opacities on ophthalmoscopic examination
- Surgery or laser therapy is most often used
Major forms of cataracts
(Images)
- Shows examples of different types of cataracts
Uveitis
- Inflammation of the choroid layer
- Iris (iriditis)
- Iris + ciliary body (iridocyclitis)
- Posterior compartment (posterior uveitis)
- Endophthalmitis (bacterial infection of entire eye, rare)
- Common types: anterior uveitis, intermediate uveitis, posterior uveitis, panuveitis
- Complications include macular edema, destruction, glaucoma, corneal damage, or cataracts
Uveitis
- Etiology: Most anterior uveitis (about 90%) is idiopathic, seronegative spondyloarthropathies IBD, sarcoidosis, JIA, lupus, Behcet's, AIDS, herpes, often immune-mediated
- Etiology: Posterior uveitis - infections (toxoplasmosis, CMV) or autoimmune/sarcoidosis frequent causes
Uveitis - history
- Anterior uveitis: Acute (pain, redness, photophobia, tearing, decreased vision) or Chronic (blurred vision, mild redness, little pain, photophobia)
- Posterior uveitis (blurred vision, floaters)
Uveitis - Physical
- Conjunctival injection, limbus inflammation
- Reduced visual acuity; funny-looking iris and pupil with anterior uveitis
- Blood/pus, flare, increased IOP
Hypopyon and hyphema
(Images)
Production of aqueous humor – review
(diagram)
Production of aqueous humor – review
- Drainage of aqueous humor impaired - leads to high intraocular pressure
- Aqueous humor secreted by ciliary processes into posterior chamber
- Moves through pupil to anterior chamber; resorption via scleral venous sinus
Glaucoma
- Progressive, pressure-sensitive optic neuropathy
- Elevated intraocular pressure, although some patients with normal IOP develop characteristic optic nerve and visual field changes
- Normal IOP is 10-21 mm Hg
- Leading cause of blindness, only half know they have it.
Glaucoma
- May be classified into two categories
- Open-Angle = aqueous humor has complete physical access to trabecular meshwork
- Closed-Angle = peripheral zone of the iris adheres to the trabecular meshwork and physically impedes drainage of aqueous humor
Primary Open-Angle Glaucoma
- Most common form, but may be difficult to diagnose clinically
- Possible causes include
- Obstructions of trabecular meshwork
- Loss of trabecular endothelial cells
- Loss of normal phagocytic activity
- Disturbances in neurologic feedback mechanisms
- High intraocular pressure (IOP) is major risk factor for progression
Primary Open-Angle Glaucoma – Clinical manifestations
- Asymptomatic, bilateral, insidious vision loss
- Usually affects temporal fields first
- Physical exam: increased IOP, flame-shaped hemorrhages, increased cup-disk ratio, optic nerve atrophy
Secondary Open-Angle Glaucoma
- Can occur due to: clogginf of trabecular meshwork, high molecular-weight lens proteins, red cells after trauma, or necrotic tumors
- Can develop quickly, and have a similar presentation to acute angle-closure glaucoma
Primary Angle-Closure Glaucoma
- 5% of all glaucoma
- Risk factors: race (Asian, Southeast Asian, Inuit), hyperopia, female sex, environmental factors (movie theaters)
- Transient apposition; obstruction of aqueous humor flow
- Marked elevation in intraocular pressure (usually exceeds 40 mmHg)
- Can damage the lens and retina
Primary Angle-Closure Glaucoma – Clinical features
- Usually very painful, photophobic, unilateral red eye
- Redness includes peripheral conjunctiva and encroaches on limbus
- Pupils are fixed in mid-dilation with decreased VA
- Haloes around lights; subcapsular opacities in lens
- Sustained high pressure causes corneal edema and degeneration
- Vision loss in hours/days is a red flag
Secondary Angle-Closure Glaucoma
- Typically associated with diabetes
- Neovascular membrane over trabecular meshwork pulling iris closer and blocking flow
- Uveitis can cause synechiae (iritis constricting membranes) that adhere iris to lens.
Glaucoma - Treatment
- Acute angle-closure glaucoma may require laser iridotomy or cataract surgery
- Medication used until surgery can be performed include topical alpha 2-adrenergic agonists, topical beta-blockers , miotic agents, prostaglandin analogues, or carbonic anhydrase inhibitors
- Primary open-angle glaucoma may be treated with the same drugs, or if there is continued optic nerve damage, consider laser trabeculoplasty.
