- •Preface
- •Acknowledgments
- •Anatomic Features
- •Anatomic Directions and Planes
- •Refractive Conditions
- •Epithelial Tissue
- •Glandular Epithelium
- •Connective Tissue
- •Muscle Tissue
- •Nerve Tissue
- •Intercellular Junctions
- •References
- •Cornea
- •Corneal Dimensions
- •Corneal Histologic Features
- •Epithelium
- •Epithelial Replacement
- •Bowman’s Layer
- •Stroma or Substantia Propria
- •Descemet’s Membrane
- •Endothelium
- •Corneal Function
- •Corneal Hydration
- •Aquaporins
- •Corneal Metabolism
- •Corneal Repair: Wound Healing
- •Epithelium
- •Bowman’s
- •Stroma
- •Descemet’s
- •Endothelium
- •Absorption of Ultraviolet Radiation (UVR)
- •Corneal Innervation
- •Corneal Blood Supply
- •Sclera
- •Scleral Histologic Features
- •Episclera
- •Sclera
- •Physiology of Scleral Changes in Myopia
- •Scleral Spur
- •Scleral Opacity
- •Scleral Color
- •Scleral Foramina And Canals
- •Scleral Blood Supply
- •Scleral Innervation
- •Limbal Histologic Features
- •Palisades of Vogt
- •References
- •IRIS
- •Histologic Features of Iris
- •Anterior Border Layer
- •Iris Stroma and Sphincter Muscle
- •Anterior Epithelium and Dilator Muscle
- •Posterior Epithelium
- •Anterior Iris Surface
- •Posterior Iris Surface
- •Iris Color
- •CILIARY BODY
- •Supraciliaris (Supraciliary Lamina)
- •Ciliary Muscle
- •Ciliary Stroma
- •Ciliary Epithelium
- •Choroid
- •Suprachoroid Lamina (Lamina Fusca)
- •Choroidal Stroma
- •Choriocapillaris
- •Functions of Iris
- •Functions of Ciliary Body
- •Aqueous Production
- •Function and Rate of Production
- •Vitreous Production
- •Blood-Aqueous Barrier
- •Functions of Choroid
- •Iris
- •Ciliary Body
- •Choroid
- •References
- •Retinal Pigment Epithelium
- •Photoreceptor Cells
- •Composition of Rods and Cones
- •Outer Segment
- •Cilium
- •Inner Segment
- •Outer Fiber, Cell Body, and Inner Fiber
- •Rod and Cone Morphology
- •Rods
- •Cones
- •Bipolar Cells
- •Ganglion Cells
- •Horizontal Cells
- •Amacrine Cells
- •Interplexiform Neurons
- •Neuroglial Cells
- •Müller Cells
- •Microglial Cells and Astrocytes
- •Retinal Pigment Epithelium
- •Photoreceptor Layer
- •External Limiting Membrane
- •Outer Nuclear Layer
- •Outer Plexiform Layer
- •Inner Nuclear Layer
- •Inner Plexiform Layer
- •Ganglion Cell Layer
- •Nerve Fiber Layer
- •Internal Limiting Membrane
- •Physiology of the rpe
- •Scotopic and Photopic Vision
- •Neural Signals
- •Number and Distribution of Neural Cells
- •Physiology of the neural retina
- •Retinal Synapses
- •Neurotransmitters
- •Phototransduction
- •Information Processing
- •Receptive Fields
- •Light and Dark Adaptation
- •Circadian Rhythm
- •Retinal Metabolism
- •Central Retina
- •Macula Lutea
- •Fovea (Fovea Centralis)
- •Foveola
- •Parafoveal and Perifoveal Areas
- •Peripheral Retina
- •Optic Disc
- •Blood-Retinal Barrier
- •References
- •Lens Capsule
- •Lens Epithelium
- •Lens Fibers
- •Epithelium-Fiber Interface
- •Lens Capsule
- •LENS Fibers
- •Fiber Components
- •Formation of Lens Fibers
- •Fiber Junctions
- •Lens Metabolism
- •Ionic Current