Layers of the retina – review
(Diagram)
Retinal detachment
- Separation of neurosensory retina from retinal pigment epithelium
- Caused by full-thickness retinal defect (tear)
- Liquedified vitreous humor seep through tear; separates retina from RPE
- Most common type is rhegmatogenous
- Causes include age, cataract surgery, inflammation in posterior chamber
Retinal detachment
- Retinal detachment without retinal break
- Complicates retinal vascular disorders
- Caused by fluid leakage from the choroid circulation that separates the retina from RPE
- Causes: trauma, hypertension, tumors, many autoimmune diseases
- Can accompany diabetes, retinal ischemia, and eye trauma
Retinal Detachment – Clinical features
- Initial symptoms may include flashing light sensation (photopsia), retinal traction and floaters and sometimes vision loss
- Symptoms progress and patient may report a shadow, may spread to involve entire visual field over days and appears as cloudy, irregular, or curtain-like
- This is an urgent condition that needs ophthalmologist attention.
Retinal Vascular Disease - Diabetes Mellitus
- Hyperglycemia effects on lens and iris mentioned earlier
- Retinal vasculopathy of diabetes may be classified into: Background (preproliferative) and proliferative diabetic retinopathy
Background (preproliferative) diabetic retinopathy
- Pathology: retinal blood vessels’ basement membrane is thickened, microaneurysms are common (widening of blood vessels), macular edema, hemorrhagic exudates
- Pathophysiology: due to local microcirculatory changes in the retina (VEGF up-regulation, retinal angiogenesis)
Proliferative diabetic retinopathy
- Appearance of new blood vessels sprouting from existing blood vessels
- Angiogenic vessels grow on the retinal surface, and on optic disc, and can lead to: neovascularization of the disc
Diabetic retinopathy – clinical features
- Initial stages are usually asymptomatic
- Progressive loss of vision (floaters, blurring, distortion)
- Early signs may include microaneurysms, a few (early) or more (late) hemorrhages (dot and flame), general retinal edema
- Later stages include hard exudates and cotton wool spots, macular edema
- Even retinal detachment can occur over time
The cotton-wool spot
- Axoplasmic transport interrupted in nerve fiber layer
- Accumulation of mitochondria at swollen ends of axons
- Cytoid bodies populate nerve fiber layer infarcts.
- Seen ophthalmoscopically as cotton-wool spots
Macular Degeneration - Intro
- Source of central vision; damaged macula causes dramatic vision loss
- Early stages often involve spots beneath the retina (drusen or tiny, round lesions) which may not change vision much
ARMD - pathogenesis
- Etiology is unclear but associated with smoking, certain nutrients or dietary factors (sometimes treated with high dose antioxidants), atherosclerosis and hypertension.
- Can be familial
ARMD – dry (atrophic, non-exudative)
- ARMD is atrophic or exudative
- Atrophic ARMD; diffuse or discrete deposits of inflammation-related proteins (drusen) in Bruch’s membrane + geographic atrophy of the retinal pigment epithelium
- Photoreceptors and vision lost mostly in macula
- Atrophic ARMD develops slowly
ARMD - dry
-
Initial clinical features; difficulty with night vision, difficulty recognizing faces, and eventually severe vision loss; fairly common worldwide
-
Treatments are not very effective; prevention is key (avoid smoking, consume omega 3 oils, and carotenoids like lutein and beta carotene in vegetables (which can quench free radicals and filter blue light).
ARMD – Wet (exudative, neovascular)
- Exudative ARMD progresses quickly and is characterized by development of a neovascular membrane.
- This membrane is full of disordered blood vessels just below the retina
- May penetrate the retinal pigment epithelium
- Blood vessels may leak; organized by retinal pigment epithelial cells into macular scars
- Clinical features similar to non-exudative ARMD, but vision worsens rapidly but is more treatable
Drusen
- Not necessarily causative lesion in dry ARMD
- More drusen correlate with worsening vision
- Hard exudates have a well-defined edge
- Soft exudates are slightly blurred/fuzzier in their appearance
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Description
Test your knowledge on cranial nerves related to eye movement and their functions. This quiz covers the effects of nerve damage, visual field defects, and related conditions affecting sight. Ideal for students studying anatomy and physiology.