- •Regulation of Fluid Volume
- •Oxidative Stress
- •Cataracts
- •The Physiology of Cataract Formation
- •Age-Related Cortical Cataract
- •Age-Related Nuclear Cataract
- •Posterior Subcapsular Cataract (PSC)
- •Steroid-Induced Cataract
- •References
- •Scleral Spur
- •Trabecular Meshwork
- •Canal of Schlemm
- •Juxtacanalicular Connective Tissue
- •Function of the Filtration Apparatus
- •Posterior Chamber
- •FACTORS AFFECTING Intraocular Pressure
- •Drugs that Effect IOP
- •Vitreous Chamber
- •Vitreal Attachments
- •Vitreous Zones
- •Vitreous Cortex
- •Intermediate Zone
- •Cloquet’s Canal
- •Composition of Vitreous
- •Collagen
- •Hyaluronic Acid (hyaluronan)
- •Hyalocytes
- •Vitreal Function
- •Age-Related Vitreal Changes
- •References
- •Optic Pits
- •Optic Cup, Lens, and hyaloid vessels
- •Optic Cup
- •Lens
- •Hyaloid Arterial System
- •Retinal Pigment Epithelium
- •Neural Retina
- •Retinal Vessels
- •Cornea
- •Sclera
- •UVEA
- •Choroid
- •Ciliary Body
- •Iris
- •Pupillary Membrane
- •Anterior Chamber
- •Vitreous
- •Optic Nerve
- •Eyelids
- •Orbit
- •Extraocular Muscles
- •Nasolacrimal System
- •References
- •Orbital Walls
- •Roof
- •Floor
- •Medial Wall
- •Lateral Wall
- •Orbital Margins
- •Orbital Foramina and Fissures
- •Paranasal Sinuses
- •ORBITAL CONNECTIVE TISSUE
- •Periorbita
- •Orbital Septum
- •Tenon’s Capsule
- •Suspensory Ligament (of Lockwood)
- •Orbital Muscle of Müller
- •Orbital Septal System
- •Orbital Fat
- •Aging Changes in the Orbit
- •References
- •Palpebral Fissure
- •Eyelid Topography
- •Eyelid Margin
- •Eyelid Structures
- •Orbicularis Oculi Muscle
- •Palpebral Portion
- •Orbital Portion
- •Orbicularis Action
- •Superior Palpebral Levator Muscle
- •Levator Aponeurosis
- •Levator Action
- •Retractor of Lower Eyelid
- •Tarsal Muscle (of Müller)
- •Tarsal Plate
- •Palpebral Ligaments
- •Glands of the Lids
- •Histologic Features
- •Skin
- •Muscles
- •Tarsal Plates
- •Palpebral Conjunctiva
- •Glands
- •Innervation of Eyelids
- •Blood Supply of Eyelids
- •Conjunctiva
- •Plica Semilunaris
- •Caruncle
- •Conjunctival Blood Vessels
- •Conjunctival Lymphatics
- •Conjunctival Innervation
- •Lacrimal Secretory System
- •Tear Film Distribution
- •Nasolacrimal Drainage System
- •Puncta and Canaliculi
- •Lacrimal Sac and Nasolacrimal Duct
- •Tear Drainage
- •References
- •Sliding Ratchet Model of Muscle Contraction
- •Structure of the Extraocular Muscles
- •Fick’s Axes
- •Ductions
- •Vergences and Versions
- •Positions of Gaze
- •Origin of the Rectus Muscles
- •Insertions of the Rectus Muscles: Spiral of Tillaux
- •Medial Rectus Muscle
- •Lateral Rectus Muscle
- •Superior Rectus Muscle
- •Inferior Rectus Muscle
- •Superior Oblique Muscle
- •Inferior Oblique Muscle
- •FIBERS OF THE Extraocular muscleS
- •ORBITAL CONNECTIVE TISSUE STRUCTURES
- •Horizontal Rectus Muscles
- •Vertical Rectus Muscles
- •Oblique Muscles
- •Movements From Secondary Positions
- •Vertical Rectus Muscles
- •Oblique Muscles
- •Yoke Muscles
- •Innervation
- •Blood Supply
- •References
- •Ophthalmic Artery
- •Central Retinal Artery
- •Lacrimal Artery
- •Posterior Ciliary Arteries
- •Ethmoid Arteries
- •Supraorbital Artery
- •Muscular Arteries
- •Anterior Ciliary Arteries
- •Medial Palpebral Arteries
- •Supratrochlear Artery
- •Dorsonasal Artery
- •Facial Artery
- •Superficial Temporal Artery
- •Maxillary Artery
- •Superior Ophthalmic Vein
- •Central Retinal Vein
- •Vortex Veins
- •Inferior Ophthalmic Vein
- •Anterior Ciliary Veins
- •Infraorbital Vein
- •Cavernous Sinus
- •References
- •Trigeminal Nerve
- •Ophthalmic Division of Trigeminal Nerve
- •Nasociliary Nerve
- •Frontal Nerve
- •Lacrimal Nerve
- •Ophthalmic Nerve Formation
- •Maxillary Division of Trigeminal Nerve
- •Infraorbital Nerve
- •Zygomatic Nerve
- •Maxillary Nerve Formation
- •Trigeminal Nerve Formation
- •Oculomotor Nerve: Cranial Nerve III
- •Oculomotor Nucleus
- •Oculomotor Nerve Pathway
- •Trochlear Nerve: Cranial Nerve IV
- •Trochlear Nucleus
- •Trochlear Nerve Pathway
- •Abducens Nucleus
- •Abducens Nerve Pathway
- •Superior Orbital Fissure
- •Control of Eye Movements
- •Facial Nerve: Cranial Nerve VII
- •Facial Nucleus
- •Facial Nerve Pathway
- •References
- •Optic Nerve
- •Optic Chiasm
- •Optic Tract
- •Lateral Geniculate Nucleus
- •Optic Radiations (Geniculocalcarine Tract)
- •Primary Visual Cortex (Striate Cortex)
- •Retina
- •Optic Disc
- •Optic Nerve
- •Optic Chiasm
- •Optic Tract
- •Lateral Geniculate Nucleus
- •Optic Radiations
- •Striate Cortex
- •Striate Cortex Maps
- •Macular Sparing
- •References
- •Sympathetic Pathway to Ocular Structures
- •Parasympathetic Pathway to Ocular Structures
- •Neurotransmitters
- •Ophthalmic Agonist Agents
- •Ophthalmic Antagonist Agents
- •Disruption in the Afferent Pathway
- •Disruption within the Central Nervous System
- •Disruption in the Efferent Pathway
- •Disruption in the Sympathetic Pathway
- •References
- •Index
104 Clinical Anatomy of the Visual System
A posterior subcapsular cataract is a disturbance located just beneath the posterior capsule (Figure 5-15). This type of cataract impacts vision early and significantly given its location along the visual axis and near the nodal point of the eye. A significant risk factor for posterior subcapsular cataracts is long-term, highdose steroid use.
Clinical Comment: Cataract Surgery
The decision for cataract removal is determined by the effect the cataract has on the patient’s everyday life. When a person is not able to perform the usual daily activities because of reduced vision caused by the opacity, the lens should be removed. Cataract extraction is a relatively safe surgical procedure usually done under local anesthesia. A small incision is made to allow entrance
of surgical instruments into the anterior chamber. The anterior lens capsule is opened and the lens epithelium and all fibers are removed, with the lens capsule remaining intact. An intraocular lens (IOL) can then be inserted into the lens capsule to replace the power of the missing lens. Multifocal IOLs that correct for presbyopia may be an option.
The Physiology of Cataract Formation
Numerous mechanisms are presumed causative for cataracts, including fluid and ion imbalance, oxidative damage, protein modification, and metabolic disruption.66 A disturbance in fluid regulation can be caused by ionic pump dysfunction and/or membrane permeability increase that allows water accumulation. If Na+/K+ ATPase pump activity decreases significantly, a rise in Na+ in the cytoplasm is accompanied by an influx of water, the lens fibers swell and transparency diminishes.69 An increased level of cytoplasmic Ca++ is also associated with a loss of transparency.69 Water accumulation between fibers can form vacuoles causing a disruption of fiber arrangement and increased light scatter. UVR and oxidative damage as a result of free radical accumulation affects cellular function, damages lens DNA, causes protein modification, and high-molecular-weight crystallin aggregations, any of which can increase light scatter.25 Alpha crystallins, as molecular chaperones, help to stabilize beta/gamma crystallin configuration but by age 40 have disappeared from the lens nucleus, although the normal lens usually remains fairly transparent for years past that age.92 But as the concentration of alpha crystallins is reduced, aggregates accumulate and with time form light-scattering opacities.
Glutathione and ascorbate maintain a reducing environment providing some protection from free radical damage and preventing protein modification. Reduced levels of glutathione allow oxidative damage to membranes and proteins.77 A decrease in glutathione
FIGURE 5-12
Grading system for age-related cataracts. Nuclear sclerotic changes are shown in cross section, with anterior surface to the left. Cortical and posterior subcapsular changes are seen in retroillumination. (From Fingeret M, Casser L, Woodcome HT: Atlas of primary eyecare procedures, Norwalk, Conn, 1992, Appleton & Lange.)
concentration is associated with cataract development.92,93 A barrier, speculated to develop in middle age and located at the interface of the cortex and nucleus, seems to impede the flow of small molecules from the cortex into the nucleus and might account for the reduction in glutathione in the nucleus.91 A modification of the connexins in gap junctions causes a disruption in communication between fibers and might be one cause of this barrier.94,95 Changes occur in aquaporin channel proteins in the innermost nuclear regions of the lens as early as age 5 and by middle age (age 40 to 50), half of such channels are lost in the region of the speculated barrier.82 These changes can lead to the occlusion of the water channels and contribute to the barrier function.
A diabetic cataract results from elevated glucose levels and can develop rapidly. With increased blood glucose, excess glucose present in the aqueous enters
CHAPTER 5 t Crystalline Lens 105
A B
FIGURE 5-13
Nuclear cataract seen with A, diffuse illumination, and B, optic section. (From Kanski JJ, Nischal
KK: Ophthalmology: clinical signs and differential diagnosis, St Louis, 2000, Mosby.)
FIGURE 5-14
Spokes of a cortical cataract visible against the red reflex. (Courtesy Pacific University Family Vision Center, Forest Grove, Ore.)
the lens. As this excess glucose is metabolized, sorbitol accumulates faster than it is converted to fructose. Sorbitol concentration increases within the lens fiber, because sorbitol does not readily pass through the fiber membrane, and thus water is drawn into the fiber. The fibers swell, the lens loses transparency, and the fibers may eventually rupture.
Age-Related Cortical Cataract
High lifetime exposure to UVR is associated with increased incidence of cortical cataracts; the paradox is that the most severe damage in cortical cataracts occurs near the equator initially, the area most protected from sunlight by the iris. Cortical cataracts are associated with increased membrane permeability and ion transporters, pumps, and exchangers are not able to maintain the
FIGURE 5-15
Posterior subcapsular cataract. (From Kanski JJ, Nischal KK:
Ophthalmology: clinical signs and differential diagnosis, St Louis, 2000, Mosby.)
homeostatic concentration.71 An increased concentration of Ca++ in the fiber cytoplasm also drives fluid accumulation.69 Affected regions of the fiber show disruption of structure and can include membrane rupture. The changes first occur in the center of the elongated fiber (that is at the equatorial region), with the apical and basal ends remaining transparent. Generally the tapered fiber ends, located at the sutures in the optical axis, are only affected very late in the life of the cortical cataract.
Age-Related Nuclear Cataract
Age-related nuclear cataracts are associated with a decline of glutathione, making the fibers susceptible to oxidative damage. Levels can be significantly reduced in the nucleus while levels in the cortex remain within the normal range.78,94 Oxidative protein modification increases significantly after age 50, contributing to the damage
